Angas Hamer

Prediction of sudden death by electrophysiologic studies in high risk patients surviving acute myocardial infarction.

Seventy patients surviving a myocardial infarction complicated by heart failure or arrhythmias, or both, were studied 7 to 20 days after the infarction. Twenty-four hour electrocardiographic ambulatory monitoring and intracardiac electrophysiologic studies were performed in each patient. Electrophysiologic studies included introduction of single right ventricular premature stimuli during sinus rhythm (70 patients), atrial pacing (35 patients) and ventricular pacing (70 patients) at a stimulating voltage of 2 V, with the use of higher stimulating voltages (up to 10 V), and double right ventricular premature stimuli in 33 patients and pacing at a second right ventricular site in 50 patients. A repetitive response was defined as two or more spontaneous ventricular depolarizations in response to the premature stimuli, with His bundle reentry and aberrant conduction of supraventricular impulses excluded by a His bundle recording. Repetitive responses were initiated in 20 patients, and 12 patients had responses that were either sustained ventricular tachycardia or self-terminating ventricular tachycardia of more than five complexes in duration. The finding of a repetitive response was not related to the occurrence of complex ventricular arrhythmias during ambulatory monitoring or in the coronary care unit. Five of the 12 patients with sustained or self-terminating responses of more than five complexes died during the 12 month follow-up period, 4 suddenly, and these responses were significantly associated with late sudden death (p less than 0.05), because only 1 of 25 patients with responses of fewer than five complexes or no response to maximal provocation died suddenly. It is concluded that induced responses of more than five complexes in duration may be an important indicator of a potentially reversible risk of sudden death after myocardial infarction.

Multiform ventricular tachycardia.

Electrophysiological studies were performed in three patients with chronic recurrent ventricular tachycardia (VT) associated with coronary artery disease. In each case the ventricular origin of the tachycardia was confirmed and induction of tachycardia by programmed stimulation suggested a re‐entry mechanism. Multiple types of ventricular tachycardia were observed which differed in cycle length, QRS morphology, timing of local epicardial and endocardial ventricular electrograms and the use of the specialized conduction system for propagation. There was evidence of one or more re‐entry circuits arising in or near previously infarcted areas, with features of cycle length alternation, change in exit points and variations in subsequent conduction through the myocardium and specialized conduction tissues. These findings suggest multiform VT can be due to a number of factors. A modified surgical approach is recommended for management of medically refractory VT when there is evidence of multiple types.

Electrophysiologic studies in survivors of late cardiac arrest after myocardial infarction

Nine patients resuscitated from life-threatening ventricular arrhythmias (VA) within 3 months of an acute myocardial infarction (AMI) underwent electrophysiologic studies (EPS) with clinical follow-up for at least 12 months. Neither reinfarction, drug therapy, nor electrolyte imbalance was a precipitating factor. VA was induced by ventricular pacing in six of nine patients. Five patients were prescribed empiric drug therapy, while the four other patients had repeated EPS to select optimal drug therapy. One patient remained unstable and died of VA in the hospital. No patient was discharged and successfully maintained on a drug known to prevent induction of VA, yet only two patients (25%) had a further recurrence of VA, one fatal. Our findings suggested that either drug therapy that is determined empirically or found not to suppress the induction of VA during EPS can be associated with a successful outcome in some of these patients, or the natural history of VA after myocardial infarction is that they are self-limiting in the absence of a new ischemic event.

Delayed neurally mediated syncope after inferior wall acute myocardial infarction

L 1 first coined the label vasovagal syncope in 1932 to explain brief loss of consciousness with hypotension and bradycardia. The normal response to a reduction in circulating blood volume or emotion is a stimulation of the sympathetic nervous system. However, neurally mediated syncope (NMS) may occur because of the activation of the Bezold Jarisch reflex, in which stimulation of cardiac stretch leads to a sudden and dramatic interruption of this compensatory sympathetic response, with a similarly dramatic increase in vagal stimulation. This results in a sudden vasodilatation and bradycardia and in turn hypotension and syncope. It has been shown that the Bezold Jarisch reflex can be triggered acutely by inferior wall acute myocardial infarction (AMI). The bradycardic, hypotensive presentation of an inferior wall AMI is familiar to all cardiologists and emergency physicians. Single case reports have also suggested the initiation of NMS with inferior ischemia and subsequent resolution with treatment of the ischemia. An association between inferior wall AMI and the later development of NMS has not been previously described.

Digitalis and Beta-Adrenergic Blocking Drugs for the Treatment of Tachycardias

Digitalis preparations and beta-adrenergic blocking drugs are well-established agents for the treatment of tachycardias. Their primary role appears to be in tachycardias in which depression of sinus and AV nodal function would benefit the patient. They appear to have less effect on the atrial and ventricular myocardia. Both groups of drugs have direct and indirect effects on the heart, the latter by way of the autonomic nervous system. Because the role of the autonomic nervous system in the genesis and maintenance of tachycardias varies in patients, the effects of these drugs may be quite unpredictable and inconsistent. It is not uncommon to use these drugs in combination with other antiarrhythmic drugs in order to control tachycardias.