I have had a heart attack. Do I need open heart surgery or a stent?

New advice on the choice between open heart surgery and inserting a stent via a catheter after a heart attack is launched today. The European Society of Cardiology (ESC) and European Association for Cardio-Thoracic Surgery (EACTS) Guidelines on myocardial revascularization are published online in European Heart Journal.

25 aug 2018--Coronary artery disease, also called ischaemic heart disease, is the top cause of death worldwide. Arteries supplying oxygen-rich blood to the heart become narrowed with fatty material, causing chest pain and increasing the risk of heart attacks and death. Patients should stop smoking, be physically active, and consume a healthy diet. They also need lifelong medication which can include a statin to control blood lipids, blood pressure lowering drugs, and aspirin.
Myocardial revascularization can be performed in patients with stable (chronic) coronary artery disease or an acute event (heart attack) to improve blood flow to the heart, reduce chest pain (angina), and improve survival. There are two types of myocardial revascularization: open heart surgery to bypass clogged arteries (coronary artery bypass grafting; CABG) and percutaneous coronary intervention (PCI) to open clogged arteries with a stent.
Patients should be involved in choosing the procedure, state the guidelines. They need unbiased, evidence-based information with terminology they can understand explaining the risks and benefits in the short- and long-term such as survival, relief of chest pain, quality of life, and requirement for a repeat procedure. In non-emergency situations, patients must have time to reflect on the trade-offs and seek a second opinion. Patients have the right to obtain information on the level of experience of the doctor and hospital in performing these procedures.
Outcomes from the two procedures vary according to the anatomical complexity of coronary artery disease. This is graded using the SYNTAX Score, which predicts whether PCI can provide similar survival as bypass. For patients with more simple disease, surgical bypass and PCI provide similar long-term outcomes. For patients with complex disease, long-term survival is better with surgical bypass. Also, patients with diabetes have better long-term outcomes with surgical bypass even with less complex disease.
A heart team of cardiologists, cardiac surgeons and anaesthetists should be consulted for patients with chronic coronary artery disease and a complex coronary anatomy, while respecting the preferences of the patient.
Professor Miguel Sousa-Uva, EACTS Chairperson of the Guidelines Task Force, Santa Cruz Hospital, Carnaxide, Portugal, said: "Despite the development of new stents, studies show that patients with complex coronary artery disease have better survival with bypass surgery and this should be the preferred method of revascularization."
In patients with stable disease, another aspect to consider when choosing the procedure is whether it is possible to bypass or insert a stent into all blocked arteries, as this improves symptoms and survival. Preference should be given to the procedure most likely to achieve this so-called complete revascularization.
When PCI is chosen, stents that release a drug to prevent clots, heart attacks, and reinterventions should be used in all procedures. Bioresorbable stents, which are absorbed by the body, should only be used in clinical trials.
Professor Franz-Josef Neumann, ESC Chairperson of the Guidelines Task Force, University Heart Centre Freiburg ? Bad Krozingen, Germany, said: "The guidelines aim to help patients and doctors make a logical decision on the type of revascularization based on the scientific evidence. They will also be consulted by governments and health insurers as the standard of care for coronary artery disease."

More information: 2018 ESC/EACTS Guidelines on myocardial revascularization. European Heart Journal. 2018. DOI: 10.1093/eurheartj/ehy394.


Provided by European Society of Cardiology

Do doctors really know how to diagnose a heart attack?

Confusion over how to diagnose a heart attack is set to be cleared up with new guidance launched today. The 2018 Fourth Universal Definition of Myocardial Infarction is published online in European Heart Journal.

25 aug 2018--"Unless there is clarity in the emergency room on what defines a heart attack, patients with chest pain may be wrongly labelled with heart attack and not receive the correct treatment," said Professor Kristian Thygesen, Aarhus University Hospital, Denmark.
"Many doctors have not understood that elevated troponin levels in the blood are not sufficient to diagnosis a heart attack and this has created real problems," continued Professor Thygesen, who is joint chair of the Task Force that wrote the document, together with Professor Joseph S. Alpert, University of Arizona, USA and Professor Harvey D. White, Auckland City Hospital, New Zealand.
The international consensus document spells out that a heart attack (myocardial infarction) has occurred when the heart muscle (myocardium) is injured and has insufficient oxygen. Troponin is a protein normally used by the heart muscle for contraction, but is released into the blood when the muscle is injured. Oxygen shortage (ischaemia) is detected by electrocardiogram (ECG) and symptoms such as pain in the chest, arms, or jaw, shortness of breath, and tiredness.
Myocardial injury on its own is now considered a separate condition. There are numerous situations which can cause myocardial injury, and therefore a rise in troponin. These include infection, sepsis, kidney disease, heart surgery, and strenuous exercise. The first step of treatment is to address the underlying disorder.
As for myocardial infarction, there are different types which require specific treatment. Type 1 is the situation which most people associate with a heart attack. Here a fatty deposit in an artery, called a plaque, ruptures and blocks blood flow to the heart which deprives it of oxygen. Treatment can include antiplatelet medication to stop platelets clumping together and forming a clot, inserting a stent via a catheter to open up the artery, or surgery to bypass the artery.
In type 2, oxygen deprivation is not caused by plaque rupture in an artery but is due to other reasons such as respiratory failure or severe hypertension. Professor Alpert said: "Some doctors have incorrectly called this type 1 and given the wrong treatment, which can be harmful. Treatment should be directed at the underlying condition, for example blood pressure lowering medications for patients with hypertension."
Efforts by doctors to correctly diagnosis myocardial infarction and its subtypes have not been helped by the lack of diagnosis codes in the International Classification of Diseases (ICD). The subtypes of myocardial infarction were first introduced by the joint Task Force in 2007, but were not incorporated into the ICD until October 2017.3,4
Professor White said: "In the consensus document we have expanded the section on type 2 myocardial infarction and included three figures to help doctors make the correct diagnosis. The incorporation of type 2 into the ICD codes is another step towards accurate recognition followed by appropriate treatment. A code for myocardial injury will be added to the ICD next year."
The international consensus document was produced by the European Society of Cardiology (ESC), American College of Cardiology (ACC), American Heart Association (AHA), and World Heart Federation (WHF).

More information: 2018 ESC/ACCF/AHA/WHF Fourth Universal Definition of Myocardial Infarction. European Heart Journal. 2018. doi: 10.1093/eurheartj/ehy462


Provided by European Society of Cardiology

Holiday treats, hectic schedules may increase risk of heart attack

Between the ubiquitous goody trays, unending to-do lists and stressful travel itineraries, it can be tough to stay on track when it comes to health during the holiday season, whether it's sticking to a diet or maintaining an exercise regimen.

11 dec 2017--Such holiday-fueled pressures may also contribute to the fact that the holidays are also the most dangerous time of year for heart attacks.

Research shows deaths from heart attacks peak during December and January, possibly due to changes in diet and alcohol consumption, stress from family interactions, strained finances, travel and entertaining, and respiratory problems from burning wood.
"We tend to exercise less and eat more during the holidays," said John Osborne, M.D., Ph.D., a Dallas-area preventive cardiologist. "It's a very stressful time. There's a lot of emotion attached to the holidays and that can be another factor to why we have more cardiovascular events."
As the holidays upend routines, taking medications as prescribed can also get lost in the shuffle, Osborne said.
"I can't tell you how often I get calls from patients who have traveled somewhere and forgot their medications," he said, adding that he worries more about the patients who don't contact him. "Some people figure they'll be fine to be off them for a week or so, but if you start missing medications, that can have a big impact on causing your blood pressure to be out of control."
For those who have already had a heart attack, the heightened risk during the holidays is particularly dangerous. That's because about one in five heart attack survivors age 45 and older will have another heart attack within five years.
Being with family during the holidays is a good time for patients to talk about their health history—not just heart attacks, but also high blood pressure and high cholesterol, experts say.
"We can dramatically lower the risk of cardiovascular events with lifestyle changes, but don't ignore your family history," Osborne said. "Genetics can catch up to you, even if you're doing all the right stuff."
Heart disease can be prevented in many cases through lifestyle factors, such as maintaining a healthy weight, exercising regularly, controlling cholesterol and blood pressure and not smoking, but "making lifestyle changes can be difficult," Osborne said.
"I admit to my patients that I don't love to exercise, but I really feel great having exercised," he said. "Getting that motivation can be painful, but it's fantastic when you get to the other side."
Osborne said tools such as mobile apps can provide education and electronic reminders to help people stay focused on heart health.
"I have a very brief period with patients," he said. "Tools like apps can encourage good health behaviors, being that gentle in-your-face technology."

More information: D. P. Phillips. Cardiac Mortality Is Higher Around Christmas and New Year's Than at Any Other Time: The Holidays as a Risk Factor for Death, Circulation (2004). DOI: 10.1161/01.CIR.0000151424.02045.F7


Provided by American Heart Association

ANTARCTIC trial antiplatelet monitoring: No benefit in elderly patients

Monitoring platelet function in order to individualize antiplatelet therapy did not improve outcomes for elderly patients after a heart attack compared to a standard, unmonitored approach, results of the ANTARCTIC trial show.

05 sept 2016--The findings, presented in a Hot Line session at ESC Congress 2016, and with simultaneous publication in the Lancet, challenge current international guidelines which recommend platelet function testing in high risk patients.
"Platelet function testing is still being used in many centres to measure the effect of antiplatelet drugs and adjust the choice of these drugs and their doses. Our study does not support this practice and these recommendations," said senior investigator Gilles Montalescot M.D, Ph.D, from Hôpital Pitié-Salpêtrière, in Paris, France.
"Although measuring the effect of antiplatelet agents makes sense in order to choose the best drugs or doses, this costly and more complex strategy does not appear to benefit patients, even when they present with extremely high risk of ischemic and bleeding events liked those enrolled in ANTARCTIC."
ANTARCTIC is the only study of platelet function testing in elderly patients at very high risk of ischemic and bleeding complications.
It enrolled 877 patients, aged 75 years or more, who presented with an acute coronary syndrome and underwent coronary stenting.
All patients were started on the antiplatelet agent prasugrel (5mg), with 442 randomised to the conventional therapy (no adjustment) and 435 to monitoring and treatment adjustment, if needed.
Patients in the monitoring arm received 14 days of the daily 5mg prasugrel dose, but then underwent a platelet function test at Day 14, followed by medication adjustment, if the test showed high or low platelet reactivity. Additional monitoring was performed at Day 28 in patients who needed treatment adjustment.
The primary end point of the trial was the composite of cardiovascular death, myocardial infarction, stroke, stent thrombosis, urgent revascularization and bleeding complication at 1-year.
This endpoint occurred at a similar rate in both arms of the study: 27.6% in the monitoring group, and 27.8% in the conventional group (hazard ratio [HR], 1.003; 95% confidence interval [CI], 0.78 to 1.29; P=0.98).
There was similarly no significant difference in rates of the main secondary end point (a composite of cardiovascular death, myocardial infarction, stent thrombosis or urgent revascularization), which occurred in 9.9% and 9.3%, respectively (HR, 1.06; 95% CI, 0.69 to 1.62; P=0.80).
"Platelet function monitoring led to a change of treatment in 44.8% of patients who were identified as being over- or under-treated, yet this strategy did not improve ischemic or safety outcomes," noted Professor Montalescot.
"ANTARCTIC confirms the ARCTIC study (NEJM 2011) in a different population with a different drug, and has addressed the potential limitations of the ARCTIC study, but finally reached the same conclusion. I expect there will be adjustments of guidelines and practice in light of this."
ANTARCTIC stands for Assessment of a Normal versus Tailored dose of prasugrel after stenting in patients Aged > 75 years to Reduce the Composite of bleeding, stent Thrombosis and Ischemic Complications.


Provided by European Society of Cardiology

Age, creatinine, ejection fraction predict post-MI survival

22 april 2015—A simple age, creatinine, and ejection fraction (ACEF) score can predict one-year mortality risk in myocardial infarction 30-day survivors who underwent percutaneous coronary intervention, according to a study published in the May 1 issue of The American Journal of Cardiology.

Jang Hoon Lee, M.D., from Kyungpook National University Hospital in Daegu, South Korea, and colleagues examined whether the ACEF score could predict one-year mortality for 12,000 post-myocardial infarction 30-day survivors who underwent percutaneous coronary intervention. Twelve risk factors were selected and ranked based on their area under the curve (AUC) value.

The researchers found that the best AUC value was indicated by age, ejection fraction, and serum creatinine levels. Nonsurvivors had a significantly higher ACEF score (1.95 ± 0.82 versus 1.28 ± 0.5); the ACEF score independently predicted one-year mortality (adjusted hazard ratio, 2.26). A prediction model including 12 risk factors had the best accuracy (AUC, 0.8), but this was not significantly different from the ACEF score (AUC, 0.79). For the ACEF_LOW, ACEF_MID, and ACEF_HIGH groups, the adjusted hazard ratios for one-year mortality were 1 (reference), 3.11, and 10.38, respectively.

"The ACEF score may be a novel valid model to stratify the one-year mortality risk in 30-day survivors who underwent percutaneous coronary intervention after myocardial infarction," the authors write.

More information: Abstract
Full Text (subscription or payment may be required)

Do heart patients fare better when doctors away?

Doctors joke that if you're going to have a heart attack, the safest place would be at a big national gathering of heart specialists. But a new study suggests some older hospitalized heart patients may fare better when these doctors aren't around.

26 dec 2014--Survival chances were better for cardiac arrest patients and for the sickest heart failure patients if they were treated at teaching hospitals during the two biggest national cardiology meetings, compared with those treated during weeks before and after the meetings. Also, some of the sickest heart attack patients got fewer invasive procedures during meeting days, versus those treated at other times—but that didn't hurt their odds of surviving, the nine-year study found.

The findings were only at teaching hospitals, typically affiliated with medical schools and involved in doctor training and sometimes research; these are the workplaces for many doctors who attend major medical meetings. No differences were seen in death rates at non-teaching hospitals.

The evidence is only circumstantial and the study lacks information on whether the patients' own doctors actually attended the meetings.

"The solution is not to get the cardiologists to have meetings every week," said Dr. Anupam Jena, a Harvard Medical School economist and internist and the study's lead author. Identifying specific treatments that were given or not given during meeting times would be a better solution that might lead to better outcomes, Jena said.

It might be that doctors who don't attend the meetings are less inclined to try the most invasive treatments, and that a less intensive approach is better for the sickest patients, Jena said.

The study was published online Monday in JAMA Internal Medicine.

The research is provocative and might help doctors figure out how to lower patients' death rates throughout the year, said Dr. Rita Redberg, the journal's editor.

Redberg is a cardiologist at a teaching hospital at the University of California, San Francisco. She usually attends the national American College of Cardiology and American Heart Association meetings, but said she does not think her absences have affected patient outcomes.

"I'm from a big academic institution so there's always coverage while I'm gone," Redberg said.

The authors analyzed 30-day death rates for Medicare patients hospitalized during the annual meetings in the spring and fall, which typically draw thousands of doctors. Data included nearly 3,000 patients at teaching hospitals during meeting days from 2002 through 2011. The comparison group was about 18,000 patients hospitalized on the same days during the three weeks before and three weeks after the meetings.

The 30-day death rates for meeting-day versus non-meeting days patients were:

—60 percent versus 70 percent for cardiac arrests.

—18 percent versus 25 percent for the sickest heart failure patients.

— No difference for the sickest heart attack patients: about 39 percent for both groups.

Among the heart attack patients, the meeting-days group had fewer heart stent procedures to open blocked arteries. The researchers found no difference in rates for a few invasive procedures for cardiac arrest and high-risk heart failure patients, but said there may have been differences in other treatments not included in the study that might explain the results.

Dr. Patrick O'Gara, president of the American College of Cardiology, said the study's observational design makes it impossible to know if the national meetings had any effect on patients' survival. He also noted that the number of heart doctorswho attend the national meetings is a fraction of the nearly 30,000 cardiologists nationwide.

The American Heart Association echoed those comments in a statement and said the group does not recommend any changes in treatment based on the study.

More information: Journal: JAMA Intern Med. Published online December 22, 2014. doi:10.1001/jamainternmed.2014.6781

American Heart Association: www.heart.org

American College of Cardiology: www.acc.org

Nonobstructive CAD associated with increased risk of heart attack, death

In a study that included nearly 38,000 patients, those diagnosed with nonobstructive coronary artery disease (CAD) had a significantly increased risk of heart attack or death one year after diagnosis, according to a study in the November 5 issue of JAMA.

05 nov 2014--Nonobstructive coronary artery disease (CAD) is atherosclerotic plaque that would not be expected to obstruct blood flow or result in anginal symptoms (such as chest pain). Although such lesions are relatively common, occurring in 10 percent to 25 percent of patients undergoing coronary angiography, their presence has been characterized as "insignificant" or "no significant CAD" in the medical literature. However, this perception of nonobstructive CAD may be incorrect, because prior studies have noted that the majority of plaque ruptures and resultant myocardial infarctions (MIs; heart attacks) arise from nonobstructive plaques. Despite the prevalence of nonobstructive CAD identified by coronary angiography, little is known about its risk of adverse outcomes, according to background information in the article.

Thomas M. Maddox, M.D., M.Sc., of the VA Eastern Colorado Health Care System, Denver, and colleagues compared heart attack and mortality rates among patients with nonobstructive CAD, obstructive CAD, and no apparent CAD. The patients included in the study were all U.S. veterans who underwent elective coronary angiography for CAD between October 2007 and September 2012 in the Veterans Affairs health care system. Patients with prior CAD events were excluded. CAD extent was defined by degree of vessel narrowing and distribution (1, 2, or 3 vessel).

During the study period, 37,674 patients underwent elective coronary angiography for indications related to CAD; of those, 22.3 percent had nonobstructive CAD and 55.4 percent had obstructive CAD. Within 1 year, 845 patients died and 385 were rehospitalized for MI. The researchers found that the 1-year MI risk progressively increased by the extent of CAD, rather than abruptly increasing between nonobstructive and obstructive CAD. Patients with nonobstructive CAD had an associated risk of MI that was 2-to 4.5-fold greater than among those with no apparent CAD. Similar observations were seen with 1-year mortality and the combined outcome of 1-year MI and death.

"These findings highlight a need to recognize that nonobstructive CAD is associated with significantly increased risk for MI, consistent with prior biologic studies indicating that a majority of MIs are related to nonobstructive stenosis [narrowing of an artery]. Correspondingly, these results reveal the limitations of a dichotomous [divided into two parts] characterization of angiographic CAD into 'obstructive' and 'nonobstructive' to predict MI and highlight the importance of preventive strategies such as pharmacotherapy treatments and lifestyle modifications to mitigate these risks," the authors write.

More information: DOI: 10.1001/jama.2014.14681

Provided by The JAMA Network Journals

Healthy lifestyle choices may dramatically reduce risk of heart attack in men

Myocardial Infarction or Heart Attack. Credit: Blausen Medical Communications/Wikipedia/CC-A 3.0

Following a healthy lifestyle, including maintaining a healthy weight and diet, exercise, not smoking and moderating alcohol intake, could prevent four out of five coronary events in men, according to a new study publishing today in the Journal of the American College of Cardiology.

24 sept 2014--While mortality from heart disease has declined in recent decades, with much of the reduction attributed to medical therapies, the authors said prevention through a healthy lifestyle avoids potential side effects of medication and is more cost effective for population-wide reductions in coronary heart disease.

For the study, researchers examined a population of 20,721 healthy Swedish men aged 45-79 years of age and followed them for 11 years. Lifestyle choices were assessed through a questionnaire exploring diet, alcohol consumption, smoking status, level of physical activity and abdominal adiposity (belly fat). Men in the study with the lowest risk were non-smokers, walked or cycled for at least 40 minutes per day, exercised at least one hour per week, had a waist circumference below 95 centimeters, consumed moderate amounts of alcohol, and followed a healthy diet with a regular consumption of fruits, vegetables, legumes, nuts, reduced-fat dairy products, whole grains and fish.

The researchers found a clear reduction in risk for heart attack for each individual lifestyle factor the participants practiced. For instance having a low-risk diet together with a moderate alcohol consumption led to an estimated 35 percent lower risk of heart attack compared to the high-risk group, those who practice none of the low-risk factors.

Men who combined the low-risk diet and moderate alcohol consumption with not smoking, being physically active and having a low amount of abdominal fat, had 86 percent lower risk. Researchers found similar results in men with hypertension andhigh cholesterol levels.

"It is not surprising that healthy lifestyle choices would lead to a reduction in heart attacks," said Agneta Akesson, Ph.D., Associate Professor at the Institute of Environmental Medicine, Karolinska Institutet, Stockholm, and lead author of the study. "What is surprising is how drastically the risk dropped due to these factors."

According to the authors, less than 2 percent of the American population conforms to what is defined as ideal cardiovascular health. The burden of cardiovascular disease could be significantly reduced through programs targeted to men and promoting low-risk lifestyle choices. Even in those who take medication, an additional reduction in risk for chronic heart disease has been observed in those with a healthy lifestyle.

"It is important to note that these lifestyle behaviors are modifiable, and changing from high-risk to low-risk behaviors can have great impact on cardiovascular health," Akesson said. "However, the best thing one can do is to adopt healthy lifestyle choices early in life."

Provided by American College of Cardiology

Heart attack survival similar among those receiving clot-busting drugs, angioplasty

The one-year survival rate after a severe heart attack was similar among people who initially received clot-busting medications and those who immediately underwent angioplasty, according to a late-breaking clinical trial presented at the American Heart Association's Scientific Sessions 2013.

20nov 2013--The Strategic Reperfusion Early After Myocardial Infarction (STREAM) Trial included 1,892 people who suffered an ST-elevation myocardial infarction (STEMI), a heart attack in which a blood vessel is totally blocked, but weren't able to undergoangioplasty with the first hour of arriving at the hospital. Researchers randomly assigned half of these patients to receive three medications, including age-adjusted bolus tenecteplase, clopidogrel and enoxaparin. If their symptoms persisted, they also underwent angioplasty, a procedure that opens blocked blood vessels. The other half received angioplasty, and standard drugs to prevent blood clots.

Both groups were treated within three hours of the onset of heart-attack symptoms.

Among those who first received the combined medications, 2.1 percent died, including from heart disease and stroke, compared to 1.5 percent of those who initially underwent angioplasty. This was not a significant difference.

In an earlier part of the study, patients who received clot-busting medications were slightly more likely to survive without complications 30 days after treatment. These latest findings represent the original study's one-year follow-up.

"In this study, the combined drug strategy proved a reasonable approach to take as an initial treatment immediately after severe heart attack when angioplasty is not immediately available," said Peter Sinnaeve, M.D., Ph.D., the study's lead author and assistant professor of cardiology at the University of Leuven in Belgium.

The American Heart Association currently recommends clot-busting medication within the first 30 minutes and angioplasty within the first 90 minutes of hospital arrival and continues to review and adapt guidelines as appropriate. The association has developed the Mission Lifeline® program to help improve timely access to appropriate care.

More information: The Strategic Reperfusion Early After Myocardial Infarction (STREAM) study. Armstrong PW, Gershlick A, Goldstein P, Wilcox R, Danays T, Bluhmki E, Van de Werf F; STREAM Steering Committee. Am Heart J. 2010 Jul;160(1):30-35.e1. DOI: 10.1016/j.ahj.2010.04.007.

Provided by American Heart Association

Tips for having a heart-healthy holiday

22 dec 2012—It's the season of joy, peace and goodwill, but it's also the time of year that brings a spike in heart attacks with most occurring on Christmas Day, Boxing Day and New Year's Day.

Dubbed by heart researchers as the "Merry Christmas Coronary," it can be triggered by stressful events or other risk factors, says cardiologist Dr. Greg Curnew, an associate clinical professor of medicine of McMaster's Michael G. DeGroote School of Medicine, on staff at Hamilton Health Sciences.

A heart attack – caused by a rupture of plaque in the wall of a coronary artery - strikes when you least suspect it, says Curnew. "It's like a volcano erupting."

Most heart deaths occur out of hospital, with one in four of those dying within one hour of their first-ever symptoms. He outlines heart attack signs as: 

• Chest pain that lasts for at least 10 minutes – coming on suddenly or slowly – and feeling like heaviness or a steel band tightening around the chest.
• Chest discomfort that spreads to the neck, throat, jaw and shoulder, the back, arms and even the hands.
• For those who don't experience chest pain, be aware of discomfort in upper parts of the body.
• A choking feeling in the throat, or arms that feel heavy or useless.
• Breathlessness, nausea or vomiting, a cold sweat, light-headedness.

"If you think you are having a heart attack, this is not the time to call telemedicine or your family doctor. Get straight to the hospital," says Curnew.

He recommends chewing two baby Aspirins or taking one or two nitroglycerine tables three to five minutes apart – but not if you are on medication for sexual dysfunction, such as Viagra – and call 911 immediately.

While it's the time of year for overindulging in rich, salty foods, Curnew warns that eating just one fatty meal constricts blood flow in arteries for the next three to four hours.

He advises anyone taking cholesterol-lowering drugs to not stop taking their prescribed dosage.

Curnew offers potential New Year's resolutions for consideration: 

• Learn basic life support skills and how to use an external defibrillator.
• Become an active participant in your health with your doctor and develop a health binder that you constantly update.
• Join the Good Food Box program; a non-profit fresh fruit and vegetable distribution program which makes fresh, high quality produce affordable and accessible to everyone.
• If you want to lose weight, join a group or find a health buddy.

"For me, this is a time of year to celebrate and to feel lucky to be here for the holidays, and with a wish to be here next year, too," says Curnew.

Provided by McMaster University

Risks: First Month After a Heart Attack Is Crucial

By ERIC NAGOURNEY

11 nov 2008--People who survive a heart attack are at much higher risk of sudden cardiac death in the next 30 days, researchers have found.

The findings, which appeared in the Nov. 5 Journal of the American Medical Association, suggest that doctors need to closely supervise patients in the month after a heart attack, and that patients also need to be alert to signs of trouble.

“The first month after a heart attack can be envisioned as a period of healing with heart tissue remodeling, which conceptually is associated with a propensity to experience sudden death,” one of the authors, Dr. Véronique L. Roger of the Mayo Clinic in Rochester, Minn., said in an e-mail message.

The researchers, led by Dr. A. Selcuk Adabag of the Veterans Affairs Medical Center in Minneapolis, followed the health of almost 3,000 people who had a heart attack from 1979 to 2005.

In the first 30 days, they found, the rate of sudden cardiac death was 1.2 percent, about four times the risk that would have been expected in the general population, once age and sex were taken into account.

But the rate improved greatly over the following 11 months, dropping to a level lower than that usually seen in the general population.

In fact, over all, the study found big improvements in the rate of sudden cardiac death for heart attack patients in the past three decades. The decline, the researchers said, was more than 40 percent. They attributed that to improved treatment for people who have just had a heart attack.

Depression, health care services and heart attacks -- what's the connection?

New data points to psychosocial factors impacting how often cardiac patients seek further care

22 oct 2008--Depression symptoms are associated with significantly higher use of healthcare services following a heart attack, according to a new study released today by the Centre for Addiction and Mental Health (CAMH). With approximately 70,000 Canadians experiencing a heart attack each year, this new data may help thousands of people get the care they need and reduce hospital visits.
"While we know that the use of health services is higher for people with depression symptoms, and depression is common for people who have had a heart attack, this is one of the first studies to quantify the relationship between depression symptoms, cardiac illness severity and their effect on health service consumption," explains Dr. Paul Kurdyak, head of CAMH's Centralized Assessment, Triage and Support research program and principal investigator for this research.
Data from almost 2000 heart attack patients showed that depression symptoms alone resulted in an increase in health service consumption with a:
Nine per cent increase in heart-related hospitalizations,
24 per cent increase in total re-hospitalization days, and
43 per cent increase in non-heart related hospitalizations visits following discharge after a heart attack.
Surprisingly, the data also showed that depression caused the greatest increase in health service use in those patients with lower cardiac illness severity, and therefore, the least need for those services. "What we're seeing is people who are clearly in distress seeking help from our healthcare system, but it may not include the right kind of help to address their distress," says Dr. Kurdyak.
While there are well-established and effective chronic cardiac care and depression intervention programs, "this data supports the need for integrating depression screening and case-management into existing cardiac care," says Dr. Kurdyak. "Integrated depression care for people who have had a heart attack can improve their quality of life and may reduce the apparent mismatch between need and service use."
###
To arrange interviews please contact Michael Torres, Media Relations, CAMH at (416) 595-6015.
The Centre for Addiction and Mental Health (CAMH) is Canada's largest mental health and addiction teaching hospital, as well as one of the world's leading research centres in the area of addiction and mental health. CAMH combines clinical care, research, education, policy development and health promotion to transform the lives of people affected by mental health and addiction issues.
CAMH is fully affiliated with the University of Toronto, and is a Pan American Health Organization/World Health Organization Collaborating Centre.

Study suggests why heart attack victims do better with social support

COLUMBUS, Ohio, 19 sept 2008 – Researchers have identified specific damages to the brain that may occur when heart attack victims are socially isolated from others.
The study in mice found that those animals that lived alone before undergoing a heart attack showed five to eight times more damage to neurons in one part of the brain than did similar animals that lived with others.
While studies in humans have shown that socially isolated heart attack victims have a lower survival rate than others, this study may help reveal the mechanisms behind that result, said Zachary Weil, co-author of the study and former doctoral student in neuroscience at Ohio State University.
"This study shows that there are basic changes that occur in the brain when a heart attack victim is socially isolated," Weil said.
"In these mice, living with others seemed to provide strong protection from some of the damaging results of a heart attack."
The study appears in the October 2008 issue of the journal Molecular Psychiatry.
In the study, mice were put into two groups – members of one group lived alone, while the others lived communally in a cage with four other mice.
After two weeks with these living arrangements, some of the mice underwent a surgically induced heart attack. Those in a control group underwent the same surgical procedure, but the researchers prevented any loss of oxygen to the brain that would occur in a typical heart attack.
Brain tissue and blood samples were later collected from the mice. Researchers compared damage in the hippocampus, the area of the brain that plays a key role in memory. A lack of oxygen during a severe heart attack – one where the victim stops breathing – can either kill or seriously damage neurons, the primary cells of the nervous system.
Results showed that the mice that were socially isolated prior to the heart attack showed five to eight times more damage to their neurons compared to mice that were housed together, said Weil, who is now a post-doctoral researcher at Rockefeller University in New York.
Socially isolated mice also showed evidence of greater inflammation in the hippocampus, when compared to socially housed and control mice.
"There was a runaway inflammatory response in the tissue of socially isolated mice, which is damaging to the brain," said Randy Nelson, a co-author of the study and professor of psychology and neuroscience at Ohio State.
Socially isolated mice showed increased activation of microglia, a type of immune cell in the central nervous system that responds to damaged neurons, the study found.
One of the ways microglia respond is by releasing tumor necrosis factor alpha (TNF-a), one of a large family of proteins called cytokines -- chemical messengers that are mobilized when the body is injured or has an infection. These cytokines cause inflammation in their effort to repair an injured or infected area of the body.
Levels of TNF-a were elevated in isolated mice, but not in socially housed mice, compared to the control mice.
The higher levels of TNF-a in the socially isolated mice, and the inflammation it caused, was the main reason for the increased neuronal damage in these animals, Nelson said.
"Inflammation is normally good, but in this case it is too much of a good thing," he said.
In addition, results showed that the isolated mice had higher levels of the stress hormone corticosterone following the heart attack. Other studies have linked elevated levels of this hormone to increased neuronal damage.
"We found that the hormonal stress response network is more activated after cardiac arrest in socially isolated animals," said Courtney DeVries, in whose lab the work was conducted and another co-author and associate professor of psychology and neuroscience at Ohio State.
"This is contributing to damage in the neurons."
DeVries said this study, and others in her lab and in labs across the country, have highlighted the importance of social isolation and relationships in health, and specifically in recovery from heart attacks and strokes.
In fact, studies have shown that social isolation is as strong a predictor of one-year survival rates among heart attack victims as more classic risk factors such as high cholesterol and hypertension.
"One of the stumbling blocks has been that we haven't found the mechanism that explains why socially isolated individuals don't fare was well when it comes to heart attacks.
"But this study shows there is a physical reason why isolated people don't do as well, and it has to do with the inflammatory response to a heart attack."
If these findings continue to be replicated, it may suggest new ways to help treat heart attack victims.
"It is very difficult to alter people's social networks, but if we can understand the exact mechanism behind why socially isolated people don't fare as well after a heart attack, we may be able to develop therapies that can improve their outcomes," DeVries said.

Fat Cell Protein Boosts Heart Attack Risk in Elderly

09 aug 2008-- A protein produced by fat cells may play a pivotal role in increasing an older American's risk for a heart attack even if they are losing weight, a new report says.
Levels of adiponectin increase in the bloodstream when people lose weight and appear to endanger the cardiovascular health of older people, according to the new study to be published in The Journal of Clinical Endocrinology & Metabolism.
This finding, though, appears odd, because past studies have shown high adiponectin concentration is associated with lower risks of diabetes and cholesterol abnormalities.
"This study is significant because previous findings have been contradictory, and the present investigation includes the largest number of heart attacks in an elderly group to date," Dr. Jorge Kizer, an associate professor of medicine and public health at Weill Cornell Medical College in New York City, said in a news release issued by the journal's publisher. "Our findings make a persuasive case that adiponectin is in fact associated with an increase in heart disease risk in older persons."
The new study looked at a sample of 1,386 adults, aged 65 to 100, from around the country. Of these, 604 had heart disease, with those with the highest adiponectin levels being most likely to suffer a heart attack.
The researchers theorized that higher adiponectin levels may indicate underlying disease, or even have direct harmful effects especially in the elderly. Previous studies show adiponectin increases energy expenditure in the central nervous system of mice -- something that could be significantly harmful if also occurring in older adults by accelerating the loss of skeletal muscle.
The findings are consistent, though, with other recent studies tying high adiponectin to mortality in the elderly.
"This study shows that this abundant product of fat cells is a marker and perhaps even a mediator of worsened outcomes in persons aged 65 years and older," Kizer said.
More information
The National Institute of Health has more about healthy aging.

Even best efforts can't prevent all heart attacks

By STEPHANIE NANO
19 june 2008--Tim Russert was a good patient, taking medications for his heart disease and exercising, his doctor said. He had no chest pains and he passed an exercise stress test weeks ago. Yet at 58, he suffered a heart attack and died.
That's not uncommon, say cardiologists. Heart disease patients can significantly reduce their chances of a heart attack, but they can't totally prevent it, said Dr. Howard Hodis of the Keck School of Medicine at the University of Southern California.
"Under the most ideal circumstances, there's still going to be individuals who succumb to the disease process. It's never going to be 100 percent," said Hodis.
Experts say that shouldn't discourage heart patients from doing everything they can to lower their risks of a heart attack: control blood pressure and cholesterol, quit smoking, lose weight, change their diet, exercise and reduce stress.
"If you have heart disease, does it mean that it's all over? No. But it really means that you have to pay attention," said Dr. Suzanne Steinbaum, a preventive cardiologist at Lenox Hill Hospital in New York.
For many patients, the hardest part is changing their diet and getting exercise, she said.
"It's easier to take a pill than it is to get up and do something," said Steinbaum. "It's very difficult. It's a big commitment."
Russert, host of NBC's "Meet the Press," had a heart attack Friday in Washington while recording voiceovers for the news program.
His physician, Dr. Michael A. Newman, said in a statement that the heart attack was caused by a clot in an artery, blocking blood flow to the heart. That led to a fatal cardiac arrest — an abnormal heart rhythm that stops the heart from pumping blood to the body.
Newman said Russert had hardening of the arteries but no symptoms, and his blood pressure and cholesterol were well controlled. Russert exercised on a treadmill regularly, including the morning that he died, Newman's statement said. An autopsy showed Russert had an enlarged heart and significant blockage in the coronary artery where the clot formed.
Newman, who declined an interview request from The Associated Press, noted Monday night on CNN that Russert was overweight.
"Tim was a good patient. Are there things all of us as patients could be better at? Sure. But Tim was a good patient," Newman said on CNN's "Larry King Live."
About 920,000 Americans have a heart attack each year and 38 percent are fatal, according to the American Heart Association. Half of men and 64 percent of women who die suddenly of heart disease have no previous symptoms.
Despite impressive advances in preventing and treating heart disease, experts say there's no easy way to know which patients are going to have a heart attack and which aren't. Most heart attacks occur when fatty deposits in the arteries rupture and a clot forms.
The goal of preventive measures is to stabilize the plaque and prevent a rupture, or to prevent a dangerous clot from developing if the plaque does burst open.
Steinbaum said patients have difficulty understanding how someone can have a normal stress test like Russert, and then have a heart attack later. She said Russert apparently didn't have enough blockage when he had a stress test in April to indicate any problems. The test shows how the heart reacts to exertion and whether there's adequate blood flow to the heart.
"A stress test is important for us to assess how well the heart is functioning, but it doesn't give you a bye." said Steinbaum.
Not all heart attacks result in the heart suddenly stopping, as in Russert's case. Dr. Paul Wang of Stanford School of Medicine said only a small percentage lead to cardiac arrest, and it's not clear why, although the size of the heart attack can be a factor.
"This is far from uncommon though, unfortunately," he said. "There's still a substantial number of people who do have cardiac arrest," after a heart attack.
Few people survive a sudden cardiac arrest; a prompt shock from a defibrillator is needed to restore a normal heartbeat. Wang said the Russert case highlights the need for workplaces to prepare for a cardiac arrest, just as they plan for fire drills.
But not everyone can be saved. Russert's doctor said on CNN that efforts to revive him began immediately and paramedics shocked his heart three times before reaching the hospital.

When Is a Heart Attack Not a Heart Attack?

By LISA SANDERS, M.D.
1. Symptoms
“I don’t think he had a heart attack,” the patient’s wife declared emphatically. “I don’t care what the doctor in the hospital said.” The patient nodded his agreement. “But we need to be sure,” she added in a distinctive Long Island accent. That’s why they had gone to see Dr. Bruce Decter in New Hyde Park, N.Y., a cardiologist just out of training — to get a second opinion from someone a little closer to the books. The patient, a lanky 42-year-old man with a chiseled jaw, retreating hairline and skinny ponytail, seemed tired and anxious and grateful to have his childhood sweetheart do all the talking.
He had chest pain off and on for most of his adult life. His internist didn’t think it was his heart, and a normal stress test done the previous year seemed to confirm that. Then the week before his visit to Decter, his chest began to hurt while making love. It spread to his left shoulder and arm. And it didn’t go away. He hardly slept at all that night because of the pain and a gnawing anxiety that this time it really was a heart attack.
First thing the next morning he went to his internist. An EKG was normal, but the patient was so worried that his doctor arranged for him to see a cardiologist that afternoon. By then the patient was pale, sweaty and shaking. “I think you’re having a heart attack,” the cardiologist told the patient and then sent him straight to the E.R. The EKG done in the hospital was normal, but a series of blood tests indicated that he was having a heart attack, and a big one. He was rushed to the cardiac catheterization lab to see if the clogged vessel could be reopened. To the doctors’ utter amazement, there was no blockage; his heart looked fine.
Still, the cardiologist was certain that the patient had some kind of heart problem. As he explained it, there was either a blockage that reopened on its own, or he had a spasm in one of the coronary arteries. In either case, the patient was lucky that his heart hadn’t been permanently damaged. The cardiologist started the patient on a beta blocker — a medication that has been shown to protect the heart. But the chest pain kept coming.

2. Investigation
At his office, a week after the trip to the E.R., Decter examined the patient, a fit middle-aged man. His blood pressure was perfect. His heart rate was regular and slow. In fact, his entire exam was completely normal. He got another EKG. Also normal. The patient’s blood tests from the E.R. seemed to indicate that he had had a heart attack, but none of the EKGs or the angiogram revealed any abnormality.
The problem for Decter was one that doctors face regularly: how to reconcile tests that contradict one another. Often patients, and even doctors, think that test results provide a definitive answer — like the solution in today’s paper to yesterday’s crossword. But every test carries a risk of being wrong, and all tests need to be interpreted. This is never clearer than when different tests seem to tell different stories. Could these apparently contradictory results be shaped into a single narrative that made sense?
The blood test in question measures an enzyme that is released when a muscle like the heart is injured. That enzyme, creatine phosphokinase, abbreviated as CPK, was normal when the patient first presented to the emergency room but rose to a level 20 times higher than normal over the next several hours. In a patient who has chest pain that comes on with exertion, an elevated CPK usually means that the patient is having a heart attack.
But damage to any muscle will cause CPK to increase, so there is an additional test that can determine whether the enzymes are leaked from a damaged heart or from damaged skeletal muscle. When Decter called the lab for results of this test, he found that the CPK hadn’t come from the heart; it had come from the muscles of the arms and legs. “You’re right,” Decter told the anxious patient. “You didn’t have a heart attack.” But at this point, the young cardiologist acknowledged, he wasn’t at all sure what the patient did have.
The patient considered himself pretty healthy, he told the doctor. He took no medicine, had never smoked and exercised daily. In fact, the only other time he’d ever been in the hospital was when he was 21 and had mononucleosis. His urine then was really dark — “the color of Coca-Cola” — and the doctors were worried.
When Decter heard that, something stirred in his memory. Cola-colored urine. Perhaps this was the key. Had he had this kind of dark urine since then? he asked. The patient told him that a couple of times a month his urine would turn brown and he’d feel achy all over. It happened whenever he was sick or tired or when he exercised too hard. He’d told lots of doctors about it, but none of them could figure out what was going on.
Decter knew he was on to something. Urine that dark is usually caused by muscle breakdown. When muscle cells are damaged, they leak CPK, but they also spill several other chemicals. One of them, the compound that gives skeletal muscle its distinctive deep red hue, can turn urine a dark brown. Were the brown urine and the elevated CPK caused by the same problem? Were they both signs of some longstanding disease process that was destroying this patient’s muscle?
Decter sent his patient to Dr. Alfred E. Slonim, a pediatric endocrinologist by training who spent his career investigating diseases of the muscle. The patient called Decter after seeing the specialist, almost speechless with excitement. Slonim spent more than an hour with him and his wife, getting the history of his strange illness. “Tell him about what happens on Yom Kippur,” his wife prompted near the end of the interview. Every year on the Jewish day of atonement, the patient would fast for a day, from sunset to sunset. And every year, he would spend the day after Yom Kippur in bed, crippled by an aching in his muscles and passing dark brown urine. Once he said that, Slonim had the diagnosis: the patient had a form of the genetic disease known as carnitine palmitoyltransferase deficiency or CPT.

3. Resolution
In this rare genetic disease, patients are missing the necessary biological equipment to burn fat for energy. Normally the body uses a type of sugar provided by the diet or stored in the liver to keep the body running. When that sugar is used up, the body switches to fat for fuel. Patients with CPT can’t do that. Instead, when they run out of sugar, their bodies are forced to turn to the second backup form of energy: muscle. When this patient’s body depleted the normal fuel — because of decreased intake (fasting or illness) or increased metabolic activity (exercise or fever) — it had to turn to the energy stored in muscle just to keep the biological motor running.
This diagnosis finally allowed the patient and Decter to make sense of the original story. The CPT gave the patient terrible, chronic heartburn; the delicate tissue of the esophagus, when injured, can cause a pain that feels to many patients very much like the classic presentation of a heart attack. Certainly this patient thought he was having one the night he had sex. He didn’t sleep and didn’t eat all the next day when he was in the E.R., and that is what triggered the attack on his muscles and elevated his CPK numbers. “It’s incredible that it took a wrong diagnosis to get to the right one,” the patient told me. There’s no cure for this disease, but frequent meals can help ward off many attacks.
As for Decter, he says he doesn’t believe that this disease is quite as rare as he was told in medical school. Over the past decade, he has seen four patients with unexplained elevations in their CPKs and no evidence of heart disease. Two have tested positive for CPT-like genetic disorders. He’s still trying to figure out the other two.

Second Trial Finds Infusion No Help in STEMI


ATLANTA, Nov. 27 -- Heart attack victims do not benefit from an infusion of glucose, insulin, and potassium soon after the event, researchers here said.
Action Points
Explain to interested patients that small studies had suggested that an infusion of glucose, insulin, and potassium would benefit patients with ST-segment elevation myocardial infarction.
Note that this report shows that the infusion does no good and may perhaps do some harm in the first few days after a heart attack.
The finding marks the second time the so-called GIK therapy has been found wanting in patients with ST-segment elevation myocardial infarction (STEMI), Abhinav Goyal, M.D., of the Emory Rollins School of Public Health, and colleagues reported in the Nov. 28 issue of the Journal of the American Medical Association.
In fact, patients getting the GIK infusion appeared to have a slightly higher risk of death during the first three days after heart attack, although at 30 days there was no difference between them and controls, the researchers said.
The findings were not a surprise, the researchers said. In 2005, many of the same investigators reported that the therapy had a neutral effect in the 20,201 patients in a large randomized, controlled trial, the CREATE-ECLA study.
The current study, dubbed Organization for the Assessment of Strategies for Ischemic Syndromes-6 (OASIS-6), was stopped early when the CREATE results were published.
Both studies were two-by-two factorial designs, in which patients were randomized in a blinded fashion to get placebo or an anticoagulant drug -- fondaparinux (Arixtra) in the OASIS-6 trial and reviparin (Clivarine) in the CREATE study -- as well as the GIK infusion or no infusion, in an open-label fashion.
In this report, Dr. Goyal said, the researchers presented data on the 2,748 patients with acute STEMI who were randomized in OASIS-6 to get either GIK or no infusion before the study was halted.
They also reported a combined analysis of all patients in both trials.
The researchers found that in the OASIS-6 study, there were no differences at 30 days between the GIK infusion and the control groups in death (P=0.36), heart failure (P=0.31), or death and heart failure combined (P=0.41).
When the two studies were combined -- yielding 22,943 patients available for analysis -- the 30-day results were much the same.
However, when the researchers looked at the first three days after the heart attack, they found:
712 deaths (or 6.2%) in the GIK group and 632 deaths (or 5.5%) in the control group, for a hazard ratio of 1.13 and a 95% confidence interval from 1.02 to 1.26, which was significant at P=0.03.
1,509 death or heart failure events in the GIK group (or 15.8%) and 1,388 events in the control group (or 14.5%) for a hazard ratio of 1.09 and a 95% confidence interval from 1.02 to1.18, which was significant at P=0.02.
There was a consistent but nonsignificant increase in the number of heart failures in the GIK group, the researchers said.
In the following 27 days, the researchers said, GIK infusion was associated with a significantly lower occurrence of heart failure and the composite outcome of death or heart failure, as well as a nonsignificant decrease in the risk of death.
Overall, however, the GIK infusion had no effect on any outcome, they said.
The finding of a short-term risk increase, followed by a longer-term benefit, was probably a case of "survivor bias," the researchers said, especially since statistically controlling for glucose, potassium, and fluid balance eliminated much of the effect.
"The early harmful effects of GIK therapy largely may be explained by its propensity to increase glucose, potassium, and net fluid gain," the researchers concluded.
The bottom line, Dr. Goyal and colleagues said, is that "GIK infusion does not produce a favorable clinical effect in patients with STEMI."
Future studies of metabolic modulations in STEMI patients should try to avoid methods that increase glucose, potassium, and fluids, they added.
The study was supported by sanofi-aventis, Organon, and GlaxoSmithKline.
Dr. Goyal reported no conflicts. However, three of the study authors -- Andrzej Budaj, M.D., Ph.D., of Grochowski Hospital in Warsaw and Shamir Mehta, M.D., and Salim Yusuf, M.B.B.S., D.Phil., both of McMaster University in Hamilton, Ont. -- reported financial links to sanofi- aventis and GlaxoSmithKline.
Primary source: Journal of the American Medical AssociationSource reference: Díaz R, et al "Glucose-insulin-potassium therapy in patients With ST-segment elevation myocardial infarction" JAMA 2007; 298(20): 2399-2405.

Study Ties Heart Attack Deaths to Weekend Care

study of nearly all heart attack patients in New Jersey finds that those who arrived at a hospital on a weekend were less likely to get aggressive treatment and were slightly more likely to die than those who arrived during the week, researchers are reporting.
The study, based on an analysis of 231,164 heart attack patients admitted to New Jersey hospitals from 1987 to 2002, found a gap of almost a percentage point in heart attack death rates over a three-year span: 12.9 percent for weekend patients versus 12 percent for weekday patients. (The deaths occurred within a month of admission.)

http://www.nytimes.com/2007/03/14/health/14cnd-heart.html?ex=1331524800&en=49ff635470635463&ei=5088&partner=rssnyt&emc=rss