The concentrations of total, low density lipoprotein (LDL), and high density lipoprotein (HDL) cholesterol, triglyceride and apoprotein B have been examined in Zen monks whose intake of animal products was almost negligible for 2 to 8 years, and in age-matched (24 to 25 years) control Japanese males who eat Western style food. The mean levels of total, LDL- and HDL-cholesterol, and apoprotein B were 135.1±16.7, 73.0±11.6, 50.4±9.6, and 70.6±15.6 mg/dl, respectively in Zen monks. These levels were 28.5, 32.8, 18.8, and 23.9% lower in Zen monks than in control Japanese males. These values are statistically significant compared to those of the controls (p < 0.01). There were no significant changes in the level of triglyceride in both groups

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We examined the relationship between late potentials and left ventricular function from a hemodynamic point of view in 50 patients with prior myocardial infarction. Late potentials were found in 15 (30%) of 50 patients. A left ventricular aneurysm was found in 28 patients. Late potentials were detected in 14 (50%) of 28 patients with the aneurysm but in 1 (5%) of 22 patients without it (p < 0.01). In the 50 patients, a hemodynamic data from the late potential positive group (n = 15) were compared to those from the late potential negative group (n = 35). The late potential positive group had a significantly lower ejection fraction, cardiac index and stroke volume than the late potential negative group. We further studied the 28 patients with left ventricular aneurysm in a similar way. The cardiac index and stroke volume were also significantly lower in the late potential positive group. The ejection fraction tended to be lower in the late potential positive group. These results suggest that left ventricular function and left ventricular aneurysm are among the factors that influence the development of late potentials.

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A dipyridamole-induced Tl-201 perfusion abnormality was evaluated from its clinical features, echocardiography and myocardial histopathology in 39 patients with hypertrophic cardiomyopathy (HCM). From the findings of Tl-201 emission computed tomography (ECT), subjects were divided into three groups: group 1 (n = 16) which did not show a perfusion abnormality in the hypertrophic region; group 2 (n = 12) which showed a perfusion defect on the initial image with complete redistribution on the delayed image; and group 3 (n = 11) which showed a persistent perfusion defect-this group included most patients who revealed that group 2 showed a marked asymmetrical septal hypertrophy and an incidental obstructive pattern, and that group 3 had a significantly dilated left ventricular diastolic dimension and a decreased percentage of fractional shortening. Group 3 also showed frequent ventricular tachycardia and a familial history of cardiomyopathy. As for the myocardial biopsy findings, group 3 had significantly advanced myocardial fibrosis, the percentage being 6.03.1% in group 1; 5.52.5% in group 2; and 11.93.4% in group 3. Thus, it was concluded that the persistent perfusion defect on dipyridamole stress Tl-201 ECT testing is an important finding corresponding to the advanced clinical and pathological aspects of HCM.

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We measured the peripheral venous pressure (VP) in supine leg exercise in 25"normal"subjects and 122 patients with primarily left-sided heart diseases (NYHA class I = 68, class II = 54 cases) to determine whether or not plasma catecholamine concentration would increase in patients with mild congestive heart failure, in response to dynamic exercise. Cardiac patients (n = 122) were divided in to 2 groups on the basis of VP increment (ΔVP): Group N had 60 patients with ΔVP less than 35 mmH₂O, and Group H had 62 patients with ΔVP in excess of 25 mmH₂O. Plasma concentrations of noradrenaline (NA) and adrenaline (A) were measured before and during leg exercise. The relation between ΔVP, NA and A, and the relation between ΔVP and increments of NA (ΔNA) and of A (ΔA) by leg exercise were studied in both the cardiac patients and the"normal"subjects (Group C). (1) NA at rest was 0.225±0.016 ng/ml (mean±SE) in Group C and 0.216±0.009 ng/ml in Group N. It was 0.468±0.026 ng/ml in Group H, which was significantly higher than in Group C (p < 0.001), or Group N (p < 0.001). (2) NA was 0.0510.009 ng/ml in Group C, 0.0670.007 ng/ml in Group N, and 0.2490.019 ng/ml in Group H. There was a statistically significant difference in NA between Groups C and H (p < 0.001) and between Groups N and H (p < 0.001). (3) There was no significant difference between the three groups in A at rest, or in A. (4) There was a correlation between VP and NA at rest (r = 0.614, p < 0.001) and between VP and NA (r = 0.708, p < 0.001). These data suggest that sympathetic nervous activity increased in the patients with high VP but without overt heart failure, and that the constriction of the capacitance vessels caused by an increase in NA could be at least one of the mechanisms involved in raising the VP in those patients.

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We administered urokinase (UK) 24 × 10⁴ unit (U.) + dextran sulfate (DS) 1, 500 or 3, 000 mg (UK₂₄), UK 48 × 10⁴U. + DS 3, 000 mg (UK₄₈) and UK 60 × 10⁴U. (UK₆₀) over 6 hrs daily for 5 consecutive days to 26 patients with pulmonary thromboembolism (PTE). The fibrinolytic effect of UK was evaluated by a combination of clinical and laboratory findings (score), isotopic perfusion defect and A-a DO₂. Prominent recovery was observed in 60% cases of the UK₄₈ and UK₆₀ groups but none in the UK₂₄ group. Fibrin degradation products (FDP) D and D-D increased significantly when α₂ plasmin inhibitor (α₂PI) decreased to less than 3 mg/dl. These results suggest that fibrinolytic therapy of PTE can be evaluated objectively using non-invasive examinations and UK treatment is successful when 48 or 60 × 10⁴U. of UK is administered over 6 hrs and a 50% decrease of α₂PI is obtained.

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To study the clinical implications of the total number of heart beats per 24 hours (THB), 24 hour ambulatory electrocardiography and treadmill test were performed by sixty patients with sick sinus syndrome (SSS, 58 ± 12 years old). who underwent overdrive suppression test. Results were compared with thirty control subjects (58 ± 12 years old). The THB was 74 ± 11 thousand beats in the SSS group and 99 ± 10 thousand beats in the control group. The THB and the maximal heart rate (MHR) achieved during the treadmill test were significantly lower in the SSS group than in the control group. However, the exercise duration in patients with SSS was similar to that of the control subjects. The exercise duration and the MHR were correlated to age, but not to the THB in the patients with SSS. There was no significant relationship between the total heart beats per 24 hours and the maximal sinus node recovery time (max. SNRT). We conclude that the THB, independent of the max. SNRT, can be a useful index in diagnosing and assessing the quantity of bradycardia in patients with SSS. The tolerance of exercise and the MHR were not correlated with the THB, in patients with SSS.

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We analyzed the effect of xamoterol (β₁-partial agonist) on myocardial energetics in 8 patients with normal left ventricular function. We measured resting systemic and coronary hemodynamics before and after a single intravenous injection of xamoterol (0.1 mg/kg). This agent increased heart rate from 70 ± 7 to 80 ± 11 beats/min (p < 0.05) and cardiac index from 2.9 ± 0.5 to 3.2 ± 0.5 L/min·m² (p < 0.01), respectively. Left ventricular peak positive dp/dt (1870 ± 350 vs 2620 ± 580 mmHg/sec (p < 0.01)) and left ventricular ejection fraction (62 ± 7 vs 70 ± 7% (p < 0.01)) also increased, while left ventricular end-diastolic pressure (9 ± 3 vs 5± 3 mmHg (p < 0.01) and volume index (70 ± 14 vs 58 ± 16 ml/m² (p < 0.01)) decreased. Coronary blood flow and total myocardial oxygen consumption did not change significantly after intervention. As a result, xamoterol enhanced left ventricular external mechanical work versus myocardial oxygen consumption ratio (mechanical efficiency) from 20 4 to 24 5% (p < 0.01). Myocardial oxygen extraction ratio decreased significantly (p < 0.01) from 66 5 to 62 5% after xamoterol. We conclude that xamoterol augments left ventricular mechanical efficiency accompanied by a decrease in coronary vascular tone in patients with normal cardiac function.

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We examined the effects of a new inotrope, OPC-8212 (OPC: 2 (1H)-quino-linone), on coronary sinus flow (CSF), myocardial oxygen consumption, myocardial lactate extraction ratio (LER), cardiac index (CI) and pulmonary arterial diastolic pressure (PADP) in eleven patients with prior myocardial infarction. Measurements were taken before (control) and 8 hours after administration of OPC (480 mg, p.o.). A cardiac function curve was obtained in each stage with rapid intravenous administration of 500 ml of saline (loaded state) after baseline measurements. There was a significant increase in the cardiac index and decrease in the pulmonary arterial diastolic pressure in the loaded state after OPC. Thus the ventricular function curve was shifted to the left and showed a steep incline, indicating an increased inotropic state. On the other hand, myocardial oxygen consumption and myocardial lactate extraction ratio were unchanged. Thus we concluded that OPC improved cardiac performance without increasing myocardial oxygen consumption.

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Nine subjects (average age 56 ± 7 years old) underwent sitting cycle ergometer exercise for four months. Exercise capacity and maximal VO₂ increased after exercise training in these subjects. Forearm vascular responses to lower body negative pressure (LBNP) at -10 and -40 mmHg were compared before and after exercise training. The magnitude of reflex forearm vasoconstriction in response to LBNP at -10 mmHg was greater after exercise training than before. The decreases in central venous pressure during LBNP at -10 mmHg were similar before and after exercise training. The pressor and forearm vasoconstrictive responses to the cold pressor test also did not differ before and after exercise training. These results suggest that mild exercise training in middle-aged subjects augments the tonic inhibitory influence of the cardiopulmonary receptors on forearm vascular resistance.

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To re-evaluate the concept of"high lateral"myocardial infarction, angiographic findings were analysed in 29 patients with remote infarction and abnormal Q waves in lead I or aVL but no abnormal Q waves in other leads and no prominent R wave in lead V1. All patients except one showed asynergy in the anterior segment on right anterior oblique left ventriculogram. Asynergies in other segments were, if present, mild or small. Critical narrowing was present in the diagonal branches or in their"parent"arteries (that is, the left anterior descending artery or left main trunk) in 28 patients but in the circumflex artery in only 3 patients. Thus, the traditional concept that a"high lateral"infarction is myocardial necrosis of the basal aspect of the left ventricle, receiving its blood supply from the circumflex artery, needs correction."High lateral infarction"corresponds to necrosis of the area between the obtuse margin and the inter-ventricular groove ordinarily supplied by the diagonal branches of the left anterior descending artery. Such infarctions are expressed by asynergy of the anterior segment rather than the posterior segment.

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Angiographic status of the saphenous vein graft (SVG) and the internal mammary artery graft (IMAG) anastomosed to the left anterior descending artery were compared at two different postoperative periods; - within 2 months and at 6 to 12 months after the operation. In 50 SVGs and 35 IMAGs which were studied at the early postoperative period, the rate of intact, stenosed and occluded grafts were almost the same in these two kinds of grafts. However, in 35 SVGs and 25 IMAGs which were studied at the later period, the stenosis of SVG increased significantly while IMAG remained intact. The rate of intact, stenosed and occluded grafts at postoperative 6 to 12 months were 71%, 23% and 6% in SVG, and 88%, 8& and 4% in IMAG, respectively. Considering the better angiographic quality of IMAG, use of IMAG to bypass the most important coronary artery should be considered especially when the patients are younger.

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In order to clarify the pathological involvement of the sympathetic nervous system in the development of cardiomyopathy, a receptor-binding study was carried out on cardiomyopathic Syrian hamsters of strain BIO 14.6 (BIO) at 21 days (prenecrotic stage); 35-42 days (onset of cardiomyopathy); and 70-84 days of life (early cardiac hypertrophy). The newly developed α₁-blocker (bunazosin hydrochloride) was initially administered at doses of 100 μg/kg or 10 mg/kg BIO hamsters at 21 days of life and continued for 70 days. At the onset of cardiomyopathy and early cardiac hypertrophy, there was an increase in the number of α₁-receptors in the BIO hamsters compared to controls, but there were no significant changes at the prenecrotic stage. On histopathological examination, 10 mg/kg bunazosin had a singnificant beneficial effect on cardiomyopathy [area of necrosis 1.38% in untreated vs 0.33% in treated animals; area of calcification 2.70% (untreated) vs 0.60% (treated); area of all myocardial injuries 6.97% (untreated) vs 3.19% (treated)]. However, 100 g/kg bunazosin had no effect. It was concluded that the increase in the number of ₁-receptors may not be involved in the pathogenesis of cardiomyopathy but that ₁-receptors could be implicated in the later progression of the condition.

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reflection to the body surface of the single beat-potentials of the His-Purkinje system (HPS) was analysed by a single beat recording of the epicardial HPS potentials from the Langendorff perfused canine heart and by the reconstruction of HPS potentials on the basis of the cable concept. Unipolar epicardial HPS potentials from 8 leads distributed equidistantly over the basal region of the ventricles were amplified by a high gain (120 dB) amplifiers with an active bandpass filter (40-2400 kHz). The waveform of these HPS potentials differed in each lead. The largest (42 ± 8 μV, mean ±SE, n = 5) of these HPS potentials, which was obtained from the anterior free wall of the right ventricle, was composed of two peaks: the initial slow- and positive-peak and the late sharp- and negative-peak. The former peak appeared 12 ± 3 msec (mean ± SE, n = 5) ahead of the spike of the His-bundle electrogram (HBE) recorded from the close bipolar electrodes which were attached intracavitally along the membrane portion of the His-bundle. The latter appeared in coincidence with the spike of HBE. The extracellular potentials generated by HPS excitation were calculated by assuming that the excitation proceeds along the three dimensionally reconstructed HPS. The simulated waveform was in agreement with those of the epicardial HPS potentials. Thus, the HPS potentials on the body surface may inscribe a diverse waveform as a reflection of the complexed architecture of the whole HPS.

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The sequential changes in 24-hour urinary norepinephrine (NE) and epinephrine (E) excretion levels were measured in spontaneously hypertensive rats (SHR) that received deoxycorticosterone acetate (DOCA) and 1% NaCl drinking water. These were compared with those from control SHR and similarly treated Wistar-Kyoto rats (WKY). Blood pressure, NE and E increased progressively in DOCA-SHR group, and NE (2392 ± 94 vs. 998 ± 49 ng/day) and E (250 ± 21 vs. 116 ± 6 ng/day) exceeded twice that of the control SHR group in the sixth week of DOCA treatment. In WKY rats, NE (1372 ± 48 vs. 968 ± 37 ng/day) and E (147 ± 9 vs. 121 ± 7 ng/day) levels were significantly higher in rats given DOCA than those in control group in the sixth week of the treatment, but were not so remarkably high as in DOCA-SHR group. A histological examination of DOCA-SHR kidneys revealed fibrinoid necrosis in the vascular walls. These data suggest that sympathoadrenal activity plays an important role in the development of malignant hypertension in DOCA-SHR group.

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