Biomedical subjects
Publications and source records attributed to J Kupersmith.
Peripartum cardiomyopathy is a congestive cardiomyopathy that occurs within the last month of pregnancy or first six months after delivery. Early diagnosis and prompt treatment are of paramount importance. Our patient did not respond to conventional therapy and needed a left ventricular assist device and subsequent orthotopic cardiac transplantation to survive.
Prism-CLR is a new single chamber unipolar pace, bipolar or unipolar sense, rate responsive pacemaker that utilizes a closed-loop system based on the analysis of the evoked potential for rate adjustment. It also has an automatic output regulation feature for capture verification and threshold search. Five patients in whom this pacemaker was implanted exhibited an appropriate rate increase with exercise and psychological stress. Automatic output regulation functioned appropriately in three of five patients. Preliminary data suggest that Prism-ClR is an effective pacemaker for patients who may benefit from rate responsive pacing. The automatic output regulation recognition algorithm may need modification in some patients.
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The dextrorotatory isomer of sotalol (d-sotalol) has class III antiarrhythmic properties with known action potential duration (APD) prolonging effects, and is largely devoid of beta-adrenergic blocking activity. We studied its electrophysiologic effects and the mechanism of its APD prolonging effects in sheep Purkinje fibers by means of standard microelectrode techniques. At all concentrations (10(-6) to 10(-4) mol/L), d-sotalol had no effect on Vmax. At 10(-6) mol/L, d-sotalol had no effect on APD. A concentration-dependent effect of 10(-5) to 10(-4) mol/L d-sotalol was found on APD. At peak effect, APD was prolonged by 56% and 49% at 50% (APD50) and 90% (APD90) of repolarization (p less than 0.01). Early afterdepolarizations (EADs) were noted at high concentration of d-sotalol (10(-4) mol/L). These EADs were increased in number by epinephrine. To assess the mechanism of APD prolongation, verapamil (2.0 X 10(-6) mol/L) was added before and after d-sotalol treatment. In the presence of verapamil, no APD prolongation was observed even at the highest d-sotalol concentration (10(-4) mol/L). Next, during APD prolongation at the highest d-sotalol concentration, we added verapamil, noticing a remarkable shortening of APD. In addition, d-sotalol-induced EADs disappeared with addition of verapamil. Thus (1) verapamil blocks d-sotalol-induced APD prolongation and EADs and (2) this may be consistent with a mechanism via slow inward current.
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The automatic implantable cardioverter defibrillator is an effective device for prevention of sudden cardiac death. Patients who require the implantation of the device often require permanent pacing for symptomatic bradyarrhythmias and may require antiarrhythmic drug therapy. Antiarrhythmic drugs may alter the defibrillation thresholds, arrhythmia cycle length and frequency, pacing thresholds and postshock excitability. Interactions between the defibrillator and the pacemaker may result in sensing problems, leading to multiple counting and inappropriate shocks, or ventricular fibrillation nondetection, sensing or capture failure post defibrillation and pacemaker reprogramming induced by defibrillator discharge. The potential for interactions will increase as the new generation of programmable defibrillators become clinically available, combining features of permanent pacemakers, antitachycardia pacemakers and defibrillators.
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The hemodynamic and antiarrhythmic interactions between nadolol and a commonly used class I antiarrhythmic agent, quinidine or procainamide, were evaluated in 18 patients with ventricular arrhythmias in a double-blind, parallel study. Patients qualified for entry into the study if their ventricular arrhythmias remained poorly controlled (greater than or equal to 10 ventricular premature complexes/hr) with the class I agent alone and they had a left ventricular ejection fraction greater than 30%. Patients received their usual therapeutic doses of quinidine or procainamide throughout the study, which consisted of 3 treatment periods; a 2-week placebo treatment period, a 2-week open-label oral nadolol dose titration period, during which the dosages of nadolol were gradually increased from 40 mg daily to a maximum tolerated dose up to 120 mg daily, and a 4-week randomized, parallel comparison period during which patients were treated with either a class I agent alone or a combination of a class I agent and nadolol. Left ventricular ejection fractions by radionuclide ventriculography and 24-hour ambulatory electrocardiographic (Holter) recordings were obtained at the end of each treatment period. A positive treatment response was defined as greater than or equal to 75% reduction in ventricular premature complex frequency. During the dose titration phase, combination therapy with nadolol (mean dose 94 mg daily) and class I agents produced a mean decrease in ventricular premature complexes of 79% (p less than 0.01), and a mean decrease in ventricular couplets of 95% (p less than 0.01). A positive response was observed in 57% of patients treated with nadolol plus a class I agent.(ABSTRACT TRUNCATED AT 250 WORDS)
Myotonic dystrophy is frequently associated with functional and anatomic derangements in the myocardium. Ten myotonic dystrophy patients (seven men and three women, ages ranging from 35 to 58 years) were evaluated with a 12-lead ECG, 24-hour Holter monitor recording, invasive electrophysiologic studies, and echocardiographic examination. Nine patients displayed abnormalities in the conduction system. ECG and Holter monitor abnormalities were first-degree atrioventricular block (n = 8), second-degree atrioventricular block (n = 1) (Wenckebach type), complete left bundle branch block (n = 2), left anterior fascicular block (n = 5), left posterior fascicular block (n = 1), sinus bradycardia (n = 6), sick sinus syndrome (n = 2), frequent premature ventricular complexes (n = 4), and ventricular tachycardia (n = 2). Electrophysiologic study abnormalities included AH interval less than or equal to 140 msec (n = 7), AH interval greater than 140 msec (n = 3), HV interval greater than 60 msec (n = 9), and ventricular tachycardia induction (n = 1). Echocardiographic examination revealed mitral valve prolapse (n = 6). We conclude that diffuse conduction abnormalities were seen in a majority of our patients with myotonic dystrophy. Ventricular arrhythmias, including ventricular tachycardia, were seen in some of these patients, and mitral valve prolapse was a frequent finding.
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When membrane potential (Vm) remains at depolarized levels for prolonged intervals, quiescence and/or repetitive activations occur. In situ such events would be associated with arrhythmias. One way for such a state to occur is abnormal delay of repolarization leading to marked prolongation of action potential (AP) duration (APD). We studied canine Purkinje fibers in which abnormal AP prolongation had been induced by hypoxic, acidic Tyrode's with or without epinephrine, or by Ni++. AP's exhibited a prolonged secondary plateau with or without early afterdepolarizations (EAD's); they were up to ten minutes in duration. With programmed stimulation, APD's displayed a markedly exaggerated interval dependence with slight increases in diastolic interval causing transitions from normal to abnormal and very long AP's. Normalization of AP's occurred during prolonged rapid pacing trains and only gradually returned to abnormality after cessation of pacing. We also induced EAD's via programmed stimulation at plateau Vm levels. Repolarization could be brought on abruptly via these stimulus-induced EAD's; in certain instances trains of EAD's were required. The above characteristics of the state for which the term "repolarization failure" seems appropriate may have implications for in situ arrhythmias, e.g. in "Torsade de Pointes" ventricular tachycardia.
Labetalol is a competitive inhibitor of alpha- and beta-adrenergic receptors and has an antihypertensive action. To determine limb haemodynamic effects, we measured calf blood flow and venous capacitance by venous occlusion plethysmography before and after oral labetalol in 10 patients 3-7 days following coronary bypass surgery. Vascular resistance was calculated as the ratio of mean arterial pressure to arterial flow. The peak effect of labetalol was taken as the point of maximum blood pressure decline, and this interval was selected for evaluation of the limb haemodynamic response. Ninety to 120 min after administration of 100-200 mg of labetalol the mean blood pressure fell from 88 +/- 3 to 79 +/- 3 mm Hg; (P less than 0.005). The mean arterial blood flow registered 5.1 +/- 1.0 ml 100 ml-1 limb tissue min-1 which was not significantly different from the control value of 4.4 +/- 0.8 ml 100 ml-1 limb tissue min-1. The calculated index of limb vascular resistance was not affected by labetalol administration, averaging 37 +/- 12 mm Hg 100-1 ml limb tissue min-1 before labetalol and 30 +/- 11 mm Hg ml-1 100 ml limb tissue min-1 at the time of peak hypotensive effect. There was a slight but statistically significant increment in limb venous volume to 1.9 +/- 0.3 from 1.5 +/- 0.3 ml 100 ml-1 limb tissue (P less than 0.025). Placebo administration produced no consistent changes in blood pressure, arterial blood flow, vascular resistance or venous capacitance.(ABSTRACT TRUNCATED AT 250 WORDS)
Abnormal delay of repolarization leading to prolonged reduction of membrane potential could lead to arrhythmias. Transmission of this type of abnormality from an "abnormal" to a "normal" segment of Purkinje fiber was studied as follows: In a double compartment bath one segment was superfused with unmodified Tyrode's solution and the other with solutions known to induce abnormal prolongation of action potential duration (manifest by prolonged step-like delays in repolarization, or "secondary plateaus" and "early afterdepolarization," that is, activations arising as a consequence of the prolonged depolarized membrane potential). Transmission of abnormalities varied. Complete transmission of secondary plateaus and early afterdepolarizations led to action potentials configurationally similar throughout the fiber. Selective transmission of early afterdepolarization led to the occurrence of new premature action potentials in the normal segment. Cycle length prolongation favored both the occurrence and the transmission of abnormalities. After addition of lidocaine or high potassium ion solutions to the normal segment, shortening of action potential duration occurred and was transmitted from normal to abnormal segment. In this way, reversal of abnormality throughout the fiber occurred via an intervention applied selectively to the normal segment. Observations in this study may be relevant to arrhythmias and their treatment.
A 31 year old woman who developed an atypical ventricular tachycardia after administration of intravenous verapamil for control of a recurrent supraventricular tachycardia is presented. Possible explanations for the observed arrhythmia, polymorphous ventricular tachycardia, are discussed. Verapamil must be considered one of the pharmacologic agents that can cause this arrhythmia.