Heart attack: Use of amino acid supplement

Use of amino acid supplement following a heart attack provides no benefit, may be harmful

Use of the amino acid supplement L-arginine following a heart attack does not improve certain cardiac functions and measurements and may be associated with an increased risk of death, according to a study in the January 4 issue of JAMA.

L-arginine is a widely available dietary supplement and is publicized as having benefits for patients with hypertension, angina, heart failure and sexual dysfunction, according to background information in the article. Prior studies suggest that L-arginine has the potential to reduce vascular (blood vessel) stiffness.

Steven P. Schulman, M.D., of Johns Hopkins Medical Institutions, Baltimore, and colleagues conducted the Vascular Interaction with Age in Myocardial Infarction (VINTAGE MI) clinical trial to test whether administering L-arginine to patients following a first ST-segment elevation myocardial infarction (STEMI; a certain pattern on an electrocardiogram following a heart attack) over a 6-month period would decrease vascular stiffness and improve ejection fraction (a measure of how much blood the left ventricle of the heart pumps out with each contraction).

The randomized, double-blind, placebo-controlled trial included 153 STEMI patients; 77 were 60 years or older. Participants were enrolled from February 2002 to June 2004. Patients were randomly assigned to receive L-arginine (goal dose of 3 g three times a day) or matching placebo for six months.

The researchers found: "The VINTAGE MI study demonstrated that 6 months of L-arginine added to standard postinfarct medications did not reduce noninvasive measures of vascular stiffness, improve ejection fraction, or improve clinical outcomes. To the contrary, we noted a possible increased risk of death in older patients after infarction while taking L-arginine compared with those taking a placebo, leading to the early termination of the study. These findings have broad public health implications given the increasing availability and use of L-arginine in patients with and without established cardiovascular diseases."

Death occurred in 6 patients (8.6 percent) in the L-arginine group died during the 6-month study period vs. none in the placebo group.

"In conclusion, L-arginine therapy should not be given to patients following a myocardial infarction. It neither alters noninvasive measures of vascular stiffness nor improves left ventricular function. L-arginine therapy in older patients with diffuse atherosclerosis may worsen clinical outcomes," the authors write.

JAMA and Archives Journals

Transcendental Meditation and heart disease

Transcendental Meditation reduce risk factors for heart disease

The Transcendental Meditation (TM) program has been shown to significantly reduce risk factors for heart disease, including hypertension, high cholesterol, anxiety, hostility, and smoking.

In a randomized study published in the journal of the American Heart Association, individuals with mild hypertension experienced significant reductions in systolic and diastolic blood pressure over a 3-month period after learning the TM technique.

These reductions in blood pressure were substantially greater than those experienced by individuals in two control groups-a "usual-care" group that received training in improved diet and exercise and a group practicing muscle relaxation.

The TM technique produced reductions in blood pressure equivalent to those produced by anti-hypertensive drugs but without their adverse side effects.

A related study of health insurance data over a five-year period found that individuals regularly practicing the TM technique required 87% less hospitalization for heart disease than the norm.

Hypertension, 26: 820-827, 1995.
Psychosomatic Medicine 49: 493-507, 1987.

Stroke ischaemic

Stroke caused by blood clots or other obstructions - ischaemic stroke - accounts for 80% of all cases.

A blockage is called a cerebral thrombus or cerebral embolism and can be caused by atherosclerosis - hardening of the arteries.
In both types of stroke - those caused by blood clots and those caused by burst blood vessels - blood supply to the brain is interrupted, depriving the cells of oxygen and other nutrients. The cells are then damaged or die.
Mini-strokes, or transient ischaemic attacks (TIAs), may be a warning sign of an imminent full-blown stroke.

Embolic
In an embolic stroke, a blood clot - or embolus - forms somewhere in the body, usually the heart, and travels through the bloodstream to the brain.
Once in the brain, the clot eventually travels to a blood vessel small enough to block its passage. The clot lodges there, blocking the blood vessel and causing a stroke.

Thrombotic
In the other form of blood-clot stroke, blood flow is impaired because of a blockage to one or more of the arteries supplying blood to the brain - a thrombus.
The process leading to this blockage is known as thrombosis and strokes caused in this way are called thrombotic strokes.
In atrial fibrillation, where the two upper chambers of the heart - the atria - quiver instead of beating properly, blood is not properly pumped out of the heart. As a result it may form clots and if the clot becomes lodged in an artery in the brain, a stroke may result.
The American Heart Association says arond 15% of strokes are caused in this way.
Blood clot strokes can also happen as the result of unhealthy blood vessels clogged with a build up of fatty deposits and cholesterol.
The body regards these build ups as multiple, tiny and repeated injuries to the blood vessel wall and reacts as it would to bleeding from a wound, by forming clots.

The symptoms of stroke:
1. Sudden numbness or weakness of the face, arm or leg, particularly if it is on one side of the body
2. Sudden confusion, trouble speaking or understanding. Sudden difficulty with walking, dizziness, loss of balance or co-ordination
3. Sudden trouble seeing in one or both eyes
4. Sudden severe headache with no known cause

Anyone identifying themselves or friends or family as having a stroke should call emergency services, not a GP, as any delay reduces the chance of a full recovery.
The speed of treatment after a stroke is extremely important as the longer the brain cells are deprived of oxygen, the more damage they will suffer.

Treatment
Clot-busting drugs can be used in the first minutes or hours - up to a maximum of three hours - after an ischaemic stroke to dissolve the clot.
After this time aspirin, which is not as powerful, may be given.
Survival rates are better for patients in specialist stroke units, because of the expert nature of staff and early use of rehabilitation, but such units are not always available. Rehabilitation programmes will be given to most stroke patients to help them recover lost mobility and speech.

http://news.bbc.co.uk

10 ways for the health of your heart

10 ways to take control of your heart health
Take action!

1. Exercise. Make exercise a regular part of your life. Each day, enjoy at least 30 minutes of physical activity that raises your heart beat. Recommended activities include brisk walking, gardening, dancing and such sports as tennis and basketball.

2. Drink lots of water - at least six glasses per day.

3. Eat healthfully. Eat plenty of fresh fruit and vegetables as well as a variety of whole grains.

4. Watch your cholesterol. Choose foods containing unsaturated or monosaturated fats. Avoid foods containing saturated fats, trans fats and cholesterol. Eat fewer fried foods. Eat lean meat and fish.

5. Reduce your salt intake. It can help to reduce your blood pressure.

6. Stop smoking. Tobacco smoking is a major risk factor for cardiovascular disease.

7. Maintain a healthy weight. By avoiding obesity and overweight, you’ll reduce your risk of heart disease, stroke and diabetes.

8. Stay on track. If you miss some exercise or eat an unhealthful meal, just get back on track!

9. Monitor your progress. Keep track of your achievements and reward yourself each time you reach a goal.

10. Check up. Ask your healthcare provider to test your blood pressure, cholesterol and glucose levels. Let him or her help you get them where they need to be.

Cardiovascular disease: Eating less salt

Eating less salt can cut cardiovascular disease risk by a quarter and fatal heart disease by a fifth, work shows

The ideal daily intake of salt is no more than six grams and ministers want everyone to achieve this by 2010.
Experts already know that too much salt can raise blood pressure and high blood pressure increases the risk of heart attack and stroke. The British Medical Journal study now gives the evidence behind this link and quantifies how much harm salt can do.

People who significantly cut back on the amount of salt in their diet reduced their chances of developing cardiovascular disease by 25% over the following 10 to 15 years. And their risk of dying from cardiovascular disease went down by 20%.
All of the 3,126 people studied by the US team from Boston had had high-normal blood pressure, or "pre-hypertension". In the trials, participants reduced their salt (sodium) intake by about 25% - 35%, from about 10g to around 7g.
And those who cut back tended to stick to a lower salt diet in the long term, the researchers from Brigham and Women's Hospital found.
Professor Graham MacGregor, a consultant in cardiovascular medicine at London's St George's hospital and chairman of the Consensus Action Group on Salt, said: "This is a very important study. "It shows that if people reduce their salt intake it will reduce the number of people suffering from heart attacks, strokes and heart failure. We did not have that type of evidence before.

"And we are only talking about quite small reductions in salt intake to have a big effect on risk."
Three-quarters of the salt we eat is already in the food we buy. The average daily consumption in the UK is 9g.
Professor MacGregor said the 6g target was achievable for most people if they were careful about the food they chose to eat. He said the onus was on food manufacturers to limit the amount of salt in products.
Sodium is usually listed in the nutritional information on food labels, and multiplying this value by 2.5 will give the salt content.
The Food Standards Agency said it would continue its work in encouraging industry to offer consumers healthier choices.
Ellen Mason, cardiac nurse at the British Heart Foundation, advised: "By simply checking the labels and switching to a lower salt option, you'll be doing your heart a favour."
The Salt Manufacturers Association said the evidence did not prove that salt reduction would have any significant health benefits for the majority of people. It conceded that individuals with high blood pressure might be advised to restrict their intake.

RECOMMENDED SALT LIMITS

1 to 3 years - 2 g salt a day (0.8g sodium)
4 to 6 years - 3g salt a day (1.2g sodium)
7 to 10 years - 5g salt a day (2g sodium)
11 and over - 6g salt a day (2.5g sodium)

Source: Food Standards Agency

http://news.bbc.co.uk/2/hi/health/6570933.stm

Thalassemia: complex vasculopathy

Endothelial function and arterial stiffness in sickle-thalassemia patients

Athanasios Aessopos (a), Dimitrios Farmakis (a), Maria Tsironi (a), Evanthia Diamanti-Kandarakis (a), Marina Matzourani (a), Christina Fragodimiri (b), Antonia Hatziliami (b) and Markisia Karagiorga (b)

a) First Department of Internal Medicine, University of Athens Medical School, Laiko Hospital, 17 Aghiou Thoma St., Athens 115 27, Greece

b) Thalassemia Unit, Aghia Sophia Children's Hospital, Athens, Greece

Background. Homozygous sickle-cell anemia and β-thalassemia are characterized by impaired endothelial function, while data on arterial stiffness have hitherto been conflicting. We sought to investigate aortic elastic properties and endothelial function in sickle-thalassemia, which combines molecular and clinical features of the above conditions.

Methods and results. Forty-seven sickle-thalassemia patients, younger than 45 years, with preserved left ventricular (LV) function and no history of smoking, systemic or pulmonary hypertension, diabetes mellitus, dyslipidemia or thyroid disease, along with 40 healthy controls were studied. Aortic strain, distensibility and stiffness index were calculated by echocardiographically-obtained aortic root diameters. Brachial artery endothelial function was assessed by ultrasonographic evaluation of flow-mediated dilatation (FMD) and nitrate-mediated dilatation (NMD). Left ventricle was assessed by echocardiography. Patients had an impaired FMD (4.2 ± 2.9% versus 9.2 ± 3.8% in controls, p <> 0.05). Aortic strain and distensibility were lower and aortic stiffness index was higher in patients compared to controls (8.1 ± 4.6 versus 5.8 ± 2.9, p <>

Conclusion. Sickle-thalassemia is characterized by a complex vasculopathy, consisting of endothelial dysfunction and increased arterial stiffness, with a global effect on cardiovascular function.

Keywords: Thalassemia; Sickle-cell disease; Endothelial function; Arterial stiffness

Atherosclerosis Volume 191, Issue 2 , April 2007, Pages 427-432

Plasma lipids and leukocytes: Relationship

Identifying leukocyte gene expression patterns associated with plasma lipid levels in human subjects

Jun Ma, Adam A. Dempsey, Dimitri Stamatiou, K.Wayne Marshall and Choong-Chin Liew
ChondroGene, Inc., 800 Petrolia Road, Unit 15, Toronto, Ont., Canada M3J 3K4

Plasma lipid levels have been known to be risk factors for atherosclerosis for decades, and in recent years it has become accepted that inflammation is a crucial event in the pathogenesis of atherosclerosis.

In this study, we investigated the relationship between plasma lipids and leukocytes by profiling and analyzing leukocyte gene expression in response to plasma lipid levels.

We discovered several interesting patterns of leukocyte gene expression:

1) the expression of a number of immune response- and inflammation-related genes are correlated with plasma lipid levels;

2) genes involved in lipid metabolism and in the electron transport chain were positively correlated with triglycerides and low-density lipoprotein cholesterol (LDL) levels, and negatively correlated with high-density lipoprotein cholesterol (HDL) levels;

3) genes involved in platelet activation were negatively correlated with HDL levels;

4) transcription factors regulating lipogenesis-related genes were correlated with plasma lipid levels;

5) a number of genes correlated with plasma lipid levels were found to be located in the regions of known quantitative trait loci (QTLs) associated with hyperlipemia.

Our findings suggest that leukocytes respond to changing plasma lipid levels by regulating a network of genes, including genes involved in immune response, and lipid and fatty acid metabolism.

Keywords: Atherosclerosis; Coronary artery disease; Leukocyte; Lipid; Gene expression

Atherosclerosis Volume 191, Issue 1 , March 2007, Pages 63-72

Brugada syndrome: Sodium channel mutations

A sodium channel pore mutation causing Brugada syndrome

Arnold E. Pfahnl MD, PhD, Prakash C. Viswanathan PhD, Raul Weiss MD, Lijuan L. Shang PhD, Shamarendra Sanyal MD, PhD, Vladimir Shusterman MD, PhD, Cari Kornblit BS, Barry London MD, PhD and Samuel C. Dudley, Jr. MD, PhD
Cardiovascular Institute, University of Pittsburgh, Pittsburgh, Pennsylvania
Ohio State University, Dorothy M. Davis Heart and Lung Institute, Columbus, Ohio.
Division of Cardiology, Atlanta Veterans Affairs Medical Center and Emory University, Atlanta, Georgia

Brugada and long QT type 3 syndromes are linked to sodium channel mutations and clinically cause arrhythmias that lead to sudden death. We have identified a novel threonine-to-isoleucine missense mutation at position 353 (T353I) adjacent to the pore-lining region of domain I of the cardiac sodium channel (SCN5A) in a family with Brugada syndrome. Both male and female carriers are symptomatic at young ages, have typical Brugada-type electrocardiogram changes, and have relatively normal corrected QT intervals.

Objectives. To characterize the properties of the newly identified cardiac sodium channel (SCN5A) mutation at the cellular level.

Results.Using whole-cell voltage clamp, we found that heterologous expression of SCN5A containing the T353I mutation resulted in 74% ± 6% less peak macroscopic sodium current when compared with wild-type channels. A construct of the T353I mutant channel fused with green fluorescent protein failed to traffic properly to the sarcolemma, with a large proportion of channels sequestered intracellularly. Overnight exposure to 0.1 mM mexiletine, a Na+ channel blocking agent, increased T353I channel trafficking to the membrane to near normal levels, but the mutant channels showed a significant late current that was 1.6% ± 0.2% of peak sodium current at 200 ms, a finding seen with long QT mutations.

Conclusions.The clinical presentation of patients carrying the T353I mutation is that of Brugada syndrome and could be explained by a cardiac Na+ channel trafficking defect. However, when the defect was ameliorated, the mutated channels had biophysical properties consistent with long QT syndrome. The lack of phenotypic changes associated with the long QT syndrome could be explained by a T353I-induced trafficking defect reducing the number of mutant channels with persistent currents present at the sarcolemma.

Keywords: Electrophysiology; Patch-clamp; Sodium channel; Arrhythmias; Brugada syndrome; Long QT

Heart Rhythm Volume 4, Issue 1 , January 2007, Pages 46-53

Women after a first myocardial infarction

Women's health after a first myocardial infarction: a comprehensive perspective on recovery over a 4-year period

Maritha Wickholm (1) and Bengt Fridlund (1,2)

1) School of Social and Health Sciences, Halmstad University, Halmstad, Sweden

2) Department of Nursing, Lund University, P.O. Box 157, 22100, Lund, Sweden

Background: Little attention has so far been focused on follow ups of women's long-term recovery after a myocardial infarction (MI), especially from a comprehensive perspective.

Aim: The aim of this study was to prospectively determine women's self-rated health after a first MI from a comprehensive perspective on recovery over a 4-year period.

Methods: Consecutively chosen women (n=240) who had suffered a first MI were asked to complete a self-rated questionnaire regarding health (including not only biophysical, but also behavioral, emotional, social and working conditions) before being discharged from hospital as well as 1 and 4 years later. The results were analyzed by descriptive and inferential statistics.

Results: Health improvements, especially during the first year, could be observed in the women's behavioral condition regarding their attitude to diet consciousness, exercise, simultaneous capability and smoking behavior as well as in the emotional condition regarding their stressful life events, depressed mood and loss of control. In the social condition, the women considered that the healthcare professionals had improved their support over time as well as treating the women's complaints more seriously. Regarding the working condition, the women felt that they were being controlled at work, especially during the first year after the MI.

Conclusions: Based on a comprehensive perspective on women's recovery after a first MI, a favorable development of the women's health was observed in the behavioral and emotional conditions while deterioration in the social and working conditions was observed over time. Thus, further efforts are needed in the two latter conditions by means of further studies in combination with greater support from healthcare professionals.
Keywords: Coronary heart disease; Comprehensive; Health; Myocardial infarction; Recovery; Risk factors; Women

European Journal of Cardiovascular Nursing Volume 2, Issue 1 , April 2003, Pages 19-25

Chest pain: interactions between nurses and men

Interactions between nurses and men admitted with chest pain

Alan K. White
School of Health and Community Care, Leeds Metropolitan University, UK


This paper reports on an analysis of the interactions that occurred between nurses and men admitted with acute chest pain.

Background and aim: Men admitted to hospital after experiencing chest pain were the focus of a study into men's transition from being well men to ill men. During the study it became apparent that nurses adopted strategies to manage the men through this early acute phase of their illness.

Methods: Data were collected through fieldwork using participant observation on an acute medical admissions ward and an intensive care unit with dedicated coronary care beds. Twenty-five men were included in the study with 10 followed through to discharge. An interpretive grounded theory was used to direct the data collection and analysis.

Results: The men and nurses were seen to be part of a complex interplay, but three main types of interaction were identified: supportive, controlling and educative/informative. Discussions with the men suggests a key factor in the men's experiences was the interactions they had with the nursing and medical staff.

Conclusions: Attention should be given to nurses’ awareness of men's coping strategies when faced with sudden health change and how their actions impact on their recovery.

Keywords: Chest pain; Interaction; Masculinity; Coronary care; Myocardial infarction

European Journal of Cardiovascular Nursing
Volume 2, Issue 1 , April 2003, Pages 47-55

Information needs of myocardial infarction patients

Information needs of myocardial infarction patients

Fiona Timmins and Michael Kaliszer

School of Nursing and Midwifery Studies, Trinity Centre for Health Sciences, Trinity College Dublin, Ireland

Department of Community Health, Trinity College Dublin, Ireland

The main objectives of this study were to assess the perceptions of patients immediately after their first myocardial infarction of their needs in a cardiac education programme and to compare these with their perceptions 6 weeks after the event and also with their nurse educators.

The data were collected by a questionnaire, the cardiac patients’ learning needs inventory which was administered to both patients and nurses. It comprised 37 ‘needs’ items grouped into seven categories, each item to be scored into one of five levels of importance. There were 27 patients interviewed on the first occasion, of whom 18 responded to a postal questionnaire on the second occasion.

A census of three groups of nurses was taken in the study, namely all nurses employed in one coronary care unit and in a cardiac ward at a large Dublin Hospital and all nurses employed as cardiac rehabilitation nurses/officers in Ireland at the time of commencement of the study. Sixty-eight nurses responded, a response rate of 80%.

A key finding was that the responses were highly skewed, with two-thirds in the top grade (‘very important’) and less than 1% in the two lowest grades (‘not important’ and ‘somewhat important’).

The overall response score distribution of the patients differed somewhat from that of the nurses, but this difference was accounted for by mainly three items, all in the ‘physical activity’ category, namely ‘when to resume driving’, ‘when to resume sexual activity’, and ‘when to resume work’, which the nurses scored high and the patients low.

Both patients and nurses gave the highest mean scores to four items, namely ‘what to do when in chest pain’, ‘what are the symptoms of a heart attack’, ‘when to call a doctor’, and ‘what to do to reduce the chance of another heart attack’. The first three of these are in the ‘symptom management’ category.

These findings support previous studies on the topic. The findings also support the need for individualised nurse/patient negotiated cardiac teaching programmes that can be tailored to suit each patient's needs.

Keywords: Information needs; Needs inventory; Myocardial infarction; Educational needs; Learning needs

European Journal of Cardiovascular Nursing

Volume 2, Issue 1 , April 2003, Pages 57-65

Kinetic therapy in patients with cardiogenic shock

Kinetic therapy reduces complications and shortens hospital stay in patients with cardiogenic shock — a retrospective analysis

Gregor Simonis, Kerstin Flemming, Enrico Ziegs, Katrin Haacke, Thomas Rauwolf and Ruth H. Strasser Department of Medicine/Cardiology, Heart Center, Dresden University of Technology, Dresden, Germany

Background. Kinetic therapy (KT) has been shown to reduce complications and to shorten hospital stay in trauma patients. Data in non-surgical patients are inconclusive, and kinetic therapy has not been tested in patients with cardiogenic shock.

Objective. The present analysis compares KT with standard care in patients with cardiogenic shock.

Methods. A retrospective analysis of 133 patients with cardiogenic shock admitted to 1 academic heart center was performed. Patients with standard care (SC, turning every 2 h by the staff) were compared with kinetic therapy (KT, using oscillating air-flotation beds).

Measurements and main results. 68 patients with KT were compared with 65 patients with SC. Length of ventilator therapy was 11 days in KT and 18 days in SC (p = 0.048). The mortality was comparable in both groups. Pneumonia occurred in 14 patients in KT and 39 patients in SC (p < p =" 0.009)">

Conclusion. The use of KT shortens hospital stay and reduces rates of pneumonia and pressure ulcers as compared to SC.

Keywords: Cardiogenic shock; Kinetic therapy; Critical care; Resource use

European Journal of Cardiovascular Nursing

Volume 6, Issue 1 , March 2007, Pages 40-45

Early atherosclerosis: Edaravone

Potent free radical scavenger, edaravone, suppresses oxidative stress-induced endothelial damage and early atherosclerosis

Hang Xi, Masahiro Akishita, Kumiko Nagai, Wei Yu, Hiroshi Hasegawa, Masato Eto, Koichi Kozaki and Kenji Toba

Department of Geriatric Medicine, Kyorin University School of Medicine, Tokyo, Japan;

Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, Japan

Objective. Effects of potent free radical scavenger, edaravone, on oxidative stress-induced endothelial damage and early atherosclerosis were investigated using animal models and cultured cells.

Methods and results. Endothelial apoptosis was induced by 5-min intra-arterial exposure of a rat carotid artery with 0.01 mmol/L H2O2. Edaravone treatment (10 mg/kg i.p.) for 3 days suppressed endothelial apoptosis, as evaluated by chromatin staining of en face specimens at 24 h, by approximately 40%. Similarly, edaravone dose-dependently inhibited H2O2-induce apoptosis of cultured endothelial cells in parallel with the inhibition of 8-isoprostane formation, 4-hydroxy-2-nonenal (4-HNE) accumulation and VCAM-1 expression. Next, apolipoprotein-E knockout mice were fed a high-cholesterol diet for 4 weeks with edaravone (10 mg/kg i.p.) or vehicle treatment. Edaravone treatment decreased atherosclerotic lesions in the aortic sinus (0.18 ± 0.01 to 0.09 ± 0.01 mm2, P < 0.001) and descending aorta (5.09 ± 0.86 to 1.75 ± 0.41 mm2, P < 0.05), as evaluated by oil red O staining without influence on plasma lipid concentrations or blood pressure. Dihydroethidium labeling and cytochrome c reduction assay showed that superoxide anions in the aorta were suppressed by edaravone. Also, plasma 8-isoprostane concentrations and aortic nitrotyrosine, 4-HNE and VCAM-1 contents were decreased by edaravone treatment.

Conclusions. These results suggest that edaravone may be a useful therapeutic tool for early atherosclerosis, pending the clinical efficacy.

Keywords: Atherosclerosis; Reactive oxygen species; Free radical scavenger; Edaravone; 4-HNE; Apolipoprotein E knockout mouse

Atherosclerosis

Volume 191, Issue 2 , April 2007, Pages 281-289

Alcohol is cardiotoxic

Binge Drinking Negates Benefits of Alcohol

SHERRY BOSCHERT (San Francisco Bureau)

Moderate consumption of alcohol can be part of a healthy lifestyle to prevent cardiac disease, but not if you drink too fast, Dr. Mary O. Gray said at a meeting sponsored by the California chapter of the American College of Cardiology.

The cardioprotective benefits of alcohol appear to be limited to one drink per day for women or two drinks per day for men (with a “drink” consisting of one glass of wine, one shot of liquor, or one bottle or can of beer). Beyond that, alcohol is cardiotoxic, said Dr. Gray of San Francisco General Hospital.

Binge drinking—defined as consuming three or more drinks in 1 or 2 hours—doubled the risk of death from any cause in a recent study of patients treated for acute MI (Circulation 2005;112:3839–45). Investigators interviewed 2,000 patients a median of 4 days after a confirmed MI and found that regular consumption of alcohol reduced their risk of death, but binge drinking blocked or attenuated this benefit.

The negative effects of binge drinking applied regardless of whether a person was a light or heavy drinker overall. The study also asked about other factors that might affect cardiovascular risk, such as vigorous activity or vigorous sexual activity, but found no correlation with mortality, she said at the meeting, also sponsored by the University of California, San Francisco.

Heavy drinking for a long time can cause alcoholic cardiomyopathy, a diagnosis made clinically through history and elimination of other etiologies. Heavy drinkers with hypertension or heart failure should be advised to stop drinking to preserve their hearts, as well as to protect other aspects of their physical and personal/social well-being.

Data on very heavy drinkers suggest that those who develop heart failure may recover cardiovascular function if they stop drinking. Recovery is more likely if the patient is relatively young and has no other risk factors for cardiovascular disease.

Heavy drinkers often are malnourished, so treatment should include attention to a healthy diet including thiamine supplementation, Dr. Gray advised. Treat cardiac arrhythmias or systemic hypertension promptly in heavy drinkers, she added.

Most heavy drinkers also are heavy cigarette smokers. Dr. Gray and associates plan to study the interplay between cigarette smoke and alcohol consumption to try to tease out their causal effects in alcoholic cardiomyopathy.

Cardiology News, Volume 5, Issue 3, Page 16 (March 2007)

http://www.ecardiologynews.com

Atrial fibrillation: Risk factor

Apnea Is Risk Factor for AF in Younger Patients

JANE SALODOF MACNEIL (Southwest Bureau)

Obesity and obstructive sleep apnea are independent risk factors for atrial fibrillation in patients younger than 65 years of age, but not in older patients, according to a retrospective cohort study of 3,542 people who had sleep studies at the Mayo Clinic in Rochester, Minn.

Heart failure was the only independent predictor of new-onset atrial fibrillation for people 65 years of age and older in the study, which followed patients a mean of 4.7 years after an initial polysomnography.

“The ability of sleep apnea to predict the development of atrial fibrillation was dependent on the age of the patient. If they were more than 65, and they were in sinus rhythm when you did the sleep study, they didn't get atrial fibrillation,” Dr. Virend K. Somers, a coinvestigator, said at a meeting on sleep medicine sponsored by the American College of Chest Physicians.

None of the patients reviewed had atrial fibrillation before or at the time of the screenings, conducted from 1987 to 2003, for possible sleep disorders. All told, 133 people developed atrial fibrillation at some point after undergoing polysomnography (J. Am. Coll. Cardiol. 2007;49:565–71).

Obstructive sleep apnea was diagnosed in 2,626 people (74%), and the investigators reported it was a strong predictor (hazard ratio 2.18) of future atrial fibrillation. A total of 4.3% of patients with obstructive sleep apnea but only 2.1% without the disorder were subsequently diagnosed with atrial fibrillation.

An age-stratified analysis showed patients younger than 65 years were more vulnerable to atrial fibrillation, however, and had more risk factors. The most significant was lower oxygen levels at night (hazard ratio 3.29), but age (2.04), male gender (2.66), coronary artery disease (2.66), and body mass index (1.07) also were predictors. In older patients, heart failure had a hazard ratio of 7.68.

Why the older patients were less susceptible to atrial fibrillation is unclear, according to the authors. Dr. Somers, a professor of medicine at the Mayo Clinic, speculated that the older patients probably had undiagnosed apnea for many years.

“If you have sleep apnea and you last to 65–70 years, you are going to be okay—you are going to live longer,” he said. “But if you are susceptible to the damage that sleep apnea does to your cardiovascular system, you will die early on.”

Dr. Somers is a consultant for Respironics and received an honorarium from the ResMed Foundation, which funded the study. He noted that it follows earlier research at the Mayo Clinic that showed an association between obstructive sleep apnea and atrial fibrillation.

In one study, he and his coinvestigators found obstructive sleep apnea was “strikingly more prevalent” (odds ratio 2.19) in atrial fibrillation patients than in general cardiology patients. About half (49%) of 151 patients who underwent electrocardioversion for atrial fibrillation had obstructive sleep apnea vs. about a third (32%) of 312 patients treated for other heart conditions (Circulation 2004;110:364–7).

In a study of patients who underwent electrocardioversion, Dr. Somers' group found atrial fibrillation was more likely to recur if obstructive sleep apnea was not treated (Circulation 2003;107:2589–94). It compared 39 patients with obstructive sleep apnea with 79 patients who did not have the sleep disorder. Within 12 months, 82% of 27 untreated or inadequately treated apnea patients had their apnea recur, vs. 42% of 12 apnea patients treated with continuous positive airway pressure and 53% of the control group.

Dr. Somers noted that within the apnea population, risk doubled when the condition went untreated Moreover, looking just at the 25 apnea patients who received no treatment, the investigators found nocturnal oxygen saturation fell to lower levels in patients who had a recurrence of atrial fibrillation.

Cardiology News, Volume 5, Issue 3, Page 12 (March 2007)

Prevent Atrial Fibrillation: New Drugs

New Drugs Show Novel Ways to Treat, Prevent Atrial Fibrillation

MITCHEL L. ZOLER (Philadelphia Bureau)

New drugs for treating or preventing atrial fibrillation are coming from new ways to change the electrical properties of the atria and to promote sinus rhythm.

The new agents differ from the approved antiarrhythmic drugs for atrial fibrillation (AF)–such as dofetilide—which also affect ventricular rhythms and cause adverse effects. New drugs target different ion-channel effects, have multiple ion effects, or work by a mechanism that doesn't involve ion channels, Dr. Peter Kowey said at an international symposium on atrial fibrillation sponsored by the Academy of Healthcare Education.

▸ Azimilide. This agent acts by blocking both rapid and slow potassium channels in myocardium, and is chemically distinct from other class III antiarrhythmic drugs like sotalol, amiodarone, and dofetilide. After a long period of testing in many studies, including phase III trials, the development of azimilide for preventing AF recurrence was dropped, despite clear evidence of efficacy, because it did not look potent enough, said Dr. Kowey, professor of medicine at Jefferson Medical College, Philadelphia, and president of the Main Line Health Heart Center at Lankenau Hospital, Wynnewood, Pa. Azimilide is under review by the Food and Drug Administration for patients with implantable cardioverter defibrillators for the indication of preventing new device events in patients with frequent events.

▸ Tedisamil. Study results showed that tedisamil, which blocks all potassium channels, is more effective than placebo for stopping AF, acting in a dose-dependent way. The big downside is that it can cause torsades de pointes. Despite this, the drug remains in development because it's especially effective for stopping AF that's lasted for days or even weeks; available drugs are primarily effective only when the AF has been going on for hours.

▸ Dronedarone. Under development for several years and now under FDA review, dronedarone is an amiodaronelike compound that lacks the iodine moiety and is much safer than amiodarone. Safety data from phase III efficacy trials showed that dronedarone lacked the pulmonary and thyroid toxicity of amiodarone and had an overall profile that was similar to placebo, and it had a clear effect on prolonging the time to first recurrence of AF. But its progress stalled when results from the ANDROMEDA (Antiarrhythmic Trial With Dronedarone in Moderate to Severe Congestive Heart Failure Evaluating Morbidity Decrease) study, which studied the drug in patients with heart failure and AF, linked dronedarone treatment with an excess of deaths resulting from heart failure. The results did not show increased mortality resulting from arrhythmias. This indication of a problem led to the ATHENA (A Trial with Dronedarone to Prevent Hospitalization or Death in Patients With Atrial Fibrillation) study, which enrolled 3,700 patients who may not have been as sick as those in ANDROMEDA. Results from ATHENA are expected next year, and will determine the FDA's future review of the drug.

▸ Vernakalant. Formerly known as RSD-1235, this is the first “atrial-selective” drug to reach the FDA for review. It is an intravenous drug that seeks labeling for terminating AF in patients whose arrhythmia is of “relatively recent onset.” Results from the phase III studies, especially the ACT III trial, showed that vernakalant was effective for converting patients to sinus rhythm when AF lasted for a week or less, but it was not significantly better than placebo for stopping AF that lasted 8 or more days. An oral formulation of the drug showed efficacy for preventing new AF episodes in one phase II study, with a safety profile that was similar to placebo, but the study included only 171 patients. The atrial-selective designation is relative: Although vernakalant and other drugs in the class have a reduced ventricular effect, increasing the dosage produces greater ventricular effects.

▸ Gap junction modulators. A new class of AF drugs under development, these agents are believed to work by restoring intercellular connections that may be arrhythmogenic when malfunctioning. Preclinical development has so far not identified a good candidate for clinical testing. In trials with other end points, the angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers have shown associations with a reduced frequency of AF in empirical observations and post hoc analyses, and this evidence warrants the running of studies designed to directly test the antiarrhythmic efficacy of these drugs. Anti-inflammatory agents, such as statins and polyunsaturated fatty acids, have also shown hints of reducing AF incidence.

As new strategies for stopping or preventing AF appear, a major challenge will be to design new ways to test these drugs. For many new agents, a trial designed to measure the time to first reoccurrence of symptomatic AF will be irrelevant, Dr. Kowey said.

Cardiology News, Volume 5, Issue 3, Page 10 (March 2007)
http://www.ecardiologynews.com