To examine the role of coronary artery spasm in patients with syncope after alcohol ingestion, we performed an intracoronary ergonovine provocation test in 7 male patients (39 to 73 years old, mean 54 years) with alcohol-related syncope which remained unexplained despite noninvasive cardiovascular and neurological examinations. No patients had structural heart disease or significant coronary artery stenosis. Ergonovine was continuously infused into each coronary artery at a rate of 10μg/min for up to 5min. Coronary artery spasm with ST-segment elevation was induced in 4 of 7 patients. Chest pain before syncope or history of chest pain were not present in 3 of 4 patients with a positive ergonovine test. Multivessel coronary artery spasm was induced in 3 patients. One patient presented with triple vessel coronary artery spasm progressing to near syncope as a result of profound hypotension and ventricular tachycardia during provocation, Coronary artery spasm was promptly relieved by intracoronary isosorbide dinitrate infusion. All patients with a positive ergonovine test were treated with calcium antagonist and did not experience syncope during follow-up.
These results suggest that coronary artery spasm is one of the important causes of syncope after alcohol ingestion.

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Bicycle ergometer exercise was used to induce ischemia in 20 patients with stable angina pectoris (SAP). Superoxide dismutase (SOD) blood concentrations, free radical generation (by the SOD-inhibitable reaction of ferricytochrome C), malondialdehyde (MDA) plasma concentrations, the unfractionated leucocyte filterability rate and the filterability rates of the granulocyte and mononuclear sub-fractions (using a positive pressure filtration system and 5μ diameter Nuclepore filters), were monitored before and after exercise in the patients and in 18 matched controls. At the onset of ischemia a significant increase in the level of MDA plasma concentrations and significant decreases in both SOD blood concentrations and the SOD-inhibitable reduction of ferricytochrome C indicated oxygen free radicals had been released in the SAP patients. These changes were associated with significant impairments of granulocyte and unfractionated leucocyte filterabilities and with morphological evidence of granulocyte activation.

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Leucocyte elastase may be involved in the structural modification observed in the atherosclerotic process. Therefore, we tested the usefulness of leucocyte elastase plasma level determination as a marker for atherosclerosis.
Plasma levels of elastase were determined by ELISA in 100 consecutive patients (mean age 56±9.8 years) admitted to hospital for coron
No significant differary angiographic investigation of chest pain. Eighty-seven patients had evidence of atherosclerosis, and 13 patients had normal coronary vessels.ence in leucocyte elastase was found between the 2 groups, nor was there any relationship between elastase levels and the severity of atherosclerosis. However, relationships between plasma leucocyte elastase levels and various lipid fractions (Apo AI, LDL) and daily tobacco consumption were found. Leucocyte elastase may thus play a role not only by direct modification of the vessel wall, but also indirectly via risk factors such as dyslipoproteinemia and leucocyte toxicity.

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Coronary angiograms recorded in the recent phase of an acute my-ocardial infarction in 73 patients were compared with those taken in the remote phase at least 12 months from the onset of the infarction. The infarct-related lesions of 23 patients (32%) showed a regression of 20% or more. Analysis of recent-phase angiograms proved that any one of several features (long-segment narrowing, intraluminal thrombus, flaplike structure or atheromatous ulceration) was present more frequently in the lesions showing a marked regression (18/23, 78%) than in the lesions without regression (15/40, 38%) (p<0.01). Thus, the narrowings of infarct-related lesions seen on the recent-phase angiograms regress frequently. The possibility of regression can be predicted from the angiographic features.

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Mitral valve surgery was performed in 59 patients with severe pulmonary hypertension (average systolic pulmonary artery pressure 77.1±18.6mmHg; range 50-115mmHg) between 1983 and 1990. Thirtyeight patients had been subjected to mitral valve replacement, 16 patients both mitral and aortic valve replacement, and 5 patients had open mitral commissurotomy, with an operative (30 day) mortality of 5.0%. These 3 deaths happened during the early postoperative period. Survivors were followed up for a period ranging from 6 months to 7 years with a mean of 36 months. Four late deaths (7.1%) occurred in patients with valve replacement. Actuarial survival was 93±3% at 5 years, and 90.7±4.4% at 7 years. Right ventricular catheterization was performed on 14 patients a mean of 38 months following operation. Systolic pulmonary artery pressure had decreased from a mean of 77.1±18.6 to 39.7±14.0mmHg (p<0.001) and 90% of the survivors were in New York Heart Association Class 1 or II compared to 23.7% preoperatively. The clinical and hemodynamic findings in this series suggest that severe pulmonary hypertension is not a contraindication, and pulmonary hypertension decreases significantly after mitral valve surgery.

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The purpose of this study was to construct a simple ergometer for the ³¹P NMR spectroscopic study of dynamic forearm exercise in a whole body magnetic resonance imaging system and to evaluate the total system and the physiological response to this type of exercise using a multistage protocol.
The system consisted of a completely nonmagnetic assembly includ
ing a rope, pulley and weights. The work of lifting weights was quanti tated. The exercise protocol of 1-min increments in work load enabled subjects to reach maximal effort. Phosphocreatine decreased linearly with an increase in work load and was accompanied by a fall in pH and an increase in lactate level in the antecubital vein of the exercising fore arm; concomitantly, there was a slight increase in whole body oxygen uptake and heart rate. Spectroscopy gave reproducible results using this exercise protocol.
These results demonstrate that this system provides a reliable means for performing ³¹P magnetic resonance spectroscopy studies during fore arm exercise.

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Acute hemodynamics of pimobendan were compared to captopril in a crossover trial in patients with chronic heart failure (NYHA II-III). Heart failure had been stabilized by conventional therapy with diuretics and digitalis for more than 2 weeks. Patients receiving vasodilators were excluded. The hemodynamics were analyzed using a Swan-Ganz catheter at the bedside during drug administration.
Following an intravenous injection of 2.5mg of pimobendan, there was a significant increase in heart rate and decrease in mean pulmonary artery pressure, total pulmonary resistance, mean arterial pressure, systemic vascular resistance and mean right atrial pressure 2 hours after the injection. Captopril (12.5mg, orally) significantly decreased mean arterial pressure, systemic vascular resistance and double product 2 hours after administration. In this study, the inotropic effect was evaluated through the relation between the stroke volume index and diastolic pulmonary artery pressure, and also between the stroke volume index and mean arterial pressure. Although decreases of diastolic pulmonary artery pressure and mean arterial pressure were seen with both drugs, the differences in stroke volume index were not significant.
In comparison with captopril, the acute hemodynamics of pimobendan are characterized as follows: 1) the systemic arteriovasodilating effects of the two drugs were equal, 2) the pulmonary arteriovasodilating effect of pimobendan was marked, 3) a venodilating effect, documented through a decrease of mean right atrial pressure, was seen only with pimobendan.
This study concluded that pimobendan is a stronger arterio-venodilator than captopril.

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The clinical features, hemodynamic changes and prognosis of 21 children with simple atrioventricular septal defect (3 associated with patent ductus arteriosus) were studied during a follow-up period of 1 month to 13 3/12 years (median 3 years). Six patients had spontaneous closure of the ventricular part of the defect within 22.2±27.7 months (Group I). The symptoms and signs of failure to thrive, frequent respiratory tract infections and congestive heart failure were more common in patients without spontaneous closure of the ventricular part of atrioventricular septal defect (Group II) than in patients in Group I. The Qp/Qs ratio, pulmonary vascular resistance and pulmonary to systemic resistance ratio were also higher in Group II than in Group I. In spite of a higher postoperative mortality rate and a higher incidence of transient complete heart block, the children in Group II also had a significantly higher (p<0.005) preoperative mortality rate than those in Group I.
In conclusion, if the ventricular part of the atrioventricular septal defect closed or was closing spontaneously, symptoms and signs were less severe and there was a better prognosis.

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An intriguing aspect of cardiac mechanoenergetics is the smaller variability of the contractile efficiency than the energy economy of force. We theoretically speculated about this dissociation by relating the mechanical efficiency with P_o/a (the curvature of the force-velocity curve) in Hill's characteristic equation of muscle; P_o/a is known to change with the energy economy and inversely with V_max, and myosin ATPase activity. The analysis showed that the variability is smaller for the mechanical efficiency than for P_o/a and that the energy economy changes approximately with (P_o/a)³. These theoretical relations may partly explain the small variability of the empirically observed contractile efficiency under various experimental conditions which are known to widely change the energy economy.

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Neuropeptide Y (NPY) has a wide and specific distribution in the central nervous system, and is colocalized with catecholamines in specific neuronal systems. In this study, in order to investigate the regulatory mechanisms of NPY and presynaptic α₂-adrenergic receptors on central noradrenergic transmission in hypertension, we have examined the effects of NPY and the α₂-agonist, UK 14, 304, on (³H)-noradrenaline (NA) release from hypothalamic slices of spontaneously hypertensive rats (SHR). Electrical stimulation (1 Hz)-evoked (³H)-NA release was significantly greater in the hypothalamic slices of SHR than in those of Wistar Kyoto rats (WKY). NPY and the α₂-agonist, UK 14, 304, inhibited the stimulation-evoked (³H)-NA release in a dose-related manner. The inhibitory effects of NPY and UK 14, 304 on NA release were significantly attenuated in SHR compared with WKY. These results suggest that NPY and α₂-adrenoceptors might be involved in the regulation of central sympathetic nervous activity in hypertension.

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Effects of FRC 8653, a new dihydropyridine derivative, on regional blood flow, cardiac function and myocardial oxygen consumption were examined and compared with those of nifedipine in anesthetized openchest dogs. Intravenous administration of FRC 8653 at doses of 1, 3 and 10μg/kg dose-dependently decreased aortic pressure and increased aortic, vertebral and coronary blood flow similar to nifedipine. No significant change was observed in left ventricular end-diastolic pressure, left ventricular positive dP/dt and heart rate following i.v. administration of FRC 8653. Myocardial oxygen consumption was dose-dependently decreased by FRC 8653. When changes in mean aortic pressure and aortic and coronary blood flow were compared at the same dose of 10μg/kg i.v., both FRC 8653 and nifedipine showed almost the same degree of reduction of mean aortic pressure, but the time from drug administration to peak responses and the duration for which half the maximal effects were maintained, were significantly longer with FRC 8653 than nifedipine. Results suggest that FRC 8653 may be useful for the treatment of patients with hypertension and ischemic heart disease.

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We present a patient with left ventricular thrombus diagnosed by two-dimensional echocardiography. Thrombosis was due to acquired transient protein C deficiency which was caused by impaired liver function due to hepatitis, sepsis and heart failure. With proper treatment the thrombus disappeared on the fourth day. Eighteen weeks later the protein C level returned to normal. We recommend echocardiographic evaluation and follow-up of suspected cases for intracardiac thrombus. The measurement of protein C level in such cases is proposed. This is the first case with left-sided cardiac thrombus associated with protein C deficiency in the medical literature.

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Electrophysiological examination in a 39-year-old male disclosed an accessory pathway between the right atrium and the right ventricle and AV nodal dual pathways. Atrial and ventricular extrastimuli induced paroxysmal supraventricular tachycardia (PSVT), which was shown to be AV reciprocating tachycardia. Double atrial response was noted during ventricular extrastimuli at V₁V₂ of 280msec and V₁V₂ of 250msec. The first atrial response is considered to have been transmitted in a retrograde fashion in the accessory pathway, and the second atrial response similarly in the slow pathway of the AV node.

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A narrow aortic root and a small aortic annulus made aortic valve replacement in a 35-year-old female patient with calcified aortic stenosis rather difficult. At the end of the procedure, it was noticed that the aortic root was badly torn. The tear started at the end of the aortotomy incision, near the commissure between the non-coronary and left coronary cusps, ran flush with the prosthetic ring and extended beneath and a few millimeters beyond the ostium of the left coronary artery. Only a thin rim of the aortic wall was left proximally, which was not strong enough to support the sutures. The aorta was repaired using a pericardium covered Goretex patch, bolstered by the left atrial appendage.

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