A great number of patients suffer and die from the sequelae of acute and chronic heart failure each year. Although advances in medical and surgical therapy have benefited many of these patients, the majority suffer from disease refractory to any definitive therapy. For these patients, cardiac transplantation is the only remaining hope. Unfortunately, because of the increasing demand for donor organs in the face of a fixed and limited supply, this option is only available to a small percentage of these patients. Even in patients accepted for transplantation, a significant waiting list mortality has been observed. A variety of ventricular assist devices (VAD) have been developed since the first successful case of mechanical cardiac assistance over 30 years ago. These devices differ in basic mechanical function, method of insertion, and degree of implantability, and thus have different indications and potential applications. While the intra-aortic balloon pump and centrifugal pumps are effective short-term support modalities, extracorporeal and implantable pulsatile devices have been used successfully for long-term support of patients with reversible and non-reversible cardiac failure. These pumps have most commonly been utilized as bridges to transplantation, but increasing clinical experience has supported the notion of long-term mechanical assistance as a definitive therapy for endstage heart disease. While complications, particularly infection and thromboembolism, pose significant challenges and long-term device reliability remains to be fully determined, available implantable devices seem capable of providing effective long-term support. As data is obtained from currently ongoing trials comparing VAD support to medical therapy for endstage heart failure, ethical and economic issues will assume increasing importance. (Jpn Circ J 1997; 61: 887 -892)

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Neointimal formation and arterial wall remodeling are pivotal causes of luminal narrowing in atherogenesis and restenosis. Arterial remodeling refers to a series of dynamic structural changes that arteries may undergo in response to various stimuli, including changes in blood flow and pressure, and acute injury. The biological mechanisms involved in arterial remodeling are poorly understood and are currently a main target for research. We have recently focused on the role of the arterial wall microcirculation (ie, vasa vasorum) in arterial remodeling after injury. In the past, a correlation between arterial wall neovascularization and the accumulation of arterial plaque has been documented; however, the dynamic role of these microvessels in arterial repair and luminal narrowing has not been examined. The type of arterial injury, the nature of the lesion that develops, and the arterial compartment in which angiogenesis occurs may determine the role of the vasa vasorum in arterial narrowing. In this review, we highlight the data that link arterial wall neovascularization with lesion formation and the process of arterial remodeling. (Jpn Circ J 1997; 61: 893 - 904)

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An enhanced method for determining cardiac output using Doppler color flow imaging techniques to measure mitral orifice diameter was developed and validated in an experimental model and in clinical patients. In an in vitro circuit model, color jet width correlated well with actual orifice dimension from 12 to 24 mm (r=0.99). In the clinical application, mitral valve area was calculated as a ×b×π/4 where a and b represent the width of the color flow stream in the mitral orifice just distal to the annulus in apical long-axis (short-diameter) and 4-chamber (90° rotated, Iong-diameter) views, respectively. Cardiac output was then computed as the product of mitral valve area and time-velocity integral of transmitral flow from the same site. Cardiac output was also measured by thermodilution and conventional echocardiographic methods using diameters and time-velocity integrals from the left ventricular outflow tract. In 30 patients with nonvalvular heart disease, cardiac output measured by thermodilution ranged from 3.40 to 8.40 L/min. Cardiac output was determined in 28 of 30 patients (93%) by the Doppler color flow imaging technique; it ranged from 3.00 to 8.36 L/min and correlated well with thermodilution: y=0.90x+0.63, r=0.91. Cardiac output was determined in 24 of 30 patients by the conventional left ventricular outflow method (80%). The cardiac output measured by the conventional method correlated less closely with thermodilution (r=0.84), although there was no statistical difference in correlation coefficiencies between the 2 methods. These results indicate that the Doppler color flow imaging technique can be used to enhance the determination of cardiac output by echocardiography, particularly when the conventioal method has resulted in technically inadequate recordings. (Jpn Circ J 1997; 61: 905 - 911)

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The presence of mitral insufficiency after acute myocardial infarction (AMI) often leads to hemodynamic impairment and heart failure. This study was designed to examine the relationship between mitral regurgitation (MR), an indicator of mitral insufficiency, and the course of recovery from AMI. We evaluated the course of MR after AMI in 223 patients by color Doppler echocardiography. MR was detected in 21% (47/223) of patients at the onset of AMI, and developed in 18% (40/223) of patients during follow-up. Patients were grouped according to the course of MR as well as the success of acute recanalization therapy. No correlation was observed between the presence or course of MR and the site of infarction. The incidence of successful recanalization was higher in patients with MR that improved during follow-up than in patients with MR that was unchanged or that worsened during follow-up. Although no significant differences in hemodynamic variables were noted among the groups at admission, the group with unsuccessful recanalization and unimproved MR (BS-) showed a significantly greater left ventricular end-diastolic diameter (LVDd), left ventricular end-systolic diameter, and left ventricular end-diastolic volume (LVEDV) as well as a lower left ventricular ejection fraction than patients with successful recanalization and no MR (CS+) during the convalescent period. The extent of change in LVDd and LVEDV between admission and convalescence was significantly greater in the BS(-) group than in the CS(+) group. The results suggest that successful recanalization after AMI reduces the incidence of MR. Acute recanalization therapy after AMI may prevent left ventricular remodeling, resulting in a secondary improvement of MR. (Jpn Circ J 1997; 61: 912 - 920)

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The purpose of this study was to evaluate ST-segment elevation induced by regional myocardial stretch without myocardial ischemia in canine hearts. A strain gauge arch (TH-601T) was sutured to the left ventricular epicardium, parallel to the short axis, to shorten the end-diastolic length of the myocardium beneath the arch (stretch zone; SZ) and to produce regional myocardial stretch in each of 6 dogs. An increase in preload caused by altering the height of a saline-filled reservoir affected prolongation or shortening of the myocardium both in the SZ and outside the arch (normal zone; NZ) to increase myocardial stretch. An epicardial electrocardiogam was recorded in both the SZ and the NZ. After suture of the strain gauge arch, the ST segment was elevated in the SZ. An increase in preload augmented stretch during systole in the SZ, resulting in additional ST-segment elevation. These results suggest that regional myocardial stretch itself plays an important role in ST-segment elevation. (Jpn Circ J 1997; 61: 921 - 926)

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To clarify the roles of subclasses of α₁-adrenoreceptors in ischemic-reperfused myocardium, we compared the effect of the nonselective α₁-blocker bunazosin with that of the α_1A-blocker WB4101 and the α_1B-blocker chlorethylclonidine (CEC) in isolated rat hearts. After 30 min of preperfusion, Langendorff-perfused hearts were subjected to 25 min of global ischemia followed by 30 min of reperfusion. Hearts were randomly divided into 4 groups, with one of the following substances being added to the perfusate: buffer alone (control), 10^-6 mol/L bunazosin, 10^-7 mol/L WB4101, or 10^-7 mol/L CEC. Bunazosin had a negative inotropic effect and preserved the postischemic ATP content, reduced the postischemic increase in intracellular Na⁺ content and then enhanced postreperfusion recovery of creatine phosphate. Bunazosin also reduced myocardial ⁴⁵Ca²⁺ uptake during reperfusion (control 5.2 vs bunazosin 2.5 μmol/g dry weight of tissue (dwt), p<0.01). However, the recovery of left ventricular developed pressure (DP) was not improved when bunazosin was added to the perfusate during reperfusion. WB4101 had neither a negative inotropic nor an energy-sparing effect, but it improved the recovery of DP (control 43% vs WB4101 56% of preischemic value, p<0.05) with no reduction in myocardial ⁴⁵Ca²⁺ uptake. CEC had a negative inotropic and energy-sparing effect and then reduced myocardial ⁴⁵Ca²⁺ uptake (CEC 3.1 μmol/g dwt, p<0.05), but it did not improve the recovery of DP. These results suggest that the preischemic administration of an α_1B-adrenoreceptor subtype blocker protected ischemic-reperfused myocardium via reduction of Ca²⁺ overload, whereas the selective blockade of the α_1A-adrenoreceptor subtype reduced myocardial damage via mechanism(s) other than Ca²⁺ metabolism. (Jpn Circ J 1997; 61: 927 - 935)

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We investigated whether impaired endothelium-dependent vasodilatory response recovers as heart failure improves. The femoral blood flow responses to intra-arterial administration of nitroglycerin (NTG) and acetylcholine (ACh) were examined in dogs with 2-week pacing-induced chronic congestive heart failure (congestive heart failure group; CHF, n=12). Thereafter, pacing was stopped and hemodynamic changes and femoral blood flow responses were re-examined either 1 week (recover 1 week group; Re 1W, n=6) or 4 weeks (recover 4 weeks group; Re 4W, n=6) after the cessation of pacing. Another group in which a pacemaker was implanted without pacing served as the control group (n=8) . In CHF, heart rate and pulmonary artery pressure increased, and echocardiography revealed increased left ventricular diastolic dimension and reduced percent fractional shortening compared with those in the control group. In Re 1W, all hemodynamic parameters returned to the basal levels and did not differ from those in the control group. Although there was no significant difference in the blood flow responses to NTG among the 4 groups, the responses to ACh in CHF were significantly reduced compared with those in the control group. Despite the recovered hemodynamics, femoral blood flow responses to ACh were still reduced in Re 1W, but they returned to the levels of the control group in Re 4W. Thus, vascular endothelial dysfunction recovers along with improvement in CHF, however, the recovery of endothelial function is delayed in comparison with improvement in cardiac function. (Jpn Circ J 1997; 61: 936 - 942)

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A previously healthy 64-year-old woman attended our hospital with chest pain, facial edema, and general fatigue. A chest radiograph revealed cardiomegaly, small bilateral pleural effusions, and hilar congestion - findings that improved after early therapy with furosemide and methyldigoxin. A chest radiograph recorded 7 years earlier had revealed no dilation of cardiac shadow. There were no findings suggesting atrial septal defect (ASD) or valvular heart disease. Echocardiography revealed a tumor-like mass adhering to the posterior wall of the left atrium. Color-flow Doppler echocardiography revealed a left-to-right shunt at the atrial level. The Q_p/Q _s ratio as measured by cardiac catheterization was 2.0. Coronary angiography revealed abnormal dilated arteries from the atrioventricular nodal branch and several feeding arteries from the left circumflex branch. We hypothesized that the left-to-right shunt could be due to the tumor, which extended to the rim of the patent foramen ovale, or to the very small, previously unrecognized, ASD. This patient died 6 months after her first admission and an autopsy was performed. Light microscopic examination of the tumor revealed spindle-shaped fibroblast-like cells arranged in a storiform or fascicular pattern. The immunohistochemical findings were consistent with malignant fibrous histiocytoma (MFH) . In the literature, Ieft-to-right shunt at the atrial level has not been reported in patients with cardiac MFH. (Jpn Circ J 1997; 61: 943 - 946)

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A 76-year-old man with abdominal aortic aneurysm (AAA) and concomitant gastric cancer, who had under-gone coronary artery bypass grafting (CABG), presented with recurrent exertional angina. Both lesions, the AAA and advanced gastric cancer, exhibited an absolute indication for urgent surgery. Coronary revascularization with percutaneous transluminal coronary angioplasty (PTCA) was carried out successfully before abdominal surgery. A one-stage abdominal operation was performed safely. The need for coronary revascularization complicates the treatment strategy for these patients with associated coronary artery disease. PTCA is the best option, especially if the patient presents with recurrent angina after prior CABG. (Jpn Circ J 1997; 61: 947 - 950)

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A 52-year-old man acquired a ventricular septal defect following non-penetrating chest trauma. Four days after the traumatic accident, he showed signs of congestive heart failure. Imaging techniques using echocardiography and left ventriculography were helpful in diagnosing the condition. Surgical repair by patch closure of the ventricular septal defect was accomplished 7 days after the traumatic accident. (Jpn Circ J 1997; 61: 951 - 953)

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A case of acute myocardial infarction associated with primary coronary dissection was followed up angio-graphically. A 46-year-old woman complained of chest oppression. Electrocardiogram on admission showed ST-segment elevation in V_1-5· Urgent coronary angiography was performed under a diagnosis of acute anterior myocardial infarction, and showed a significant stenosis with multiple filling defects in segments 7-8 (99% with severe delay) in the left anterior descending artery. There was no organic lesion in the right coronary artery. Intracoronary thrombolytic therapy was unsuccessful, and thereafter she was treated with aspirin, warfarin and isosorbide dinitrate. Coronary angiography performed 1 month later revealed a long dissection with double lumens in segments 7-8. The septal branches emerged from the smaller lumen. Two months later, the 2 lumens were almost equal in size. These findings indicated that coronary dissection produced a false lumen with an entry in segment 7 and a reentry in segment 8, and that the false lumen was responsible for the greater flow. Four months later, the flow in the true lumen had improved remarkably while that in the false lumen had almost disappeared. She remained in stable condition during the follow-up period of 4 months. (Jpn Circ J 1997; 61: 954 - 957)

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Chronic pulmonary thromboembolism is known to be associated with poor prognosis with conservative medical treatment. Pulmonary thromboendarterectomy for chronic pulmonary thromboembolic disease is a potentially lifesaving procedure that prevents right-sided cardiac failure as a result of secondary pulmonary hypertension caused by pulmonary thromboembolism. We report a rare case of systemic lupus erythematosus with antiphospholipid syndrome in a patient who presented with pulmonary hypertension secondary to chronic proximal multiple pulmonary thromboembolism. To our knowledge, this is the first case report of chronic pulmonary thromboembolism complicated by systemic lupus erythematosus with antiphospholipid syndrome. Thromboendarterectomy was performed with satisfactory results. (Jpn Circ J 1997; 61: 958 - 964)

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