We estimated the magnitude of the left atrial contraction in 28 patients with ischemic heart disease by calculating the biplane cineangiographic volumes of the left atrium. The left atrial contraction contribution to the left ventricular stroke volume (ml/m², Y axis) correlated inversely with the left ventricular ejection fraction (%, X axis), yielding an equation : Y=-0.31 X + 43.7 (n=28, r=-0.56, p<0.001). The result indicates that the left ventricular filling is compensated by the augmented atrial contraction in case of impaired left ventricular function. We defined the left atrial volume at the beginning of the atrial contraction (LAVd, ml/m²) as the "preload" of the left atrium, and we also defined the volume expelled by the active atrial contraction (ΔLAVa, ml/m²) as the stroke volume of the left atrium. The stroke volume (Y) correlated positively with the "preload" (X), yielding an equation : Y=0.48 X -1.3 (n=28, r=0.80, p<0.001). We then defined the left ventricular end-diastolic pressure, the peak of the a-wave, as the "afterload" of the left atrium, and we studied the "afterload"-stroke volume relations in the left atrium. However as expected, a reasonable relationship between them was difficult to form. Consequently, we showed that an increase in the "preload" of the left atrium augmented the stroke volume of the left atrium, which means that Frank-Starling mechanism is operative in the left atrium.

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We studied the acute hemodynamic effects of dopamine, dobutamine, and isoproterenol in infants and young children with large ventricular septal defect (VSD). Dopamine (5 μg/kg/min) had no significant hemodynamic effects. Dobutamine (5 μg/ kg/ min) administration resulted in modest increases in heart rate and systemic arterial pressure and a decrease in left atrial pressure. This drug decreased the pulmonary blood flow, and the pulmonary-to-systemic blood flow (Qp/Qs) ratio, although these changes were not statistically significant. Isoproterenol, infused at doses of 0.03 and 0.06 μg/kg/min, increased the heart rate and lowered left atrial pressure. Only the high dose of isoproterenol lowered systemic and pulmonary arterial pressure. The low dose infusion of this drug increased the pulmonary blood flow as well as the systemic flow, whereas the high dose infusion resulted in a decrease of the Qp/Qs ratio without an increase in the pulmonary blood flow. Right atrial pressure was lowered by dobutamine and the high dose of isoproterenol, but the mean change was only 1 to 2 mmHg. The difference of the effects among these catecholamines is due to their relative strength of action on the vascular bed and the myocardium. Although the doses and durations of the drug infusions were limited, these acute hemodynamic effects should be taken into account when they are to be given to congested infants and young children large VSD.

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To clarify the clinical significance of regional myocardial perfusion abnormality of the left ventricle in dilated cardiomyopathy (DCM), 20 patients with DCM underwent dipyridamole Tl-201 emission computed tomography (ECT). The subjects were divided into 2 groups: group 1 had (n=9) reversible defects and group 2 (n=11) had persistent defects only. Group 2 patients significantly advanced heart failure and significantly poorer prognoses than group 1 (55% vs 11% in 2 years survival rate, p<0.05). The echocardiographic left ventricular end-diastolic dimension was larger in group 2 than group 1 (68.3±8.2 mm vs 61.9±4.0 mm, p<0.05) and % fractional shortening was smaller in group 2 than group 1 (18.0±4.5% vs 24.5±6.9%, p<0.05). Moreover, 12 of the 13 segments with reversible defect showed fairly well preserved left ventricular wall motion, whereas 35 of 58 segments with persistent defect had severely impaired wall motion (1/13 vs 35/58, p<0.01). Dipyridamole Tl-201 ECT demonstrated conclusively that the two types of defects (reversible and persistent) are useful to evaluate not only the abnormal myocardial perfusion but also myocardial damage and the prognosis in DCM.

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Oxygen toxicity in the non-ischemic and non-hypoxic heart has not been reported. In an experiment on isolated rat heart lung preparation, the effects of superoxide dismutase (SOD) on oxygen toxicity during hyperoxic perfusion were evaluated with intramyocardial high energy phosphates and the release of creatine phosphokinase (CPK) in the perfusate blood. Although there were non significant differences in high energy phosphates between SOD-treated and untreated hearts, the CPK release from the SOD-treated hearts was significantly less than from the untreated hearts. SOD increased the oxygen pressure of perfusate blood, too. These results indicate that hyperoxia induced cardiac and lung cell damage which was protected by SOD.

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Nitrendipine, a new calcium entry blocker, was administered to renovascular hypertensive rats (2KlC Goldblatt) (RHR, n=8) and sham operated control rats (ShC, n=8) to evaluate the effects on left ventricular hypertrophy and regional blood flow using radioactive microspheres. Nine untreated RHR and 8 untreated ShC served as control groups. After 6 weeks treatment (20 mg/kg subcutaneously, every other day), blood pressure reduced significantly in both RHR and ShC associated with a reduction in total peripheral resistance. Significant reversal of left ventricular hypertrophy was noted in RHR (1278±41 to 1024±19 mg, p<0.01), but not in ShC. There was a significant relationship between blood pressure and left ventricular mass in both untreated rats (r=0.955, p<0.001) and treated rats (r=0.729, p<0.005). Nitrendipine increased coronary blood flow in RHR (430±30 to 566±47 ml/m/100g, p<0.05) as well as in ShC (375±15 to 508±29 ml/m/100g, p<0.05), without increasing cardiac oxygen demand. Renal blood flow was unchanged, whereas cerebral blood flow was significantly increased in both RHR (128±6 to 164±13 ml/m/100g, p<0.01) and ShC (124±7 to 173±5 ml/m/100g, p<0.01). Thus, long treatment of nitrendipine effectively regressed cardiac hypertrophy toward normal. Nitrendipine reduced total peripheral resistance; however, the effects on regional blood flow were not uniform among various organs.

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Atrial septal aneurysms are rare, usually associated with congenital heart disease causing atrial pressure elevation. We describe here a case of atrial septal aneurysm with no other cardiac abnormalities that was diagnosed by two-dimensional echocardiography.

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In order to define indications for newly developing aggressive managements for patients with acute myocardial infarction, an analysis of therapeutic results was made on 1, 060 patients admitted to our coronary care unit (CCU). The total mortality was 14.9%, and 143 patients (13.5%) died from cardiac complications. These 143 patients were divided according to causes of death listed in Killip's classification. In the Killip class 4 group, mortality was as high as 86.6%, and all patients with previous infarction and/or hemodynamic abnormality of Forrester's subset 4 died. Pump failure caused death in 100 patients, of whom 69 were in a state of cardiogenic shock at the time of their admission. On the other hand, 58 patients, accounting for 40.6% of the cardiac deaths, were in Killip's class 1 or 2 at admission. In these 58 patients, 23 died from free wall rupture and/or perforation of the interventricular septum. Another 27 patients expired from reinfarction or infarct size extension and/or post-infarction angina. Thus, we can say that the major causes of death of patients in CCU are cardiogenic shock, reinfarction and cardiac rupture. We could not save these patients by using conventional CCU managements. Newly developing aggressive techniques, such as intracoronary thrombolysis and artificial hearts, seem to be indicated for these potentially fatal patients, while the effectiveness of these techniques should be verified as to such patients.

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The elective simple coronary revascularization in the last consecutive 200 patients were analyzed in this study. Despite of the increase in older patients who have more high risk factors, including low left ventricular ejection fraction (LVEF) and multiple vessel disease, there were no operative deaths in the second 100 patients. The use of calcium antagonist in patients with a history of spastic angina eliminate episodes of spastic angina in the perioperative period. In the late postoperative period, there were no cardiac deaths during the 7-year follow-up period. Angina remained in two of three patients with the patent grafts, who had a history of spastic angina. Hyperlipidemia and diabetes mellitus influenced occlusion of the grafts and progression of atherosclerosis of native coronary arteries an then four of five reoperations. Exercise tolerance in patients, even those with preoperative low LVEF, has been improved although their was some increment of left ventricular end-diastolic pressure during excercise. Patency rate in sequential grafting with saphenous vein grafts or internal mammary artery grafts were 92% in the average follow-up period of 11 months. The increase of flow rate with nitroglycerine and atrial pacing in internal mammary artery grafts (IMAG) were comparable with saphenous vein grafts.

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Coronary artery bypass grafting utilizing the internal mammary artery (IMA) was performed in 108 patients with an operative mortality (less than 1 month) of 0% and a hospital mortality of 1.9%. The IMA was used most often in the left anterior descending artery system in combination with saphenous vein grafts (SVG) to the right and left circumflex artery systems. Although the IMA flow was smaller than the SVG flow when measured intraoperatively by an electromagnetic flow meter, postoperative clinical, electrocardiographic, isotopic, angiographic and coronary sinus flow-metric studies all demonstrated that the IMA can respond well to myocardial blood flow demand both at rest and during exercise, resulting in excellent clinical improvements with no detectable signs of flow deficiency. In addition, no signs of ischemia were detected in any of the 15 patients with stenosis in the left main trunk treated with an IMA graft. The IMA graft appears to have a great adaptive capacity to meet increased myocardial demand. Postoperative angiography performed at an average of 3 months after surgery in 60 unselected patients demonstrated an IMA patency rate of 98% in comparison with 88% patency in SVGs to the left anterior descending artery (p<0.05). Not only the patency rate, but also the graft wall characteristics were much better in IMA grafts than in SVGs. Some SVGs showed marked wall irregularity as early as 3 months after surgery. Postoperative changes in the IMA caliber (enlargement when the run-off is great) and the lower rate of progression of stenosis in the native recipient coronary artery receiving an IMA graft have led us to conclude that the IMA graft is a "living conduit" with great adaptive capacity, acting like a very large collateral vessel created by surgery: it responds well to coronary blood flow demand in a cooperative manner with native coronary artery flow and also shows good potential for long-term patency.

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Ninety one patients with untable angina were evaluated by clinical and angiographic study. Of 91 patients, 42 (46%) responded poorly to the intensive medical treatment. Emergency coronary arteriography was then performed on these patients. The important pathoanatomical mechanisms contributing to instability of angina pectoris and/or refractoriness to the intensive medical treatment were observed in 19 of 42 patients (45%). These include: 1) More severe disease with left main lesion; 2) Refractory coronary spasm; 3) Coronary dissection; 4) Rapid progression of atherosclerosis; 5) Ulcerating plaque and 6) Coronary thrombus. Our results presented here suggest that an appropriate knowledge regarding pathophysiology might improve the approach to treatment.

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The efficacy of intracoronary urokinase (UK) in an acute myocardial infarction has not been firmly established in a randomized fashion. Two hundred and ten patients were randomized to UK therapy (107 patients) and placebo (103 patients). Successful recanalization was achieved in 74% of the UK group vs 17% in the placebo group (p<0.01). The success rate was dose dependent up to 960, 000 I.U. Clinical course was favorable and left ventricular enddiastolic pressure was reduced significantly in the UK group compared with the placebo group (p<0.05). Ejection fraction one month after the study was better in the reopened group than in the occluded group. Thus, early administration of UK can establish coronary reflow in a high proportion of patients and appears to favor the clinical course.

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Contraction band necrosis (CBN), coagulation necrosis (CN) and infarct size, expressed as CBN + CN, were quantitatively analyzed in 15 pig hearts without collateral circulation. The left anterior descending coronary artery was ligated for 60 and 120 minutes and then reperfused for eight hours (group 1 and 2, respectively). Five hearts were not reperfused (group 3). There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method, decreased to almost zero after occlusion but recovered during reperfusion. Percent infarct area of the perfused area in group 1, 2 and 3 were 80±9, 96±2% and 95±3%, respectively. The percent area of CBN was 68±11% in group 1, 2±1% in group 2 and 2±2% in group 3. We conclude that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even in reperfusion following one-hour occlusion. Therefore, in patients with acute myocardial infarction, coronary thrombolysis should be performed within one hour after the onset of the infarction to reduce the infarct size.

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In order to know the feasibility of coronary reperfusion by thrombolysis or aorto-coronary bypass graft in the early stages of the acute myocardial infarction, we studied the effect of the coronary artery reperfusion to acutely ischemic myocardium induced by the coronary artery occlusion in ninety-five anesthetized open-chest dogs. The major factors determining the extent of the myocardial salvage by the reperfusion were the duration of the occlusion time and the degree of the reperfusion injury. These two determinants were analysed by coronary circulation, the regional myocardial function, the mitochondrial metabolism, mitochondrial Ca and Mg contents, and morphological findings of the myocardium by electron-microscopy. The regional myocardial contractility (% systolic shortening) and the mitochondrial metabolism (oxydative phosphorylation) were significantly damaged by the reperfusion more in 60 minute occlusion than in 30 minute occlusion, although the coronary circulation (coronary blood flow, regional myocardial blood flow and coronary vascular resistance) and myocardial gas contents (PO₂, PCO₂ and pH) in the ischemic myocardium induced by less than 60 minute occlusion were almost recovered to the pre-occluded level by 60 minutes after reperfusion. By 120 minute reperfusion, the ischemic damage calculated from mitochondrial Ca and Mg contents (MC index: 1-[Mg/Ca] ischemia/[Mg/Ca] non-ischemia) was not changed in 30 minute occlusion but was significantly deteriorated in 60 minute occlusion. Therefore, coronary reperfusion must be started within 60 minute or less after occlusion. A supplementary way to protect the myocardium from ischemia is needed as soon as possible before reperfusion. Ca⁺⁺ antagonist, diltiazem, administered 10 μg/kg/min intravenously during the coronary occlusion and reperfusion significantly improved the myocardial contractility, the mitochondrial metabolism, MC index and morphological findings by electron-microscopy in reperfusion after 60 minute occlusion. Therefore, it is useful to administer Ca⁺⁺ antagonist, diltiazem, to protect the myocardium from ischemia until thrombolysis or aorto-coronary bypass graft is successful.

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Balloon technology has advanced to incorporate the skills of angioplasters while efforts to enhance their skills continue. These factors have contributed to the expansion of percutaneous transluminal coronary angioplasty (PTCA) indications. We have analyzed the comparison of short and long term results between PTCA and CABG revascularization procedures. In the development of revascularization procedure, one graft surgery has significantly declined in use since 1983 (2 years after the start of PTCA) while there has been an increase of multi graft surgery (more than 2 grafts). On the other hand, PTCA has showed a linear increase since 1982 and reached 160 cases in 1985. The growth of complex angioplasty other than PTCA for single discrete lesions is parallel to that of PTCA and has been used in 44% of overall cases. The growth curve of angioplasty crossed over that of revascularization surgery in 1983. PTCA was successful in 246 patients out of 300 overall cases representing 88% success rate and in 340 lesions representing an 81% success. For CABG the patency rate was 89.5% which means a out of 638 grafts were successful. PTCA was conducted in 137 cases with multiple lesion. That data could be interpreted as mean patient success of 120/137, lesion success was 196/265 with a success rate of 88% and 73%, respectively. Primary results in 284 multi CABG cases were good with a patency rate of 91% (487 patent grafts out of 536 anastomoses). However, in-hospital deaths were 3.5% higher (10 cases with CABG group). The effective dilatation of high-grade organic lesion was found to be closely related to the improvement of clinical symptoms and a marked decrease in incidence of ergonovine induced spasms at the angioplasty site in patients with vasospastic angina (VSA). Thus PTCA can be accepted as an alternative therapy to CABG in VSA. In the long term follow up, work load response parameters such as exercise time, % predicted HR, PRP, Mets and the modified treadmill exercise scores improved significantly after the successful PTCA.

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Necropsy studies of coronary arteries were made in 14 patients who died after percutaneous transluminal coronary angioplasty (PTCA). Eight patients died shortly after PTCA, while the other six patients died some considerable time later. A total of 9, 920 serial step sections of necropsied coronary arteries at the site of PTCA were prepared and examined histopathologically by light microscope to determine the mechanism of luminal enlargement in PTCA, as well as the occurrence of restenosis. Of the eight patients who died shortly after PTCA, two had disruption of the intima and the media in the arterial wall located opposite the site that had atheroma, in spite of the fact that the former wall is more normal than the latter. Dissection of the media was camed out in four patients and intimal desquamation performed in six. All the patients revealed fresh thrombus formation. Of the six patients who survived for a longtime after PTCA was performed, two had disruption of the intima and the media located opposite the site with atheroma. In one, the media was dissected and in another, intimal desquamation was camed out. In one patient, release of atheroma into the lumen was suspected. Proliferation of intimal cells was revered in three patients indicating that restenosis had occurred. No compression of the atheroma was observed in any of the 14 patients. The above findings led to the conclusion that the mechanisms of luminal enlargement in PTCA are 1) intimal and medial disruption in the arterial wall located opposite the atheroma; 2) medial dissection; 3) intimal desquamation; 4) release of atheroma into the lumen; and 5) any combination of 1) - 4). With regard to restenosis, all patients in our study revealed fresh thrombus formation, which suggests the early occurrence of restenosis after PTCA. Three of the six patients who survived long after PTCA showed proliferation of intimal cells. This suggests the possibility that even if the stenosed artery were dilated by PTCA, stenosis may have again occurred as a result of excessive proliferation of intimal cells repairing arterial lesions.

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Nine patients with familial hypercholesterolemia (FH), 6 with homozygotes and 3 with heterozygotes, were treated with long term repetitive LDL-apheresis. The techniques are simple plasma exchange with human albumin solution, double membrane filtration, and selective LDL-adsorption by dextran sulfate-cellulose gel. The average term was 3.5 years except for the two homozygotes for whom the treatment was only initiated in our facility. Plasma total cholesterol levels were controlled between pretreating level, 320 to 500 mg/dl, and posttreating level, 100 to 160 mg/dl, by biweekly treatments. All patients showed remarkable improvement of cutaneous and tendinous xanthomas. One homozygous patient died at 31 years old of myocardial infarction after 2 years of treatment. A homozygous patient who has been treated since 5 years old for 6 years was reexamined by angiography and was shown to have atheromatous lesions regressed in the aortic valve region and in the left renal artery.

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