Kensuke Kaseno

Electrophysiologic Effects of Diltiazem, a Calcium Antagonist, in Patients With Impaired Sinus or Atrioventricular Node Function

The electrophysiologic effects of diltiazem, a calcium antagonistic agent, were studied in 30 subjects with various degrees of sinus or AV node dysfunc tion. After diltiazem was administered, sinus activity was not depressed in con trol subjects, whereas marked inhibition was observed in some of the patients with sick sinus syndrome. Ventricular automaticity was little affected by this drug. The AV conduction system was significantly depressed, and there was no difference in degree between controls and AV block patients. The depression of the AV conduction system became more marked as the basic atrial cycle length was shortened. The drug had no apparent effects on atrial refractoriness, atrial echo zone, or the accessory pathway system. Conclusively, diltiazem affects mainly sinus and AV conduction systems. Its effect on the sinus node may provide a hazardous problem in patients with the sick sinus sysdrome patients, while its effect on the AV node will have thera peutic value in patients with AV nodal re-entrant arrhythmias.

Transient ST-segment elevation in subarachnoid hemorrhage

Electrocardiographic manifestation mimicking the hyperacute phase of myocardial infarction and the electrical alternans of the elevated ST-segment in association with subarachnoid hemorrhage were reported in two patients with no evidence of heart disease. In both cases the ST-segment changes were transient and there were no persistent changes suggestive of underlying myocardial damage or ischemia. These findings suggested that the electrocardiographic changes were probably secondary to subarachnoid hemorrhage and not an expression of primary myocardial disease. The electrocardiographic abnormalities could be explained by altered autonomic activity to coronary arteries or directly to the myocardium.

Primary hemangiopericytoma of the heart associated with pseudoaneurysm of the pulmonary artery--a case report.

A thirty-three-year-old male with malignant hemangiopericytoma of the right ventricular outflow tract and the pulmonary artery associated with pseudoaneurysm formation at the latter is presented. Contrast computed tomography was helpful in diagnosing the pseudoaneurysm of the pulmonary artery. The positional change of the murmur, with a tumor plop caused by the pedunculated tumor of the right ventricular outflow tract, was detected.

Acute effects of low aortic pressure on cardiac performance

SummaryAortic pressure has dual effects on the heart: One as the afterload pressure for the left heart and the other as a determinant of coronary perfusion pressure. As aortic pressure becomes subphysiological, these two effects may come to an imbalance. In dogs in which aortic pressure, aortic flow and heart rate were controlled at constant levels, a critical level of low aortic pressure (CAP) was studied below which an acute and progressive rise of left atrial pressure was observed. In normal heart, an elevation of CAP was observed from 15 to 36 mm Hg, as aortic flow was increased from 30 to 180 ml/min/kg. The elevation was less marked in response to the increase of heart rate from 100 to 250 beats/min. Coronary ligation or administration of a large amount of propranolol (1 to 2 mg/kg) caused a significant elevation of CAP. The results obtained from the present study is suggestive of the role of low aortic pressure in the development of cardiac deterioration during shock.

Influence of Changes in Heart Rate, Aortic Pressure and Flow Rate upon Experimental Coronary Insufficiency

This study was designed to evaluate the role of heart rate, aortic pressure, and aortic flow in the development of coronary insufficiency following acute coronary stenosis. In dogs, each of these parameters was controlled at a predetermined level while the left anterior descending coronary artery was constricted with a small screw clamp. The critical coronary pressure (CCP), i.e. the pressure below which a rise of left atrial pressure could be detected, was determined at various levels of hemodynamic load. Increases in aortic pressure, elevation of the heart rate and an increase in aortic flow rate were all associated with an elevation of the CCP and an increase in tension-time index (TTI). The changes in CCP were most striking when TTI was increased by aortic flow rate change. These findings suggest that with high aortic pressure, further constriction of coronary artery is required to precipitate coronary insufficiency, that the level of pacing required to induce coronary insufficiency is a useful index in assessing the degree of coronary stenosis, and that an augmentation of aortic flow rate is an important factor in the initiation of coronary insufficiency.