A questionnaire study on the effect of p-blockade in dilated cardiomyopathy was performed. In 89 cases obtained from 24 institutions, either metoprolol (72 patients, 41.4±29.3 mg/day, 14.1±13.2 months, mean±SD), propranolol (5 patients, 23.8±24.3 mg/day, 25.0±25.3 months), carteolol (4 patients, 7.5±2.9 mg/day, 9.0±2.8 months) or another p-blockers (8 patients) was administered. Nine patients died during the follow-up period. Overall effectiveness as evaluated by the attending physicians showed improvement in 51 patients (57.3%), no change in 26 patients (29.2%), deterioration in 11 patients (12.4%) or was indeterminate in one patient. New York Heart Association (NYHA) functional class improved significantly from 2.6 to 2.3 (p<0.01). Heart rate decreased from 83.1 to 70.1 (p<0.01). Cardiothoracic ratio decreased from 55.5% to 53.9% (p<0.01). Left ventricular ejection fraction of the left ventricle measured by echocardiogram increased from 29.8% to 37.8% (p<0.01). Exercise tolerance during a treadmill test and ventricular arrhythmias in Holter electrocardiograms improved significantly. There was no change in blood pressure. When the patients in different functional classes were compared, the patients of NYHA class III improved more frequently than those of NYHA class II (69% vs 53% p<0.01). Improvement of left ventricular end-diastolic dimension and left ventricular ejection fraction was more prominent in patients of class III than in those of class II. NYHA functional class and cardiothoracic ratio were significantly improved only in class III. NYHA functional class began to improve at 2 weeks, but ejection fraction increased significantly after 3 months. It is concluded that β-adrenergic blockade has a beneficial effect in most patients with dilated cardiomyopathy.

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The influence of advancing age on the electrophysiological changes of the atrial muscle induced by programmed atrial stimulation, such as fragmented atrial activity (FAA), interatrial conduction delay (ICD), and repetitive atrial firing (RAF), was investigated in 42 patients with neither documented episodes of paroxysmal atrial fibrillation nor sick sinus syndrome. The induction rates of FAA, ICD, and RAF were not affected by age. The zones of FAA, ICD and RAF, did not show any correlation with age. However, the longest coupling interval giving rise to FAA (longest CI-FAA) or ICD (longest CI-ICD) showed a significant correlation with age (10ngest CI-FAA; r=0.428, p<0.01, longest CI-ICD; r=0.398, p<0.01). Although the longest coupling interval giving rise to RAF did not show a direct correlation with age (r=0.267), it was significantly longer in patients over 60 years of age than in those under 60 (p<0.05). These results suggest that aging affects the electrophysiological properties of the atrial muscle, which can help to explain why atrial fibrillation is seem more frequently in the elderly.

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The effects of reperfusion on left ventricular (LV) function and volume were studied in patients with evolving acute myocardial infarction (AMI). We analyzed the LV ejection fraction and volume in patients who had been admitted within 24 h of the onset of their first AMI with culprit lesion of #6, #7 and # 1 (American Heart Association classification). Sixty-five patients (Re group) received successful reperfusion therapy within 6 h after the AMI. The other 60 patients (Oc group), who were admitted from 6 to 24 h after the AMI, received conservative therapy. Patients with reobstruction of the culprit lesion after reperfusion therapy were excluded from the Re group. Patients with spontaneous recanalization following conservative therapy were excluded from the Oc group. The LV ejection fraction (LVEF), LV end-systolic volume index (LVESVI), and LV end-diastolic volume index (LVEDVI) were measured using a modified Dodge's formula by left ventriculography performed 4 weeks after the AMI. LVEF in the Re group was significantly greater than in the Oc group (57±12 vs 49±11%) (mean±SD, p<0.01). LVESVI in the Re group was significantly smaller than in the Oc group (30±13 vs 38±16ml/m², p<0.01). Although LVEDVI was not significantly different between the 2 groups, in patients with a responsible coronary lesion of segment #6, LVEDVI in the Re group was significantly smaller than in the Oc group (67±14 vs 77±18 ml/m², p<0.05). Although LVEF and LV volume correlated in both groups, the correlation was weak (r=0.40-0.42), suggesting that LV volume was not dependent solely on LV fuctional recovery. The incidence of ventricular aneurysm in the Re group was significantly lower than in the Oc group (15.4 vs 45.0%, p<0.01). Multi-variate analysis selected reperfusion of the responsible coronary artery as one of the factors significantly associated with a reduction of LVEDVI. LVESVI, an improvement of LVEF, and a decrease in the rate of aneurysm formation. In summary, our results indicated that reperfusion improved EF, reduced LV volume, and decreased the rate of aneurysm formation as compared to non-reperfusion, which suggests that reperfusion therapy is beneficial for both functional recovery and ventricular remodeling.

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To clarify the relationship between clotting and lytic activities of intracardiac thrombi, and to elucidate whether this could be used to evaluate the embolic risk the ratio of indium-111 radioactivity accumulated on thrombi to that in the blood pool using dual-tracer technique %IE as a parameter of the clotting activity, and D-dimer, which is a fibrin specific degradation product, as a parameter of lytic activity were measured in 37 patients with intracardiac thrombi. Fifteen of the 37 patients had past histories of arterial embolization. The values of D-dimer correlated significantly with those of %IE (r=0.758, p<0.01), e, g., the higher the values of D-dimer the higher the values of %IE. 37 patients were divided into 2 groups using the regression line for the D-dimer and %IE domains. Eleven patients above the regression line had thrombosis in excess of fibrinolysis but the remaining 26 patients under the regression line had fibrinolysis in excess of thrombosis. The incidence of past embolic episodes was 82% (9/11) in patients with thrombosis in excess of fibrinolysis but 23% (6/26) in patients with fibrinolysis in excess of thrombosis. These results demonstrated that intracardiac thrombi were under the dynamic process between the clotting and the lytic activities and moreover patients with intracardiac thrombi and thrombosis in excess of fibrinolysis had a substantial risk of arterial embolization.

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The present study investigated the effects of phentolamine (PH) and nitroglycerin (NG) on the hemodynamics of the right heart in patients with cardiac disease. The patients were divided into a well-functioning left heart group (W group, n=15) and a poorly-functioning left heart group (P group, n=15). Right cardiac hemodynamic parameters and plasma noradrenaline (NA) and adrenaline (A) concentrations were measured before and after administering PH (0.1 mg/kg, i.v.) or NG (0.6 my, sublingual). In a parallel animal study we obtained a systemic venous return curve by measuring mean circulatory pyressure (MOP), mean right atrial pressure ((RAP)^^^- ) and cardiac output, before and after administering PH (0.1 mg/kg, i.v.) or NG (12.5 μg/kg, i.v.) to anesthetized open-chest dogs (n=14). We used MOP data (W group: 7.5 mmHg, P group: 10 mmHg) obtained in a separate series of human studies in our laboratory. We constructed the venous return curve by connecting the MOP point on abscissa with the cardiac index (CI)-(RAP)^^^- plot obtained in the clinical study. We also constructed the right ventricular output curve by connecting the point of -2 mmHg on the abscissa with the CI-(RAP)^^^- plot. We obtained the following results: (1) PH shifted the CI-(RAP)^^^- plot to the left and upwards, while NG shifted the CI-(RAP)^^^- plot to the left almost horizontally on the CI-(RAP)^^^- plane, where CI was plotted on ordinate and (RAP)^^^- on abscissa. The length (|(CHP)^^^ →|, C=control point, PH=point after PH) of the shift of CI-(RAP)^^^- plot due to PH was greater in the P group than in W group, while there was no difference in the length (|(CNG)^^^→|, C=control point, NG=point after NG) of the shift of CI-RAP plot due to NG between P and W groups. (2) Both PH and NG significantly elevated plasma NA and A concentrations in both the W and P groups. In the P group, PH increased the plasma NA concentration significantly more than did NG, but both drugs increased plasma A concentration to a similar extent. (3) Both PH and NG significantly decreased the mean pulmonary arterial pressure with NG doing so significantly more than PH. (4) In anesthetized open-chest dogs, PH 100 μg/kg i.v. rotated the venous return curve clockwise and shifted it to the left, while NG 12.5 μg/kg i.v. shifted the venous return curve parallel to the left. We interpreted the changes in the CI-RAP plot caused by PH and NG in human studies on the basis of venous return curve changes obtained in the dog experiments. It is suggested that the PH-induced increase in cardiac output is due to (a) stimulation of β-adrenoceptors in the systemic capacitance vessels (a decrease in resistance to venous return) by PH-induced increase in plasma NA level and (b) an improvement in pumping function of the right heart by the stimulation of cardiac β-adrenoceptors by a PH-induced increase in plasma NA level.

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Cardiogenic shock still remains a highly lethal complication of acute myocardial infarction (AMI). This study reviews our hospital experience in treating AMI complicated by cardiogenic shock to evaluate whether coronary angioplasty improves survival or not. We have treated 523 AMI patients from 1985 to 1990, and among these, 26 patients with AMI complicated by cardiogenic shock who underwent percutaneous transluminal coronary angioplasty (PTCA) compose the study group. In 16 patients, PTCA was successful (Groups S) and in 10 patients, unsuccessful (Group F). There were no statistical differences between the Groups with respect to clinical background, intraaortic balloon counterpulsation (IABP) or emergency coronary bypass graft surgery. Before PTCA, hemodynamic variables including cardiac index, pulmonary capillary wedge pressure and systolic blood pressure were similar in the 2 groups. After PTCA, cardiac index in Group S patients was better than in Group F patients (2.18±0.61 versus 1.62±0.65, p<0.05). Thirty day and 1 year survivals were also better in Group S than in Group F (30 day survival: Group S 56.2%, Group F 10%, 1 year survival: Group S 31.2%, Group F 0%, p<0.05). Multi-variate analysis showed that age under 75 years old, systolic blood pressure over 90 mmHg after PTCA and successful PTCA were independent predictors of 30 day survival (p<0.05). It was suggested that PTCA was an effective procedure to reduce mortality in patients with cardiogenic shock.

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The purpose of this research was to evaluate the left ventricular systolic function behavior after cardioversion and defibrillation. The study included 18 adult patients who had direct current cardioversion or defibrillation performed for conversion of spontaneous or induced arrhythmias. All patients were submitted to a careful medical evaluation and an M-mode echocardiogram before cardioversion or defibrillation. The clinical and echocardiographic evaluations were repeated immediately after, and 6 and 12 h following the countershock. Six hours after cardioversion or defibrillation a statistically significant (p =.04) decrease in contractility (circumferential fiber shortening and ejection fraction) was observed without significant changes in preload (end diastolic volume), heart rate or afterload (end systolic stress and diastolic arterial pressure). Within 12 h, the left ventricular systolic dysfunction disappeared. The impairment of systolic function was independent of the amount of energy used, the type of arrhythmia, the rhythm after cardioversion or defibrillation and the etiologic cardiac diagnoses. There was a significant (p =.03) direct, negative and linear correlation between left ventricular systolic indices (ejection fraction and circumferential fiber shortening) before the countershock and the amount of decrease in systolic function after the countershock. In spite of the fact that most patients had a low ejection fraction, none of them presented clinical signs of heart failure. Defibrillation and cardioversion produce a transient decrease in cardiac contractility which is independent of the amount of energy used and does not produce clinical signs of heart failure.

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We examined serum lipids, lipoproteins, apolipoproteins (Apo), lipoprotein(a) (Lo(a)), C4b-binding protein (C4dp) and lathosterol in 22 normolipidemic (serum total cholesterol <220 mg/dl and serum triglycerides < 150 mg/dl) male patients with coronary artery disease (CAD) and 33 normal male subjects. Many of the patients in the CAD group with normal total cholesterol (T-Ch) and triglycerides (TG) had higher TG, low-density lipoprotein (LDL)-Ch, β-lipoprotein (Lipo) and Apo B values and lower high-density lipoprotein (HDL)-Ch. Apo A-I and Apo A-II values than those of the control group. Differences were also observed in the β-Lipo/HDL-Ch. Apo B/Apo A-I, and HDL-Ch ratios and the atherogenic index [A.I.=(T-Ch-HDL-Ch)/HDL-Ch], all of which are generally accepted as indices for atherosclerosis. Even in CAD patients with normolipidemia, the HDL-Ch/T-Ch ratio and A.I. seemed to be important risk factors. In addition, Lo(a) and lathosterol, an accepted indicator of whole-body cholesterol synthesis, were higher in the CAD group. The CAD group also appeared to have a higher C4by value, suggesting that this parameter is correlated with other lipids.

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To elucidate the site of hypoxic pulmonary vasoconstriction (HPV) in the dynamic lung, we studied the effect of alveolar hypoxia (O4% O2) on excised canine lung lobes with pulsatile perfusion from artery to vein (antegrade perfusion: AP) or vein to artery (retrograde perfusion: RP), and compared responses to hypoxia with those to serotonin and histamine. In our preparation, increases in the pulmonary vascular resistance (R) resulted in a wide range of decreases in the flow wave amplitude at the lobar inflow site (FA). These decreases in FA reflected reductions in the compliance of the vasculature proximal to the main site of resistance. The FA/R ratios of serotonin were 2.29 in AP and 0.24 in RP indicating the predominant arterial constriction, those of histamine were 0.07 in AP and 1.24 in RP indicating the selective venous constriction. In contrast, the responses to hypoxia were 0.38 in AP and 0.42 in RP. These results suggest that HPV occurs not only on the arterial side but on the venous side in the dynamic lung, and the main site of HPV is located in the peripheral pulmonary vasculature, between muscular arteries and veins which are constricted by serotonin and histamine.

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In anesthetized open-chest dogs, an intravenous bolus injection of endothelin-1 (ET-1, 400 pmol/kg) caused transient hypotension (initial hypotensive phase; phase 1), followed by a continuous elevation of blood pressure (late hypertensive phase; phase 2). The constriction and dilation of the systemic capacitance and resistance vessels were evaluated from the change in mean circulatory pressure (MCP) and in total peripheral resistance (TPR) in phases 1 and 2. To examine the modification of the action of ET-1 on the blood vessels by the baroceptor reflex or by the endothelium-derived relaxing factor (EDRF) released by ET-1 in phase 1, we performed experiments in dogs under total spinal anesthesia (TSA group), methylene blue-treated dogs (MB group) as well as in the untreated dogs (control group). ET-1 decreased the TPR significantly, and increased the MCP significantly in phase 1 in the control (n=8) and TSA (n=8) groups; there was no difference between the groups. ET-1 had no significant effect on TPR but increased the MCP significantly in MB group (n = 8) during phase 1. The percentage increase of MCP in the MB group significantly ex-ceeded that of the control group. ET-1 increased both the TPR and MCP significantly in phase 2 in the control group (n=8). This study indicated that the vasocostrictor action of ET-1 on the systemic capacitance vessels in phase I did not result from a baroceptor reflex, and that the vasodilator action of ET-1 on the systemic resistance vessels may be at least in part mediated via EDRF released by ET-1. We suggest that the vasoconstrictor action of ET-1 on the systemic capacitance vessels is strong, but the vasodilator action of EDRF on the systemic capacitance vessels is weak.

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We examined the effect of low Na concentrations (25 mM) in Ca-free solutions on the myocardial damage induced by the Ca paradox in guinea pigs using electron microscopy and electrophysiological methods. Ultrastructural damage consist of contraction bands, swelling of mitochondria and disappearance of major part of contractile apparatus induced by the Ca paradox was prevented by reducing Na from 145 to 25 mM in the Ca-free solution. The penetration of lanthanum into the myocardial cells, which was induced by the Ca paradox, was also prevented by reducing Na concentration during the Ca depletion period. Perfusion with Ca-free solution containing normal Na (145 mM) for 10min caused a significant prolongation in the action potential duration (APD) of left ventricular papillary muscle, and reperfusion with Ca containing solution caused depolarization. The perfusion with Ca-free solution containing low Na concentration (25 mM) significantly reduced APD, but APD returned almost to control values without depolarization after reperfusion with Ca-containing solution for 5 min. These results suggest that the Na concentration in a Ca-free solution plays an important role in the pathogenesis of the Ca paradox phenomenon in guinea pig hearts.

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Acute ligation of proximal left coronary artery was performed on forty male Sprague-Dawley rats. Five min later, occlusion was released in order to evaluate the effectiveness of the 3 antiarrhythmic drugs in eliminating reperfusion ventricular arrhythmias. The drugs evaluated were moricizine (5 mg/kg), disopyramide (DSP) (5 mg/kg) and mexiletine (MXT) (5 mg/kg), which were administered intravenously 5 min before ligation of the coronary artery. Compared to control rats that underwent identical experimental procedures, all 3 drugs significantly lowered the mortality rate from 90% of the control group to 20, 20 and O% for moricizine, DSP and MXT groups. The incidence of ventricular fibrillation (Vf) was also decreased significantly by these drugs. The duration of ventricular tachycardia (VT) and Vf of surviving rats in drug groups were 111.7±35.0 sec, 71.6±29.4 sec and 32.9±14.6 sec for moricizine, DSP and MXT, respectively. Many of the drug treated rats could be restored to the normal sinus rhythm and survived. All 3 drugs slowed the heart rate significantly, but as for the blood pressure only MXT showed significant suppressing effect. In conclusion, moricizine has the same significant preventive effect on reperfusion induced ventricular tachyarrhythmias as DSP and MXT.

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A 60-year-old woman on chronic dialysis consulted our department for closer examination of transient atrial fibrillation and a mitral regurgitant murmur. Echocardiography revealed a left atrial abnormal dense echogenic spherical mass, the diameter of which was 2 cm. She died of cerebral bleeding 3 months later. At autopsy, the submitral mass-like structure consisted of light-gray pasty material, which was liqtlefaction necrosis of a mitral annular calcification. These findings were different from those of the so-called mitral annular calcification found in the elderly or in chronic renal failure patients. The existence of such calcification must be kept in mind and not be mistaken for cardiac tumor.

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