Exercise induced "Mobitz type II" second degree AV block in a patient with chronic bifascicular block (right bundle branch block and left anterior hemiblock).

A 55 year old healthy man with chronic bifascicular block (right bundle branch block and left anterior hemiblock) had a near syncopal episode. A treadmill test showed exercise induced Mobitz type II AV block manifested clinically by paradoxical slowing of the heart rate and decreased blood pressure. True His Purkinje block and pseudo AV block due to His extrasystoles were documented by an electrophysiological study.

Double-blind crossover randomized trial of intravenously administered verapamil. Its use for atrial fibrillation and flutter following open heart surgery.

Fourteen patients with onset of atrial fibrillation (11) or flutter (three) and ventricular rate over 120 beats per minute following cardiac surgery were treated with intravenous (IV) doses of verapamil hydrochloride or placebo in a double-blind crossover protocol. Patients with poor left ventricular function, hypotension, atrioventricular block, and taking beta-blockers and disopyramide were excluded. The dosages were 0.075 mg/kg and 0.15 mg/kg given 15 minutes apart, with termination of study on achieving an end point (conversion to sinus rhythm or slowing of ventricular rate to below 100 beats per minute). None reached the end point with placebo but all with verapamil. Baseline ventricular rate was 144 +/- 20 beats per minute, after placebo 143 +/- 16 beats per minute, and after verapamil 89 +/- 7 beats per minute (mean +/- SD). Thus, IV verapamil briefly slows the ventricular rate of atrial tachyarrhythmias following cardiac surgery.

Effects of oral dipyridamole on coronary dynamics and myocardial metabolism at rest and during pacing-induced angina in patients with coronary artery disease.

The effects of oral dipyridamole administration (150 mg) on coronary hemodynamics, myocardial metabolism, and pacing threshold were studied in 10 patients with significant coronary artery disease (CAD). Following dipyridamole through 120 minutes, there was no significant change in resting heart rate, arterial pressure, coronary venous flow, coronary resistance, myocardial lactate extraction, or myocardial oxygen consumption. Rapid atrial pacing performed before and at 60, 90, and 120 minutes after dipyridamole failed to demonstrate any significant reduction in pacing threshold or evidence of increased ischemia after dipyridamole. Blood dipyridamole levels showed variable and slow absorption which probably explains the difference between intravenous and oral dipyridamole on coronary dynamics and myocardial response to pacing.

Left-to-right shunt via left superior vena cava communication with left atrium.

The findings in a 22-year-old man with Ebstein's anomaly of the tricuspid valve, Wolff-Parkinson-White syndrome, and a persistent left superior vena cava are reported. This is the first reported case of this combination of anomalies in which the atrial septum was intact and the left superior vena cava communicated with the left atrium. Uniquely, blood was shunted left to right via the left superior vena cava from the left atrium. Only one previous case of left-to-right shunting via a left superior vena cava (in the absence of mitral valvular disease or cor triatriatum) has been reported (associated with aortic coarctation). Angiograms demonstrated the left atrial connection of the left superior vena cava to be at the entrance of the right superior pulmonary vein into the left atrium. In the absence of demonstrable left-sided heart disease, this anatomic juxtaposition is suggested as a possible explanation for the direction of shunting.

Bi-morphic atrial flutter.

A case of atrial flutter whose classic "saw-tooth" morphology, resistant to full doses of digoxin and quinidine, was changed to an unusual form by low energy direct current shock is presented. The atrial and ventricular rates remained identical in spite of the different F wave pattern before and after attempted cardioversions. 0.5 mg digoxin was given after cardioversion failed and the patient reverted to normal sinus rhythm. This case strengthens the theory of rapidly discharging atrial focus as a mechanism of atrial flutter and the case for a change in intra-atrial conductions as cause for change in atrial electrograms.