Search

A patient with intermittent tachycardia-dependent left posterior hemiblock is reported. Electrocardiographic patterns of complete and incomplete block were documented. Identification of the electrocardiographic characteristics of intraventricular conduction defects is aided when they are intermittent. The difficulty in diagnosing incomplete left posterior hemiblock, and the possible masking of the signs of previous inferior infarction by left posterior hemiblock are emphasised. [ABSTRACT FROM PUBLISHER]

The electrophysiologic effects of encainide were studied in 10 patients with Wolff–Parkinson– White syndrome after intravenous (1 mg kg in 60 minutes) and oral administration of two dose regimens (75 and 150 mg daily). Under control conditions atrial fibrillation (AF) with a rapid ventricular response was induced in all patients andatrioventricular reciprocating tachycardia (A VRT) in 9 patients. After intravenous encainide AF was no longer induced in 3/9 patients; in 3 of the remaining the accessory pathway (AP) was totally blocked and in the others the shortest RR interval increased from 213 ±6 to 297 ±91 ms and the mean RR interval from 293 ± 39 to 362 ± 79 ms. The lower dose of oral encainide prolonged the shortest RR interval from 206 ± 24 to 273 ± 64 ms and the mean RR interval from 280 ± 48 to 368 ±52 ms in 6 patients; in 2 cases no preexcitedbeats were recorded and in 1 AF was not inducible. After the higher dose of oral encainide A F was still inducible in 7/8 cases; in 3 the A P was blocked and in the others the shortest and mean RR intervals increased from 202 ±30 to 280 ± 24 ms and from 276 ±59 to 436 ± 80 ms, respectively. After intravenous encainide antegrade conduction over the A P was blocked in 4/9 patients and the antegrade effective refractory period (ERP) was prolonged in another 4. Oral encainide blocked A P conduction in 4 cases and prolonged ERP considerably in the others. Induction of A V RT was prevented in 1/8 patients after intravenous and in 5/9 patients after oral encainide; in the 4 patients in whom AVRTremained inducible cycle length increasedfrom 306±31 to 3 54 ±49 ms after intravenous encainide and to 392 ±46 ms after oral administration. All patients were discharged on encainide (mean maintenance dose, 127 mg daily) and followed for 21 ±7 months; no recurrence of AF was observed; two patients complained of transient mild side effects. These data show that in patients with Wolff-Parkinson- White syndrome encainide prolongs refractoriness and slows conduction over the AP; it prevents induction of AVRT and markedly slows ventricular response during AF, thus protecting patients against life-threatening arrhythmias [ABSTRACT FROM PUBLISHER]

Over a five-year period 57 patients (pts) with sustained, recurrent, post-infarction ventricular tachycardia (VT) refractory to conventional antiarrhythmic treatment were evaluated. In 28 (49%) pts VT was controlled by amiodarone (A) in a dose of 3000 mg week. During long-term follow-up 5/28 (18%) pts died; no severe side-effects were observed with this dosage. In 17 of the 29 pts not controlled by this regimen, the dosage of A was increased to 6000–8000 mg week; short-term control of VT was achieved in 9/17 (53%) pts, but over a long-term follow-up 5/9 (56%) died and severe side-effects (11% polmonary fibrosis and 11% hepatitis) occurred in 22%. Twenty pts, resistant to a low (12 pts) or high (8 pts) doses of A, underwent map-guided surgical treatment. In conclusion A is superior to conventional drug's in the treatment of sustained, recurrent, post-infarction VT, but when high doses are necessary to prevent VT, long-term results are poor and severe side-effects frequent. In pts refractory to standard doses of A, map-guided surgery is the treatment of choice. [ABSTRACT FROM PUBLISHER]

A case of a patient with variant angina associated with severe ventricular tachyarrhythmias studied by continuous electrocardiographic and haemodynamic monitoring is reported. Severe ventricular arrhythmias developed both during maximal ST-segment elevation, in association with haemodynamic signs of acute ischaemic cardiac dysfunction and after nitroglycerin-induced reversion of ischaemia and return of the haemodynamic variables to the basal state. Thus, in this patient, ventricular arrhythmias during acute ischaemia could be related not only to acute vasospastic coronary occlusion but probably also to reperfusion after relief of coronary spasm. [ABSTRACT FROM PUBLISHER]

Two patients with vasospastic angina at rest developed ST segment elevation both in the anterior and inferior leads during spontaneous and ergonovine-induced attacks. In both cases the acute myocardial ischemia secondary to multivessel coronary spasm led to reversible electromechanical dissociation. Coronary arteriography showed normal coronary arteries in one case and severe three-vessel disease in the other; spasm of the right coronary artery was demonstrated in both patients. These cases show that in patients with vasospastic angina coronary spasm may simultaneously involve different arteries and lead to ischemic electromechanical dissociation. Ergonovine testing is contraindicated in those patients with suspected or proved multivessel coronary spasm. [ABSTRACT FROM PUBLISHER]