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The study investigated whether patients hospitalized for unstable angina pectoris (UAP), who subsequently develop complete coronary thrombosis (acute transmural myocardial infarction (AMI)) despite medical treatment, exhibit platelet hyperaggregability in an assay system that does not employ agonist stimulation. The study comprised 89 patients with UAP (Braunwald type B). Unfractionated heparin and nitrate were administered to all patients via continuous intravenous drip together with aspirin taken orally. Citrated platelet-rich plasma (230-250x 10(3)/microl) was obtained on admission and again, in some patients, following the AMI. Platelet aggregability was measured in an optically modified cone-plate viscometer that enables the detection of platelet aggregation without agonist stimulation. A continuous shear rate of 1,200/s was employed. Of the 89 patients, 85 were finally stabilized, while 4 developed an AMI accompanied by persistent ST-segment elevation with increased levels of plasma creatine kinase within 3 h after starting the treatment. The extent of platelet aggregation on admission was significantly greater in these 4 patients compared with the 85 who were stabilized (87.8+/-6.8%, n=4 vs 26.8+/-9.1%, n=85; mean+/-SD). These data suggest that platelet hyperaggregability mediated mainly by fibrinogen binding to the activated glycoprotein IIb/IIIa complex occurs before a complete thrombotic occlusion and this evaluation may provide important information before the onset of myocardial infarction.

We investigated alterations in the beta-adrenergic receptor-adenylate cyclase system in rabbits with congestive heart failure induced by adriamycin cardiotoxicity. A dose of 24 mg/kg adriamycin was administered over 16 weeks in 16 rabbits. Five of them died and 4 of them could not tolerate the full dose of adriamycin. Complete data were obtained in the remaining 7 rabbits. Another 7 rabbits received physiological saline for the same period and served as controls. Plasma norepinephrine concentration increased in adriamycin-treated rabbits, but not in the control rabbits. Cardiac output was lower in the adriamycin-treated group than in the control group. Both the left and right ventricular end-diastolic pressure were higher in the adriamycin-treated group. The density of myocardial beta-adrenergic receptors and the norepinephrine content were reduced in both ventricles in the adriamycin-treated group. Basal and isoproterenol-, sodium fluoride- and forskolin-stimulated adenylate cyclase activities were lower in the adriamycin-treated group. Thus, alterations in beta-adrenergic signaling occurred in both ventricles in animals with chronic biventricular failure induced by adriamycin. These may be the result of post-receptor abnormalities, including abnormalities of guanine nucleotide-binding proteins or of the catalytic unit of adenylate cyclase.

This study investigated the therapeutic efficacy of a new beta-blocker, nipradilol, a non-selective agent with vasodilating activity, for the treatment of idiopathic dilated cardiomyopathy (DCM). The New York Heart Association functional class improved in the nipradilol group (n = 9, p < 0.01), but not in the control group who received conventional therapy (n = 9). The observation period was 19 +/- 7 months in the nipradilol group, and 20 +/- 9 months in the control group. Before therapy there was no difference in heart rate between the 2 groups (76 +/- 12 vs 79 +/- 15 beats/min). The end-diastolic and end-systolic left ventricular dimensions decreased in the nipradilol group (p < 0.05), but not in the control group. Radionuclide ventriculography revealed that the left ventricular ejection fraction increased in the nipradilol group (27 +/- 8 to 41 +/- 18%, p < 0.05), but not in the control group (27 +/- 11 to 27 +/- 8%). Plasma norepinephrine tended to be lowered, although not significantly, whereas plasma alpha atrial natriuretic peptide significantly decreased after the therapy (p < 0.01) in the treatment group. Lymphocyte beta-adrenoceptors were up-regulated in the nipradilol group (p < 0.05). None of these parameters changed during the observation period in the control group. Thus, nipradilol improved symptoms and cardiac function with a favorable effect on neurohumoral factors in patients with DCM.

Objectives: Protons produced during ischemia may increase intracellular Na+ (Na+i) through Na+/H+ exchange, and may lead to Ca2+ overload through Na+/Ca2+ exchange to cause myocardial stunning. This study investigated whether an increase in the H+ buffering capacity of the perfusate or a reduction of H+ production by a brief hypoxic preperfusion before ischemia would reduce myocardial stunning. We also investigated whether the protective effect of these maneuvers depends on the free [Ca2+] of the perfusate., Methods: Isolated rat hearts were preperfused with oxygenated or hypoxic buffer (pH 7.4) containing 100 mM of either sucrose or HEPES for 10 min, followed by 15 min of total ischemia and 30 min of reperfusion. To investigate the dependence of the effects of HEPES or a brief hypoxic preperfusion, the free Ca2+ concentration in the buffer was changed from 1.25 mM to 2.5 mM in some hearts., Results: Oxygenated preperfusion with buffer containing HEPES and 1.25 or 2.5 mM Ca2+ improved the metabolic and functional recovery with a decrease in the accumulation of Na+i during ischemia and in 45Ca2+ uptake during reperfusion. A brief hypoxic preperfusion with 1.25 mM Ca2+ provided a similar protective effect whereas no protective effect was observed when the [Ca2+] was raised to 2.5 mM., Conclusions: An increase in the H+ buffering capacity or a brief hypoxic preperfusion reduced myocardial stunning with improved metabolic recovery, and reduced Ca2+ uptake. However, the effects of these interventions were affected differently by the free [Ca2+] of the perfusate, which suggests that they work, at least in part, through some different mechanism(s).

The purpose of this study was 1) to clarify whether augmented myocardial contraction after a brief coronary occlusion, i.e. post-ischemic hypercontraction, depends on a transient increase in coronary blood flow or preceding myocardial ischemia, and 2) to identify the role of catecholamines or calcium flux in this phenomenon. Sixteen mongrel dogs were examined in open-chest anesthetized condition. One-minute reperfusion after two-minute total coronary occlusion of the left anterior descending artery resulted in a transient increase in segment shortening. Intracoronary administration of adenosine caused hyperemia without any changes in segment shortening. Two minutes of total coronary occlusion with adenosine caused post-ischemic hypercontraction to the same degree, but without any additional hyperemia. Two minutes of partial occlusion with 75% flow reduction caused less post-ischemic hypercontraction. Post-ischemic hypercontraction did not occur after partial occlusion with 50% flow reduction, irrespective of hyperemia with adenosine during reperfusion. Propranolol or verapamil did not prevent this phenomenon. Thus, post-ischemic hypercontraction is not dependent on the transient increase in coronary blood flow, but is related to the preceding myocardial ischemia. Local release of catecholamines is not likely to be the cause. A calcium antagonist, verapamil, did not modify this phenomenon. The precise mechanism of this phenomenon is still uncertain, although some alterations in cellular hemostasis, such as ionic changes, are likely to be the cause.

Two hundred and five patients treated for infective endocarditis over the last 10 years were reviewed. There were 185 cases of native valve endocarditis (NVE) and 20 of prosthetic valve endocarditis (PVE). In the NVE group there were 175 clinically active patients and 10 non-active patients. The mortalities among 108 non-surgical and 57 surgical patients were 15.7% and 14.0%, respectively. Leading causes of deaths in the former were cardiac failure, embolism and cerebral hemorrhage. Patients with embolism showed significantly higher mortality. Culture negative endocarditis resulted in almost the same incidence of hospital death and urgent operation as staphylococcal endocarditis, and a higher incidence than streptococcal endocarditis. In 9 of 33 patients operated at our hospital, surgery was performed on an urgent basis and one NYHA class IV patient died. Indications for operation were intractable cardiac failure, uncontrollable infection and angina. In the PVE group, 3 of 4 patients operated in the active stage died of severe cardiac failure generated preoperatively. The only survivor was a patient operated early under stable hemodynamics. These results suggest that culture negative endocarditis should be observed as closely as staphylococcal endocarditis and early operation should be considered for patients with progressive cardiac failure, embolism and uncontrollable infection.

The pathophysiology and treatment of pump failure with right ventricular overload due to chronic pulmonary diseases were discussed. When right ventricular overload occurs hypertrophy and dilatation of right ventricle follows and the heart as a whole, including left ventricle, is altered in morphology and function. Therapeutic measures for right ventricular overload are the key to management and treatment of pump failure. Pulmonary hypertension, as an etiological factor, is discussed and is divided into two categories, that is, mild to moderate pulmonary hypertension with hypoxia due to chronic obstructive lung disease, and severe pulmonary hypertension due to pulmonary vascular disease. In each category, effects of oxygen inhalation and vaso-dilating agents were evaluated. Oxygen did not decrease pulmonary vascular resistance in the state of chronic hypoxia, though a vasodilating agent was effective. In pulmonary vascular disease, vaso-dilating agents were effective to decrease pulmonary vascular resistance and pulmonary artery pressure, though the effect was less than 30% down in resistance.

Echocardiographic and electrocardiographic findings in 74 adults with hypertrophic cardiomyopathy (HCM) were analyzed to identify the pattern of myocardial hypertrophy as a possible determinant of abnormal Q waves. The pattern of septal hypertrophy along the left ventricular long axis was divided into 3 types based on the site of maximum septal hypertrophy: basal, diffuse and apical types. Abnormal Q waves defined by the revised Minnesota Codes (either I-I, I-II or I-III) were noted in 31 cases (42%). The total incidence of abnormal Q waves in the basal type (15/26, 58%) and in the diffuse type (12/22, 55%) was significantly higher (p less than 0.001 and p less than 0.01, respectively) than that in the apical type (4/26, 15%). The abnormal Q waves defined by the strict criteria of Code I-I were significantly more prevalent (p less than 0.05) in the basal type than in the diffuse type, although there was no significant difference in the total incidence of abnormal Q waves between these 2 groups. Thirty-six patients with an extension of hypertrophy to the right ventricle (RVH) had a significantly higher incidence of abnormal Q waves than 22 patients without RVH (56% vs 27%, p less than 0.05). Furthermore, close relationships of RVH to the location of abnormal Q waves were documented. In conclusion, the abnormal Q waves in HCM may be related to the pattern of septal hypertrophy along the left ventricular long axis and to RVH.