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A 35-year-old man had a history of recurrent syncope for more than a decade. During a witnessed episode, an ambulatory electrocardiographic recording showed ventricular flutter/fibrillation that lasted for 2 1/2 [...]

The evolution of second-degree atrioventricular block in the His-Purkinje system was studied in four patients with acute myocardial infarction, utilizing continuous electrocardiographic monitoring and serial His bundle recordings. Three patients had anterior wall infarction; all developed acute right bundle-branch block and two also showed a left anterior hemiblock one to four hours prior to onset of second-degree atrioventricular block. The fourth patient had an old anteroseptal infarction and chronic right bundle-branch block and left anterior hemiblock; he developed second-degree atrioventricular block following an acute lateroposterior infarction. His bundle electrograms were obtained during the insertion of a temporary ventricular pacemaker within the first 24 hours of onset of chest pain. A second His bundle electrogram was obtained during removal of the temporary pacemaker 7 to 14 days after the first recording. In all cases the block was localized in the His-Purkinje system. In three patients the first His bundle recording showed second-degree atrioventricular block with minimal increment of delay in conduction (3 to 10 msec) prior to the blocked beat (equivalent of Mobitz type 2 block). The second His bundle electrogram showed the development of significant increment of delay in conduction (35 to 210 msec) prior to block (equivalent of Wenckebach conduction). The fourth patient illustrated the reverse order of the observations seen in the other three. Three patients showed resumption of 1:1 atrioventricular conduction; however, when one patient was challenged with rapid atrial pacing, he developed repetitive block in the His-Purkinje system.

Of 1125 patients with acute myocardial infarction admitted to Mount Sinai Medical Center in 1971 and 1972, 292 (28.8 percent) had intraventricular conduction defects. In 210 of the 292 patients with intraventricular conduction defect, it was possible to determine if the conduction defect was present before the infarction (Group 1, 123 patients) or developed acutely with the infarction (Group 2, 87 patients). Of the 210 patients, 52.8 percent died (mean age 72.1 years). Fifty-three patients in Group 1 and 18 patients in Group 2 had isolated left axis deviation (LAD). The mortality was 35 percent and 28 percent respectively. This difference was not significant (p > 0.60). Sixty-four of the 210 patients presented with a left bundle branch block (LBBB) pattern. The overall mortality of 54 percent was the same in both groups. Right bundle branch block (RBBB), with either normal axis, left (LAD) or right axis deviation (RAD), was found in 74 patients. Of 40 patients in Group 1, 62 percent died, and of 35 patients in Group 2, 80 percent expired. Again this difference was not significant (p > 0.10). In 13 of 25 patients with RBBB in Group 1, death was possibly related to progression of the conduction defect The use of prophylactic temporary pacing is suggested for these patients.

The ST alternans was recorded during at least one ischemic attack with ST elevation in nine of 65 patients with variant angina. The magnitude and duration of ST elevation during ischemic attacks were significantly greater in patients with than in those without ST alternans. It always appeared during the occlusion phase and disappeared during the reperfusion phase of ischemic attacks. In patients with episodic ST alternans, the ischemic attacks showed a greater ST elevation and a longer duration in the presence of ST alternans than in its absence. The incidence of occlusion phase ventricular arrhythmias was greater in patients with than in those without ST alternans; the incidence of reperfusion phase ventricular arrhythmias was similar in the two groups. The ST alternans always preceded the onset of occlusion phase arrhythmias. Thus, in variant angina, ST alternans represents an index of the severity of ischemia and a precursor of ventricular arrhythmias.