Although the "holiday heart syndrome," highlighted by rhythm disturbances after acute alcohol ingestion, is well known, the potential arrhythmogenic effects of alcohol have not been studied. Fourteen patients (two with congestive cardiomyopathy) with a history of rhythm disturbances and alcohol consumption were studied electrophysiologically. One patient had nonsustained ventricular tachycardia, one had nonsustained atrial fibrillation, one had paired ventricular responses, and the remainder had no response to the extrastimulus technique. After 90 mL of 80-proof whiskey, 10 of the 14 patients developed sustained or nonsustained atrial or ventricular tachyarrhythmias. Significant prolongation of His-ventricular conduction was seen after alcohol intake; this was noteworthy as one of the patients had previously shown Mobitz II atrioventricular block after acute alcohol consumption. Alcohol in modest doses has the potential to produce rhythm disturbances in patients with a history of chronic alcohol consumption and heart disease.

No abstract

Electrophysiological studies were performed during sinus rhythm on 21 patients who had demonstrated the spontaneous occurrence of sustained atrial flutter. The purpose was to determine if atrial conduction disease is a prediposing factor for the development of atrial flutter. Patients with atrial enlargement were excluded from the series. The control group consisted of 11 age-matched patients with normal electrocardiograms and electrophysiology studies. The flutter group showed prolongation of the mean right intra-atrial conduction time at 50 msec (control of 37 msec, P less than 0.05), the mean interatrial conduction time at 92 msec (control of 44 msec, P less than 0.001) and the mean P wave duration at 132 msec (control of 112 msec, P less than 0.01). The flutter group also demonstrated a higher incidence of sinus node dysfunction and ventricular conduction disease compared to the control group. These data indicate that patients who develop atrial flutter have atrial conduction disease. Atrial conduction disease appears to be 1) a major prediposing factor for the development of atrial flutter and 2) a part of the fibro-degenerative conduction disease spectrum.

No abstract

No abstract

No abstract

No abstract

Symptoms suggesting autonomic instability and increased adrenergic effect were identified in 53 patients with primary disorders of impaired wakefulness. Urine and plasma catecholamine concentrations were significantly increased in patients with sleep apnea. Excessive increases in heart rate during isoproterenol infusions suggested adrenergic hyperresponsiveness as an alternative explanation for symptoms of catecholamine excess in some individuals. Twenty-two patients demonstrated mitral valve prolapse (MVP), implicating primary neurologic disturbances as potential factors in the fatigue and lassitude often associated with MVP. The catecholamine abnormalities may explain some of the difficulties frequently encountered in using stimulants to treat sleep disorders.