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Abstract:
Ventricular premature beats (VPBs) are the most common cardiac arrhythmia. Simple VPBs have one form. Complex VPBs are repetitive, bigeminal, frequent, have different forms, or occur in the T wave of the previous beat. VPBs are seen frequently in patients with normal hearts, coronary artery disease, and mitral valve prolapse. In patients with normal hearts, VPBs are discovered with higher incidence when ambulatory or exercise electrocardiography is used to supplement the standard ECG. Patients with normal hearts and VPBs have a benign prognosis, and drug treatment is seldom needed. Most patients with stable angina pectoris and/or healed myocardial infarctions have VPBs on ambulatory and exercise electrocardiographic testing. These patients die sooner when VPBs are found than when none occur; complex VPBs suggest an even worse prognosis. Treatment of VPBs may relieve such symptoms as palpitations, but change in the prognosis by successful suppression has not yet been demonstrated. VPBs often occur during episodes of Prinzmetal's vasospastic angina. Treatment is directed principally toward relief and prevention of the spasm. All patients with acute myocardial infarction (AMI) have VPBs. Their incidence is highest at the onset of the illness. The number and complexity of the VPBs rise when myocardial damage is greater. VPBs should be prevented and, if present, vigorously suppressed to prevent ventricular fibrillation from developing during AMI. VPBs can be detected with exercise and ambulatory electrocardiography in most patients who have survived an acute episode of myocardial infarction. The prognosis is adversely affected by the presence of simple VPBs and even more ominous when complex VPBs are found. That the prognosis can be improved by suppression of VPBs after myocardial infarction has not been conclusively established. Survivors of cardiac arrest usually have simple and complex VPBs. The likelihood that further arrests will occur can be decreased by administration of antiarrhythmic drugs in sufficiently high doses to produce therapeutic blood levels or prevent induction of ventricular arrhythmias during electrophysiologic studies. A majority of patients with mitral valve prolapse have VPBs. Few require specific treatment for the arrhythmia.