From May 1975 to December 1988, 62 patients underwent 66 replacements of prosthetic heart valves, due to structural valve failure in 37, prosthetic valve endocarditis (PVE) in 17, periprosthetic leak in 5, thrombosed valve in 3, hemolysis in 2, and prophylactic removal in 2. Before reoperation, 3 patients were in NYHA Class I. 24 in Class II. 21 in Class III, and 18 in Class IV. Replacements of valve prostheses were at the mitral position in 33 patients, at the aortic position in 16, at the aortic and mitral position in 9, at the mitral and tricuspid position in 5, at the tricuspid position in 2, and at the pulmonary position in 1. There were 6 early deaths (9.1%), and 13 late deaths (7.2± 0.4%patient-year). Clinical improvement of the current survivors was good. The follow-up duration was 4 months to 11.4 years (mean 3.5 years), and the cumulative follow-up was 180 patient-years (100% complete). Patients undergoing replacement of 2 prostheses showed a higher early mortality rate (35.7%) than those who received replacement of I prosthesis (1.9%) (p<0.01). The actuarial survival including early deaths was compared using the generalized Wilcoxon test. survival was better in patients with replacement of one prosthesis than in those with replacement of 2 prostheses (p<0.001), and was better in NYHA Class I to III patients than in Class IV patients (p<0.05). Replacement of 1 prosthesis for patients with primary tissue failure of bioprostheses showed no operative mortality and a good 5 year survival rate (96±4%). High risk factors for replacement of prosthetic valves included double valve replacement. NYHA Class IV and PVE.

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To clarify the clinical significance of resting thallium-201 (Tl) delayed SPECT for assessing the viability of infarcted regions, we studied resting Tl initial and delayed Tl SPECT one week after exercise (Ex) Tl SPECT in 38 patients (40 regions) with old myocardial infarction (OMI) and 35 patients (37 regions) with effort angina pectoris (EAP). Analysis of resting Tl and Ex Tl SPECT divided the patients with OMI into 3 groups. Twenty-three patients whose perfusion defect (PD) on resting delayed image was same as that of Ex delayed image were divided into 12 patients with Ex Tl redistribution (RD) (G1) and 11 patients without Ex Tl RD (G3). Fifteen patients showed a decrease of PD on resting delayed image compared with Ex delayed image (G2):, Thirty-five patients with EAP were divided into 18 patients who had no PD oh Ex delayed image (G1) and 17 patients whose PD did not disappear on Ex delayed image but disappeared on resting delayed image (G2). The increase of pulmonary artery wedge pressure on Ex was higher in G2 than in G1 of both OMI and EAP (OMI; G1 15±16mmHg vs G2 27±7mmHg; p<0.01, EAP; G1 12±7 mmHg vs G2 22±6 mmHg; p<0.05). The percent Tl uptake of the PD on Ex Tl initial images was lower in G2 than in G1 of both OMI and EAP (OMI: G1 63±7% vs G2 55±9%; p<0.05, EAP: G1 72±7% vs G2 65±9%; p<0.05). That of the PD on resting Tl delayed images was higher in G1, and G2 than in G3 of OMI (G1 78±7%. G2 74±8%. G3 41±10%; G1 vs G3, G2 vs G3 p<0.001). The prevalence of akinetic or dyskinetic wall motion on left ventriculography was higher in G2 than G1, and in :G3 than G2 (G1, 24.3%. G2 52.2%. G3 85.7%; p<0.001). Thus, in patients with OMI the decrease of Tl PD on resting Tl delayed images compared with Ex delayed images may indicate severe ischemia induced by stress as well as in patients with EAP, and furthermore the presence of viable muscle. On the other hand, the infarcted region without decrease of Tl PD on resting delayed images may lack viable muscle.

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To demonstrate serial changes of left ventricular (LV) function during coronary artery bypass grafting surgery, transesophageal echocardiography (TEE) was used in 17 patients. The cross-sectional image of the left ventricle at the level of the papillary muscles was monitored, and was analyzed immediately in the operating room using a computer-assisted cine-memory function. Global LV funtion was evaluated by measuring LV end-diastolic and end-systolic area and computing the fractional area change (FAC). Segmental wall motion abnormalities (SWMA) were graded according to a scoring system. During the operative procedure before sternal closure. 5 patients showed SWMA with a simultaneous decrease in FAC to under 40%, and 9 patients showed SWMA without FAC depression. Two-thirds of new SWMA improved after myocardial revascularization. All 17 patients showed a change of interventricular septal movement at the end of the operation. FAC improved from a mean value (±SD) after intubation of 47.6±10.7% to a mean value after revascularization of 58.5±13.0% (p<0.05) and to a mean value at the end of the operation of 55.9±12.2% (p<0.05). Thus: 1) global and regional LV function improved immediately after myocardial revascularization with administration of inotropic agents; 2) a significant change of interventricular septal movement occurred after sternal closure; and 3) intraoperative TEE monitoring is a safe, simple. and effective method for evaluating LV global and regional function.

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This clinical study was undertaken to evaluate resting left ventricular early diastolic function relating to perioperative myocardial damage after coronary artery bypass graft (CABG) with radionuclide ventriculography. Forty-eight cases undergoing CABG were divided into two groups-Group I: not complicated with perioperative myocardial infarction (PMI), and Group II: complicated with PMI. In Group I (42 cases), early diastolic parameters such as peak filling rate (1/3 PFR) and mean filling rate (1/3 FR(m)) during first third diastole were not impaired in the postoperative and follow up periods. In contrast, in Group 11 (6 cases), early diastolic parameters were significantly de-creased to 157±74% EDV/sec of 1/3 PFR(pre op: 234±74, p<0.05) and 153±80% EVD/sec of 1/3 FR(m) (pre op: 231±86, p<0.05) in the postoperative period, and these parameters were still decreased in follow up period. The time to peak filling rate, normalized to diastolic time (TPFR/DT) of Group II cases, was severely prolonged in both periods. From these results, the complication of perioperative myocardial infarction was suggested by the decrease of early diastolic function and the prolongation of the time to peak filling rate. Early diastolic function was a more sensitive parameter than systolic function in the detection of impaired cardiac function in those cases with perioperative myocardial damage after CABG.

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To evaluate the clinical characteristic of pulmonary gas exchange in patients with low pulmonary capillary wedge pressure (PCW<18mmHg) in the early phase of acute myocardial infarction. we investigated 48 patients admitted with-in 24h from the onset of chest pain. The alveolar-arterial oxygen tension difference (AaDO₂) and arterial blood gas parameters were obtained while breathing room air on admission. The disturbance of pulmonary gas exchange. as revealed by the high value of AaDO₂, existed without left ventricular dysfunction. and AaDO₀2 had no significant relationship with any of the hemodynamic para-meters including the difference between plasma colloid osmotic pressure and PCW. Multiple regression analysis was performed using 9 variables related to pulmonary gas exchange, to identify those which were important. As a result. QRS score (p<0.01) and age (p<0.05) were identified as significant variables related to AaDO₂. Thus. the disturbance of pulmonary gas exchange in patients with low PCW was caused by mechanisms other than left ventricular failure which may reflect the extent of ischemic myocardium.

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Proarrhythmic responses were evaluated in repeated electrophsiologic studies (EPS) in 27 patients with inducible ventricular tachycardia (VT). Class Ia drugs were administered to 23. Ib to 6. Ic to 4. III to 5 and IV to 9 patients. The mean age was 53 years, and 18 patients had structural heart diseases. Pleomorphism was observed in 11 patients. In 4 patients (15%), the VT cycle length (CL) shortened by 50ms or more in EPS during the administration of antiarrhythmic drugs. VT was inducible by a less aggressive induction mode than the control study in 9 patients (33%). In 4 patients (15%), the induced VT changed to the incessant form, and the other 2 patients (7%) required DC shocks due to hemodynamic deterioration. Patients with pleomorphic VT and/or structural heart diseases seemed to develop proarrhythmia more frequently. In total, some proarrhythmic response was observed in 13 (48%) of the 27 patients. Therefore, it should be kept in mind that proarrhythmic effects are frequently observed during antiarrhythmic therapy in patients with sustained VT. The action of the drugs on the slow conduction zone may vary. which may provide a basis for the development of proarrhythmia.

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Four child patients (1 male and 3 females) with homozygous familial hypercholesterolemia (FH) were examined. They were 4y4m to 9y8m of age on admission. A female patient at age 5y7m on admission had already experienced anginal attacks. Ischemic change was found on exercise ECG in 2 patients. Grade 1/6 to 3/6 (Levine) systolic ejection type murmur was audible in all patients. Cardiac catheterization was carried out in all patients. Supravalvular aortic stenosis was found and so-called atherosclerotic wall thickening was also noticed in 3 of them. Narrowing of the coronary arteries was found in only l patient who complained of anginal pain. Supravalvular aortic stenosis was more prevalent than coronary artery disorders in FH children and this lesion was also detected by echocardiography. Therefore. follow-up by echocardiography seems to be very useful in assessing the progression of atherosclerosis in patients with severe hypercholesterolemia.

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A patient suffering from tsutsugamushi disease underwent endomyocardial biopsy for the purpose of diagnosis of myocarditis. Proliferation of Rickettsia tsutsugamushi was observed in the vascular endothelial cells of the myocardium. There have been no reports describing the identification of Rickettsia tsutsugamushi endomyocardial biopsy. This report indicates that endomyocardial biopsy may be a useful adjunct to the clarification of myocardial involvement of Rickettsia tsutsugamushi.

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A 55-year-old male presented with hypotension and marked elevation of jugular venous pressure suggesting impaired ventricular filling. Echocardiography demonstrated a moderate amount of pericardial effusion and dense and shaggy fibrinous strands attached to the pericardia. Pericardiocentesis was performed under the diagnosis of cardiac tamponade, but normal ventricular filling could not be restored even after pericardiocentesis. Hemodynamic evaluation after pericardiocentesis revealed persisting low cardiac output. elevation and equilibration of right atrial, right ventricular end-diastolic and pulmonary capillary wedge pressures, and deep y descent. Later, surgical removal of the thickened pericardium was required. This case appeared to be typical effusive-constrictive pericarditis. Regarding etiology, a rare organism. Streptococcus milleri, proved to be responsible, while the case history and clinical situation were suggestive of a tuberculous or tumorous origin.

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Infective aneurysm showing dilatation of all three coronary sinuses of Valsalva due to infective endocarditis is extremely rare. We present the first report of such a case complicated by left single coronary artery. The patient was a 55-year-old man with a past history of untreated diabetes mellitus, cerebral infarction, aortic regurgitation and high-grade fever. He was admitted with a complaint of easy fatigability. In a treadmill exercise test, asymptomatic ischemic depression of the ST segment was observed. Two-dimensional echocardiography revealed marked dilatation of all three sinuses of Valsalva, and a mural thrombus within the dilated right sinus of Valsalva. On magnetic resonance imaging, an abnormal signal in the markedly dilated right sinus of Valsalva was revealed. Coronary arteriography showed left single coronary artery (L1 type by Sharbaugh's classification). The histopathological features of the affected aorta were thought to represent the healing stage of infective endocarditis. With regard to the myocardial ischemia in this patient, it was thought to have arisen mainly through aortic regurgitation and coronary atherosclerosis due to single coronary artery, and partly influenced by untreated diabetes mellitus.

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Effects of a high-salt diet on blood pressure, extracellular fluid volume, and the renin-angiotensin system in rats with the two types of Goldblatt hypertension were examined. Both in one-kidney, one clip (1K1C) rats and in one-kidney, sham-clipped (1K) rats, systolic blood pressures of rats which received a high-salt diet for 4 weeks were higher than those of rats of respective groups on a normal-salt diet, suggesting an increased sensitivity of blood pressure to changes in salt intake. Whereas sodium space was increased in 1K rats on the high-salt 1K1C rats receiving the high-salt did not have significnatly increased sodium space. These results suggest that acceleration of 1K1C hypertension with salt load could not be explained only by changes in extracellular fluid volume. In contrast, both in two-kidney, one clip (2K1C) rats and in two-kidney. sham-clipped (2K) rats, the high-salt diet produced no change in blood pressure de-spite the increase in sodium space, suggesting a decreased salt sensitivity. Although on the normal-salt diet the blood pressure of 2K1C rats tended to correlate with plasma renin activity, on the high-salt diet plasma renin activity was markedly decreased, and then blood pressure highly correlated with sodium space. Accordingly, the lesser salt sensitivity in 2K1C rats is probably attributable to the counterbalance of the suppressed renin-angiotensin system against volume expansion. Evidence presented suggests, therefore, that 1K1C rats have greater salt sensitivity of blood pressure than 2K1C rats. Moreover, neither volume expansion nor stimulation of the renin-angiotensin system may be the sole cause for blood-pressure rise with salt loads, although they are important factors regulating salt sensitivity in Goldblatt hypertensive rats.

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The role of thromboxane A2 (TXA2) in myocardial necrosis during coronary occlusion and reperfusion was investigated by using a new long-acting TXA2 synthetase inhibitor. DP1904. A rabbit coronary branch was occluded for 30 min and then reperfused for 72h. Infarct size and area at risk were determined histologically and by fluorescent particles, respectively, for 4 groups; a saline receiving control group (C group), a DP1904 treated group (DP group), a heparin treated group (H group), and a DP1904 plus heparin treated group (DP-H group). The H group and DP-H group were included to examine the influence of heparinization on the effect of DP1904. In the DP and DP-H groups. 10mg/kg of DP1904 was injected i.v. 2h before coronary occlusion, as well as 24 and 48h after reperfusion. This dose of DP1904 (10mg/kg i.v.) was able to inhibit serum thromboxane B2 formation ex vivo to 1.1% of the control level 2h after its administration, and to 39.5% at 24h, in the rabbit (n=5). The H and DP-H groups received 1000 units of heparin i.v. 3 min prior to coronary occlusion. The size of the area at risk, heart rate, blood pressure, and rate-pressure products were comparable between the 4 groups. Mortality was not significantly different in any group. Myocardial infarct size as the percentage of area at risk was 43.63.9% in C group (n=10), 41.1±4.4% in DP group (n=9), 47.8±3.0% in H group (n= 13), and 44.7±4.0% in DP-H group (n=10), which were not significantly different. These findings suggest that TXA2 does not contribute directly to myocardial necrosis during coronary occlusion and reperfusion in the rabbit.

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