The Difference Between Sudden Cardiac Arrest and Heart Attacks

Cardiac Arrest Survival

Cardiac Arrest Survival (Photo credit: GEEKSTATS)

, director of cardiology at Johns Hopkins Hospital, talks about the difference between sudden cardiac arrest and a heart attack and what those at risk can do.

Question: What is sudden cardiac arrest?

Answer: Sudden cardiac arrest refers to collapse and loss of consciousness due to a dramatic fall in blood pressure. This is often but not always the result of a life-threatening arrhythmia or an abnormality of the normal rhythmic activity of the heart. An excessively fast or slow heart rate can cause a profound drop in the blood pressure and sudden cardiac arrest. [It] is not a heart attack or myocardial infarction, which refers to a critical blockage in a blood vessel that supplies blood, oxygen and nutrients to the heart muscle. A blockage in a blood vessel can cause part of the heart muscle to die and be replaced by scar.

Q: How common is it, and who is at risk?

A: The risk factors for sudden cardiac arrest include the presence of heart disease, a family history and many of the factors that increase the risk for a heart attack, such as smoking, obesity, physical inactivity, high blood pressure, high cholesterol, high blood sugar or diabetes, and a poor diet. If someone has heart disease, particularly with weakness of the heart muscle, they may be at particularly high risk for sudden cardiac arrest and may benefit from implantation of an Implantable Cardioverter Defibrillator. [The defibrillators] may also benefit patients with a family history of sudden cardiac arrest and/or a genetic tendency to arrhythmias.

Q: How can you prevent sudden cardiac arrest?

A: In some cases, sudden cardiac arrest can be brought on by exertion, but this is not always the case, as sudden cardiac arrest often occurs when one is at rest. Physical activity is generally good for all of us. Those with known heart disease should consult their health care provider about the details of their own physical activity, but generally, even patients with heart disease should try to remain active. It’s wise to avoid extreme activity, particularly in harsh environmental conditions, such as heat or cold. For anyone who exercises, symptoms such as profound dizziness or lightheadedness, chest pain, shortness of breath, extreme fatigue and/or palpitations should prompt cessation of exercise and depending upon the severity of the symptoms and get prompt medical attention.

Q: How is sudden cardiac arrest different from a heart attack?

A: Heart attacks are caused by blockage of the arteries, which supply oxygen and nutrients. These most often are accompanied by chest pain and/or shortness of breath. Sudden cardiac arrest can be a complication of a heart attack, but it can occur without a heart attack. The treatment of a heart attack is to limit the damage to the heart by promptly opening up the involved blood vessel by a procedure known as angioplasty and by placing a stent to keep that vessel open. The treatment of sudden cardiac arrest is restoration of the heart’s normal rate of contraction and rhythm, and this typically involves a shock to the chest that’s known as cardioversion or defibrillation.

Q: How quickly do you need to be treated to survive?

A: The most common arrhythmias or irregularities of the heart that cause sudden cardiac arrest are rapid heart rhythms from the heart’s lower chamber. These are called ventricular tachycardia and ventricular fibrillation. If these arrhythmias are not promptly corrected by a shock to the chest, the individual will die. In the case of ventricular fibrillation, this may take only minutes. One can buy time by performing effective CPR. Just chest compressions, or so-called “hands-only” CPR, can be lifesaving.

Adapted from The Baltimore Sun

Patient Outcomes Significantly Improved By L-Carnitine Following Heart Attack

myocardial infarction - Myokardinfarkt - scheme

myocardial infarction – scheme (Photo credit: Wikipedia)

L-carnitine significantly improves cardiac health in patients after a heart attack, say a multicenter team of investigators in a study published in Mayo Clinic Proceedings. Their findings, based on analysis of key controlled trials, associate L-carnitine with significant reduction in death from all causes and a highly significant reduction in ventricular arrhythmias and anginal attacks following a heart attack, compared with placebo or control.

Heart disease is the leading cause of death in the United States. Although many of the therapies developed in recent decades have markedly improved life expectancy, adverse cardiovascular events such as ventricular arrhythmias and angina attacks still occur frequently after an acute myocardial infarction (heart attack).

It is known that during ischemic events L-carnitine levels are depleted. Investigators sought to determine the effects of targeting cardiac metabolic pathways using L-carnitine to improve free fatty acid levels and glucose oxidation in these patients. By performing a systematic review and meta-analysis of the available studies published over several decades, they looked at the role of L-carnitine compared with placebo or control in patients experiencing an acute myocardial infarction.

L-carnitine is a trimethylamine which occurs in high amounts in red meat and is found in certain other foods, and is also widely available as an over-the-counter nutritional supplement which is claimed to improve energy, weight loss, and athletic performance. Its potential role in treating heart disease was first reported in the late 1970s.

A comprehensive literature search yielded 153 studies, 13, published from 1989-2007, were deemed eligible. All the trials were comparison trials of L-carnitine compared with placebo or control in the setting of acute myocardial infarction.

This systematic review of the 13 controlled trials in 3,629 patients, involving 250 deaths, 220 cases of new heart failure, and 38 recurrent heart attacks, found that L-carnitine was associated with:

  • Significant 27% reduction in all-cause mortality (number needed to treat 38)
  • Highly significant 65% reduction in ventricular arrhythmias (number needed to treat 4)
  • Significant 40% reduction in the development of angina (number needed to treat 3)
  • Reduction in infarct size

There were numerically fewer myocardial reinfarctions and heart failure cases associated with L-carnitine, but this did not reach statistical significance.

First author James J. DiNicolantonio, PharmD, Wegmans Pharmacy, Ithaca, NY, observes, “Although therapies for acute coronary syndrome (ACS), including percutaneous coronary intervention, dual antiplatelet therapy, b-blockers (BBs), statins, angiotensin-converting enzyme inhibitors (ACEIs), omega-3 fatty acids, and cardiac rehabilitation, have markedly improved clinical outcomes, adverse cardiovascular (CV) events still occur too frequently after ACS. One promising therapy for improving cardiac health involves using L-carnitine to improve free fatty acid levels and glucose oxidation.”

“The potential mechanisms responsible for the observed beneficial impact of L-carnitine in acute myocardial infarction are likely multifactorial and may, in part, be conferred through the ability of L-carnitine to improve mitochondrial energy metabolism in the heart by facilitating the transport of long-chain fatty acids from the cytosol to the mitochondrial matrix, where b-oxidation occurs, removing toxic fatty acid intermediates, reducing ischemia induced by long-chain fatty acid concentrations, and replenishing depleted carnitine concentrations seen in ischemic, infarcted, and failing myocardium,” says DiNicolantonio.

L-carnitine is proven to be safe and is readily available over the counter. The investigators agree that the overall results of this meta-analysis support the potential use of L-carnitine in acute myocardial infarction and possibly in secondary coronary prevention and treatment, including angina. They advocate for a larger randomized, multicenter trial to be performed to confirm these results in the modern era of routine revascularization and other intensive medical therapies following acute myocardial infarction. But, says DiNicolantonio, “L-carnitine therapy can already be considered in selected patients with high-risk or persistent angina after acute myocardial infarction who cannot tolerate treatment with ACE inhibitors or beta blockers, considering its low cost and excellent safety profile.”

These findings may seem to contradict those reported in a study published earlier this month in Nature Medicine by Robert A. Koeth and others (Koeth, R. A. et al. Nature Med.*), which demonstrated that metabolism by intestinal microbiota of dietary L-carnitine produced trimethylamine N-oxide (TMAO) and accelerated atherosclerosis in mice. They also noted that omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine, and suggested a possible direct link between L-carnitine, gut bacteria, TMAO, and atherosclerosis and risk of ischemic heart disease.

“The Nature Medicine paper is of interest,” agrees senior investigator Carl J. Lavie, M.D.,FACC,FACP,FCCP, Medical Director of the Cardiac Rehabilitation and Prevention Center at the John Ochsner Heart and Vascular Institute at the University of Queensland School of Medicine in New Orleans, “but the main study reported there was in animals, and unlike our study, lacks hard outcomes.” He also notes that “there are various forms of ‘carnitine’ and our relatively large meta-analysis specifically tested L-carnitine on hard outcomes in humans who had already experienced acute myocardial infarction.”

from Sciences, E. (2013, April 16). “Patient Outcomes Significantly Improved By L-Carnitine Following Heart Attack.” Medical News Today. Retrieved from