William S. Frankl

Probable postcardiotomy syndrome following implantation of a transvenous pacemaker: Report of the first case

The syndrome of fever and pericarditis is reported following implantation of a transvenous pacemaker in a 72-year-old man. The pacemaker was placed for prophylactic reasons (i.e., presence of bifascicular block). The syndrome resolved spontaneously after over four weeks of fever and a pericardial friction rub. Perforation of the right ventricle, although not recognized in this patient, is a complication which occurs with passage of a transvenous pacemaker. There was no other antecedent events to explain the syndrome such as myocardial infarction or trauma to the chest.

Electrophysiologic effects of hydralazine on sinoatrial function in patients with sick sinus node syndrome.

The electrophysiologic effects of hydralazine were evaluated in nine hypertensive patients with sinoatrial dysfunction. Intravenous hydralazine, 0.15 mg/kg, caused no significant reduction in arterial blood pressure. Yet this dose of hydralazine increased heart rate from 61.9 +/- 4.1 beats/min (mean +/- standard error of the mean) to 68.6 +/- 4.9 (P less than 0.001). Sinus nodal recovery time upon termination of atrial pacing shortened from 3,207 +/- 1,098 to 2,064 +/- 573 msec (P less than 0.05) and second escape cycles shortened as well (P less than 0.025). Acceleration of heart rate and abbreviation of recovery time did not closely correlate with change in blood pressure (r = 0.41 and 0.18, respectively). Junctional escape beats became more frequent and junctional escape time shortened from 2,525 +/- 692 to 1,705 +/- 382 msec (P less than 0.05). Sinoatrial conduction time tended to shorten, but a significant change was not observed. Atrial tachyarrhythmias did not occur and atrial refractoriness was unchanged. Thus, a minimal blood pressure response to hydralazine was associated with enhanced automaticity. Hydralazine merits clinical trial for treatment of sick sinus syndrome with concomitant hypertension.

Effect of procainamide on induced ventricular tachycardia.

Ventricular extrastimulation was performed in 11 patients evaluated for chronic recurrent ventricular tachycardia, before and after a 1‐gm procainamide infusion. Extrastimulation caused only nonsustained extra beats (<4) in 3 patients. Sustained tachycardia was induced in 7 patients in the basal state, of which 6 continued to have inducible tachycardia after procainamide was given (5.2 to 9.8 mg/L). The zone of coupling intervals that initiated tachycardia was unchanged or widened in these 6 patients because ventricular refractoriness was unchanged or because the tachycardia zone shifted to later diastole by an interval at least equivalent to the prolongation of ventricular refractoriness. Post‐procainamide tachycardia cycle length was prolonged in all patients, by an average 51 msec. The one patient who responded to procainamide had a shartened ventricular refractory period, but the greatest slowing of tachycardia. Finally, sustained ventricular tachycardia could be induced in the eleventh patient only following procainamide administration, consistent with his clinical history. These results suggest that procainamide often may be ineffective in preventing sustained ventricular tachycardia, and that slowed conduction, rather than prolonged refractoriness, is the basis for the procainamide antiarrhythmie effect. Our data emphasize that antiarrhythmie drug effectiveness be evaluated in terms of effect on sustained arrhythmia rather than suppression of isolated ectopic beats.

Variant Angina Pectoris

A case of Prinzmetal’s angina pectoris (variant angina pectoris) is reported. The presentation provided two somewhat unusual elements in that relief of pain was sometimes obtained by jogging and elevated ST segment alternans occurred on the exercise test. However, there were many aspects of the case which were classical, and these are described. Because of the high incidence of myocardial infarction and the presence of a single obstructive lesion amenable to surgery attributed to this form of angina pectoris, coronary angiography was performed and revealed just such a lesion. The patient was subjected to saphenous vein bypass with subsequent relief of pain. Some notes on the rationale for the surgical approach and therapy are presented.

Effect of lidocaine on right ventricular muscle refractoriness.

The effect of clinical doses of lidocaine on ventricular refractoriness was investigated in man. Effective refractory period (ERP) and functional refractory period (FRP) were determined in 11 normokalemic patients via a catheter at the right ventricular apex using programmed extra‐stimuli and a ventricular electrogram recorded from the pacing catheter. No subject had recent ischemia or infarction. Measurements were repeated after clinical doses of lidocaine that produced therapeutic blood levels. Lidocaine caused no significant change in ERP or F RP during ventricular or atrial drive, or sinus rhythm with unchanged cycle length (CL). During sinus rhythm ERP/CL was unchanged. In 4 of 5 patients, lidocaine did not abolish echo phenomena observed during ventricular drive. This study demonstrates that ventricular refractoriness can be safely measured in man. Clinical doses of lidocaine did not alter right ventricular refractory periods. Lidocaine action is not explained by alteration of ventricular refractoriness, at least in muscle remote from the site of acute infarction.

Differential echocardiographic patterns in mitral regurgitation.

* Professor of Medicine, Chief, Cardiology Division, Department of Medicine, The Medical College of Pennsylvania. † Resident in Cardiology, Cardiology Division, Department of Medicine, The Medical College of Pennsylvania. ‡ Assistant Professor of Medicine, Director, Cardiac Graphics Laboratory, Cardiology Division, Department of Medicine, The Medical College of Pennsylvania. There have been a number of reports on the systolic click-late systolic mur-