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Biomedical subjects

R A Massumi

Publications and source records attributed to R A Massumi.

At least 19 recordsLinked to original sources

Verapamil-mediated atrioventricular nodal reentrant tachycardia and the uncovering of dual-pathway AV nodal conduction.

In a 67-year-old man with multiple myocardial infarctions in the past, the use of oral verapamil for control of angina pectoris was followed by the appearance of two previously undiagnosed abnormalities, namely, a dual-pathway AV node conduction pattern, and paroxysms of AV nodal reentrant tachycardia precipitated by premature ventricular beats (PVB). It is probable that the differential effects of verapamil on the fast and slow AV node pathways, and the interplay of PVB with its concealment within the AV node, created the necessary circumstances in the AV node to precipitate the tachycardia. Observed off verapamil over several months, the patient remained in normal sinus rhythm but continued to have numerous premature ventricular beats (PVB's). Nevertheless, neither the clinical electrocardiographic features of dual-pathway AV node conduction nor the AV nodal reentrant tachycardia could be found. The proarrhythmic effect of verapamil and its ability to provoke the very arrhythmia against which it is most effective are of particular interest in view of a similar behavior exhibited by the Class I antiarrhythmic agents.

Aged↗

Intermittent fascicular extrasystoles producing pseudo AV block: electrophysiologic effects of beta agonists and antagonists.

This report describes a patient with pseudo-type II second-degree AV block due to an intermittent parasystolic focus located in the left bundle branch. A paradoxical increase in the fascicular rate was seen following intravenous propranolol, and fascicular extrasystoles were suppressed after intravenous isoproterenol treatment. All propagated fascicular extrasystoles were conducted to the ventricle with incomplete or complete right bundle branch block and a decrease in the H'-V interval compared to the H-V interval during sinus rhythm. Treatment with oral quinidine abolished fascicular extrasystoles without worsening of AV conduction.

Bundle-Branch Block↗

Mechanically mediated pacemaker pseudomalfunction.

A case is described of pacemaker pseudomalfunction caused by intermittent displacement of the ventricular lead. The displacement was shown to be caused by critically timed atrial contractions, dislodging the looped ventricular lead, and resulting in intermittent failure to stimulate the heart.

Aged↗

Myocardial performance and N2O analgesia in coronary-artery disease.

Inhalation of 40 per cent N2O by nine patients who had occlusive disease in two or more coronary arteries with elevation of left ventricular end-diastolic pressures (LVEDP) significantly decreased arterial pressure (average 5 per cent) and myocardial contractility as measured by dP/dt/CPIP (average 14 per cent), and increased LVEDP (average 21 per cent). N2O had no significant effect in four patients who had angina without angiographically demonstrable coronary arterial disease. It is concluded that N2O depresses myocardial function in patients who have occlusion of the coronary arteries and impaired left ventricular function.

Adult↗

Prolonged His-Q interval in chronic bifascicular block. Relation to impending complete heart block.

Although prolonged infra-His conduction time in bifascicular block is suspected of denoting trifascicular disease, adquate documentation is lacking concerning the correlation between lengthened His-Q interval (H-Q) and the risk of development of complete heart block (CHB). H-Q in conducted sinus beats in patients with bifascicular block associated with Mobitz II or intermittent CHB represents the approximation of maximal H-Q prolongation prior to onset of trifascicular block. To assess this relationship between prolongation of H-Q and trifascicular block, His bundle electrocardiography (HBE) was performed in 50 patients with chronic bifascicular block exhibiting Mobitz II block or transient CHB. Mobitz II or episodic CHB was shown in all patients: within two days prior to HBE in 45/50 patients; in 39/50 patients during HBE; and following HBE in five patients. In 49/50 patients H-Q was prolonged (greater than 55 msec) and in 47 this interval was substantially lengthened (65 msec or greater). Since marked H-Q prolongation in conducted sinus beats was documented in nearly all patients with bifascicular block associated with intermittent complete trifascicular block, we conclude that a considerably lengthened H-Q interval in bifascicular block is not only a usual prerequisite but strong evidence, for impending complete heart block.

Adult↗

Electrophysiologic properties of perhexiline.

Perhexiline maleate (Pexid), a promising clinical antiarrhythmic and antianginal drug, was evaluated for its electrophysiologic effects on the entire conduction system of the intact canine heart throughout a wide range of therapeutic and potentially toxic doses. Intracardiac conduction times were measured by bipolar intramyocardial and transvenous endocardial electrodes before and following the intravenous administration of each dose of perhexiline maleate, 3 mg/kg every 30 min for a total of 4 doses in 7 open-chest anesthetized dogs. Eight animals served as controls in which similar operative technique and electrophysiologic variables were recorded after infusion of the maleate diluent. In addition, the effects of perhexiline on atrial and ventricular thresholds to electrical stimulation were recorded, as well as the QRS and QT intervals, sinus rate, and rhythm disorders. It was observed that perhexiline did not significantly (p greater than .05) alter sinus rate, QT interval, QRS duration, PR interval, intra-atrial conduction time, atrioventricular nodal conduction time, and His-Purkinje conduction velocity. The drug did not affect the cardiac threshold to electrical stimulation of less than 0.1 ma. No ectopic atrial or ventricular activity emerged during the accumulated influence of the agent. From this study, it is concluded that perhexiline does not exert deleterious actions on the conduction system of the intact canine heart. In view of the negligible toxic effects and its efficacy in treating ventricular tachyarrhythmias in patients, the drug deserves further clinical evaluation.

Animals↗

Lack of sensing by demand pacemakers due to intraventricular conduction defects.

A previously unrecognized form of failure of normally functioning noncompetitive R-inhibited or R-triggered pacemakers to sense is described in 30 patients. The failure was produced by the delayed arrival of ventricular depolarization due to intraventricular conduction disturbances at the site of pacemaker sensing electrodes. These patinets with late activation of the right ventricle exhibited right bundle branch block (RBBB) during conducted sinus beats or had ectopic beats arising from the left ventricle. In both these situations, several late occurring QRS complexes were not sensed by the pacemaker electrodes in the right ventricular apex (RVA) and thereby the R-inhibited pacemaker spike discharged into the initial portion of the QRS complex. Activation of the RVA was delayed up to 65 msec in sinus beats with RBBB and even longer in premature beats arising from the left ventricle. The depolarization front of such beats reached the myocardium around the right ventricular pacemaker electrodes late in the QRS and thereby were not sensed up to 65 msec after the QRS onset as seen on the surface electrocardiogram (ECG). It was found in this study that if the inscription of such QRS complexes began up to 65 msec before the next due pacemaker impulse, these complexes were not sensed, allowing discharge of normally functioning R-inhibited pacemakers within the QRS which mimicked pacemaker malfunction. Failure to sense due to this phenomenon was observed in patients with noncompetitive pacemakers, both R-inhibited and R-triggered; temporary and permanent; with unipolar as well as bipolar electrodes. Similarly, patients with left ventricular epicardial electrodes and left bundle branch block in sinus beats also exhibited this phenomenon. Complete evaluation proved that pacemaker function was normal in the entire patient group. Recognition that failure to sense was the result of intraventricular conduction disorder prevented the untimely replacement of the pulse generator. This phenomenon of nonsensing by noncompetitive pacemakers should be considered in the presence of wide QRS complexes before the pacemaker is concluded to be malfunctioning.

Aged↗

Calcified left ventricular aneurysm and non-atherosclerotic myocardial infarction in a child.

A 14-year-old boy, admitted with intractable chest pain, was found to have an enlarged heart and calcification in the apical region, with electrocardiographic features of massive inferolateral myocardial infarction. Left ventricular angiography revealed a large left ventricular aneurysm. He died following resection of the aneurysm and post mortem examination showed changes of a non-specific chronic myocarditis. A vasculitis involving small coronary arterioles was also found in the vicinity of the aneurysm, and the possibility of a rheumatic vasculitis was suggested by a transient episode of an erythema marginatum-like eruption. It is concluded that the association of infarction pattern on the electrocardiogram together with calcification of the heart in children is highly suggestive of a ventricular aneurysm secondary to a myocarditis or a vasculitis involving small, intramyocardial branches of the coronary arteries.

Adolescent↗