Archief Roodbont

The incidence of anticoagulant-associated intracerebral hemorrage (AAICH) quintupled in our population during the 1990s.The majority of this change can be explained by increasing warfarin use. Anticoagulant-associated intracerebral hemorrhage now occurs at a frequency comparable to subarachnoid hemorrhage.


Subarachnoid Hemorrhage
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When a cerebral aneurysm ruptures, blood will fill the space surrounding the brain.

What is it? Subarachnoid hemorrhage occurs when a blood vessel just outside the brain ruptures. The area of the skull surrounding the brain (the subarachnoid space) rapidly fills with blood. A patient with subarachnoid hemorrhage may have a sudden, intense headache, neck pain, and nausea or vomiting. Sometimes this is described as the worst headache of one's life. The sudden buildup of pressure outside the brain may also cause rapid loss of consciousness or death.

What causes it? Subarachnoid hemorrhage is most often caused by abnormalities of the arteries at the base of the brain, called cerebral aneurysms. These are small areas of rounded or irregular swellings in the arteries. Where the swelling is most severe, the blood vessel wall become weak and prone to rupture. View an interactive tutorial on cerebral aneurysms from the Toronto Brain Vascular Malformation Study Group. (Requires Flash.)
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Surgical treatment of aneurysms involves placing clip on neck of aneurysm.

Who gets it? The cause of cerebral aneurysms is not known. They may develop from birth or in childhood and grow very slowly. Some people have not one, but several aneuryms. Subarachnoid hemorrhage can occur at any age, including teenagers and young adults. Subarachnoid hemorrhage is slightly more common in women than men.

Pulse Pressure and Risk of New-Onset Atrial Fibrillation
Gary F. Mitchell, MD; Ramachandran S. Vasan, MD; Michelle J. Keyes, MA; Helen Parise, ScD; Thomas J. Wang, MD; Martin G. Larson, ScD; Ralph B. D’Agostino, Sr, PhD; William B. Kannel, MD, MPH; Daniel Levy, MD; Emelia J. Benjamin, MD, ScM


JAMA. 2007;297:709-715.

Context Atrial fibrillation (AF) is responsible for considerable morbidity and mortality, making identification of modifiable risk factors a priority. Increased pulse pressure, a reflection of aortic stiffness, increases cardiac load and may increase AF risk.

Objective To examine relations between pulse pressure and incident AF.

Design, Setting, and Participants Prospective, community-based observational cohort in Framingham, Mass, including 5331 Framingham Heart Study participants aged 35 years and older and initially free from AF (median age, 57 years; 55% women).

Main Outcome Measures Incident AF.

Results AF developed in 698 participants (13.1%) a median of 12 years after pulse pressure assessment. Cumulative 20-year AF incidence rates were 5.6% for pulse pressure of 40 mm Hg or less (25th percentile) and 23.3% for pulse pressure greater than 61 mm Hg (75th percentile). In models adjusted for age, sex, baseline and time-dependent change in mean arterial pressure, and clinical risk factors for AF (body mass index, smoking, valvular disease, diabetes, electrocardiographic left ventricular hypertrophy, hypertension treatment, and prevalent myocardial infarction or heart failure), pulse pressure was associated with increased risk for AF (adjusted hazard ratio [HR], 1.26 per 20-mm Hg increment; 95% confidence interval [CI], 1.12-1.43; P<.001). In contrast, mean arterial pressure was unrelated to incident AF (adjusted HR, 0.96 per 10-mm Hg increment; 95% CI, 0.88-1.05; P = .39). Systolic pressure was related to AF (HR, 1.14 per 20-mm Hg increment; 95% CI, 1.04-1.25; P = .006); however, if diastolic pressure was added, model fit improved and the diastolic relation was inverse (adjusted HR, 0.87 per 10-mm Hg increment; 95% CI, 0.78-0.96; P = .01), consistent with a pulse pressure effect. Among patients with interpretable echocardiographic images, the association between pulse pressure and AF persisted in models that adjusted for baseline left atrial dimension, left ventricular mass, and left ventricular fractional shortening (adjusted HR, 1.23; 95% CI, 1.09-1.39; P = .001).

Conclusion Pulse pressure is an important risk factor for incident AF in a community-based sample. Further research is needed to determine whether interventions that reduce pulse pressure will limit the growing incidence of AF.


Author Affiliations: Cardiovascular Engineering Inc, Waltham, Mass (Dr Mitchell); Evans Department of Medicine (Drs Vasan and Benjamin), Whitaker Cardiovascular Institute (Drs Vasan and Benjamin), and Section of Preventive Medicine, Boston University School of Medicine, Boston, Mass (Drs Vasan, Kannel, and Benjamin); Department of Mathematics and Statistics, Boston University (Ms Keyes, Drs Parise and Larson), Cardiology Division, Massachusetts General Hospital, Boston (Dr Wang); National Heart, Lung, and Blood Institute's Framingham Study, Framingham, Mass (Drs Vasan, Wang, Larson, D’Agostino, Kannel, Levy, and Benjamin); National Heart, Lung, and Blood Institute, Bethesda, Md (Dr Levy).

RELATED ARTICLE

This Week in JAMA
JAMA. 2007;297:673.
FULL TEXT

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

High Pulse Pressure: Risk Factor for New-Onset AFib?
Journal Watch Cardiology 2007;2007:2-2.
FULL TEXT

January 17, 2007 — The US Food and Drug Administration (FDA) has approved safety labeling revisions to advise about the need for individualization of warfarin sodium therapy to minimize the risk of bleeding and to advise about the risks of worsening depression and emergence of suicidality in patients receiving quetiapine fumarate for the treatment of depression and other conditions.

Warfarin Sodium (Coumadin) Requires Individualized Dosing to Minimize Bleeding Risk
On October 4, 2006, the FDA approved safety labeling revisions for warfarin sodium tablets and injection (Coumadin, made by Bristol-Myers Squibb) to warn about the risk for major or fatal bleeding associated with their use.

The most serious risks for anticoagulant therapy with warfarin are hemorrhage in any tissue/organ and less frequently (incidence, < 0.1%) necrosis and/or gangrene of skin and other tissues. In some cases, hemorrhage and necroses have resulted in death or permanent disability.

The risk of bleeding is highest during treatment initiation and with higher doses. Risk factors include a high intensity of anticoagulation (international normalized ratio [INR], > 4.0); age, 65 years or older; highly variable INRs; a history of gastrointestinal bleeding; hypertension; cerebrovascular disease; serious heart disease; anemia; malignancy; trauma; renal insufficiency; concomitant drugs; and long duration of warfarin therapy.

The FDA emphasizes the need for individualized treatment with warfarin because of its low therapeutic index and potential effects from other drugs and dietary vitamin K intake. Pharmacokinetic mechanisms for drug interactions include synergism (impaired hemostasis, reduced clotting factor synthesis), competitive antagonism (vitamin K), and altered physiologic control loop for vitamin K metabolism (hereditary resistance). Pharmacodynamic interactions are based on enzyme induction/inhibition and reduced plasma protein binding.

Regular monitoring of INR is recommended for all patients. Those at high risk of bleeding can benefit from more frequent monitoring, careful dose adjustments to achieve desired INR, and a shorter duration of therapy.

To minimize the risk of bleeding, patients should be advised to avoid initiating or discontinuing other medications, including salicylates (eg, aspirin and topical analgesics), other over-the-counter medications, and herbal products. Maintenance of a balanced diet with a consistent amount of vitamin K is advised; drastic changes in diet (eg, eating large amounts of green leafy vegetables) and consumption of cranberry juice/products should be avoided.

According to the FDA, bromelains, danshen, dong quai (Angelica sinensis), garlic, Ginkgo biloba, ginseng, and cranberry products are associated most often with an increased effect of warfarin. Coenzyme Q10 (ubidecarenone) and St. John's Wort are associated most often with a decrease in the effects of warfarin.

Some botanicals can cause bleeding events when taken alone (eg, garlic and Ginkgo biloba) because of anticoagulant, antiplatelet, and/or fibrinolytic properties, which would be expected to provide an additive effect when taken with warfarin. Conversely, other botanicals (eg, mistletoe, agrimony, goldenseal, and yarrow) can have coagulant properties when taken alone or might decrease the effects of warfarin.

Patients should be advised to contact their healthcare professional immediately if unusual bleeding or related symptoms occur, such as pain, swelling/discomfort, prolonged bleeding from cuts, increased menstrual flow or vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or dark brown urine, red or tar black stools, headache, dizziness, or weakness.

Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension and pulmonary embolism and thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement. It can also be used to reduce the risk for death, recurrent myocardial infarction, and thromboembolic events (such as stroke or systemic embolization) after myocardial infarction.

Research article
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Maintenance treatment with esomeprazole following initial relief of NSAID-associated upper GI symptoms - the NASA2 and SPACE2 studies
Christopher J Hawkey , Nick J Talley , James M Scheiman , Roger H Jones , Goran Langstrom , Jorgen Naesdal , Neville D Yeomans and Nasa/space Author group

Arthritis Research & Therapy 2007, 9:R17 doi:10.1186/ar2124

Published 9 February 2007


Abstract (provisional)



The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.



Non-steroidal anti-inflammatory drugs (NSAIDs), including selective cyclo-oxygenase (COX)-2 inhibitors, cause upper gastrointestinal (GI) symptoms that are relieved by treatment with esomeprazole. We assessed esomeprazole for maintaining long-term relief of such symptoms. 610 patients with a chronic condition requiring anti-inflammatory therapy who achieved relief of NSAID-associated symptoms of pain, discomfort or burning in the upper abdomen during two previous studies were enrolled and randomised into two identical, multicentre, parallel-group, placebo-controlled studies of esomeprazole 20 mg or 40 mg treatment (NASA2 and SPACE2, study codes SH-NEN-0002 and SH-NEN-0004, respectively) performed at various rheumatology, gastroenterology and primary care clinics. 426 patients completed the 6-month treatment period. The primary measure was the proportion of patients with relapse of upper GI symptoms, recorded in daily diary cards, after 6 months. Relapse was defined as moderate-to-severe upper GI symptoms (a score of ^33 on a 7-grade scale) for 3 days or more in any 7-day period. Esomeprazole was significantly more effective than placebo in maintaining relief of upper GI symptoms over 6 months treatment. Life table estimates (95% confidence intervals) of the proportion of patients with relapse at 6 months (pooled population) were: placebo, 39.1% (32.2-46.0%); esomeprazole 20 mg, 29.3% (22.3-36.2%) p=0.006 vs. placebo; esomeprazole 40 mg, 26.1% (19.4-32.9%) p=0.001 vs. placebo. Patients on either non-selective NSAIDs or selective COX-2 inhibitors appeared to benefit. The frequency of adverse events was similar in all three groups. Esomeprazole maintains relief of NSAID-associated upper GI symptoms in patients taking continuous NSAIDs, including selective COX-2 inhibitors. ClinicalTrials.gov identifiers: NASA2, NCT00241514 and SPACE2, NCT00241553

Beta blockers prevent atrial fibrillation in systolic HF

16 February 2007

Beta blockers appear to prevent atrial fibrillation (AF) in patients with systolic heart failure (HF), say researchers.

Imad Abi Nasr (Assistance Publique-Hôpitaux de Paris, France) and colleagues came to this conclusion after conducting a meta-analysis of seven randomized, placebo-controlled trials including 70% of all HF patients involved in beta-blocker studies.

The benefits of beta blockers in HF may involve prevention of AF, but only one randomized trial directly suggests such an effect, Abi Nasr and team explain. "A systematic review of published and unpublished data is timely and could allow estimating the effectiveness of beta blockers to prevent chronic HF-related AF," they write.

The team looked for all studies that provided information on the incidence of AF during follow-up among those patients in sinus rhythm at baseline.

This revealed seven studies, including 11,952 patients who were receiving background treatment with angiotensin-converting enzyme inhibitors.

During an average follow-up period of 1.35 years, there were 227 versus 313 incident cases of AF in the beta-blocker and placebo arms, respectively. These translated into AF incidences of 28 per 1000 patient-years in the beta-blockers arm and 39 per 1000 patient-years in the placebo arm.

Analysis of this data indicated that beta-blockers significantly reduced the incidence of AF onset, with a relative risk (RR) reduction of 27% (RR=0.73, p<0.001).

Robustness analysis ruled out the possibility of publication bias, owing to the inclusion of unpublished neutral trials, the authors note.

A similar effect was seen with non-selective and selective beta blockers, according to heterogeneity tests, provided one trial – the SENIORS trial – was excluded. An old population (>70 years), a higher prevalence of baseline AF, and a high proportion of patients with diastolic HF may explain the absence of effect in SENIORS, Abi Nasr et al comment.

"Our meta-analysis suggests that beta blockers should be used as the first-line agents on preventing occurrence or recurrence of HF-related AF, with a similar and additional benefit in comparison with ACE-inhibitors and angiotensin II receptor antagonists," the authors conclude.

Eur Heart J 2007; 28: 457-462

Guidelines for Antithrombotic Therapy in Atrial Fibrillation Frequently Not Followed

Atrial fibrillation patients frequently do not receive antithrombotic therapy according to guidelines, a population-based study in Archives of Internal Medicine finds.

Researchers analyzed the medical records of some 570 patients, aged 30 to 84, with newly diagnosed atrial fibrillation (AF); three quarters of them met age and cardiovascular criteria for high stroke risk. Although guidelines call for warfarin anticoagulation for all high-risk AF patients, only 41% of such study participants received it. Indeed, AF classification, rather than stroke risk factors, was the strongest predictor of warfarin use. And even among participants who did receive warfarin, the target international normalized ratio (INR) range was maintained less than half the time.

Journal Watch Oncology and Hematology Associate Editor Dr. David Green offers one explanation for the underuse of warfarin: "Physicians often are reluctant to prescribe warfarin anticoagulation to frail elders because of concerns about bleeding; however, such bleeding is most likely to occur in patients whose INRs exceed the therapeutic range."

Archives of Internal Medicine article (Free abstract; full text requires subscription)

ACCP guidelines (Free)

ACC/AHA/ESC guidelines (Free)

WASHINGTON (Reuters) -- Ninety percent of the people infected with bird flu have been under the age of 40, and 60 percent of them have died, according to the latest analysis from the World Health Organization.

But the WHO researchers stressed their analysis did not suggest why this might be and noted there are several theories on why the H5N1 virus seems to attack younger people.

The H5N1 avian influenza virus has infected 272 people in 10 countries since it re-emerged in 2003. It has killed 166 of them.

It remains mostly a virus of birds and has killed or forced the culling of more than 200 million chickens, ducks, geese, turkeys and other fowl.

But its occasional attack on a human being has researchers worried. They fear it could mutate into a form more like seasonal flu, in which case it would be spread around the world by people and could kill millions.

So WHO is watching it very carefully and keeping statistics on every case. This kind of work, called epidemiology, can help scientists understand diseases, who they infect and who is most in danger.

WHO's Weekly Epidemiological Record analyzes all laboratory-confirmed human cases of H5N1 infection reported between late November 2003 and late November 2006.

The analysis said the median age of people confirmed infected was 18 years old and ranged from 3 months to 75 years.

"Just over half of all cases (52 percent or 132 out of 256) were aged under 20 years, and 89 percent were aged under 40 years."

This could be because it usually requires intense contact with a sick bird for a person to become infected, and in most countries, it is younger people, often children, who tend to poultry.

But there could be other reasons, such as immune system response to infection, scientists say.

The WHO researchers found that H5N1 has killed 60 percent of its victims and found big differences in fatality by age.

"The highest case fatality rate (76 percent) was found among those aged 10 to 19 years; the lowest case fatality rate (40 percent) was found among those aged over 50 years," the report reads.

Bird flu killed 44 percent of victims under the age of 5 and 66 percent of those aged 30 to 39.

WHO scientists plan a meeting in Turkey next month to talk about why such differences may exist.

Copyright 2007 Reuters. All rights reserved.This material may not be published, broadcast, rewritten, or redistributed.

* Sleep Apnea - Atrial fibrillation can be caused by sleep apnea, a condition where patients stop breathing for prolonged periods of time while sleeping. Patients with atrial fibrillation who are overweight, or have a history snoring or excessive sleepiness during the daytime, should be evaluated with a sleep study. Treatment for sleep apnea can eliminate atrial fibrillation in some patients.

Some patients with atrial fibrillation have no apparent cause. When this occurs in patients under age 60 to 65, it is called lone atrial fibrillation. The cause is not well understood, but the risk of blood clots is much lower in these patients.

DIAGNOSIS — Atrial fibrillation is diagnosed by obtaining an electrocardiogram (ECG or EKG), which records the heart's electrical activity. Other tests are performed to establish a cause for the atrial fibrillation, including measuring blood pressure to evaluate for hypertension and measuring thyroid stimulating hormone (TSH) in order to rule out an overactive thyroid gland. Other tests, such as an echocardiogram (ultrasound), may be performed to look for other causes of atrial fibrillation such as heart failure or heart valve problems, while lung function tests are sometimes used to look for underlying lung disease.

Patients who have symptoms suggesting atrial fibrillation, but who cannot be diagnosed with AF or other rhythm disorders based upon an office electrocardiogram, may need further monitoring. Continuous monitoring (eg, Holter monitor, show figure 3) or a recording device (eg, event monitor, show figure 4) that can be turned on by the patient when they feel palpitations are often used

SYMPTOMS AND RISKS— Three main factors determine the symptoms and risks of atrial fibrillation: how fast the ventricles are beating; the presence or absence of underlying heart disease; and the formation of blood clots, particularly in the left atrium, that can break off and enter the systemic circulation, possibly leading to a stroke or blockage of arteries going to other important organs.

Symptoms — Patient awareness of atrial fibrillation is highly variable; some patients have no symptoms while others may have debilitating shortness of breath. Most patients who are well controlled on medical therapy have no or mild symptoms; more severe symptoms occur when the ventricular rate is not well controlled. Mild symptoms include:

* Unpleasant palpitations or irregularity of the heart beat
* Mild chest discomfort (sensation of tightness) or pain
* A sense of the heart racing
* Lightheadedness
* Mild shortness of breath and fatigue that limit the ability to exercise

As the ventricles beat more rapidly or irregularly, symptoms may be more severe and include:

* Difficulty breathing
* Shortness of breath with exertion
* Fainting, or near fainting, due to a reduction in blood flow to the brain
* Confusion, due to a reduction in blood supply to the brain
* Chest discomfort
* Fatigue

Chest discomfort generally results from inadequate blood flow to meet the needs of the heart (called angina); this can be due to an increase in the heart's need for oxygen and/or a decrease in the heart's supply of blood and oxygen. In some cases, chest pain is due to the rapid heart rate itself or perhaps to stretching of the heart's chambers.

If the heart rate is very rapid, or if the patient has underlying heart disease, more serious symptoms of heart failure can develop:

* Shortness of breath at rest or at night
* Swelling of the legs
* Rapid weight gain due to fluid accumulation
* Angina or even a heart attack, primarily in patients with underlying coronary disease

Worsening heart failure or the development of angina may also produce other types of serious and potentially life-threatening arrhythmias.

Risk of stroke — A serious complication associated with atrial fibrillation is stroke, which can lead to permanent brain damage. A stroke can occur if a blood clot forms in the left atrium because of sluggish blood flow and a piece of the clot (also called an embolus) breaks off. The embolus enters the blood circulation and can obstruct a small blood vessel. The most dangerous place for this to occur is the brain, resulting in a stroke, but the embolus may also go to the eye, kidneys, spine, or important arteries of the arms or legs.

Like atrial fibrillation, the risk of stroke increases with age. Without preventive treatment (eg, blood thinners), stroke occurs in approximately 1.3 percent of patients aged 50 to 59 years and increases gradually to 5.1 percent each year for those aged 80 to 89 years. These percentages are average rates; for each patient the risk is also influenced by a number of other factors, including the presence of hypertension and additional heart disease. In some patients with multiple underlying medical conditions, the annual risk of a stroke can be as high as 8 to 10 percent.

The administration of a blood thinner (usually warfarin [Coumadin®]) lowers the risk of stroke by 50 to 65 percent in intermediate to high risk patients. Warfarin therapy is typically referred to as anticoagulation (see "Warfarin therapy" below). In patients at intermediate to high risk for stroke, no other therapy lowers the risk of a stroke as much as warfarin.

Low-risk patients have a stroke rate of less than 1 percent per year (usually patients under 60 to 65 years of age with one or no additional risk factors). Patients with this low-risk profile may be treated with aspirin instead of warfarin.

TREATMENT — There are four main issues that must be addressed in the treatment of atrial fibrillation: the need for hospitalization; conversion to and maintenance of normal sinus rhythm; rhythm versus rate control; and prevention of embolus formation and stroke.

Hospitalization — Most patients who have atrial fibrillation do not need to be admitted to the hospital. Situations in which hospitalization might be indicated include:

* Symptoms of chest pain or pressure associated with electrocardiogram (ECG) changes that suggest the person is having a heart attack or angina due to a reduction in blood supply to the heart.

* Patients who have other serious complications of atrial fibrillation, including low blood pressure, trouble breathing, heart failure, or stroke.

* An underlying medical condition that caused the atrial fibrillation and that needs treatment itself.

* When patients are cardioverted from atrial fibrillation to a normal sinus rhythm.

* Patients who may be safer in a hospital while medications are started.

* Patients who are at a particularly high risk of developing a thrombus in the atrium or who should be observed for potential bleeding problems while anticoagulation is started.

Conversion to normal rhythm — Patients with paroxysmal (intermittent) atrial fibrillation have episodes of varying duration that resolve spontaneously. Careful monitoring has shown that up to 90 percent of recurrent episodes are not recognized by the patient, including some that last more than two days.

Spontaneous conversion to normal sinus rhythm is much less likely in patients with chronic (persistent) atrial fibrillation. In these patients, atrial fibrillation is converted to sinus rhythm using either electrical cardioversion or medications.

Electrical cardioversion — Electrical cardioversion involves the use of an electrical shock from a cardioverter, delivered by paddles placed on the chest, to "reset" the heart rhythm. Urgent cardioversion is recommended if atrial fibrillation is interfering with heart's ability to supply blood and oxygen to vital organs. Signs of this include a fall in blood pressure, angina (chest pain), shortness of breath, and/or heart failure.

Some patients with newly diagnosed atrial fibrillation can undergo electrical or medical cardioversion (using an antiarrhythmic drug) immediately. However, due to the risk of stroke from left atrial blood clots, doctors frequently recommend waiting to cardiovert until the patient has been treated with a blood thinner. This medication, (usually warfarin [Coumadin®]) is given for three to four weeks, which allows 85 percent of preexisting blood clots in the left atrium to resolve.

Even though normal electrical activity is restored with the cardioversion, the atria may not resume normal muscle contraction for several days or weeks. Thus, there is still a risk of clot formation in the period immediately after cardioversion. For this reason, a blood thinner is recommended for at least four weeks after cardioversion.

Repeat cardioversion is a reasonable treatment for patients with atrial fibrillation that has recurred after a long duration of normal heart rhythm; it is most likely to be successful in younger patients with a short history of atrial fibrillation.

Transesophageal echocardiogram — An alternative to waiting involves a procedure called transesophageal echocardiogram (TEE). TEE uses a small ultrasound device that is swallowed to visualize the left atria, looking for evidence of clots or slowed blood flow. If the atria appear to be without clots or slowed blood flow, cardioversion can be performed safely without warfarin pretreatment. Although there is still a risk that cardioversion may dislodge a clot that was not seen on the TEE, the risk is quite small.

Other treatment options — For patients with intermittent or chronic atrial fibrillation, there are two long-term treatment options: rhythm control and rate control. Two large clinical trials have addressed the effectiveness and safety of these two approaches. Before discussing these trials, it is useful to review the meaning of rhythm control and rate control and both the benefits and risks of long-term warfarin therapy.

Rhythm control — Rhythm control refers to electrical or medical cardioversion followed by an antiarrhythmic drug to lower the risk of recurrence of atrial fibrillation. After successful conversion to normal sinus rhythm, only 20 to 30 percent of patients are in sinus rhythm after one year. This can be increased to between 40 and 80 percent by adding an antiarrhythmic drug.

The advantages to rhythm control are improved cardiac function and, for some patients, reduced symptoms. Selected patients who are effectively maintained in normal rhythm may be allowed to stop chronic anticoagulation. However, rhythm control is more likely to reduce the frequency of AF than eliminate it entirely. Thus most patients treated with antiarrhythmic medications should continue anticoagulation therapy indefinitely.

The disadvantages of rhythm control are the high rate of recurrent atrial fibrillation and side effects associated with antiarrhythmic drugs, including the development of new abnormal heart rhythms.

Rate control — In patients who are treated with rate control, atrial fibrillation is allowed to continue; the patient uses a medication (a beta blocker, a calcium channel blocker, or digoxin) to slow conduction through the AV node, thereby slowing the ventricular rate into the normal range. All patients require chronic therapy with a blood thinner since there is a continued risk of blood clot formation and possible stroke.

There are two major disadvantages with the rate control strategy: it is sometimes difficult to adequately control the rate and relieve symptoms; and chronic anticoagulation, which carries a risk of bleeding, is mandatory, .

Nonpharmacologic treatments — There are alternatives to medicines to achieve rhythm or rate control. Nonpharmacologic treatments include radiofrequency catheter ablation, use of a pacemaker or implantable atrial defibrillator, and several surgical treatments. Radiofrequency ablation can result in a cure when performed by an experienced physician in carefully selected patients. (See "Patient information: Radiofrequency catheter ablation" and see "Patient information: Pacemakers" and see "Patient information: Implantable cardioverter-defibrillators").

Surgical procedures, including the maze procedure and the corridor operation, may be considered in some patients with atrial fibrillation, especially those who must undergo open-heart surgery for other reasons.

Warfarin therapy — Chronic warfarin therapy reduces the rate of stroke by approximately 50 to 70 percent in patients with atrial fibrillation who are at intermediate to high risk. The potential benefit is actually greater since as many as one-half of strokes in treated patients are due to a less than optimal degree of blood thinning. (See "Patient information: Warfarin (Coumadin®)").

The major problem with warfarin therapy is that anticoagulation can lead to bleeding. In a large review of studies of patients with atrial fibrillation, the incidence of major bleeding events with warfarin was increased by 0.9 percent per year compared to aspirin (2.2 versus 1.3 percent per year). The major concern is bleeding into the brain.

The major risk factors for bleeding into the brain are:

* Age greater than 70 years
* Uncontrolled high blood pressure
* History of prior stroke
* Excessive anticoagulation.

However, the risk of bleeding into the brain is substantially smaller than the benefit of preventing strokes in patients who use warfarin.

Patients taking warfarin must be carefully and continuously monitored with periodic blood tests to make certain that the degree of blood thinning is sufficient to protect against stroke but not too great to promote bleeding.

Clinical trials — In the past, most physicians preferred rhythm control because of the presumed advantages of better heart function and a much lower risk of stroke in patients in normal sinus rhythm. However, two major trials directly compared rhythm control and rate control. There were two major conclusions:

* The outcomes were generally similar, but both studies showed a trend toward a better outcome with rate control compared to rhythm control (show figure 4 and show figure 5).

* Contrary to expectations, rhythm control was associated with a trend toward a higher risk of stroke compared to rate control. However, the majority of strokes occurred in patients receiving no or suboptimal warfarin therapy. This finding suggests that patients treated with rhythm control should usually continue anticoagulation. In other words, choosing rhythm control should be based upon the desire to improve symptoms, not an effort to avoid chronic anticoagulation.

Patients should talk to their healthcare provider about which approach is best. A 2003 guideline from two major medical societies recommends rate control with chronic anticoagulation for the majority of patients. The type of blood thinner therapy (warfarin or aspirin) recommended depends upon a patient's risk of stroke, which can be determined with a healthcare provider.

Newer therapies — There are limitations to current medical therapy of atrial fibrillation: normal sinus rhythm cannot be maintained in most patients with antiarrhythmic drugs, which also have side effects; rate control that control symptoms cannot be attained in all patients; and all patients except those at low risk require chronic warfarin therapy, which has a risk of bleeding.

Surgery and radiofrequency catheter ablation have been used for rate control and cure of atrial fibrillation. Patients with symptomatic atrial fibrillation that cannot be adequately controlled with medicines may be candidates for catheter ablation to cure the atrial fibrillation.

WHERE TO GET MORE INFORMATION — Your healthcare provider is the best source of information for questions and concerns related to your medical problem. Because no two patients are exactly alike and recommendations can vary from one person to another, it is important to seek guidance from a provider who is familiar with your individual situation.

This discussion will be updated as needed every four months on our web site (www.patients.uptodate.com). Additional topics as well as selected discussions written for healthcare professionals are also available for those who would like more detailed information. Some of the most pertinent include:

Professional Level Information:
Causes of atrial fibrillation
Overview of the presentation and management of atrial fibrillation
Paroxysmal atrial fibrillation
Anticoagulation to prevent embolization in atrial fibrillation
Control of ventricular rate in atrial fibrillation: Nonpharmacologic therapy
Control of ventricular rate in atrial fibrillation: Pharmacologic therapy
Restoration of sinus rhythm in atrial fibrillation: Recommendations

A number of web sites have information about medical problems and treatments, although it can be difficult to know which sites are reputable. Information provided by the National Institutes of Health, national medical societies and some other well-established organizations are often reliable sources of information, although the frequency with which they are updated is variable.

* National Library of Medicine

(www.nlm.nih.gov/medlineplus/healthtopics.html)

* National Heart, Lung, and Blood Institute

(www.nhlbi.nih.gov/)

* American Heart Association

(www.americanheart.org)

* Harvard Center for Cancer Prevention

(www.yourdiseaserisk.harvard.edu/)
Includes a calculator for estimating the risk of stroke

* Atrial Fibrillation Foundation

(www.affacts.org)

* Heart Rhythm Society

(www.hrsonline.org)

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9. Roy, D, Talajic, M, Dorian, P, et al. Amiodarone to prevent recurrence of atrial fibrillation. Canadian Trial of Atrial Fibrillation Investigators. N Engl J Med 2000; 342:913.
10. Wyse, DG, Waldo, AL, DiMarco, JP, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. The atrial fibrillation follow-up investigation of rhythm management (AFFIRM) investigators. N Engl J Med 2002; 347:1825.
11. Van Gelder, IC, Hagens, VE, Bosker, HA, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med 2002; 347:1834.
12. Snow, V, Weiss, KB, LeFevre, M, et al. Management of newly detected atrial fibrillation: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Intern Med 2003; 139:1009.

Atrial fibrillation
Heart problems often come with obstructive sleep apnea

By Helen Fields

10/7/04
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More than 2 million Americans have atrial fibrillation, a condition in which part of the heart quivers instead of contracting regularly. With blood puddling in the heart, a clot can form and travel to the brain to cause a stroke. Atrial fibrillation often occurs in people with obstructive sleep apnea, temporarily stopping breathing while they sleep, which afflicts some 40 percent of obese adults. Treating sleep apnea can help reduce the risk of atrial fibrillation coming back. Researchers at the Mayo Clinic looked at atrial fibrillation patients to find out how many of them have obstructive sleep apnea.

What the researchers wanted to know: How many atrial fibrillation patients have obstructive sleep apnea?

What they did: The researchers looked at 151 patients who came to the Mayo Clinic to get their fibrillating atria electric-shocked into proper behavior (a procedure called cardioversion). They were compared with 312 people who were referred to a cardiologist but had never had atrial fibrillation. All were given a questionnaire to determine whether they had obstructive sleep apnea—the questions are mostly about snoring and sleepiness during the day. The researchers sent a letter to patients who were found to have obstructive sleep apnea, suggesting they see a doctor about it.

What they found: Nearly half of the patients with atrial fibrillation had obstructive sleep apnea, compared with only 32 percent of the other heart patients. Atrial fibrillation was more strongly associated with obstructive sleep apnea than the traditional risk factors, such as neck circumference and high blood pressure, which were also considered in this study. The authors speculate that the nightly interference with air flow and the oxygen content of your blood could cause atrial fibrillation—or that atrial fibrillation causes obstructive sleep apnea in some cases, by sending impulses to the parts of the nervous system that control breathing.

What the study means to you: People with atrial fibrillation might consider getting checked for obstructive sleep apnea; treating it may help their hearts.

Caveats: The researchers used a questionnaire to diagnose sleep apnea, while the best diagnosis is actually having someone sleep in a lab all night. (But they double-checked by having some people sleep in the lab and found the questionnaires were accurate.)

Find out more: The American Heart Association's page on atrial fibrillation includes links to explanations of atrial fibrillation and cardioversion. An explanation of sleep apnea, from The Sleep Channel: www.sleepdisorderchannel.net/osa/

Read the article: Gami, A.S., et al. "Association of Atrial Fibrillation and Obstructive Sleep Apnea." Circulation. July 27, 2004, Vol. 110, No. 4, pp. 364-367.

Abstract online: http://circ.ahajournals.org

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Obstructive Sleep Apnea and the Recurrence of Atrial Fibrillation
Ravi Kanagala, MD; Narayana S. Murali, MD; Paul A. Friedman, MD; Naser M. Ammash, MD; Bernard J. Gersh, MB ChB, DPhil; Karla V. Ballman, PhD; Abu S. M. Shamsuzzaman, MD, PhD; Virend K. Somers, MD, PhD

From the Mayo Clinic, Rochester, Minn.

Correspondence to Virend K. Somers, MD, D Phil, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail somers.virend@mayo.edu

Background— We tested the hypothesis that patients with untreated obstructive sleep apnea (OSA) would be at increased risk for recurrence of atrial fibrillation (AF) after cardioversion.

Methods and Results— We prospectively obtained data on history, echocardiogram, ECG, body mass index, hypertension, diabetes, NYHA functional class, ejection fraction, left atrial appendage velocity, and medications in patients with AF/atrial flutter referred for DC cardioversion. Forty-three individuals were identified as having OSA on the basis of a previous sleep study. Data regarding the use of continuous positive airway pressure (CPAP) and recurrence of AF were obtained for 39 of these patients. Follow-up data were also obtained in 79 randomly selected postcardioversion patients (controls) who did not have any previous sleep study. Twenty-seven of the 39 OSA patients either were not receiving any CPAP therapy (n=25) or were using CPAP inappropriately (n=2). Recurrence of AF at 12 months in these 27 patients was 82%, higher than the 42% recurrence in the treated OSA group (n=12, P=0.013) and the 53% recurrence (n=79, P=0.009) in the 79 control patients. Of the 25 OSA patients who had not been treated at all, the nocturnal fall in oxygen saturation was greater (P=0.034) in those who had recurrence of AF (n=20) than in those without recurrence (n=5).

Conclusions— Patients with untreated OSA have a higher recurrence of AF after cardioversion than patients without a polysomnographic diagnosis of sleep apnea. Appropriate treatment with CPAP in OSA patients is associated with lower recurrence of AF.

Correspondence to Virend K. Somers, MD, DPhil, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905. E-mail somers.virend@mayo.edu

Received February 20, 2004; revision received April 13, 2004; accepted April 15, 2004.

Background— Obstructive sleep apnea (OSA) is associated with recurrent atrial fibrillation (AF) after electrocardioversion. OSA is highly prevalent in patients who are male, obese, and/or hypertensive, but its prevalence in patients with AF is unknown.

Methods and Results— We prospectively studied consecutive patients undergoing electrocardioversion for AF (n=151) and consecutive patients without past or current AF referred to a general cardiology practice (n=312). OSA was diagnosed with the Berlin questionnaire, which is validated to identify patients with OSA. We also assessed its accuracy compared with polysomnography in a sample of the study population. Groups were compared with the 2-tailed t, Wilcoxon, and {chi}2 tests. Logistic regression modeled the association of AF and OSA after adjustment for relevant covariates. Patients in each group had similar age, gender, body mass index, and rates of diabetes, hypertension, and congestive heart failure. The questionnaire performed with 0.86 sensitivity, 0.89 specificity, and 0.97 positive predictive value in our sample. The proportion of patients with OSA was significantly higher in the AF group than in the general cardiology group (49% versus 32%, P=0.0004). The adjusted odds ratio for the association between AF and OSA was 2.19 (95% CI 1.40 to 3.42, P=0.0006).

Conclusions— The novel finding of this study is that a strong association exists between OSA and AF, such that OSA is strikingly more prevalent in patients with AF than in high-risk patients with multiple other cardiovascular diseases. The coinciding epidemics of obesity and AF underscore the clinical importance of these results.

Improve Bones and Blood Pressure with Potassium Citrate
Potassium citrate might help reverse the negative effect of the high-protein Western diet on bone health while also lowering blood pressure.

Chronic metabolic acidosis has long been suspected to decrease bone mass. The authors of this study hypothesized that the high-protein acidogenic Western diet contributes to the pathophysiology of osteoporosis and that dietary supplementation with alkali in the form of potassium citrate (Kcitrate) might slow the osteoporotic process. To examine this hypothesis, they randomized 161 Swiss postmenopausal women who had low bone mass and had not received any osteoporosis treatment to receive 30 mEq per day of either Kcitrate or potassium chloride (KCl; control) for 12 months. Both groups also received calcium (500 mg/day) and vitamin D (400 IU/day).

Lumbar spine BMD increased progressively and significantly in the Kcitrate group but decreased in the KCl group, yielding an intergroup difference of 1.87% (P<0.001) at 12 months. Interestingly, the Kcitrate group also showed a decrease from baseline in systolic and diastolic BP of 7.9±1.8 mm Hg and 6.4±1.1 mm Hg, respectively. The KCl group showed a similar but slightly smaller drop in BP.

Comment: The increase in net lumbar spine BMD observed by these authors is similar to that reported for raloxifene (see N Engl J Med 1997; 337:1641) but less than that reported for ibandronate (see Bone 1996; 19:527). However, the BP reductions are the first to be reported in long-term K-supplemented, normotensive individuals. Despite some weaknesses (no controls for diet, calcium intake, or exercise, and little ethnic or racial diversity), the study poses an interesting proposition: Simple, inexpensive supplementation with Kcitrate might reverse the negative effect of the high-protein Western diet on bone health while also improving BP. This strategy certainly deserves further study.

— Wendy S. Biggs, MD

Published in Journal Watch Women's Health January 11, 2007


Citation(s):
Jehle S et al. Partial neutralization of the acidogenic Western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia. J Am Soc Nephrol 2006 Nov; 17:3213-22.
Original articleMedline abstract

Cochrane Review: Beta Blockers Should Not Be First Line for Hypertension
from Heartwire — a professional news service of WebMD


Sue Hughes
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Important Considerations

February 2, 2007 (Yaoundé, Cameroon) - The available evidence does not support the use of beta blockers as first-line drugs in the treatment of hypertension, according to a new Cochrane review [1].

The review, published online January 24, 2007, bases this conclusion on “the relatively weak effect of beta blockers to reduce stroke and the absence of an effect on coronary heart disease when compared with placebo or no treatment" and “the trend toward worse outcomes in comparison with calcium-channel blockers, renin-angiotensin-system inhibitors, and thiazide diuretics."

It adds that most of the evidence for these conclusions comes from trials where atenolol was the beta blocker used, and it is not known at present whether there are differences between the different subtypes of beta blockers or whether beta blockers have differential effects on younger and elderly patients.

As background, the authors, led by Dr CS Wiysonge (Ministry of Public Health, Yaoundé, Cameroon), explain that two recent systematic reviews found first-line beta blockers to be less effective in reducing the incidence of stroke and the combined end point of stroke, MI, and death compared with all other antihypertensive drugs taken together, but beta blockers might be better or worse than a specific class of drugs for a particular outcome measure, so that comparing beta blockers with all other classes taken together could be misleading. In addition, these systematic reviews did not assess the tolerability of beta blockers relative to other antihypertensive medications. They therefore undertook this review to reassess the place of beta blockade as first-line therapy for hypertension relative to each of the other major classes of antihypertensive drugs.

For their review, they included 13 randomized trials (in a total of 91 561 patients) that assessed the effectiveness of beta blockers compared with placebo, no therapy, or other drug classes, as monotherapy or first-line therapy for hypertension, on mortality and morbidity end points. Four trials (with 23 613 participants) compared beta blockers with placebo or no treatment; five trials (with 18 241 participants) compared beta blockers with diuretics; four trials (with 44 825 participants) compared beta blockers with calcium-channel blockers; and three trials (with 10 828 participants) compared beta blockers with renin-angiotensin-system inhibitors.

Results showed that the risk of all-cause mortality was not different between first-line beta blockers and placebo, diuretics, or inhibitors of the renin angiotensin system but was higher for beta blockers compared with calcium blockers.

Relative risk of all-cause mortality for beta blockers vs placebo or other treatments Comparative drug
RR of all-cause mortality for beta blockers
95% CI

Placebo
0.99
0.88–1.11

Diuretics
1.04
0.91–1.19

ACE inhibitors/ARBs
1.10
0.98–1.24

Calcium blockers
1.07
1.00–1.14

The risk of total cardiovascular disease was lower for first-line beta blockers compared with placebo but was significantly worse for beta blockers compared with calcium blockers. There was no significant difference in this end point with beta blockers when compared with either diuretics or ACE inhibitors/ARBs.

Relative risk of total cardiovascular disease for beta blockers vs placebo or other treatments Comparative drug
RR of total CV disease for beta blockers
95% CI

Placebo
0.88
0.79–0.97

Diuretics
1.13
0.99–1.13

ACE inhibitors/ARBs
1.00
0.72–1.38

Calcium blockers
1.18
1.08–1.29

The lower risk of total cardiovascular disease with beta blockers compared with placebo was primarily a reflection of the significant decrease in stroke, whereas coronary heart disease (CHD) risk was not significantly different between beta blockers and placebo. Similarly, the increase in total cardiovascular disease with beta blockers compared with calcium blockers was due to an increase in stroke with the beta blockers. There was also an increase in stroke with beta blockers as compared with inhibitors of the renin angiotensin system. CHD was not significantly different between beta blockers and diuretics, calcium blockers, or renin-angiotensin-system inhibitors.

Relative risk of stroke for beta blockers vs placebo or other treatments Comparative drug
RR of stroke for beta blockers
95% CI

Placebo
0.80
0.66–0.96

Diuretics
1.17
0.65–2.09

ACE inhibitors/ARBs
1.30
1.11–1.53

Calcium blockers
1.24
1.11–1.40

In addition, patients on beta blockers were more likely to discontinue treatment due to side effects than those on diuretics and renin-angiotensin-system inhibitors, but there was no significant difference with calcium blockers.

Relative risk of discontinuing treatment for beta blockers vs placebo or other treatments Comparative drug
RR of stopping treatment for beta blockers
95% CI

Placebo
2.34
0.84–6.52

Diuretics
1.86
1.39–2.50

ACE inhibitors/ARBs
1.41
1.29–1.54

Calcium blockers
1.20
0.71–2.04

The authors conclude that “beta blockers are inferior to various calcium-channel blockers for all-cause mortality, stroke, and total cardiovascular events and to renin-angiotensin-system inhibition for stroke."

Is age important?

Noting that a previous meta-analysis (by Khan and McAlister) found beta blockers to be inferior to all other therapies only in elderly patients, they point out that this claim relies heavily on the Medical Research Council trial in elderly hypertensive patients, in which the dropout rate was 25%. They say: “At present, there are insufficient data to make a valid comparison of beta-blocker effects on younger vs elderly patients, although this is an important hypothesis."

Are there differences between beta blockers?

They point out that of the 40 245 participants using beta blockers in this review, atenolol was used by 30 150 (75%). “Due to the paucity of data using beta blockers other than atenolol, it is not possible to say whether the effectiveness (or lack thereof) and (in)tolerability of beta blockers seen here is a property of atenolol or is a class effect of beta blockers across the board.”

Similarly, the authors note that the information reported in the trials considered in this review was insufficient to explore the effect of race or ethnicity, as most trial participants were white.

Wiysonge CS, Bradley H, Mayosi BM, et al. Beta blockers for hypertension. Cochrane Database Syst Rev 2007; 1:CD002003.
The complete contents of Heartwire, a professional news service of WebMD, can be found at www.theheart.org, a Web site for cardiovascular healthcare professionals.


--------------------------------------------------------------------------------Sue Hughes is a journalist for Medscape. She joined the heart.org, a website recently acquired by WebMD, in 2000. She was previously science editor of Scrip World Pharmaceutical News. Graduating in pharmacy from Manchester University, UK, she started her career as a hospital pharmacist before moving as a journalist to a UK pharmacy trade publication. She can be reached at Shughes@webmd.net.


Heartwire 2007. © 2007 Medscape

















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Tissue Plasminogen Activator (tPA)

AHA/ASA Recommendation
We strongly urge people to seek medical attention as soon as possible if they believe they're having a stroke or heart attack. The sooner tPA or other appropriate treatment is begun, the better the chances for recovery.

What is tPA?

Tissue plasminogen activator (tPA) is a thrombolytic agent (clot-busting drug). It's approved for use in certain patients having a heart attack or stroke. The drug can dissolve blood clots, which cause most heart attacks and strokes.

How does tPA help people having a heart attack?

Studies have shown that tPA and other clot-dissolving agents can reduce the amount of damage to the heart muscle and save lives. However, to be effective, they must be given within a few hours after symptoms begin. Administering tPA or other clot-dissolving agents is complex and is done through an intravenous (IV) line in the arm by hospital personnel.

How does tPA help people having a stroke?

tPA has been shown to be effective in treating ischemic stroke. This kind of stroke is caused by blood clots that block blood flow to the brain.

In 1996 the U.S. Food and Drug Administration (FDA) approved the use of tPA to treat ischemic stroke in the first three hours after the start of symptoms. This makes it very important for people who think they're having a stroke to seek help immediately. If given promptly, tPA can significantly reduce the effects of stroke and reduce permanent disability.

tPA or other thrombolytics can reduce disability from a heart attack or stroke, but there is also a higher risk of bleeding.

Related AHA publications

Original Message -----brief van zoon van Chris Willems voor Cor Swijgers
From: H.P.J. Willems
To: Chris Willems
Sent: Monday, February 05, 2007 4:47 PM
Subject: Re: Hoe zit dit?

Geachte opponens, beste pa

Inderdaad is het aantal carcinogene mutaties groter met het stijgen van de leeftijd, mogelijk door veranderingen in methylering van het DNA. Ik ben daar zeker geen expert in overigens. Een aantal cytostatica is foliumzuurantagonist, het belangrijkste daarvan is methotrexaat hetgeen bekend moet zijn bij Cor. Als je methotrexaat in hoge doses toedient wordt de DNA opbouw onmogelijk gemaakt, dit geeft het cytostatische effect. Dit wil echter niet zeggen dat foliumzuur carcinogeen is. Zoals besproken tijdens mijn promotie kan het zijn dat foliumzuur de carcinogenese beinvloedt en de groei van bestaande tumoren versnelt. Dit is echter zeker niet bewezen. Evenmin trouwens het gegeven dat foliumzuur het gehoor doet verbeteren. Jane Durga, van wie dit afkomstig is, geeft dit zelf al aan in haar artikel dat er strikte selectiecriteria zijn gehanteerd, dat de resultaten niet extrapoleerbaar zijn naar iedereen en dat het resultaat bevestigd dient te worden in andere studies. Dus harde aanwijzingen om foliumzuur te slikken zijn er niet, maar harde aanwijzingen om lage doses foliumzuur te laten staan uit angst voor een carcinoom zijn er overigens ook niet.

Kun je mij jou inlogaam en wachtwoord geven voor het NRC, ik heb die niet gekregen bij mijn weekendabonnement, dan kan ik zelf even op zoek gaan.

Groet, Huub

Abonnee-artikel
Verenigde Staten: Voorbeeldige immigranten
Aziaten doen het sociaal-economisch veel beter dan andere etnische groepen. Dat komt onder meer door hun uitzonderlijke ondernemingszin

Arnold Schwarzenegger veroorzaakte in oktober opschudding met zijn uitspraak dat Mexicanen moeten assimileren zoals de Aziaten dat doen. Maar de Californische gouverneur had wel een punt: al sinds de jaren zestig gelden Aziaten als 'model-minderheden' in de Verenigde Staten. En dat beeld klopt zeker voor een aantal Aziatische bevolkingsgroepen. Zo zijn Japanners, Indiërs en Taiwanezen gemiddeld hoger opgeleid en verdienen ze meer dan Latino's, zwarten en indianen. Ook bezitten Aziaten als groep vaker een eigen huis dan andere minderheden.

Ze hebben zelfs een hoger opleidingsniveau dan hun blanke mede-Amerikanen, blijkt uit het rapport A Community of Contrasts, dat diverse Aziatische organisaties opstelden. Ruim 40 procent van de Aziaten in de Verenigde Staten heeft een universitair diploma, terwijl dat onder blanken slechts een kwart is. Japanners, Indiërs, Taiwanezen en Sri Lankanen hebben individueel tevens hogere inkomens dan blanken. Per gezin bekeken – in Aziatische gezinnen werken doorgaans minstens drie mensen – komen nog eens vier Aziatische nationaliteiten boven het blanke gemiddelde uit.

Met de Latino's zijn de Aziaten de snelst groeiende groep in de Verenigde Staten. Bijna de helft woont in...

Het complete artikel bevat 781 woorden.

Medicatie die gebruikt wordt om een beroerte te voorkomen
Plaatjesremmers (aspirine, clopidogrel (plavix), dipyridamole)dipiridamole samen met aspirine heet aggrenox en assantin)

Klonters ontstaan op plaatsen waar bloedvaten beschadigd zijn, bijvoorbeeld door aderverkalking. Een klonter bestaat uit een kluwen van fibrine (een soort lijm) en samenklevende bloedplaatjes. Klontervorming kan door aspirine of producten zoals clopidogrel (Plavix) en Aggrenox (een combinatie van aspirine met dipyridamole) tegengegaan worden door het samenkleven van bloedplaatjes te verhinderen. Aspirine of aanverwante producten kunnen de kans op een beroerte verminderen, vooral bij patiënten die een beroerte gehad hebben.

Deze producten moeten meestal levenslang ingenomen worden.

Bloedverdunners (coumarines)acenacoumarol, marcousin en warfarin

Bloedverdunners worden vooral gebruikt door patiënten met voorkamerfibrillatie. Ze verminderen in belangrijke mate de kans op een beroerte. Bloedverdunners zijn slechts veilig als ze correct gebruikt worden. De mate van bloedverdunning varieert nogal: soms is het bloed onvoldoende verdund en soms is het bloed te verdund. Als het bloed onvoldoende verdund is kunnen klonters ontstaan en als het bloed te verdund is kunnen bloedingen ontstaan. Om deze problemen te vermijden moet de mate van bloedverdunning, zeker bij het begin van de behandeling, vaak gecontroleerd worden. De huisarts moet hiervoor een bloedstaal nemen. Neem contact op met je arts als er toch een bloeding optreedt. Verwittig je arts bij het optreden van zwarte stoelgang of rood verkleurde urine. Laat je bloed controleren als er bloeduitstortingen ontstaan. Hoofdpijn is ook een alarmsymptoom.

Dear Jan Goossens,

Thank you for your question.

I assume you sent it to me because you learnt about the study that I am
undertaking comparing aspirin to warfarin for people aged over the age
of 75 who have atrial fibrillation.

We are currently finishing the analysis of our study, and the results
will be in the public arena at the end of May this year. I hope that
then I will be able to answer your question!

I will send you a copy of the results when they have been published.

Yours sincerely,

Jonathan Mant

-----Original Message-----
From: Jan Goossens [mailto:roodbont@zonnet.nl]
Sent: 29 January 2007 17:12
To: j.w.mant@bham.ac.uk
Subject: atrium fibrillation

Dear Dr. Mant.

My medical doctor diagnosed a atrium flatter 23 November 2006, and
prescribed me Marcoumar. By blood controle the INR has to be between 2
and 3.
I am a simple veterinary surgeon, 82 years old and have to use now and
than a couple of celebrex pills, when gout comes up. Moreover I use
omeprazole to keep my stomach quiet. To keep my blood pressure adequate
I use 5mg amlodipine and 4mg perindopril and since my atrium flatter 50
mg atenolol. I have no troubles with my atrium fibrillation and if my
doctor would not have told me, I would not have noticed it.
Reading an article in Neurology 2007; 68: 116-121 by M.L. Flaherty et
al.: The increasing incidence of anticoagulant-associated intracerebral
hemorrhage, I think maybe it is better to use 80mg aspirin with or
without persantin (pirydamole) to avoid anticoagulant-associated
intracerebral hemorrhage .
I would be much obliged to you, if you let me know if you can agree with
my supposition and I can discus it with my doctor.
sincerely yours Jan Goossens.

For over 100 years, aspirin has been used as a pain reliever. Since the 1970s, aspirin has also been used to prevent and manage heart disease.

How does aspirin benefit the heart?

Aspirin benefits the heart in several ways:
Decreases pain. Aspirin fights pain and inflammation associated with heart disease by blocking the action of an enzyme called cyclooxygenase. When this enzyme is blocked, the body is less able to produce a substance called prostaglandin, which is a chemical that signals an injury and triggers pain.
Inhibits blood clots. Some of the prostaglandins in the blood trigger a series of events that cause blood platelets to clump together and form blood clots. Thus, when aspirin inhibits prostaglandins, it inhibits the formation of blood clots as well. Blood clots are harmful because they can clog the arteries leading to the heart, increasing the risk of heart attack and stroke. Aspirin has been shown to reduce the risk of heart attack and reduce the short-term risk of death among people suffering from heart attacks.
Reduces the risk of polyp recurrence in people with a history of colon polyps.
Reduces the risk of death. Research has shown that regular aspirin use is associated with a marked reduction from death due to all causes, particularly among the elderly, people with heart disease and people who are physically unfit.

Who benefits from aspirin therapy?

People with coronary artery disease or atherosclerosis anywhere in the body (such as the brain or legs)
People who have had a heart attack*
People who have undergone bypass surgery to treat heart disease, or have angina (chest pain)
People with any risk factor for heart disease or a heart attack
Men over the age of 40 and women over the age of 50
Postmenopausal women
People who have had a transient ischemic attack (TIA) or ischemic stroke
* If you are experiencing symptoms of a heart attack, call 9-1-1. If you do not have a history of aspirin allergy, emergency personnel may advise that you chew one aspirin slowly. It's especially effective if taken within 30 minutes of the onset of symptoms.

What are the risks and benefits of aspirin therapy?

Benefits
Aspirin can significantly reduce heart damage during a heart attack and can prevent the occurrence of future heart problems.
Aspirin can reduce the risk of stroke.
Risks
Aspirin can increase the risk of stomach ulcers and abdominal bleeding.
During stroke, aspirin can increase the risk of bleeding into the brain.

How much aspirin should I take?

Always speak to your doctor about the benefits and risks of aspirin therapy before beginning a regular regimen.Recent research indicates an appropriate dose of aspirin is between 80 and 160 mg per day. This is actually half of the standard 325-milligram aspirin commonly prescribed. Many studies show the lower dose works just as well as the higher dose, while reducing the risk of internal bleeding. A baby aspirin contains 81 mg. There are similarly lower-dose adult aspirin varieties available. But check with your doctor first to find out what dose is right for you.

How should I take aspirin?

It's helpful to follow these guidelines:
Aspirin should not be taken on an empty stomach. Take aspirin with a full glass of water with meals or after meals to prevent stomach upset.
Do not break, crush, or chew extended-release tablets or capsules--swallow them whole. Chewable aspirin tablets may be chewed, crushed or dissolved in a liquid.
Before this medication is prescribed, tell your doctor if you are allergic to aspirin, ibuprofen, or naproxen.
Do not drink alcoholic beverages while taking this medication. Taking aspirin with alcohol increases the chance of stomach bleeding.
While taking aspirin, ask your doctor what other medicines you may take for pain relief or minor colds. Read the labels of all pain relievers and cold products to make sure they are aspirin-free. Other medicines containing aspirin or non-steroidal anti-inflammatory drugs may cause bleeding problems when taken in combination with your regular aspirin therapy.Before any surgical or dental procedure or emergency treatment, tell the doctor or dentist that you are taking aspirin. You might need to stop taking this medicine for five to seven days before dental work or surgery. However, do not stop taking this medicine without first consulting with your doctor.

Are there any side effects?

Yes. Some common side effects include nausea, upset stomach, nervousness, and trouble sleeping. Call your doctor if any of these symptoms become severe or do not go away. If you have any of the following side effects, contact your doctor right away:
Severe stomach pain or heartburn.
Severe nausea or vomiting
Any signs of unusual bleeding, such as blood in the urine or stools, nosebleeds, any unusual bruising, heavy bleeding from cuts, black tarry stools, coughing up of blood, unusually heavy menstrual bleeding or unexpected vaginal bleeding, vomit that looks like coffee grounds.
Facial swelling (usually indicates an allergy).
Asthma attack (also indicates an allergy).
Ringing in the ears.
Severe headache pain
Confusion

Who should not take aspirin?

Children under the age of 18 who are recovering from a viral infection such as the flu or chicken pox.
Pregnant women (unless otherwise directed by your doctor).
People who are about to undergo surgery.
Heavy drinkers.
People with ulcers or any bleeding problem.
People taking regular doses of other pain medications such as Motrin.
People who are allergic to aspirin.

For a complete guide to heart disease for your patient visit WebMD Health
Reviewed by the doctors at The Cleveland Clinic Heart Center.
Edited by Cynthia Haines, MD, WebMD, October 2005
SOURCES: The Cleveland Clinic Heart Center. The American Heart Association. WebMD Medical News, "Baby Aspirin Safer for Preventing a Heart Attack." The Centers for Disease Control
Copyright © 2006, The Cleveland Clinic.

Warfarin, which goes by the brand name Coumadin, is an anticoagulant medication. This means that it helps prevent clots from forming in the blood. You have been prescribed warfarin because your body may be making blood clots or you may have a medical condition known to promote unwanted blood clots. It is often prescribed for patients with atrial fibrillation (an irregular heart rhythm), pulmonary embolism, and after artificial heart valve surgery or orthopedic procedures.

Blood clots can move to other parts of your body and cause serious medical problems, such as a heart attack. Warfarinwill not dissolve a blood clot; however, over time, the blood clot may dissolve on its own. Warfarin may also prevent other clots from forming or prevent clots from becoming larger. Warfarin will not dissolve a blood clot, but it may prevent other clots from forming and keep existing clots from getting larger. There are other blood thinners that you may be given in the hospital or even at home for a short amount of time: Heparin, Lovenox, or Fragmin. These drugs are administered either by vein (intravenous) or just under the skin into the subcutaneous fat.

Blood testing

In order for your health care provider to determine the correct dose of warfarin, it will be necessary for you to have blood tests. The tests are performed in a laboratory, usually once a week to once a month, as directed by your doctor. The prothrombin time (PT or protime) test is used to calculate your International Normalized Ration (INR). Your INR will help your health care provider determine how fast your blood is clotting and whether your medication dose needs to be changed. Illness, diet, medication changes and physical activities may affect your INR. Tell your health care provider about changes in your health, medications (prescription and over-the-counter) or lifestyle so appropriate dosage adjustments can be made in your warfarin therapy.

What does warfarin look like?

Coumadin brand tablets are round and scored, which means they can be broken in half. Each tablet color represents a different strength. The strength of the tablet is measured in milligrams (mg) as follows:
1 mg (pink)
2 mg (lavender)
2.5 mg (green)
3 mg (tan)
4 mg (blue)
5 mg (peach)
6 mg (teal or blue-green)
7.5 mg (yellow)
10 mg (white)
Other brands of warfarin should have the same colors and strengths as the Coumadin brand tablets. However, other brands of warfarin tablets may have a different shape or appearance. For example, they may be oval or square.

How should I take warfarin?

Take your warfarin dose as instructed once a day. Try to take it at the same time every day. A good time to take your warfarin is early in the evening (such as between 5 and 6 p.m.). Warfarin can be taken with or without food. Do not take a double dose to make up for a missed dose. Also, never change your dose without first discussing the change with your doctor.

How should I store warfarin?

As with any medication, store your warfarin at room temperature, away from extreme cold, heat, light or moisture. Bathroom cabinets are usually NOT suitable for storing medications because of the dampness. All medications, including warfarin, should always be kept out of the reach of children and pets.

What precautions should I take?

It is important that you follow these precautions when taking warfarin to reduce the risk of side effects and improve the effectiveness of your medication.

Medications and Dietary Supplements

Many medications and dietary supplements can affect the way warfarin works. These may include:
Prescription medications
Nonprescription medications such as aspirin, nonsteroidal anti-inflammatory drugs or NSAIDs (some examples are ibuprofen, naproxen or ketoprofen), cough or cold remedies and medications for pain or discomfort
Herbal products, natural remedies or nutritional supplements
Products containing vitamin K
Before taking any new medication, including over-the-counter medications, herbal products, vitamins, nutrition supplements, or medication prescribed by another doctor or dentist, check with the doctor who monitors your warfarin medication. Your warfarin doctor may need to adjust your warfarin dosage or may recommend another medication less likely to interfere with warfarin.

Diet
Eat a sensible, well-balanced diet.
Talk with your doctor if you are planning any major dietary changes such as following a weight-reducing diet or adding nutritional supplements.
Large amounts of food high in vitamin K (such as broccoli, spinach and turnip greens) may change the way warfarin works. Try to keep the amount of these foods in your diet about the same from week to week.
It is best to avoid alcohol while taking warfarin. Alcohol interferes with the effectiveness of warfarin.
Some herbal teas may cause the INR to become high or low.
Activities
Check with your doctor before starting any exercise or sports program. Your doctor may want you to avoid any activity or sport that may result in a serious fall or other injury.
Use a soft toothbrush. Brush and floss gently to prevent bleeding from the gums.
Be careful when using razors. We suggest using an electric razor or hair-removing cream to minimize the chance of cuts. If you do cut yourself, follow the guidelines below.
Illness and Emergencies
If you cut yourself and the cut is small, apply constant pressure over the cut until the bleeding stops (this may take up to 10 minutes). If the bleeding doesn't stop, continue to apply pressure and go to the nearest emergency room.
If the cut is large, apply constant pressure and get help immediately either by phone or by going to the nearest emergency room.
Call your doctor if you have any symptoms of illness such as vomiting, diarrhea, infection or fever. Illness can change the way warfarin works.
It is recommended that you wear or carry identification that states you are taking warfarin.
Avoid situations where you may get injured at home or at work.
Pregnancy

If you are a woman who is taking warfarin and is planning to become pregnant, talk with your doctor about the possible risks and ways to reduce those risks. Tell your doctor right away if you become pregnant.

Surgery and Dental Work
Before any treatment is provided, tell all your doctors and dentists that you are taking warfarin. Before having a surgical or dental procedure, you may need to have a blood test, and you may need to stop taking warfarin for a few days. Do not stop taking warfarin without first consulting with the doctor who monitors your warfarin/INR.

Travel
Check with your doctor before you travel. Before you go on vacation, you may need to have a blood test and your warfarin dose may need to be adjusted. While traveling, carry your medications with you at all times. Do not put medications in checked baggage, and do not leave your medications in the car.

When should I call my doctor?

Call your doctor if you notice any of the following signs of bleeding or illness that can affect the way your warfarin works:
Feeling more weak or tired than usual or looking pale (symptoms of anemia).
Bleeding from cuts that won't stop after applying pressure for 10 minutes.
Coughing or vomiting blood (which may look like coffee grounds).
Bleeding from the nose, gums or ears.
Unusual color of the urine or stool (including dark brown urine, or red or black, tarry stools).
Unusual bruising (black and blue marks on your skin) for unknown reasons.
Menstrual bleeding that is heavier or lasts longer than normal.
A fever or illness that gets worse.
A serious fall or a blow to the head.
Unusual pain or swelling.
Unusual headache.
Dizziness.
Difficulty breathing.
If you notice any of these symptoms, your doctor may want to do a blood test, stop the warfarin or prescribe medication to stop the bleeding. Also contact your doctor if you have any other symptoms that cause concern.

Antiarrhythmia drugs are used to treat abnormal heart rhythms resulting from irregular electrical activity of the heart. There are many different types of antiarrhythmic drugs. Examples include:

Tambocor (flecainide)
Procanbid (procainamide)
Cordarone (amiodarone)
Betapace (sotalol)

In addition, there are other types of heart medications that can be used to treat arrhythmias, including:

Beta-blockers such as metoprol or Toprol XL, which reduce the heart's workload and heart rate.
Calcium channel blockers such as Calan, which reduce the workload of the heart by blocking the uptake of calcium into the cells (this helps the heart contract harder).

There are also a variety of medications used by the doctor in an emergency situation to control or convert an abnormal heart rhythm.

Why do I need to take an antiarrhythmic?

Your doctor had determined that you have an abnormal heart rhythm that would be best treated with medications alone or in addition to a procedure such as ICD placement. Because these medications only control arrhythmias not cure them, you may have to take them for life.

Can I take other medications while taking antiarrhythmics?

If you are taking an antiarrhythmic, talk to your doctor before taking any other drugs (prescription or over-the-counter), herbal remedies, or supplements.

Are there side effects associated with antiarrhythmics?

Yes. Notify your doctor immediately if you experience any of the following side effects:
Worsening arrhythmias
Allergic reaction
Chest pain
Fainting
Swelling of the feet or legs
Blurred vision
Shortness of breath
Abnormally fast heartbeat
Abnormally slow heartbeat
Dizziness or lightheadedness
Bitter or metallic taste or change in taste
Loss of appetite
Cough
Increased sensitivity to sunlight
Diarrhea or constipation
When first taking antiarrhythmics, avoid operating heavy machinery (for example, driving) until you know how the medication will affect you.

For a complete guide to heart disease for your patient visit WebMD Health
Reviewed by the doctors at The Cleveland Clinic Heart Center.
Edited by Cynthia Haines, MD, WebMD, October 2005.
Copyright © 2006, The Cleveland Clinic.

Ablation is used to treat abnormal heart rhythms. It can be performed both surgically and non-surgically. The type of ablation performed depends upon the type of arrhythmia and the presence of other heart disease.

Non-surgical ablation , used for many types of arrhythmias, is performed in a special lab called the electrophysiology (EP) laboratory. During this non-surgical procedure a catheter is inserted into a specific area of the heart. A special machine directs energy through the catheter to small areas of the heart muscle that causes the abnormal heart rhythm. This energy "disconnects" the pathway of the abnormal rhythm. It can also be used to disconnect the electrical pathway between the upper chambers (atria) and the lower chambers (ventricles) of the heart.

Surgical ablation procedures used for treating atrial fibrillation can be "minimally invasive" or traditional "open" surgery and may be combined with other surgical therapies such as bypass surgery, valve repair, or valve replacement. Surgical ablation procedures include:

The Maze procedure. During this traditional open-heart surgical procedure, the surgeon makes small cuts in the heart to interrupt the conduction of abnormal impulses and to direct normal sinus impulses to travel to the atrioventricular node (AV node) as they normally should. When the heart heals, scar tissue forms and the abnormal electrical impulses are blocked from traveling through the heart.
Minimally invasive surgical ablation. Unlike traditional heart surgery, there is no large chest wall incision and the heart is not stopped. These techniques utilize smaller incisions and endoscopes (small lighted instruments that contain a camera).
The modified Maze procedure. The surgeon uses a special catheter to deliver energy that creates controlled lesions on the heart and ultimately scar tissue. The scar tissue blocks the abnormal electrical impulses from being conducted through the heart and promotes the normal conduction of impulses through the proper pathway. One of four energy sources may be used to create the scars: radiofrequency, microwave, laser or cryothermy (cold temperatures). The modified Maze procedure involves a single incision in the left atrium.

Why do I need ablation therapy?

Doctors recommend ablation therapy to treat:
Atrial fibrillation and atrial flutter
AV Nodal reentry tachycardia (AVNRT)
Accessory pathways
Ventricular tachycardia
In addition to re-establishing a normal heart rhythm in people with certain arrhythmias, ablation therapy can help control the heart rate in people with rapid arrhythmias, and reduce the risk of blood clots and strokes.

How should I prepare for ablation?

The procedure preparation may vary depending on whether you are having surgical or nonsurgical ablation. These are general guidelines; your doctor or nurse will give you specific instructions.To prepare for ablation, there are several steps you should take. Among them:
Ask your doctor which medications you should stop and when to stop them. Your doctor may ask you to stop certain medications (such as those that control your heart rate or aspirin products) one to five days before your procedure. If you are diabetic, ask your doctor how you should adjust your diabetic medications.
Do not eat or drink anything after midnight the evening before the procedure. If you must take medications, drink only with a small sip of water.
When you come to the hospital, wear comfortable clothes. You will change into a hospital gown for the procedure. Leave all jewelry and valuables at home.

What can I expect during nonsurgical catheter ablation?

During nonsurgical catheter ablation, the following things will occur:
The procedure will take place in a special room called the EP (electrophysiology) lab. Before the test begins, a nurse will help you get ready. You will lie on a bed and the nurse will start an IV (intravenous) line. This is so the doctors and nurses can give you medications and fluids through your vein during the procedure. You will be given a medication through your IV to help you relax. Depending on the type of ablation you have, you may or may not be awake during your procedure. If you are awake, you will be asked to report any symptoms, answer questions or follow instructions given to you by your doctor. If you are uncomfortable or need anything, please let your nurse know.
The nurse will connect you to several monitors.
After you become drowsy, your groin area will be shaved and your neck, upper chest, arm and groin will be cleansed with an antiseptic solution. Sterile drapes will be placed to cover you from your neck to your feet.
The doctor will numb the insertion site by injecting a medication. You will feel an initial burning sensation, and then it will become numb. Then, several catheters (special wires that can pace the heart and record its electrical activity) will be inserted through a small incision into a large blood vessel(s) and/or artery (in your groin, neck or arm) and advanced to your heart. If you are awake, it is important that you remain still and resist the temptation to raise your head to see what the doctor is doing while the catheters are being placed.
After the catheters are in place, the doctor will look at the monitor to assess your heart's conduction system.
Then, the doctor will perform the ablation procedure.
During traditional ablation, the doctor will use a pacemaker-like device to send electrical impulses to the heart to increase your heart rate. You may feel your heart beating faster or stronger when the pacemaker delivers the impulses. If your arrhythmia occurs during the procedure, the nurse will ask you how you are feeling. It is very important to tell the doctor or nurse the symptoms you feel. The doctor will then move the catheters around your heart to see which area(s) your arrhythmia is coming from. Once the doctor finds the area of your arrhythmia, energy is applied. You may feel some discomfort or a burning sensation in your chest, but you must stay quiet, keep very still and avoid taking deep breaths. If you are feeling pain, ask your doctor or nurse to give you more medication.
During pulmonary vein ablation (for atrial fibrillation), the doctor delivers energy through a catheter to the area of the atria that connects to the pulmonary vein (ostia), producing a circular scar. The scar will then block any impulses firing from within the pulmonary veins, thus preventing atrial fibrillation from occurring. The process is repeated to all four pulmonary veins. In some cases, ablation may also be performed to other parts of the heart such as the subclavian veins and coronary sinus. The catheter is a special "cool tip" catheter. Fluid circulates through the catheter to help control the intensity of the temperature.
Once the ablation is complete, the electrophysiologist will use monitoring devices to observe the electrical signals in the heart to ensure that the abnormal heart rhythm was corrected.
The procedure usually takes about four to eight hours, but may take longer.

What happens after nonsurgical catheter ablation?

After your non-surgical catheter ablation:
The doctor will remove the catheters from your groin and apply pressure to the site to prevent bleeding. You will be on bed rest for one to six hours. Keep your legs as still as possible during this time to prevent bleeding.
After your procedure, you will be admitted to the hospital. During your recovery, a special monitor, called telemetry, will be used to follow your heart rate and rhythm. Telemetry consists of a small box connected by wires to your chest with sticky electrode patches. The box causes your heart rhythm to be displayed on several monitors on the nursing unit. The nurses will be able to observe your heart rate and rhythm. In most cases, you will be able to go home the next day after the catheter ablation procedure but in some cases you may be able to go home the same day of the procedure.
You and your family will receive the results of the procedure after the procedure. Your doctor will also discuss when you can resume activities and how often you will need to visit your doctor.
Temporarily, many individuals experience heart palpitations on and off for a few weeks after the procedure. Sometimes you may also feel as if your abnormal heart rhythm is returning, but then it stops. These sensations are normal and you should not be alarmed. When these symptoms occur during your recovery, it is important to document them by calling your doctor or nurse as directed. Also call your doctor or nurse if you feel as if your abnormal heart rhythm has recurred.
You may be required to take medications for a certain period of time after your procedure.
If you have any other questions, please ask your doctor or nurse. Ask your health care provider how often you will need to go for follow-up appointments.

How should I care for the wound site?

You will have a small dressing on your wound. It may be removed the next day. Keep the area clean and dry.Call your doctor if you notice any redness, swelling or drainage at the incision site.

What can I expect during surgical ablation?

During the ablation, you can expect the following to take place:
General anesthesia (the patient is asleep) or local anesthesia with sedation (the patient is awake but relaxed and pain-free) may be used, depending on the individual case.
During minimally invasive surgery, the surgeon views the outer surface of the heart using an endoscope. Specialized instruments are used to locate the areas needing ablation and to create the lines of conduction block. Unlike traditional heart surgery, there is no large chest wall incision, and the heart is not stopped.
The Maze procedure requires an incision along the sternum (breast bone). The incision may be traditional (about 6 to 8 inches long), or in some cases, minimally invasive (about 3 to 5 inches long). The heart is stopped during this procedure. A heart-lung machine oxygenates the blood and circulates it throughout the body during surgery.
The modified Maze procedure involves using one of four energy sources to create the lines of conduction block (radiofrequency, microwave, laser or cryothermy). The energy probe of choice is inserted, and under direct vision, used to create the lesion lines. As in the classic Maze procedure, these lesions create lines of conduction block that interrupt the abnormal impulses and restore the normal sinus rhythm. This procedure is used primarily in patients who have atrial fibrillation and other indications for surgery.


What happens after surgical ablation?

If your ablation surgery was combined with valve, bypass or another surgical procedure, your post-procedure care may be different.After surgical ablation:
The patient is usually transferred to an intensive care unit (ICU) for close monitoring for about one to two days after the surgery. When the patient's condition is stable, he or she is transferred to a regular unit (called a telemetry unit).
The monitoring during recovery includes heart, blood pressure, and blood oxygen monitoring and frequent checks of vital signs and other parameters, such as heart sounds.
Most patients stay in the hospital about 5 to 7 days after the procedure, depending on their rate of recovery. Patients who had minimally invasive surgery may be able to go home 2 to 3 days after surgery. Your health care team will follow your progress and help you recover as quickly as possible.
Full recovery from surgery takes about 6 to 8 weeks. Most patients are able to drive in about 3 to 8 weeks after surgery. Your health care team will provide specific guidelines for your recovery and return to work, including specific instructions on activity, incision care, and general health after the surgery.
Many patients may experience skipped heartbeats or short episodes of atrial fibrilliation during the first three months after the procedure. This is common due to inflammation (swelling) of the heart tissue and is treated with medications. After the heart has healed, these abnormal heartbeats should subside.
A small number of patients require a pacemaker after surgery due to an underlying abnormal rhythm which previously was undetected.
Medications after surgery may include:
Anticoagulants (blood thinners), such as Coumadin, to prevent blood clots.
Antiarrhythmic medication to control abnormal heartbeats.
Diuretics to reduce fluid retention.
Your doctor will monitor your recovery and determine when or if these medications can be discontinued.

For a complete guide to heart disease for your patient visit WebMD Health

Reviewed by the doctors at The Cleveland Clinic Heart and Vascular Institute (2006).

Edited by Cynthia Haines, MD, March 2006, WebMD.

SOURCES: American Heart Associaton. Heart Rhythm Association.


Copyright © 2006, The Cleveland Clinic.

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More Printable Patient FAQ's
Abnormal Heart Rhythm with


An arrhythmia (also called dysrhythmia) is an irregular heartbeat. Heart rates can also be irregular. A normal heart rate is 50 to 100 beats per minute. Arrhythmias and abnormal heart rates don't necessarily occur together. Arrhythmias can occur with a normal heart rate, or with heart rates that are slow (called bradyarrhythmias -- less than 60 beats per minute). Arrhythmias can also occur with rapid heart rates (called tachyarrhythmias -- faster than 100 beats per minute).



What causes an arrhythmia?


Arrhythmias may be caused by many different factors, including:
Coronary artery disease.
Electrolyte imbalances in your blood (such as sodium or potassium).
Changes in your heart muscle.
Injury from a heart attack.
Healing process after heart surgery.
Irregular heart rhythms can also occur in "normal, healthy" hearts.



What are the types of arrhythmias?


The types of arrhythmias include:
Premature atrial contractions. These are early extra beats that originate in the atria (upper chambers of the heart). They are harmless and do not require treatment.
Premature ventricular contractions (PVCs). These are among the most common arrhythmias and occur in people with and without heart disease. This is the skipped heartbeat we all occasionally experience. In some people, it can be related to stress, too much caffeine or nicotine, or too much exercise. But sometimes, PVCs can be caused by heart disease or electrolyte imbalance. People who have a lot of PVCs, and/or symptoms associated with them, should be evaluated by a heart doctor. However, in most people, PVCs are usually harmless and rarely need treatment.
Atrial fibrillation. AF is a very common irregular heart rhythm that causes the atria, the upper chambers of the heart to contract abnormally.
Atrial flutter. This is an arrhythmia caused by one or more rapid circuits in the atrium. Atrial flutter is usually more organized and regular than atrial fibrillation. This arrhythmia occurs most often in people with heart disease, and in the first week after heart surgery. It often converts to atrial fibrillation.
Paroxysmal supraventricular tachycardia (PSVT). A rapid heart rate, usually with a regular rhythm, originating from above the ventricles. PSVT begins and ends suddenly. There are two main types: accessory path tachycardias and AV nodal reentrant tachycardias (see below).
Accessory pathway tachycardias. A rapid heart rate due to an extra abnormal pathway or connection between the atria and the ventricles. The impulses travel through the extra pathways as well as through the usual route. This allows the impulses to travel around the heart very quickly, causing the heart to beat unusually fast.
AV nodal reentrant tachycardia. A rapid heart rate due to more than one pathway through the AV node. It can cause heart palpitations, fainting or heart failure. In many cases, it can be terminated using a simple maneuver performed by a trained medical professional, medications or a pacemaker.
Ventricular tachycardia (V-tach). A rapid heart rhythm originating from the lower chambers (or ventricles) of the heart. The rapid rate prevents the heart from filling adequately with blood; therefore, less blood is able to pump through the body. This can be a serious arrhythmia, especially in people with heart disease, and may be associated with more symptoms. A heart doctor should evaluate this arrhythmia.
Ventricular fibrillation. An erratic, disorganized firing of impulses from the ventricles. The ventricles quiver and are unable to contract or pump blood to the body. This is a medical emergency that must be treated with cardiopulmonary resuscitation (CPR) and defibrillation as soon as possible.
Long QT syndrome. The QT interval is the area on the electrocardiogram (ECG) that represents the time it takes for the heart muscle to contract and then recover, or for the electrical impulse to fire impulses and then recharge. When the QT interval is longer than normal, it increases the risk for "torsade de pointes," a life-threatening form of ventricular tachycardia. Long QT syndrome is an inherited condition that can cause sudden death in young people. It can be treated with antiarrhythmic drugs, pacemaker, electrical cardioversion, defibrillation, implanted cardioverter/defibrillator or ablation therapy.
Bradyarrhythmias. These are slow heart rhythms, which may arise from disease in the heart's electrical conduction system. Examples include sinus node dysfunction and heart block.
Sinus node dysfunction. A slow heart rhythm due to an abnormal SA (sinus) node. Sinus node dysfunction is treated with a pacemaker.
Heart block. A delay or complete block of the electrical impulse as it travels from the sinus node to the ventricles. The level of the block or delay may occur in the AV node or HIS-Purkinje system. The heart may beat irregularly and, often, more slowly. If serious, heart block is treated with a pacemaker.




What are the symptoms of arrhythmias?


An arrhythmia can be silent and not cause any symptoms. A doctor can detect an irregular heartbeat during a physical exam by taking your pulse or through an electrocardiogram (ECG). When symptoms occur, they may include:
Palpitations (a feeling of skipped heart beats, fluttering or "flip-flops," or feeling that your heart is "running away").
Pounding in your chest.
Dizziness or feeling light-headed.
Fainting.
Shortness of breath.
Chest discomfort.
Weakness or fatigue (feeling very tired).




How are arrhythmias diagnosed?


Tests used to diagnose an arrhythmia or determine its cause include:
Electrocardiogram
Holter monitor
Event monitor
Stress test
Echocardiogram
Cardiac catheterization
Electrophysiology study (EPS)
Head-up tilt table test




How are arrhythmias treated?


Treatment depends on the type and seriousness of your arrhythmia. Some people with arrhythmias require no treatment. For others, treatments can include medication, making lifestyle changes and undergoing surgical procedures.



What medications are used to treat arrhythmias?


A variety of drugs are available to treat arrhythmias. These include:
Antiarrhythmic drugs. These drugs control heart-rate, and include beta-blockers.
Anticoagulant or antiplatelet therapy. These drugs reduce the risk of blood clots and include warfarin (a "blood thinner") or aspirin.
Because everyone is different, it may take trials of several medications and doses to find the one that works best for you.



What lifestyle changes should be made?


If you notice that your irregular heart rhythm occurs more often with certain activities, you should avoid them.
If you smoke, stop.
Limit your intake of alcohol.
Limit or stop using caffeine. Some people are sensitive to caffeine and may notice more symptoms when using caffeine products (such as tea, coffee, colas and some over-the-counter medications).
Stay away from stimulants used in cough and cold medications. Some such medications contain ingredients that promote irregular heart rhythms. Read the label and ask your doctor or pharmacist what medication would be best for you.




What is electrical cardioversion?


If drugs are not able to control a persistent irregular heart rhythm (such as atrial fibrillation), cardioversion may be required. After administration of a short-acting anesthesia, an electrical shock is delivered to your chest wall that synchronizes the heart and allows the normal rhythm to restart.



What is a pacemaker?


A pacemaker is a device that sends small electrical impulses to the heart muscle to maintain a suitable heart rate. Pacemakers primarily prevent the heart from beating too slowly. The pacemaker has a pulse generator (which houses the battery and a tiny computer) and leads (wires) that send impulses from the pulse generator to the heart muscle. Newer pacemakers have many sophisticated features that are designed to help manage arrhythmias and optimize heart-rate-related function as much as possible.



What is an implantable cardioverter-defibrillator (ICD)?


An ICD is a sophisticated device used primarily to treat ventricular tachycardia and ventricular fibrillation, two life-threatening heart rhythms. The ICD constantly monitors the heart rhythm. When it detects a very fast, abnormal heart rhythm, it delivers energy to the heart muscle to cause the heart to beat in a normal rhythm again. There are several ways the ICD can be used to restore normal heart rhythm. They include:
Anti-tachycardia pacing (ATP). When the heart beats too fast, a series of small electrical impulses may be delivered to the heart muscle to restore a normal heart rate and rhythm.
Cardioversion. A low energy shock may be delivered at the same time as the heart beats to restore normal heart rhythm.
Defibrillation. When the heart is beating dangerously fast or irregularly, a higher energy shock may be delivered to the heart muscle to restore a normal rhythm.
Anti-bradycardia pacing. Many ICDs provide back-up pacing to prevent too slow of a heart rhythm.




What is catheter ablation?


During an ablation, high-frequency electrical energy is delivered through a catheter to a small area of tissue inside the heart that causes the abnormal heart rhythm. This energy "disconnects" the pathway of the abnormal rhythm. Ablation is used to treat most PSVTs, atrial flutter, atrial fibrillation and some atrial and ventricular tachycardias. Ablation may be combined with other procedures to achieve optimal treatment.



What is heart surgery?


Heart surgery may be needed to correct heart disease that may be causing the arrhythmia. The Maze procedure is a type of surgery used to correct atrial fibrillation. During this procedure, a series (or "maze") of incisions are made in the right and left atria to confine the electrical impulses to defined pathways. Some people may require a pacemaker after this procedure.






For a complete guide to heart disease for your patient visit WebMD Health


Reviewed by the doctors at The Cleveland Clinic Heart Center.


Edited by Tracy Shuman, MD, October 2005.


Copyright © 2006, The Cleveland Clinic.





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