We retrospectively examined 8 patients who had classical physical signs of tricuspid regurgitation associated with congestive heart failure, the cause of which was not identified by echocardiography. Exclusion criteria were as follows; 1) peak velocity of tricuspid regurgitation greater than 3 m/sec, 2) disturbance of left ventricular wall motion, 3) severe mitral regurgitation and/or aortic regurgitation by color Doppler echocardiography, and 4) structural abnormalities of tricuspid and mitral valve complexes. The subjects had a mean age of 81 years and all showed atrial fibrillation without tachycardia. Radiocardiography showed no significant left-to-right shunt. Two-dimensional echocardiography showed a markedly enlarged right atrium and slight enlargement of the right ventricle in all patients. A signal of tricuspid regurgitation was seen throughout the markedly enlarged right atrium on color Doppler echocardiography. Although neither hypoxemia nor hypercapnea were found in any of the patients, pulmonary function tests done in 6 patients were all abnormal. In chest x-ray films, 6 of the patients showed evidence of marked protrusion of the right heart border progressing over the course of several years. Right atrial enlargement due to both long-standing atrial fibrillation and presumably, to right ventricular diastolic dysfunction caused by aging made the tricuspid valve annuls annulus dilate to produce tricuspid regurgitation. In addition, concomitant mild lung disease produced a vicious cycle which led to more severe tricuspid regurgitation resulting in severe congestive heart failure. This pathophysiology can be a cause of congestive heart failure in the elderly.

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Twenty-seven patients with stable coronary artery disease were continuously monitored with an ambulatory radionuclide ventricular function monitor (VEST) during exercise to determine the prevalence of silent ischemia and the temporal sequence of events during ischemic episodes. Exercise-induced ejection fraction abnormality was considered a <6% increase in the control value lasting for more than 60 sec. Patients performed exercise for 424±111 sec during VEST recording. Seventeen exercise-induced ejection fraction abnormalities were observed in 17 patients, of which eight (47%) were silent electrocardiographically and 12 (71%) were silent symptomatically. In all of the patients, exercise-induced ischemia occurred in a temporal sequence of ejection fraction abnormalities, ST depressions and then symptoms. In nine patients with ejection fraction and ST abnormalities, ejection fraction abnormalities occurred earlier (199±87 sec) than ST depressions (321±117 sec; p<0.01). In five patients with symptoms (399±151 sec), the sequence was ejection fraction abnormalities (205±64 sec; P<0.05) followed by ST depressions (266±101 sec; P<0.05, ) and symptoms (399±151 sec; P<0.01). After termination of exercise, ejection fraction (49±12 sec) recovered sooner than symptoms (102±27 sec; p <0.01) or ST abnormalities (191±96 sec; p<0.01). Thus, hemodynamic monitoring by VEST may be helpful in detecting ischemic episodes in coronary artery disease which remain electrocardiographically or symptomatically silent. Furthermore, exercise-stress induces a cascade of temporal changes in ischemic events which may be helpful in understanding the pathophysiology of ischemia.

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We evaluated the usefulness of a combination of QRS voltage and the pattern of ST-T abnormality in the electrocardiographic diagnosis of left ventricular hypertrophy (LVH) in 100 middle-aged men: 32 normals, 59 with hypertension (HT), and 9 with hypertrophic cardiomyopathy (HCM) with evidence of LVH (RV₅ or RV₆&ge;2.6 mV, SV₁+RV₅ or SV₁+RV₆&ge;3.5 mV). They The subjects were classified into three groups based on ST-T pattern: normal (group N), early strain (group ES), and strain (group S) . Echocardiographic evidence of LVH was present in 52.0% (52/100) of the subjects: 72.8% (43/59) of the patients with HT, all 9 patients with HCM, and none of the 32 normals. Echocardiographic evidence of LVH was present in 31.3% (20/64) of group N, 73.3% (11/15) of group ES, and all 21 subjects of group S. In patients with HT, the incidence of echocardiographic LVH was higher in group S (100%) than in both group ES (78.6%) and group N (60.6%). QRS voltage (RV₅, RV₆, RV₅ + SV₁, and RV₆ + SV₁) was significantly correlated with interventricular spetal thickness (IVST), IVST+LVPWT/2, and LV mass, as determined by echocardiography, in patients with LVH (IVST or left ventricular posterior wall thickness (LVPWT) of &ge;l2mm) (r=0.55 to r=0.75, p<0.05), but not in patients without LVH (IVST and LVPWT<12 mm). There were significant correlations between QRS voltage indices (RV₅, RV₆, RV₅+SV₁, and RV₆+SV₁) and IVST, IVST+LVPWT/2, and LV mass in group S (r=0.68 to r=0.86, p<0.05), but not in group N. Values for IVST and LV mass were significantly greater in group S than in groups ES or N. The combination of QRS criteria and ST-T findings reflected the echocardiographic assessment of LVH, especially in patients with HT. The electrocardiographic diagnosis of LVH thus appeared to be improved by evaluating both the QRS voltage and ST-T abnormality pattern.

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To assess myocardial metabolism during ischemia and reperfusion, 36 rabbits were divided into 4 groups; a control group (Control), an ischemia group in which the circumflex branch was ligated for 30 min (Ischemia), a 5 min reperfusion group (5-RP) and a 30 min reperfusion group (30-RP). The concentrations of metabolites (lactate, alanine and free-carnitine) in the myocardium determined by ¹H-magnetic resonance spectroscopy (MRS). The concentration of free carnitine was lower in Ischemia than in Control (2.0±0.4 vs 5.2±1.4μmol/wet·g, p<0.01), and remained reduced in 30-RP (3.0±0.6μmol/wet·g, p<0.01). On the other hand, the concentrations of lactate and alanine were higher in Ischemia than in those of Control (54.9±8.5 vs 8.8±0.8, 6.5±1.0 vs 2.5±0.5 μmol/wet·g, respectively; p<0.01), and remained elevated in 30-RP. These findings indicate that recovery from an ischemia-induced disturbance in myocardial metabolism to the pre-ischemic level apparently requires a prolonged period after reperfusion, and that ¹H-MRS is a useful new method for evaluating myocardial ischemia.

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To explore the role of calcium-dependent protease in the stunned myocardium, open-chest dogs underwent 15 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. Dogs received a single bolus intravenous injection of either the protease inhibitor NCO-700 (n=6) or saline (n=6) 1 min before reperfusion followed by a 30-min infusion at the same dose. Regional myocardial function was assessed in terms of systolic wall thickening with an epicardial Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions and similar degrees of dyskinesis during occlusion. After reperfusion, recovery of contractile function, expressed as a percentage of the baseline value, was significantly greater in NCO-700-treated dogs as than in control dogs: -14.3±10.6 vs -48.9±7.2 (p<0.05) at 15 min, 10.8±10.3 vs -31.1±9.0 (p<0.05) at 30 min, 42.5±10.1 vs -16.4±9.1 (p< 0.005) at 1 h, and 47.5±8.3 vs -14.9±9.4 (p<0.001) at 2 h. The data suggest that the protease inhibitor markedly improved contractile function in stunned myocardium by inhibiting intracellular protease activity.

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Atrioventricular (AV) septal defect with a common AV orifice was found in two near-term rat fetuses, which are descendants of an inbred strain, known to genetically develop tetralogy of Fallot, hypertrophic cardiomyopathy, etc. In one fetus the anterior bridging leaflet was almost entirely committed to the left ventricle but in the other it protruded slightly into the right also, coinciding with type A or type B in humans, respectively. The latter fetus had also a subaortic ventricular septal defect with overriding of the aorta and a double aortic arch. Both fetuses had a narrow pulmonary infundibulum with a muscular band, a dysplastic pulmonary valve, and a markedly hypoplastic ductus arteriosus. Complete AV septal defect and tetralogy of Fallot may be linked genetically, with some common underlying developmental processes.

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We experienced 2 patients in whom conventional percutaneous methods were not useful for acute occlusions sequel to coronary angioplasty. Acute occlusions seemed to be caused by large dissections. Pulling an inflated balloon at the dissected lesions achieved reentry from the false lumen to the true lumen, thus resolving collapse of the true lumen and recanalizing the occluded coronary artery.

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We report a case of cardiac lipoma found by chance as a cause of ST-T changes which suggested left ventricular hypertrophy. A 38-year-old man was completely asymptomatic and was incidentally found to have an abnormal electrocardiogram during a regular physical examination. Echocardiography revealed an oval mass located in the inferior wall of the left ventricle near the apex, and there was no finding of left ventricular hypertrophy. Computed tomography and magnetic resonance imaging, rather than echocardiography, were useful in determining the characteristics of the lipoma in this case. The tumor was resected by operation and the histology showed lipoma with no evidence of malignancy .

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A woman with a pheochromocytoma crisis initiated by cardiogenic shock showed severely impaired left ventricular contraction at the time of admission. Heart failure was improved rapidly, and an endomyocardial biopsy performed on the 11th day of admission showed findings compatible with "catecholamine cardiomyopathy:' Regarding the pathogenesis of short-duration left ventricular dysfunction, catecholamine-induced cardiotoxicity would probably be the initial consideration. However, in this case, after considering the electrocardiogram on admission and a series of left ventriculograms, "myocardial stunning" following diffuse coronary vasospasm induced by catecholamine crisis may have also contributed to the dysfunction.

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