To evaluate the differences in shape and phase lag of the flow velocity curves in the superior (SVC) and inferior (IVC) venae cavae and the hepatic vein (HV), Doppler echocardiographic examination was performed in 40 healthy adults (aged 20 to 67 years, mean SD:, 39±12 years). Flow velocity patterns in each vein were characterized by 4 major deflections: S wave, a systolic forward flow; D wave, a diastolic forward flow; A wave, a small backward flow or reduction of diastolic forward flow due to atrial contraction: and O wave, a small back-ward flow or reduction of forward flow after the second heart sound. Except for a reduced phasic flow in a collapsed IVC, the venous flow velocity recordings in each vein demonstrated very similar pulsatile patterns and small differences in mean time lags of less than 50 msec. In general, the lowest values of peak A/peak S, peak O/peak S and peak D/peak S were observed in HV flow and the highest in IVC flow. Backflows of A and O waves were prominent in HV flow, but small and least frequent in IVC flow. These data suggest that the baseline of the central venous flow recordings might shift downward in HV flow and upward in IVC flow. However, even if both the baseline shift and amplitude of the flow curve were normalized in each venous flow velocity curve, apparent differences in shape of the flow velocity curves would remain. We concluded that the characteristics and differences of each central venous flow velocity pattern should be noted in studies of these areas.

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Stunned myocardium of right ventricle was studied by radionuclide angiography (RNA) and Thallium myocardial scintigraphy (TL) in 39 patients with inferior myocardial infarction with and without right ventricular myocardial infarction (RVMI). RNA was performed within 1 week of the onset (acute phase) and after 1 month, when exercise cardiac scintigraphy (EX-TL) was also performed. The ejection fraction (EF) of each ventricle calculated from RNA and the phase and amplitude evaluated visually and quantitatively by Fourier analysis were compared between the acute phase and 1 month after the onset of myocardial infarction. The degree of visualization of right ventricle was examined in EX-TL 1 month after the oneset. (1) In RNA obtained in the acute myocardial infarction, abnormalities in the right ventricle (delayed phase or low amplitude image) were observed in 18 (46%) but not in 21 (54%) of the 39 patients (N group). Of those 18 patients, the abnormalities in the right ventricle alleviated in 11 (RVMI-A group) but persisted in 7 (RVMI-B group) in RNA obtained 1 month after the onset. (2) In the acute phase, the right ventricular ejection fraction (RVEF) was 39.4±10.4% in N group, 30.8±5.3% in RVMI-A group, and 29.68.9% in RVMI-B group, with significant differences between N group and the other two groups (P<0.05) but no significant difference between RVMI-A and RVMI-B groups. (3) After 1 month. RVEF was 40.1±10.1% in N group. 42.2±8.4% in RVMI-A group, and 32.2±9.8% in RVMI-B group, being improved in RVMI-A group and showing a significant difference as compared with RVMI-B group (p<0.05). (4) In EX-TL of RVMI-A group, the right ventricle was visible although the uptake of TL was reduced in the en-tire right ventricle. In RVMI-B group, only part of the right ventricular free wall was visible with defects in the other areas of right ventricle. The sign of RVMI showed improvements in many of the patients after the acute phase, and their condition was considered to have been so-called stunned myocardium, which is a complex of symptoms of reversible myocardial ischemia, rather than RVMI.

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Comparative long-term performance characteristics of St. Jude Medical (SJM) and bioprosthetic valves were conducted retrospectively for patients who under-went prosthetic valve replacement in the right side of the heart from 1975 to 1988. Fifty-four patients received either SJM (n=18) or bioprosthetic (n=37) valves. The cumulative follow-up for SJM valves was 91 valves-years (range 3.9 to 7.2 years) and that for bioprostheses was 282 valve-years (range 1.3 to 14.8 years). Follow-up rate was 100%. The actuarial survival rate excluding hospital deaths at 5 years was 81±10% for SJM and 97±3% for bioprosthetic valve recipients (p=ns). The rates of freedom from thrombosis or anticoagulant-related hemorrhage, structural valve failure, prosthetic valve endocarditis, reoperation, and overall valve-related complications at 5 years were 72±11%, 100%, 100%, 83±9%, and 72±11% for SJM valve recipients, and 100%, 97±3%. 97±3%, 94±4%, and 94±4% for bioprosthetic valve recipients, respectively. Structural valve failure, prosthetic valve endocarditis and reoperation occurred at a similar incidence in each of the two types of prostheses. Thrombosis and overall valve-related events occurred more frequently in SJM valve recipients (5.5±2.5 vs 0%/valve-year; p<0.02, 6.6±2.7 vs 1.1±0.6%/valve-year; p<0.03, respectively). The bioprosthetic valve which did not need warfarin anticoagulation therapy had low incidence of valve-related complications and showed good long-term durability even in the younger age group. The bioprosthetic valve was superior to the SJM valve in the right side of the heart.

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A case of intraaortic balloon entrapment is reported. To our knowledge, this is the tenth case in the literature. We conclude that balloon entrapment can occur without any signs of rupture of the balloon and that the balloon should be removed surgically.

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Knowledge of the mechanical properties of the small arteries is important for understanding physiological and pathophysiological conditions in the human peripheral circulation. We have recently developed a new method for the noninvasive measurement of arterial elastic properties in human fingers using photoelectric plethysmography. In this study, the pressure-volume relationship. an index for expressing arterial elasticity, was measured by this method in the finger arteries of 91 healthy subjects and 102 patients with coronary artery disease. Aging effects on the elastic properties of finger arteries were examined in healthy subjects classified into three groups: under 30. 31-49, and over 50 years of age. The pressure-volume curve shifted downward with increase in age, indicating that the elasticity of finger arteries decreased with age. Patients with 75% or greater coronary stenosis, as compared with age-matched healthy subjects, showed distinctly lower elasticity of finger arteries. As the number of diseased coronary arteries increased, the elasticity of finger arteries tended to decrease steadily. The elasticity of finger arteries decreased in coronary disease patients with hypertension much more than in those without hypertension. These results suggest that age-related changes in arterial elasticity can occur in peripheral small arteries, and that peripheral arteries in patients with coronary atherosclerosis are less elastic than those in healthy subjects.

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In order to evaluate the right atrial function in patients with ischemic heart-disease, we studied the superior vena caval blood flow velocity using pulsed Doppler echocardiography. The subjects included 31 patients with anteroseptal infarction (ANT). 23 with inferior or inferoposterior infarction (INF+POS), 27 with effort angina pectoris (EAP) and 15 with vasospastic angina pectoris (VAP). Th systolic peak flow velocity (PFVs) was significantly reduced only in INF+POS compared with those in ANT, EAP and VAP (36.8±1.8cm/sec vs 46.9±2.1cm/sec. 46.4±2.1cm/sec and 42.6±1.9cm/sec, p<0.05, respectively). No significant difference in diastolic peak flow velocity (PFVd) was found between the 4 groups. PFVs/PFVd was significantly reduced only in INF+POS compared with those in ANT. EAP, and VAP (1.390.05 vs 1.75±0.08, 1.76±0.09, and 1.62±0.09, p<0.05, respectively). These results suggested that INF+POS caused impairment of the right atrial reservoir function.

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The technique of retrograde blood flow has been shown to decrease collateral flow into the ischemic myocardium, and to cause severe myocardial ischemia in dogs. Ischemia with retrograde blood flow in dogs is similar to ischemia in human hearts. Therefore, we examined the effect of retrograde blood flow on myocardial blood flow, ST segment elevation, alternans of ST segment elevation, conduction delay and ventricular arrhythmia in dogs. Sixty dogs were divided into two groups. In group A (N=32), the left anterior descending coronary artery was occluded for 10 min. In group B (n=28), ischemia was induced by the technique of retrograde blood flow for 10min. During ischemia, the myocardial blood flow at the ischemic zone measured by a H₂ gas clearance method was 11.21.6 in group A and 5.7±0.7ml/min/100g in group B (p<0.01). The maximal ST segment elevation was 13.6±1.9 in group A and 27.2±2.1mV in group B (p<0.001); the maximal alternans of ST segment elevation was 5.3±1.1 in group A and 10.1±1.4mV in group B (p<0.01); the maximal conduction delay was 51.6±8.4 in group A and 111.1±6.2 msec in group B (p<0.001); and the incidences of ventricular premature beats (>5/min), ventricular tachycardia and fibrillation were 34%, 41% and 22% in group A, and 68%, 79% and 25% in group B (p<0.01, p<0.01 and not significant, respectively). It is concluded that ischemia with retrograde blood flow can be used to examine occlusive and reperfusion ventricular arrhythmia in dogs. because the incidences of ventricular premature beats and ventricular tachycardia were high, but that of ventricular fibrillation was not high despite the severe ischemia.

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To evaluate the mechanism of excimer laser recanalization and compare the results with those of laser-assisted thermal probe recanalization and mechanical recanalization, a total of 42 human atherosclerotic totally occluded arterial segments (2-15cm long) were recanalized by excimer laser with a 400-800 micron quartz fiber pulsed at 20 Hz with 50 mJ/mm² of energy (n=21). an Argon heated thermal probe at 10-12 watts (n=11), a guidewire directed through a 6 Fr multipurpose catheter, or an angioplasty balloon catheter (n=10). On histologic examination, the excimer laster created a single round lumen or multiple lumens ("Swiss-cheese" like appearance) with no evidence of thermal injury at the perimeter of the lumen. The incidence of perforation in vitro was less with an excimer laser catherter (8/21 or 38%) than with the thermal prove (10/11 or 91%) (p<0.01). However. serial histologic cross-sectional examination showed that the pathway of the devices were essentially the same in all recanalization procedures. The pathway of the device was located outside the atheroma but proximal to the internal elastic membrane in 13 arteries with the excimer laser (62%), in 10 arteries with the thermal probe (91%). and 8 arteries with mechnical devices (80%). These results indicate that although the eximer laser could recanalize human atherosclerotic arteries without thermal injury, the fiber frequently deflected around firm atherosclerotic plaque and advanced in a dissection plane between the plaque and media. A similar course was noted for the thermal probe or during mechanical recanalization with a guidewire and catheter. To insure the safety of an excimer fiber or a thermal probe to reopen complete occlusions. better guidance systems must be developed.

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In order to study the effects of residual stenosis on myocardial salvage, we created 99% coronary stenosis with or without contrast washout delay at reperfusion in six groups of dogs. In Group A (n=8), the artery was occluded for 1h before being fully reperfused. In Group B (n=9), the artery was occluded for 1h, then subjected to 6h of 99% stenosis without contrast washout delay. In Group C (n=8), the artery was occluded for 1h, followed by 1 week of 99% stenosis without contrast washout delay. In Group D (n=10). again the artery was occluded for 1h, then subjected to 6h of 99% stenosis with contrast washout delay. In Group E (n=8). the artery was occluded for 7h, then fully reperfused for 1 week. Finally, in Group F (n=8). the occlusion lasted for a full week. All dogs were sacrificed 1 week after occlusion. In Group A, myocardial creatine phosphokinase activity (CK) in the inner layer was 43.8±12.5% that of non-infarcted myocardium. Myocardial CK in Group B (46.5±7.4%) was little different but in Group C it dropped to 26.6±8.4%, suggesting that 99% residual stenosis is not deleterious if it is continued for 6h or less but that it will result in considerable depletion of myocardial CK, if it is sustained for 1 week. In Group D, myocardial CK dropped markedly to 11.3±3.7%, little different from that for either Group E (13.3±2.6%) or Group F (9.3±3.3%). This suggests that contrast washout de-lay following 99% stenosis is not beneficial to myocardial salvage. Infarct size, as determined using triphenyl tetrazolium chloride as a stain was smallest for Group A (6.8±3.6%) and largest for Group F (62.6±9.8%). Group B showed smaller infarct size (13.2±3.7%) than did either Group D (27.0±5.5%) or Group E (25.3±6.3%). From this. we came to the conclusion that 99% residual stenosis without contrast washout delay is not deleterious provided it is sustained for 6h or less.

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To examine the role of oxygen free radicals and extracellular calcium ions in reperfusion-induced ventricular arrhythmias, we evaluated the effects of hypoxic reperfusion. oxygen free radical scavengers, allopurinol and hypocalcemic reperfusion on reperfusion-induced ventricular arrhythmias. The hearts of male Sprague-Dawley rats were perfused in the working heart mode. Whole heart ischemia was induced for 15 min and then reperfused. Rats were divided into 5 groups: control group, scavenger group, allopurinol group. hypoxia group and hypocalcemia group. Scavenger, hypoxic and hypocalcemic perfusions were undertaken only during the period of perfusion. The incidence of reperfusion-induced ventricular fibrillation (Vf) was reduced in the scavenger group (100% to 38%) and the hypoxia group (100% to 50%). Spontaneous reversion of Vf to regular sinus rhythm was recognized in the hypoxia and hypocalcemia groups. In conclusion, oxygen free radicals would play an important role in the genesis of the reperfusion arrhythmias, and extracellular calcium concentration would also play an important role in sustaining the reperfusion arrhythimias. Notably, hypoxic reperfusion had protective effects on both processes.

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Low doses (10^-16 -10^-10 M) of endothelin-3 (ET-3) elicited continuous vasodilation of mesenteric arteries preconstricted with norepinephrine (NE) but not with KCl. In arteries perfused with Ca²⁺ free solution. ET-3 did not affect the perfusion pressure. In endothelium-denuded arteries preconstricted with NE, ET-3 significantly elevated the perfusion pressure in a dose-related manner. The levels of cyclic GMP and cyclic AMP from the intact arteries were significantly elevated by ET-3; the cyclic GMP elevasion disappeared with methylene blue. Following endothelium-denudation, cyclic GMP elevation was abolished, but cyclic AMP elevation was unaffected. Levels of 6-Keto-PGF_1α in the arteries were not changed appreciably by ET-3. These data indicate that the vasodilating effects of ET-3 depend on the presence of extracellular Ca²+ and the existence of endothelium. They are accompanied by elevations of cyclic nucleotides and the elevation of cyclic GMP depends on the endothelium. It is possible that the vasodilating effects of low doses of ET-3 are associated with endothelium-derived relaxing factor.

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An animal experimental model which simulates human effort angina, especially in terms of diastolic abnormalities, was developted using isovolumically beating perfused rat hearts. Using this model, we studied the effects of nifedipine, a Ca²⁺ channel blocker. on diastolic properities during pacing-induced ischemia. When the preload of the left ventricle was set at a low level, low-flow ischemia (coronary perfusion pressure of 40mmHg) plus tachycardia (480 beats/min for 4 min) did not induce an increase in left ventricular end-diastolic pressure (LVEDP). However, with a high preload, low-flow ischemia plus pacing tachycardia indused an increase in LVEDP of 8.4±5.4mmHg (p<0.01) and a prolongation of the time constant of ventricular pressure decline (6.8±4.6msec, p<0.05) immediately after pacing tachycardia. Pretreatment with nifedipine (3×10^-8M) prevented the rise in LVEDP induced by pacing tachycardia. Thus, in isolated perfused hearts, diastolic abnormalities similar to those seen in angina pectoris were obtained by low-flow ischemia plus pacing tachycardia. The response to nifedipine suggested that an alteration of Ca²⁺ movement may play an important role in the increase in left ventricular stiffness under these conditions.

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We compared the effects on the proliferation of bovine vascular smooth muscle cells (VSMC) of serum from 36 patients without restenosis (group A). and 21 patients with restenosis (group B) after percutaneous transluminal coronary angioplasty (PTCA). Baseline characteristics were similar in both groups. except for the greater number of patients with unstable angina at the time of PTCA (52 vs 22%, p=0.020) and the shorter interval between PTCA and repeat angiography in group B (106±30 vs 153±112 days, p=0.022). Cultured bovine VSMC were stimulated with patient serum (5%) obtained at repeat angiography in either Ca²⁺-containing or Ca²⁺-free culture medium. DNA synthesis was assessed by [³H]thymidine, incorporation. The following indices of VSMC proliferation were used: S(+)= [³H]thymidine uptake stimulated by 5% serum in Ca²⁺-containing medium/[³H]thymidine uptake stimulated by 5% fetal calf serum (FCS) in Ca²⁺-containing medium. S(-)=[³H]thymidine uptake stimulated by 5% serum in Ca²⁺-free medium/[³H]thymidine uptake stimulated by 50% FCS in Ca²⁺-free medium, and D=S(-)-S(+). D represented the preserved DNA synthesis in Ca²⁺-deprived medium. S(-) was lower than S(+) in group A (1.35±0.56 vs 1.57±0.58, p<0.0001), whereas it was higher than S( +) in group B (1.64±0.66 vs 1.50±0.58, p=0.010). D was significantly higher in group B than in group A (0.14±0.23 vs -0.22±0.28, p<0.0001), and was not associated with any continuous variables including serum calcium level on univariate regression analysis. However, multivariate analysis revealed unstable angina as an independent variable for D. Thus, it is suggested that serum from patients with restenosis stimulates VSMC proliferation while not requiring as much extracellular Ca²⁺ as serum from those without restenosis. This serum property appears to be associated with the angina pattern at PTCA. This finding concerning serum in patients with restenosis may contribute to the understanding of the pathophysiological mechanisms underlying restenosis.

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The relationship between sulthydryls and cGMP has been observed in several biological processes. Captopril is a sulfhydryl-containing angiotensin converting enzyme (ACE) inhibitor, that decreases PGI₂ production in cultured human vascular endothelial cells. Enalapril does not appear to have this property. The role of cyclic GMP (cGMP) and sulthydryls in the regulatory mechanisms in captopril-induced PGI₂ production and Ca⁺⁺ kinetics was investigated. Brady-kinin and Ca ionophore A23187 enhanced PGI₂ production, and increased the cytosolic free Ca⁺⁺ concentration ([Ca^<++gtn]_i). It was observed that 8-bromo cGMP increased intracellular cGMP concentration ([Ca⁺⁺]_i), and decreased PGI₂ production without changing [Ca⁺⁺]_i. Sulthydryl containing compounds such as captopril. N-acetylcysteine and glutathione decreased PGI₂ production via increased [cGMP]_i. Enalapril, an ACE inhibitor without sulthydryls, has no effect on PGI₂ production, [Ca^<++gtn]_i and [cGMP]_i. These results suggested that the presence of sulfhydryl groups is an important factor in the ability of vasoactive substances to induce PGI₂ production.

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