Heart Associates     Commonly Asked Questions

"Could you predict sudden cardiac arrest?"

Foretelling the future of a disease process in a patient is one of the foremost duties of a physician. However, when it comes to the issue of coronary artery disease and sudden cardiac death, it is extremely difficult to predict the possibility of sudden cardiac death with any level of accuracy. As we have discussed before, of the half a million lives lost each year from coronary artery disease, approximately 250,000 of them did not have any symptoms or evidence of coronary artery disease or cardiovascular events in the past. In general, people who have a constellation of conventional as well as novel cardiac risk factors have a much higher incidence of coronary artery disease, and therefore SCD. In addition, a high resting heart rate of more than 84 beats per minute, diminished pumping function of the heart, a depressed heart rate variability, a high frequency of premature ventricular complex rates, left ventricular hypertrophy (LVH) on 12-lead EKG, nonspecific T wave inversions on the resting EKG, abnormal signal-average EKGs with late potentials, presence of significant plaque load on the carotid artery by ultrasound examination, ankle brachial index of less than 0.7, the presence of coronary calcification on ultrafast scanning, and high levels of fibrinogen and C-reactive proteins are all markers for coronary artery disease that are helpful to predict future coronary events in a subject.

If a person already has sustained a myocardial infarction it is easier to predict subsequent coronary events by identifying the following predictors:

  1. Ventricular fibrillation and ventricular tachycardia. Patients with acute myocardial infarction developing VT or VF in the convalescent phase are at very high risk to develop sudden cardiac death. Thirty-three percent of these patients sustain sudden cardiac arrest per year in the succeeding years.

  2. Out of hospital cardiac arrest. If a patient is a survivor of an out of hospital cardiac arrest, he or she has about a 27% chance of developing a sudden cardiac death per year of survival; a situation considered to be very high risk.

  3. Poor pumping function and ventricular irritability. Survivors of acute myocardial infarction with poor pumping function of the heart (ejection fraction 30% or below), and significant ventricular irritability (more than 10 premature ventricular beats per hour detected by an ambulatory Holter monitor evaluation) have a combined 50% risk of mortality for the next three years. However, survivors of acute myocardial infarction with good pumping function and having no ventricular irritability are also at a relatively high risk for sudden cardiac arrest – a cumulative 5% for the succeeding three years. It is important to note that this subset constitutes a very large number of patients, and therefore the total life loss is very high in this group.

  4. Poor heart rate variability. In normal subjects, the beat-to-beat heart rhythm shows minor variations based on an intact sympathovagal system. This variability is quite marked with each respiration, physical activity, ischemia, and circadian rhythm. The heart’s rhythm, contractility, and electrical stability are maintained by a balanced rich supply of sympathetic and parasympathetic fibers from the nervous system. The vagal reflex (parasympathetic activity mediated through the tenth cranial nerve), has a protective effect on ventricular irritability and fibrillation. Blunted heart rate variability is a manifestation of poor vagal tone. In survivors of an acute myocardial infarction, poor heart rate variability is associated with a high incidence of sudden cardiac death. There is a subset of patients who have distinctly poor heart rate variability response (HRV) in the early morning hours of the circadian rhythm, which correlates with the observation of an increased incidence of acute myocardial infarction and sudden cardiac arrest in the early morning hours. Now, we have the capabilities to assess poor heart rate variability with present day Holter monitors.

  5. Late potentials and repetitive ventricular forms. In addition to poor heart rate variability, the presence of late potentials in a signal-average EKG, and repetitive ventricular forms are also independent markers of sudden cardiac arrest in survivors of acute myocardial infarction. However, the prognostic value is blunted by their poor specificity.

Can we predict a sudden cardiac arrest in the asymptomatic individual?

Of the 300,000 sudden cardiac deaths in the United States, the vast majority of them never experienced a cardiac event. The overall incidence of sudden cardiac death in the population at large is 0.1% to 0.2%, approximately one victim per year per 1000 population. For the high cardiac risk factor groups (i.e., individuals with high blood pressure, diabetes, hypercholesterolemia, smoking, family history, etc.), who never sustained a cardiac event, the incidence of sudden cardiac death is about 16 per 1000 population (1.6% per year). But the travesty of the situation is that a large section of the population is harboring high blood pressure, diabetes, and hypercholesterolemia even without being detected. They continue to smoke with a sense of impunity and never exercise, and thereafter will not know whether they have any exercise-induced symptoms at all.

As of now, we neither have a skin test to detect CAD nor a vaccine to prevent the disease. The risk factors must be screened and rectified. The individual’s responsibility must be addressed and accepted.

In general, I can say that the following situations are predictors of coronary artery disease and consequently sudden cardiac arrest with very wide ranges of sensitivity and specificity.

  1. Strong family history of premature coronary artery disease.
  2. Smoking.
  3. Diabetes.
  4. High blood pressure.
  5. Hyperlipidemic syndrome.
  6. Obesity.
  7. Postmenopausal state.
  8. Sedentary habits.
  9. Type A personality.
  10. High dietary salt intake.
  11. Novel cardiac risk factors. (See Chapter 3)
  12. Left ventricular hypertrophy.
  13. Abnormal resting heart rate (above 84 beats/min).
  14. Carotid and peripheral vascular disease.
  15. Reduced ankle brachial blood pressure index.
  16. Poor chronotropic response with an exercise test.
  17. Inappropriate heart rate recovery immediately after an exercise test (i.e., less than 12-beat reduction of the pulse rate in one minute after the peak exercise).
  18. Elevated C-reactive protein and fibrinogen levels.
Above all, the individual’s awareness of coronary artery disease and its implications deserve maximum attention.

Heart attacks without chest pain

About 33% of all heart attacks are without any chest pain. The incidence is very high if you are: an older person, a female, a diabetic, and have a history of congestive heart failure.

The impact: These patients reach the hospital late; more chance of misdiagnosis; less thrombolytic therapy; less primary angioplasty; less aspirin treatment; less beta blocker treatment; less heparin treatment; and less bypass graft surgery.

Phone: (585) 338-2322

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