The purpose of this study was to clarify whether the infarct expansion with cardiac rupture following acute myocardial infarction pathomorphologically differed from expansion without rupture. Eighteen autopsied patients with rupture were classified into acute phase (time between the onset of myocardial infarction and death &le;36 h) and subacute phase (>36 h). These patients were compared with 25 patients with no rupture using new parameters of expansion: radius index, cavity index, expansion area index and thinning-dilatation index of the left ventricle. In the acute phase, each parameter was significantly higher in the ruptured group than in the non-ruptured group (radius index: 0.49±0.28 vs 0.14±0.16, p<0.005, cavity index: 0.21±0.09 vs 0.08±0.06, p<0.005, expansion area index: 0.75±0.25 vs 0.34±0.23, p<0.001, thinning-dilatation index: 2.89±1.31 vs 1.53±0.52, p<0.001). However, in the subacute phase there were no differences in these parameters between the two groups. These data suggest that in the acute phase, but not the subacute phase, the degree of expansion and the proportion of expansion to infarcted area are associated with rupture.

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Acute coronary occlusion can occur following percutaneous transluminal coronary angioplasty (PTCA) upon return to the coronary care unit (CCU), and is sometimes life-threatening. To identify high-risk patients for acute occlusion following PTCA, we analyzed 11 patients with post-lab acute occlusion. All of the patients had some evidence of intimal tear or dissection at the site of dilatation. During the study period, 1343 patients (1998 lesions) with angina pectoris underwent PTCA. Of these, 331 vessels (17%) had some degree of intimal tear or dissection at the site of dilatation. From these 331, 50 patients (50 vessels) without evidence of acute occlusion were randomly selected to serve as the control group. Patients in the acute occlusion group had more extensive dissection (p<0.05) and less water balance (drip-infused water-urine, ml) during angioplasty (p<0.1) than those in the control group. Furthermore, a significantly higher percentage of patients in the acute occlusion group complained of chest discomfort upon arrival at the CCU (72% vs 8%, p<0.0001). These variables may be useful in identifying high-risk patients for post-lab acute occlusion, particularly in the presence of an intimal tear or dissection at the target site.

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Changes in hemodynamics and plasma norepinephrine levels during supine bicycle exercise after myocardial infarction were measured to investigate the mechanism of exercise-induced ST-segment elevation. Seventy-eight patients were divided into groups which showed either ST elevation (STE), ST depression (STD), or no ST changes (STU). Most of the STE group had anterior myocardial infarction (90.6%) and single-vessel disease (76.7%). The STE group achieved a significantly higher workload (119.5 ±4.0 watts, mean±SEM) than the STD group (82.3±2.8, p<0.01). Heart rate and cardiac output at maximal workload were significantly higher in the STE group (136.6±3.4 beats/min, 7.44±0.28 l/min/m²) than in the STD group (110.0±3.9, 4.83±0.36, p<0.01). Pulmonary artery pressures were less elevated in STE than STD patients. Plasma norepinephrine levels increased significantly at maximal workload in STE patients, as compared to the other groups. In conclusion, the STE group achieved a higher exercise level associated with augmented sympathetic activity, which may be a possible mechanism of exercise-induced ST elevation after myocardial infarction.

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Radiofrequency catheter ablation of atrioventricular accessory pathways was performed in 125 cases of the Wolff-Parkinson-White syndrome (type-A: 54, type-B: 29, concealed: 42) complicated with drug-refractory and symptomatic atrioventricular reentrant tachycardia and/or paroxysmal atrial fibrillation. A total of 135 accessory pathways were identified: 50 left free-wall manifest, 34 left free-wall concealed, 21 right free-wall manifest, 2 right free-wall concealed, 15 posteroseptal manifest, 10 posteroseptal concealed, 2 right anteroseptal manifest and 1 right anteroseptal concealed. Accessory pathway conduction was successfully eliminated in 133 of these 135 accessory pathways (99%). Two right posteroseptal pathways were eventually ablated with direct current. Successful ablation required a mean 5.2 applications of radiofrequency current, a mean total energy of 2615 J and a mean fluoroscopic time of 52 min. The mean number of applications, applied energy and fluoroscopic time were greater in the right free-wall pathways than in the left free-wall pathways, and in the concealed pathways than in the manifest pathways. None of the procedures produced complications. During a mean follow-up period of 11.5 months, 1 right free-wall accessory pathway recurred and was ablated successfully in a repeat session. These results suggest that radiofrequency catheter ablation of accessory pathways is highly effective and safe irrespective of the accessory pathway location and properties, although these factors can affect the difficulty of this procedure. This technique may be an alternative to surgical therapy for Wolff-Parkinson-White syndrome with drug-refractory and symptomatic supraventricular tachyarrhythmias .

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The vasodilatory response is known to be diminished in chronic heart failure. In the present study, we used dogs with chronic heart failure to investigate whether endothelium-dependent vasodilation in the resistance vessels in the hindlimb is decreased in chronic heart failure, and if so, to determine if endothelium-derived relaxing factor (EDRF) is involved in the mechanism. We induced heart failure in dogs by continuous rapid ventricular pacing. Under anesthesia, an internal carotid artery-femoral artery bypass system was established and perfusion pressure to the femoral artery was kept constant. Changes in hindlimb blood flow in response to various concentrations of acetylcholine (ACh), adenosine 5'-diphosphate disodium salt (ADP) and nitroglycerin (NTG) were examined in dogs with and without heart failure. The vasoconstrictive responses to L-N^G-monomethyl L-arginine monoacetate (L-NMMA) were also studied. In dogs with heart failure, vasodilatory responses to both of the endothelium-dependent vasodilators, ACh and ADP, were decreased, while there were no differences in the responses to the endothelium-independent vasodilator NTG. The vasoconstrictive response to L-NMMA was diminished in heart failure. Thus, endothelium-dependent vasodilation in hindlimb resistance vessels is impaired in dogs with congestive heart failure. This impairment may be related to diminished EDRF/NO production or release in these vessels.

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The effects of intracoronary administration of leukotriene D₄ (LTD₄) on myocardial blood flow (MBF) and myocardial energy metabolism in anesthetized open-chest dogs were examined, and compared with those of coronary ligation. Two series of experiments were conducted. In the first, LTD₄ (0-3.0μg/kg) was injected into the left anterior descending coronary artery (LAD) and MBF was measured. While no changes in MBF were observed after 0.5 μg/kg of LTD₄, a significant decrease in MBF in the LAD area was apparent after 1.0 μg/kg of LTD₄, with a return to baseline values by within 10 min after the injection. With 3.0 μg/kg of LTD₄, MBF remained decreased up to 15 min after the injection. In the second study, myocardial high energy phosphate concentrations in the LAD area were determined 5 min after LTD₄ administration and compared to those after ligation. ATP levels in the 1.0-3.0 μg/kg LTD₄ groups were significantly less than those in the ligation group, although there were no associated significant differences in MBF values in the LAD area. These results indicate that LTD₄ brings about changes in myocardial energy metabolism which are not secondary to reduced blood flow.

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This study was designed to determine the role of calcium in the cycle length-de-pendent changes in the action potential duration (APD) and the contractile force in guinea pig papillary muscle. APD correlated with the contractile force during the steady state, with [Ca²⁺]_o ranging from 0.3-7.2 mM. High [Ca²⁺]_o increased the force and shortened APD, while low [Ca²⁺]_o had the opposite effect. During the steady state, as the cycle length of stimulation was decreased, the increase in the contractile force was inversely related to the increase in APD within a [Ca²⁺]_o range of 0.9-5.4 mM and at diastolic intervals of &le;600 msec. At longer diastolic intervals, the relationship between changes in contractile force and changes in APD was variable and non-linear at each [Ca²⁺]_o. Changes in the postextrasystolic force were not related to APD. The phenomenon of APD overshoot, i.e., an APD that was longer during short than during basic cycles, was observed at <5.4 mM [Ca²⁺]_o and was most pronounced at the lowest [Ca²⁺]_o. Assuming that the contractile force reflects [Ca²⁺]_i, we concluded that the cycle length-dependent APD curve during the steady state is influenced by [Ca²⁺]_i in a manner consistent with the inverse relationship between APD and the contractile force.

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A simple excision of pulmonary venous obstruction (PVO) was carried out following a radical operation for total anomalous pulmonary venous drainage (TAPVD, Darling Ia). The results were quite satisfactory. This technique can be performed easily and effectively although hitherto relief of PVO has been considered to be very difficult.

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