Correlations between left ventricular (LV) function and infarct size estimated by computer-assisted thallium (Tl)-201 scintigraphy were studied in 16 patients in the acute or convalescent phase of the first attack of transmural myocardial infarction (MI). Tl-201 estimation of the infarct size was done using a "corrected" circumferential profile method, by which the total defect score could be obtained. The LV function was evaluated by radionuclide angiography, echocardiography and cardiac catheterization study. The following results were obtained : 1) A close inverse relationship was found between the defect score and the ejection fraction (r=-0.649, r<0.01). 2) The linear correlation diastolic pressure and -0.616 (p < 0.02) between the defect score and the cardiac index. 3) There was a linear correlation between the defect score and the LV end-diastolic dimension (r= -0.852, p < 0.001). However, there was no relation between the defect score and the left atrial dimension. When the LV indices were compared between the small (S) and the large (L) defect score group, the L defect group had faster heart rate, larger LV chamber size and the smaller stroke volume index than the S defect group. However, there was no significant difference in the cardiac index between these 2 groups. These results suggest that the LV dilatation in acute or convalescent phase of the first attack of transmural MI is an ominous sign because it was usually accompanied by large infarct size. The present study also indicates that LV dilatation accompanying a large infarct does not satisfactorily compensate for LV dysfunction by Frank-Starling mechanism, because the stroke volume index decreased in proportion to the infarct size and the cardiac index was maintained by an increase in heart rate in cases with LV dilatation.

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Using two-dimensional (2-D) echocardiography we evaluated the applicability of the left ventricular (LV) short axis view combined with manual scanning technique for the detection and evaluation of aneurysms of the membranous ventricular septum (AMS). In 12 patients with angiographically proven AMS, we recorded from the left sternal border the short axis view of the left ventricle continuously displayed from the aortic to the ventricular level by tilting the transducer manually along the LV long axis plane. We then compared the detectability of AMS by this method with that by other standard fixed 2-D echocardiographic views. This method proved to be best for the detection of AMS (12/12), followed by an apical four-chamber view (10/12), a parasternal LV long axis view (8/12) and an apical two-chamber (2/12) view. Fro the detection of AMS and for three-dimensional evaluation of the structure of the AMS and the original orifice of ventricular septal defect the method was shown to be clinically applicable.

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Measurements of the right ventricular volume were performed using biplane cineangiocardiography on 17 patients with mitral stenosis, ranging in age from 34 to 62. The right ventricular end-diastolic volume index ranged from 69 to 130 ml/m² (99 ± 18, mean ± SDM), and the right ventricular ejection fraction ranged from 0.33 to 0.69 (0.51 ± 0.08). There was an inverse relationship between the right ventricular end-diastolic volume index and the right ventricular ejection fraction (r=-0.52, p < 0.05). The cardiac index measured by the dye-dilution method ranged from 1.61 to 4.40 L/min/m² (2.56 ± 0.72) and correlated with the right ventricular ejection fraction (r=0.78, p < 0.001). The right ventricular end-diastolic volume was larger in 11 patients with tricuspid regurgitation than those without (p < 0.05). It was larger in 11 patients with atrial fibrillation than those with sinus rhythm (p < 0.05). The right ventricular ejection fraction was lower in 8 patients with low cardiac output (0.47 ± 0.08) than those with normal cardiac output (0.47 ± 0.08 vs 0.55 ± 0.07, p < 0.05). It was lower in 11 patients with atrial fibrillation than those with a sinus rhythm (0.48 ± 0.07 vs 0.57 ± 0.09, p < 0.05). The right ventricular ejection fraction was also lower in 7 patients with restenosis of the mitral valve following a commissurotomy than those without a previous operation (0.46 ± 0.08 vs 0.55 ± 0.07, p < 0.02). The left ventricular ejection fraction was lower in 8 patients with low cardiac output than those with a normal one (0.49 ± 0.09 vs 0.56 ± 0.04, p < 0.05). These results indicate that the right ventricular function is abnormally depressed in patients with mitral stenosis associated with low cardiac output.

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A procedure for observing blood flow during early reactive hyperemia, which uses prolonged venous occlusion following 3 min of arterial occlusion, is described. A mercury strain gauge was applied around the mid-calf and 3 tracings were simultaneously recorded during reactive hyperemia : the change in venous volume, its derivative and amplified pulse waves. The method was evaluated in animals, normal volunteers and in patients with symptoms of arterial insufficiency. This bedside procedure was found to be convenient curacy comparable to the ankle/arm pressure index in distinguishing between normal, stenotic or occluded lower extremity arterial systems. In addition, it proved more accurate than pressure measurements in diabetic patients with incompressible calcified vessels.

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The circadian rhythm of blood pressure in 11 patients with primary aldosteronism (ALD) and 15 patients with unilateral renovascular hypertension (RVH) was analyzed using the cosinor method which fits a cosine function to a series of data. In ALD, both systolic (SP) and diastolic blood pressures (DP) increased in the late evening ; the amplitude and acrophase of the circadian rhythm for SP were 7.3 (5.3 to 9.3, mean and 95% confidence limits) mmHg and 20 : 47 (19:42 to 21:52) hours, respectively, and for DP 2.6 (1.3 to 3.9) mmHg and 21:34 (19:40 to 23:28) hours, respectively. After excision of an adrenal adenoma in 6 patients, the circadian rhythm of SP and DP was abolished. In RVH, the acrophase of the circadian rhythm of SP and DP differed by about 12 hours ; the amplitude and acrophase for SP were 5.7 (3.9 to 7.5) mmHg and 17:49 (16:35 to 19:02) hours, respectively, and for DP 1.5(0.2 to 2.7) mmHg and 6:08 (2:44 to 9:31) hours, respectively. After various surgical interventions in 8 patients, the circadian rhythm of SP persisted with little change in acrophase, while that of DP disappeared. The difference in circadian rhythm suggests a difference in mechanisms of blood pressure control in ALD and RVH.

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Hemodynamics in supine position were studied echocardiographically in 56 young patients with borderline hypertension and 56 age-matched normotensive subjects. In hypertensive patients, the cardiac index (CI) did not increase, but the total peripheral resistance (TPR) increased significantly (p < 0.005). The hypertensive patients were classified into 2 groups, according to the level of the CL. In patients in group A ("normal" CI), the CI, heart rate and the mean circumferential fiber shortening velocity (mV_CF) were normal, but the TPR was increased significantly. In patients in group B ("high" CI), the CI, heart rate and the mV_CF increased significantly (hyperkinetic state), but the TPR was normal. Plasma renin activity (PRA) was significantly higher in patients in group B than the normal subjects, but the level of PRA in patients in group A was normal. These findings support the hypothesis that sympathetic nervous activity increases in patients in group B, but not in those in group A. Therefore, this study provides evidence that the TPR is abnormal in patients with borderline hypertension, and an impaired neurogenic activity seems to be important in the early stage of hypertension, as in borderline hypertension associated with a hyperkinetic circulatory state (group B).

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The blood pressure (BP) response to supine rest for one hour and to an isometric handgrip exercise (3 min, 30%, of maximum) was investigated in 18 healthy normotensive men (N) (casual BP 117 ± 6 / 73 ±5 mmHg, 39± 3 years old) (mean ± SD) and 50 men with essential hypertension (H) (162 ± 13 / 105 ±9 mmHg, 41 ± 4 years old). Casual BP was decreased by rest to resting BP (113 ± 7/70 ±7 in N and 140 ± 15/ 93 ± 11 mmHg in H). H was divided into 3 groups of H-1 (resting BP of 124 ± 7 / 80 ± 4 mmHg), H-2 (137 ± 9 / 92 ± 4) and H-3 ( 154 ± 10 / 104 ± 4). The decreases in BP with rest were significantly greater in Groups H-1 (30 mmHg in systole / 20 mmHg in diastole, p < 0.001), H-2 (23/11, p < 0.001) and H-3 (16/8, p < 0.001/0.05) as compared with those in N (4/3), and this decrease significantly correlated with the resting systolic BP in H (r=-0.601, p < 0.001) and with diastolic BP (r=-0.604, p < 0.001). The handgrip exercise increased BP (42/28, 55/35 39/26 and 30/26 mmHg in Group H-1, H-2, H-3 and N, respectively). The increase in systolic BP was significantly greater in Groups H-1, H-2 and H-3 than in N (p < 0.001, p < 0.001 and p < 0.01, respectively), and the increase in diastolic BP was significantly greater in Groups H-2 than in N (p < 0.05), but not in Group H-1 and H-3. The significant decrease in BP with rest and the significant increase in BP by the exercise may represent the pathophysiological nature of the cardiovascular response in the early stage of essential hypertension.

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Systolic time intervals and cardiac output were measured in 10 normal subjects (group I), 25 patients with angina pectoris (group II) and 32 patients with old myocardial infarction who were subdivided into 3 groups (group III : ejection fraction (EF) &ges;50% without congestive heart failure (CHF), group IV : EF < 50% without CHF and group V with CHF irrespective of the level of EF). Because the number of the patients of group V was too small and only this group was undergoing treatment during the study, the results obtained from this group were used for comparison only. The ET/PEP ratio was 2.41 ± 0.28 in group I, 2.70 ± 0.34 in group II (p < 0.02 as compared with group I), 2.35 ± 0.30 in group III and 2.11 ± 0.18 in group IV (p < 0.01 as compared with group I). The ejection time (ET) showed no significant difference between group I and group III or IV. The pre-ejection period (PEP) showed no significant difference between groups I and II. In groups III and IV, the PEP was prolonged as the EF decreased. These results indicate that the increase of the ET/PEP ratio in group II was mainly due to the prolongation of the ET, and the decrease of the ET/PEP ratio in group IV was not directly related to the ET but to the PEP prolongation. Both the stroke index (SI) and the mean systolic ejection rate (MSER) in groups III and IV were significantly low as compared with those in group I, but those in group II showed no significant difference as compared with those in group I. These findings suggest that the prolongation of ET in groups II, III and IV indicates a compensatory mechanism to maintain the SI.

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The electrophsiological effects of nicardipine-HCl, a new calcium antagonist and potent vasodilator, were studied in the isolated sinoatrial (SA) and atrioventricular (AV) nodes of the rabbit in an oxygenated Tyrode solution at 35°C using an intracellular microelectrode technique. Nicardipine-HCl decreased the spontaneous rate of the SA node and prolonged sinus recovery time, dose-dependently. The effective refractory period (ERP) and functional refractory period (FRP) of the AV node and AV conduction time (A-H interval) were also prolonged by nicardipine-HCl in a dose-dependent manner. In conclusion, nicardipine-HCl has electrophysiological effects on the SA and the AV node similar to those of other calcium antagonists in the excised and superfused rabbit heart.

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This study was done to discover whether or not the oxygen-induced depression of sympathoadrenal activity contributes to a reduction of myocardial contractile force during oxygen breathing. In 10 open-chest dogs, myocardial contractile force was measured using a myocardial strain gauge arch during air and oxygen breathing before denervation (intact heart) and after bilateral vagotomies, sympathectomies and adrenalectomies with the intravenous administration of propranolol, phenoxybenzamine and atropin (denervated heart). One hundred percent oxygen breathing caused similar increases in arterial pO₂ in both the intact (from 94 ± 10 to 442 ± 25 mmHg) and the denervated dogs (from 113 ± 11 to 456 ± 15 mmHg). Coronary blood flow measured at the left anterior descending coronary artery was reduced by oxygen breathing from 28.4 ± 3.4 to 21.7 ± 2.3 ml/min in the intact dogs, and from 19.4 ± 3.4 to 14.9 ± 2.6 ml/min in the denervated dogs. Myocardial contractile force was significantly reduced by oxygen breathing in the intact dogs (a reduction of 5.8 ± 1.4%). In the denervated dogs, on the other hand, no significant changes in myocardial contractile force was seen. This study suggests that the reduction in myocardial contractile force is mediated through sympathoadrenal activity, and thus, is abolished by sympathoadrenal blockade.

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In order to clarify the protective mechanism of verapamil, the following experiment was performed. Twenty-four anesthetized dogs were divided into 3 group of 8 animals each. In the first, the left anterior descending coronary artery (LAD) was occluded for 15 min ; in the second, 5-min reperfusion was done following a 15-min occlusion ; in the third, prior to 5-min reperfusion, verapamil (0.4 mg/kg) was infused for 5 min. In each group, heart mitochondria were prepared from the normal and occluded or reperfused areas and their functions were estimated polarographically. The contents of calcium, phospholipids and fatty acids in the mitochondria were also measured by atomic absorption spectrophotometry, Allen's method and gas chromatography, respectively. Although occlusion induced mitochondrial dysfunction, the dysfunction was exacerbated by reperfusion. Occlusion alone did not alter the contents of calcium, phospholipids and fatty acids in mitochondria, while occlusion and subsequent reperfusion increased calcium and fatty acids and decreased phospholipids in mitochondria. Verapamil prevented these reperfusion responses. These results suggest that reperfusion injury of mitochondria is based on the degradation of mitochondrial phospholipids, which is caused by an activation of phospholipase, being triggered by a calcium increase. Verapamil, a calcium antagonist, might protect against reperfusion injury by inhibiting the activation of phospholipase.

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The effect of lipid peroxide (15-hydroperoxy arachidonic acid) on the activity of lipoprotein lipase was investigated. The activities were examined in 2 enzyme species : the lipoprotein lipase bound to the coronary vessels of the rat heart and that solubilized in the human post-heparin plasma. As a substrate, ³H-labelled human chylomicron was used. Lipid peroxide decreased the maximal velocity of the reaction between the chylomicron and lipoprotein lipase on the vascular surface. In the post-heparin plasma, the lipid peroxide decreased the maximal hydrolysis rate, but did not change the half life time in the unsaturated reaction. It is suggested that lipid peroxide directly damages a part of the membrane-bound lipoprotein lipase, and that the degeneration of cell membranes and the vasoconstriction caused by lipid peroxide will additionally disturb the hydrolysis of the plasma triglyceride on the vascular surface.

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