Mitral valve prolapse (MVP) is a clinical syndrome of which mitral regurgitation and congestive heart failure are the late sequelae. It can be usually diagnosed by echocardiography. In this study, we reevaluated the patients with acute rheumatic fever (ARF) who were followed-up regularly for aspects of MVP. Physical examination, echocardiography and Doppler study were performed for all the patients. One hundred twenty-seven cases of polyarthritis (54.7%), and 105 cases of valvular involvement (45.3%) were diagnosed. Echocardiography demonstrated MVP in 46.8% with isolated mitral insufficiency, in 38.2% with combined valvular defect and in 12.6% with only polyarthritis. One hundred healthy children comprised the control group. Statistical analyses revealed a significant difference in favor of valvular involvement between the groups.

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Pulsed Doppler echocardiography was used to study left ventricular diastolic filling pattern (LVDFP) over the convalescent stage of acute myocardial infarction (AMI) in 25 patients. Twelve normal subjects served as a control group. The patients were divided on the basis of enzymatically estimated infarct size into 2 groups: 7 as the large AMI group, and the other 18 as the small AMI group. Peak early diastolic filling velocity (E) and the ratio of E to peak filling velocity at atrial contraction (E/A ratio) were determined from the Doppler transmitral flow velocity recordings at 1 and 4 weeks after the onset of AMI. At 1 week E and E/A ratio were significantly lower in the small AMI group com-pared to the control and the large AMI groups, however, there was no significant difference in E and E/A ratio between the control and the large AMI groups. E/A increased with cumulative CK release among the patients (r=0.54, p<0.01). In the following 3 weeks E and E/A ratio decreased only in the large AMI group, and E and E/A ratio at 4 weeks weakly correlated with pulmonary capillary wedge pressure (r=0.63, p<0.01 and r=0.65, p<0.01) and ejection fraction (r=0.50, p<0.05 and r=0.62, p<0.01) among the patients. There was no significant difference in E or E/A ratio between patients with and without coronary thrombolysis.
Thus, LVDFP in the early convalescent stage of AMI was characterized by low E and E/A ratio in patients with small AMI, however, a "pseudonormalized" pattern was observed in patients with large AMI. The effect of the infarct size on LVDFP diminished in the late convalescent stage of AMI. LVDFP in patients with AMI appears to be influenced by the infarct size and by the time of study. The effect of coronary thrombolysis on LVDFP was not evident throughout the convalescent stage of AMI in this study.

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We studied 16 patients with chronic mitral regurgitation by echocardiography before, and at 3 weeks, at 6-8 months and at 1-9 years after mitral valve replacement (MVR) to investigate serial changes in left ventricular (LV) function and reversal of ventricular dilatation. All patients at an average of 2.6 years after, and 8 patients before MVR were also studied by echocardiography and, except for 3 patients by measuring plasma catecholamines from the right atrium during bicycle exercise. Before operation, all patients were divided into group A (n=12) with end-systolic dimension (ESD)<4cm and systolic blood pressure (SBP)/ESD>3, and group B (n=4) with ESD>4cm and SBP/ESD<3. Maximum reduction in end-diastolic dimension (EDD) occurred at 3 weeks in all patients after MVR (from 60.5±3.7 to 49.0±4.5mm, p<0.05). ESD was reduced significantly (p<0.5) only in group A. LV function was normal in group A, but it was depressed in group B at early and late periods after MVR. The slopes of the relationship between the mean velocity of circumferential fiber shortening (Vcf) and plasma norepinephrine (NE) during exercise in all patients in group B decreased along with the depression in LV function. After operation, all patients in group A reached New York Heart Association (NYHA) functional class I, while patients in group B were in NYHA class II. It is concluded that the surgical outcome after MVR for chronic MR will be better if preoperative ESD<4cm and SBP/ESD>3. The relationship between mean Vcf and plasma NE during exercise seemed to be a useful index to evaluate the inotropic reserve of the LV.

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To examine whether atrial natriuretic factor (ANF) is secreted adequately in the early phase of myocardial infarction, plasma ANF concentration and clinical parameters, including hemodynamic variables, were studied in 118 patients with acute myocardial infarction (AMI). The patients were divided into 2 subgroups according to the absence (group A, n=41) or presence (group B, n=77) of a history of valvular heart disease, previous myocardial infarction, hypertension, or renal failure. Although no significant difference in atrial pressure after the infarction was found between the 2 groups, the plasma ANF level was significantly lower in group A than in group B (76±6vs. 185±26pg/ml; mean±SEM, p<0.01). Plasma ANF was correlated with pulmonary capillary wedge pressure in group B (r=0.54, p<0.001), whereas no relationship with hemodynamic parameters was observed in group A. In 56 of the 118 patients (group A, n=18; group B, n=38), the pulmonary arterial plasma level was significantly higher in group A (p<0.05), whereas the difference was not significant in group B. Seven of the 8 expired cases among these 56 patients had peripheral plasma ANF levels of more than 150pg/ml, which were higher than those in pulmonary arterial plasma.
These observations suggest firstly that the plasma level of ANF is lower in patients with a new onset of myocardial infarction compared to those with a history of cardiac or renal diseases, and secondly that stimulated ANF release originates not only from the right side of the heart, but also from additional site(s), particularly in patients with chronic ventricle overload and a poor prognosis.

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This study was undertaken to investigate the accuracy and reliability of videodensitometry (VDM) in measuring the magnitude of coronary arterial stenosis on coronary angiogram (CAG). CAG taken after administration of sublingual nitroglycerin was analyzed with VDM (XR-70 Coronary Analyzer, Vanguard). The magnitude of stenosis in coronary segments with four different classes of stenosis was consecutively measured 10 times by the same observer, and the values were 89.0±1.4, 70.9±2.1, 59.5±2.5, and 22.8±3.4%. The coefficients of variation (CVs), indicating intraobserver variability, were low for severe to moderate lesions (1.6, 2.9, and 4.3%, respectively), but was higher for low-grade lesions (14.8%). When the same lesions were measured by 2 observers, the measurements were highly correlated (r=0.971, p<0.01). The results of VDM were consistent with those of conventional gross examination for moderate to severe lesions, and the discrepancy was mainly found in low-grade lesions. The magnitude of stenosis of the same lesion was measured from the right and the left anterior oblique views, and the cineangle was found not to affect the results of VDM. Moreover, cardiac cycle did not affect the videodensitometric measurements of % area stenosis. In order to further investigate the accuracy of VDM, the magnitude of stenosis was measured in nine phantom arteries, and the value measured by VDM significantly correlated with the actual stenosis (r=0.969, p<0.001). These results indicate that the values of coronary arterial stenosis on CAG measured by VDM are accurate and clinically acceptable, even though variability is somewhat high for low grade lesions. VDM may be useful for evaluation of the outcome of PTCA and the anti-atherogenic action of some agents.

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The clinical significance of collaterals visible on angiography immediately after successful percutaneous transluminal coronary angioplasty (PTCA) was analyzed in 221 patients who underwent successful PTCA for coronary arteries receiving collaterals. Filling of the collaterals was classified as good; filling the entire epicardial segment of the stenosed site, fair; partially filling the epicardial segments distal to the stenosed site, and faint; visible but not filling the epicardial segments of the diseased vessel. Fifteen of 41 good collaterals remained good or fair on angiography immediately after PTCA. Among the 114 fair collaterals, 26 remained fair and 20 of 66 faint collaterals remained visible on the angiogram immediately after PTCA. There was no relationship between the degree of residual stenosis after PTCA and the degree of residual collaterals. Repeat coronary angiography was obtained in 156 patients. There was no correlation between the presence, absence or degree of collaterals observed on angiography immediately after successful PTCA and the rate of restenosis. Thus, collaterals to the vessels dilated by PTCA often remain on the angiogram immediately after PTCA and are dependent primarily on their degree before dilation. They do not indicate inadequate dilation or predict restenosis.

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The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.

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The effects of mexiletine (300mg/day, 24 patients) and disopyramide (300mg/day, 20 patients) on ventricular premature contractions (VPCs) were studied using a 24-hour ambulatory electrocardiogram. The VPC frequency was evaluated as a function of the underlying heart rate (HR). The VPC-HR correlation was classified into 2 major types, depending on whether the frequency of the VPC increased with the increased HR (positive type) or not (nonpositive type). The effects of the drugs were assessed based on the VPC-HR correlation and on the percent reduction of the VPC frequency.
Mexiletine and disopyramide significantly decreased the frequency of the VPCs of both the positive and nonpositive types. Each drug was assumed to be effective when the percent reduction of the VPC frequency exceeded 70%. Mexiletine (300mg/day) was 58.5% effective in positive type patients and 33.3% effective in nonpositive type patients, with a total efficacy of 45.8%. Disopyramide was effective in 50% of total cases with 44.4% in positive type patients and 54.5% in nonpositive type patients. However, the efficacy of these drugs on the 2 different types of VPCs was the same statistically. The findings strikingly contrasted those obtained with diltiazem and atenolol, which predominantly suppressed VPCs of the positive type which share similar characteristics with a triggered activity in vitro.
We conclude that the mode of action of class I antiarrhythmics on the VPCs differs from that of class II or IV antiarrhythmics, as viewed from the VPC-HR relationship, and that the difference probably comes from the different arrhythmogenesis for positive and nonpositive types of VPCs, in addition to the different electrophysiological actions of mexiletine and disopyramide.

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Anoxic perfusion prior to sustained ischemia (anoxic preperfusion), reportedly improves postischemic functional recovery of the heart, but its mechanism has not been well understood. The present study aimed to characterize the cardioprotective effects of anoxic preperfusion and its relationship to extracellular Ca⁺⁺ levels. Following 10min of aerobic perfusion, isolated rat hearts were assigned to a 10min aerobic perfusion or to a 10min anoxic perfusion. The hearts were then subjected to 30min of global ischemia and 30min of aerobic reperfusion. When the perfusate-free Ca⁺⁺ concentration was 2.0mM, postischemic recovery of left ventricular developed pressure was significantly improved by anoxic preperfusion (91.9±2.9% of baseline value vs. 50.5±12.9% after 30min reperfusion in the controls). However, the improvement of postischemic ventricular function by anoxic preperfusion was abolished when perfusate Ca⁺⁺ was reduced to 1.0mM and the contractile function was rather suppressed during early reperfusion by anoxic preperfusion when the Ca⁺⁺ level was 0.7mM (87.5±11.8% vs. 115.6±13.9% after 10min of reperfusion). On the other hand, lactate accumulation during the global ischemia was significantly less in anoxic preperfused hearts compared with untreated hearts both when perfusate Ca⁺⁺ was 0.7mM (61.3±5.1 vs. 85.9±6.8μmol/g dry) and when it was 2.0mM (43.8±2.0 vs. 140.3±14.1μmol/g dry). The amount of myoglobin released after global ischemia was not different between untreated and anoxic preperfused hearts regardless of the perfusate Ca⁺⁺ level. The results suggest that anoxic preperfusion does not reduce ischemic myocardial necrosis, but it attenuates myocardial stunning. That effect of anoxic preperfusion on the stunning is dependent on the extracellular Ca⁺⁺ level and is not totally explained by suppression of ischemia-induced lactate accumulation.

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The purpose of this study was to investigate the cellular distribution of carnitine and its acyl derivatives in the normal and ischemic myocardium, and the effects of exogenous l-carnitine on this distribution and mitochondrial function in the ischemic dog heart. Under nonischemic conditions, about 93% of the total cellular carnitine was located in the cytosolic compartment and 6.5% in the mitochondrial compart-ment. Sixty minutes of ischemia induced a decrease in the cytosolic free carnitine content, but caused the accumulation of long-chain acylcarnitine in the cytosolic and mitochondrial compartments.
Treatment with l-carnitine (30 or 100mg/kg, i.v.) inhibited the mitochondrial accumulation of long-chain acylcarnitine. Free fatty acid (FFA) metabolism in the mitochondria differs from that in the cytosol. So, it is necessary to investigate the changes in FFA metabolism in both of these cellular compartments. Our results suggest that l-carnitine has a protective effect on the ischemic heart by selectively reducing mitochondrial accumulation of long-chain acylcarnitine.

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The aim of this study was to investigate the correlation between hypoxic myocardial cell injury and intracellular protease activity. Cardiac myocytes were isolated from neonatal rat hearts and cultured in Eagle's modified minimum essential medium. Myocytes were incubated in hypoxic conditions for 6 hours. The cell death rate during hypoxia rose to 80% after 6 hours. Extracellular protease activity was elevated to 4 units during hypoxia, much higher than the 0.7 units in aerobic states at 6 hours. This extracellular protease activity in hypoxic conditions was markedly inhibited by leupeptin and EDTA, and weakly inhibited by the cysteine protease inhibitor, NCO-700, but phenylmethyl sulfonyl fluoride did not inhibit the protease activity. To identify the protease activated during hypoxia, calpain-specific inhibitors were added to the incubation mixture. Calpain inhibitor 1 and calpastatin, an endogenous selective calpain inhibitor, markedly inhibited extracellular protease activity during hypoxia. NCO-700 also inhibited intracellular protease activity. NCO-700 reduced hypoxic cell death to 30% after 6 hours of hypoxy-genation. These observations indicate that calpain is activated during hypoxia and leads to irreversible cell membrane degradation after 6 hours of hypoxygenation.

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The distribution of calmodulin was investigated in dog myocardium after coronary artery occlusion by an immunoperoxidase technic and compared with the distribution of myoglobin and the findings of hematoxylin-eosin (H-E) staining. After 60min or more of coronary artery ligation, calmodulin diffused clearly from myocardium in the region of hypereosinophilia (H-E) or stained intensely in regions of a contraction band or hydropic appearance. Similar findings were observed in the myocardium of cases of sudden cardiac death. The intense staining for calmodulin would reflect the association of calmodulin with membranes in response to the calcium overload that plays an important role in myocardial injury. Calmodulin staining provided more information than myoglobin staining, which only detected diffusion from necrotic cells. This method would be useful to elucidate the implications of calcium and calmodulin during the development of myocardial injury.

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We examined the possible alterations in calcium handling through the calcium channels of spontaneously hypertensive rats (SHR) using ⁴⁵Ca²⁺ uptake measurements in cultured aortic cells. Primary cultures of vascular smooth muscle cells (VSMC) were obtained by enzymatic dissociation of the thoracic aortas from 8-week-old SHR and age-matched Wistar-Kyoto rats (WKY). The functions of voltage sensitive calcium channels (VSCC) and receptor operated calcium channels (ROCC) were estimated from the activated ⁴⁵Ca²⁺ uptake in VSMC with high K⁺ depolarization and argininc vasopressin (AVP), respectively. Compared to basal conditions, depolarization with 55mM KCl increased ⁴⁵Ca²⁺ uptake at 20min by 94±17 (SE)% in SHR and 38±6% in WKY. The activated ⁴⁵Ca²⁺ uptake was significantly greater in SHR than in WKY (p<0.01). There was no significant difference in ⁴⁵Ca²⁺ uptake at 20min in the presence of 5×10^-8M AVP between SHR and WKY. These results suggest that calcium uptake, at least through VSCC, is increased in VSMC of SHR. This enhanced activity may be implicated in the hypertensive mechanisms in this model of hypertension.

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A 29-year-old woman with a long-term history of Graves' disease was admitted for thyroidectomy. Torsade de pointes occurred after the subtotal thyroidectomy. The level of her serum calcium was lower than normal. After administration of calcium gluconate intravenously, torsade de pointes disappeared and was no longer recorded. It is assumed that her torsade de pointes was caused by hypocalcemia as a complication of subtotal thyroidectomy.

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