Exercise-Induced PVDs
November 1, 2000 4 minutes read
Exercise-Induced PVDs
Abstract & Commentary
Synopsis: Frequent ventricular premature depolarizations during exercise in asymptomatic, middle-aged men are associated with a long-term increase in cardiovascular death.
Source: Jouven X, et al. N Engl J Med 2000;343: 826-833.
Jouven and colleagues from paris report results from a long-term study on risk factors in employees of the Paris Civil Service. The study enrolled 7746 male government workers between 42 and 53 years of age. These subjects underwent electrocardiography, provided a medical history, and had a physical examination with selected laboratory studies to exclude clinically apparent cardiovascular disease, including moderate to severe hypertension and any ECG abnormality. Subjects were then exercised using an accelerated bicycle protocol that included three workloads: two minutes at 82 W, six minutes at 164 W, and two minutes at 191 W. The test could be stopped before completion for severe symptoms, a systolic blood pressure over 250 mm Hg, a heart rate over 180 beats per minute, any ischemic changes on ECG ( > 1 mm ST depression), or ventricular tachycardia. Subjects with a run of two or more consecutive ventricular beats or with more than 10% of all beats ventricular in origin, were classified as having frequent ventricular premature depolarizations (VPDs). Patients were then followed long-term for up to 27 years. Mortality data during the time the subjects were used were provided by the government department in which the subjects worked. After retirement, cause of death was obtained from the death certificate.
Complete baseline data and follow-up data were available from 6101 of the original subjects. Of these, 4.4% had ischemia and 0.8%, 2.3%, and 2.9% had frequent VPDs as defined above either before, during, or after exercise. Among the subjects with frequent VPDs dur- ing exercise and among those with evidence for ischemia, cardiovascular and total mortality rates were significantly higher than in those without. There was no increased risk associated with infrequent VPDs or with frequent VPDs before or after exercise. The crude comparative cardiovascular mortality rates were as follows: 6.4% if ischemia and frequent VPDs were both absent; 16% if ischemia with frequent VPDs was present; 16.1% if frequent VPDs without ischemia was present, and 25% if both these findings were present. The cumulative, all-cause mortality rates were 26.2%, 33.1%, 40.7%, and 50.0% for the same four groups, respectively. Patients with frequent VPDs consumed more tobacco daily but were similar to the other groups in most other clinical variables. Patients with ischemic responses to exercise were slightly older and had slightly higher mean levels of cholesterol and triglycerides than did the other groups.
Jouven et al concluded that frequent VPDs during exercise in asymptomatic, middle-aged men are associated with a long-term increase in cardiovascular death.
Comment by John P. DiMarco, MD, PhD
For a number of years, it has been standard teaching that asymptomatic ventricular arrhythmias in patients with normal ventricular function are associated with a good prognosis; therefore, they did not require therapy. In the paper by Jouven et al, asymptomatic arrhythmias during exercise were associated with a 2.5-fold increase in the risk for cardiovascular death. Should these observations lead us to change our approach to patients in whom asymptomatic ventricular ectopy is detected? I believe the answer is no.
This was a very unusual study. A large cohort of men without cardiac symptoms or history were identified, tested, and then followed for a very long period of time. Even in the groups with positive findings, the annual cardiovascular mortality rates were considerably less than 1% per year through the first 20 years of the study. This low-event rate means that any response to the risk factors identified must be both safe and inexpensive to warrant implementation. Treatment of standard risk factors such as increased lipids, hypertension, and tobacco use would qualify, but antiarrhythmic therapy certainly would not.
Why were the frequent VPDs associated with increased mortality in this cohort? Several explanations might be considered. Standard ECG stress testing has a sensitivity of only 60-70% for detecting angiographically documented coronary lesions. Therefore, some of the VPDs might have been due to ischemic heart disease not detected by the test. The subjects only underwent a limited screen for cardiac disease. Mild or moderate hypertensive heart disease or an early nonischemic cardiomyopathy would not have been detected but could be associated both with PVCs and an increased mortality during follow-up. Tobacco abuse can result in increased vascular reactivity even before clinically detectable fixed coronary obstruction develops and this also may result in increased ectopy.
The Cardiac Arrhythmia Suppression Trial showed that treating ventricular ectopy, a known risk factor, in moderate to high risk populations was counterproductive. Treating VPDs in an asymptomatic individual based on the data shown here would also be incorrect.
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