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Ten patients with chronic effort angina and coronary artery disease (luminal diameter reduction greater than 75%) were stressed by atrial pacing (140 beats/minutes) before and 15 minutes after intravenous propranolol (mean dose 7.4 mg). Myocardial substrate exchange of oxygen, blood lactate, plasma free fatty acids, citrate, glucose, glutamate, and alanine as well as coronary sinus blood flow were measured. Coronary sinus blood flow, oxygen consumption, and systemic haemodynamics did not change after propranolol. Propranolol did not influence arterial lactate concentration, and it reduced the arterial concentration of free fatty acid by 37% and increased that of glutamate by 21%. During pacing myocardial lactate extraction increased in all 10 patients; in two lactate release was converted to lactate uptake. Propranolol reduced free fatty acid uptake and increased glutamate uptake during pacing. For both substances the changes in aortocoronary sinus differences or in uptake or both correlated positively with the changes in their delivery to the heart from extracardial sources (arterial concentrations/loads). In the unstressed state before pacing, aortocoronary sinus lactate differences correlated inversely with free fatty acid differences and positively with those of glutamate. During pacing the relation between lactate and glutamate differences remained positive while the inverse correlation between lactate and free fatty acid differences was lost. Myocardial citrate release was halved during pacing and recovery. Propranolol did not influence alanine or glucose exchanges. An improved myocardial lactate extraction after propranolol administration may be secondary to decreased free fatty acid uptake or increased glutamate uptake or both. In the unstressed state both mechanisms may be of importance. During pacing induced ischaemia, increased glutamate uptake is more likely than reduced free fatty acid uptake to be the mechanism responsible for the improvement in myocardial lactate extraction. The propranolol mediated alterations in myocardial substrate exchanges may reflect the extracardial effects of the drug. [ABSTRACT FROM PUBLISHER]

A retrospective study was carried out to assess the incidence of cardiomyopathy in western Denmark (Jutland and Funen) (population 2 798 000) during a two year period (1980-81). The WHO/ISCF classification was strictly followed, and rigid criteria for exclusion and inclusion of patients were adopted. Thus cases in which specific heart muscle disorders (myocarditis, alcoholic heart disease, hypertension etc) were merely suspected were excluded. Forty one patients had dilated cardiomyopathy (overall incidence 7.3/10(6) population/year) and 20 hypertrophic cardiomyopathy (overall incidence 3.6/10(6) population/year). In men aged 40-59 years the occurrence of dilated cardiomyopathy was 23.4/10(6) population/year. Only one case of Löffler's endomyocardial disease was diagnosed during the study period. Since the investigation was retrospective and was a study of diseased persons and not a population, and since a specific set of criteria for exclusion and inclusion was rigidly applied, the results represent the minimum frequency of these diseases. [ABSTRACT FROM PUBLISHER]

Intracardiac electrography and 24 hour ambulatory electrocardiographic monitoring were carried out in 20 patients with calcific aortic stenosis (mean pressure gradient 86 mm Hg) to investigate (a) the role of bradycardia and tachycardia in the pathogenesis of syncope in aortic stenosis, (b) the relation between haemodynamic data and electrophysiological abnormalities, and (c) whether valve replacement corrects electrophysiological abnormalities. Intracardiac electrograms showed impaired sinus node function in five patients and a prolonged HV interval (greater than or equal to 50 ms) in 11 but there was no difference in the findings of 13 patients with syncope and seven without. Ambulatory monitoring showed short pauses in three patients and brief episodes of tachycardia in four, but there was no difference in the findings of patients with and without syncope. The HV interval correlated inversely with the left ventricular ejection fraction, whereas no correlation was found between the HV interval and the pressure gradient. Nine patients were re-evaluated 15 months after aortic valve replacement. No change was found in sinus node function, but the HV interval had increased by 7.8 ms. It is concluded that in calcific aortic stenosis neither bradycardia nor tachycardia is shown to be a frequent cause of syncope, a prolonged HV interval is a frequent finding and further prolongation occurs after valve replacement, and contractility and conductivity appear to deteriorate in parallel. [ABSTRACT FROM PUBLISHER]

Ten patients with stable angina pectoris and obstructed coronary arteries (greater than 75% reduction in diameter) were studied before and during two periods of pacing, the second of which was preceded by sublingual administration of glyceryl trinitrate (mean dose 0.78 mg). Coronary sinus blood flow measurements and aortocoronary sinus blood sampling for metabolite determinations were carried out. Although the rate of pacing was increased by 10 beats/minute after glyceryl trinitrate administration, the onset of angina was delayed in eight patients during pacing. Drug administration decreased coronary sinus blood flow by 42% and myocardial oxygen uptake by 41% during pacing and induced a shift in mean lactate extraction towards a net release (from 3.1% to -12.6%). It increased the number of patients producing lactate from three to five. Glyceryl trinitrate administration decreased myocardial glucose uptake throughout the study, decreased lactate extraction during recovery, and increased the aortocoronary sinus citrate gradient at rest and during recovery, while the exchange of free fatty acids remained unchanged. A decrease in aortocoronary sinus lactate difference during pacing after glyceryl trinitrate administration correlated positively with the fall in coronary sinus blood flow. The metabolic data do not indicate an augmented myocardial lactate production after glyceryl trinitrate administration. A decrease in coronary sinus blood flow seems, therefore, to be of primary importance in explaining the elevated coronary sinus lactate concentration. Our finding that coronary sinus lactate concentration increased during pacing after glyceryl trinitrate administration despite clinical improvement questions the validity of its use as a quantitative index of ischaemia. [ABSTRACT FROM PUBLISHER]

Dangerous or long lasting ventricular arrhythmias developed in three patients who had sustained an electrical injury in which current passed through the thorax. In all three cases there was a delay of 8-12 hours between the injury and the onset of symptoms. The ventricular arrhythmias were severe and long lasting. In two of the three patients, ventricular tachycardia or ventricular fibrillation or both occurred and in one patient ventricular parasystole developed. No enzymatic evidence of myocardial necrosis was found but the results of an endomyocardial biopsy carried out in two of the three patients showed focal myocardial fibrosis and increased numbers of Na, K-pumps. The two patients with ventricular tachycardia became symptom free after appropriate antiarrhythmic treatment and in the third patient ventricular parasystole disappeared spontaneously within two years. Patients sustaining electrical injury in which current passes through the thorax should be monitored electrocardiographically for at least 24 hours, and patients with unexpected arrhythmias should be questioned about previous electrical injury. [ABSTRACT FROM PUBLISHER]