A 32-year-old B-type male weighing 60 kg suffered from end-stage dilated cardiomyopathy. Although aggressive medical treatment with dobutamine 21μg/kg/min, dopamine 17μg/kg/min, digoxin 0.25mg iv once daily. furosemide 40mg iv every 6 h, and bumetanide 0.5mg iv every 6 h were given. he was finally ventilator dependent for the last 3 weeks until a B-type donor weighing 42.5kg was found. Because of the 29.2% weight mismatch, a heterotopic heart transplantation was performed. Posterior plication mitral annuloplasty was also performed to correct the severe mitral regurgitation of the recipient heart. Postoperatively the patient remained respirator dependent for 17 days and was finally discharged in good condition on the 46th postoperative day.

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The cardiac response to dietary salt loading was assessed by Doppler echocardiography during various sodium intakes (52-345 mEg per day) in 30 patients with essential hypertension. The Mitral flow velocity integral in the rapid filling phase (IntR) and the atrial contraction phase (IntA) was measured from the transmitral flow pattern, and the sum of IntR and IntA (IntR+IntA), the ratio of IntA to IntR (IntA/IntR), cardiac output (CO) and total peripheral resistance (TPR) were calculated. With salt loading, the mitral flow pattern remained almost unchanged in the nonsalt-sensitive (NSS) patients. Fourteen of the 19 salt-sensitive (SS) patients showed significant increases in IntR+IntA and CO with salt loading (IntR+ IntA, from 13.9±2.8 to 17.9±3.6cm, p<0.01; CO, from 6021±2130 to 8305±1699ml/min, p<0.01), and were termed "salt-sensitive CO-dependent" (SS [COdep]), suggesting that the apparent pressor response to sodium loading was mediated by an increased CO. In the remaining five SS patients termed "salt-sensitive CO-independent" (SS [COindep]). IntA/IntR increased significantly with sodium repletion (from 0.66±0.23 to 0.90±0.31, p<0.01), without a significant change in IntR+IntA. Increments in IntA/IntR observed in the SS [COindep] patients were considered to be due to an elevation of total peripheral resistance (TPR), since changes in IntA/IntR were significantly correlated with those in TPR in all subjects (r=0.617, p<0.01).

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To assess the influence of autonomic regulation on automaticity in patients with intrinsic sinus node dysfunction, heart rate responses to autonomic drugs were evaluated in 28 patients with sick sinus syndrome and in 8 normal subjects. Heart rates before and after intravenous administration of isoproterenol (Isp), propranolol, atropine, and methoxamine were measured. To compare the results with electrophysiologic data, heart rate and automaticity recovery time (ART) before and after pharmacologic autonomic blockade (AB) were evaluated. Seventeen patients without syncope showed a similar heart rate response after administration of Isp to that of normal subjects, but 11 patients with syncope showed a significantly lower response than patients without syncope. Responses to atropine and methoxamine were lower and response to propranolol was larger in patients as compared to normal subjects. However, no significant difference was observed between patients with and without syncope. Twelve patients showed severely prolonged max ART exceeding 5000 msec after AB. Seven of them showed preserved response to Isp and max ART be-fore AB was significantly shorter than that after AB. The other 5 patients with lower response to Isp showed no significant change in max ART before and after AB. In conclusion, sympathetic regulation in patients with preserved response to Isp might compensate for the impaired intrinsic automaticity in preventing syncope even in patients with severely impaired intrinsic sinus node function.

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To investigate the mechanism of cardiac dysfunction in myocarditis, myoglobin, an intracellular oxygen-transport, was immunohistochemically examined in biopsy specimens obtained from the right side of the ventricular septum and left ventricular free wall in 58 patients with myocarditis and 19 controls. Sections 4 pm thick were stained by the indirect immunoperoxidase method using a polyclonal antibody to human myoglobin as the primary antibody. Under light microscopy, the intensity of myoglobin immunoreactivity in the tissue section was semiquantitatively classified from grade 0 to grade 3. Then, the grade of myoglobin staining was compared with clinical, hemodynamic and histopathologic parameters. In right and left ventricular specimens, the grade of myoglobin staining was positively correlated with ejection fraction, but inversely with left ventricular end-diastolic and end-systolic volume indices. The percentage of myocytes with grade 0 was correlated with the number of mononuclear cells in the specimens. In addition, the grade of myoglobin staining in right ventricular specimens was positively correlated with the duration of illness but inversely correlated with the number of mononuclear cells. In 4 patients who had serial biopsies, the ejection fraction was improved and the grade of myoglobin staining was in-creased in the convalescent stage. These results indicate that myoglobin staining reflects the intensity of myocarditis and a decrease of myoglobin may be important as one of the pathogenetic factors of cardiac dysfunction in myocarditis.

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The coronary artery response to ergonovine ( EM ) and nitrate of the proximal. middle and distal segments of the three major coronary artery branches and the main trunk was quantified in 67 patients without coronary spasm and in 69 patients with coronary spasm without significant organic stenosis. The changes in control diameter and diameter after EM administration compared to diameter after nitrate were used as the index of coronary artery tone. EM increased coronary artery tone regardless of the occurrence of coronary spasm (p<0.01). In all segments, basal coronary artery tone was greater in patients with spasm than in patients without spasm (p<0.01) in a way similar to the coronary responses to EM (p<0.01). In patients with spasm, both coronary artery tone after EM and basal coronary tone were greater in the spastic segments than in the nonspastic segments (p<0.01), which were greater than those in patients without spasm (p<0.01). Our data suggest that patients with spasm may have in-creased basal tone, and that coronary artery spasm may be based on increased coronary tone. Clinically, evaluation of the basal tone and response to EM in the entire coronary artery tree may be useful for predicting the presence of coronary artery spasm.

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Acceleration of blood flow ejected from the ventricle into the aorta and the hydraulic power state of blood flow in the aorta may be affected by asynchronous or locally depressed contraction of the left ventricle as well as by arterial impedance. In order to evaluate the effect of an infarcted heart on the hydraulic power state of blood flow, the aortic input impedance spectrum and the hydraulic power spectrum were calculated from simultaneous recordings of pulsatile aortic pressure and flow velocity at the aortic root in 6 normal controls (group 1), 6 patients with old myocardial infarction (OMI) without aneurysm (group 2), and 6 patients of OMI with aneurysm (group 3). The ratios (Rh) of power in high harmonics to that of fundamental harmonics, that is, Rh=(E2+E3+ ···E10)/E1, where E represents hydraulic power and the numbers represent harmonic numbers, were 0.64±0.17, 0.23±0.09, and 0.22±0.10 in groups 1, 2 and respectively (p<0.001 between groups 1 and 2; p<0.001, between groups 1 and 3). As the acceleration of ejecting flow of blood by the left ventricle is inversely related with arterial impedance, Rh will be also inversely related with arterial impedance. Then, the product of Rh and the characteristic impedance (Zc) would be an indicator of the left ventricular contractility. In fact, the products were 64±15, 32±14, and 31±13 dyne·sec·cm^-5 in groups 1, 2, and 3 respectively (p<0.005, between groups 1 and 2; p<0.005, between groups 1 and 3). These results suggest that asynchronous or locally depressed contractions of the left ventricular wall are closely related to depressed Rh and further to depressed values of the products of Rh and Zc. It is con-cluded that analysis of the power spectrum of blood flow in the root of the aorta provides information of the left ventricular contractility in connection with arterial impedance.

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A rare case of epicardial cyst diagnosed at surgery was presented. A 64-year old woman was admitted for evaluation of a mediastinal mass shown by echocardiography to be adjacent to both ventricles. Computed tomography (CT) and magnetic resonance imaging (MRI) studies were per-formed. On CT. there was evidence of an abnormal mass lesion at the lateral side of the outlet of the right ventricle. The CT number of the mass was 24.7, suggesting cystic lesion. MRI revealed that the intensity of the lesion signal was higher than that of subcutaneous fat on the T2 weighted image. On the T1 weighted image. a low intensity was identified in the same region. During operation a mass originating from the epicardium was diagnosed as an epicardal cyst.

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While there have been many reports of the significant role of cytoplasmic free calcium ion in myocardial injury, these have been carried out in multicellular preparations. Since cell injury may occur inhomogeneously, it is necessary to observe the 'history' of an individual myocyte in order to investigate the de-tailed role of the calcium ion in the process of myocardial injury. We have observed the natural history of individual myocytes isolated from the left ventricle of rats with respect to changes in shape and cytoplasmic free calcium concentration ([Ca²⁺]_i) measured with fura-2. We can discriminate four phases in the time course of cell deterioration. In the first phase (phase O), the myocyte is rod shaped, quiescent and responsive to electrical stimulation. The [Ca²⁺]_i is stable. In the next phase (Phase 1), once initiated, the myocyte exhibits an asynchronous wavy contraction and gradually decreases in length. The [Ca²⁺]_i gradually increases with some fluctuation. Phase 2 is characterized by rapid depelopment of contracture with a marked in-crease in [Ca²⁺]_i. In the Period following establishment of contracture (Phase 3), changes in [Ca²⁺]_i vary from cell to cell, possibly because of leakage of the dye caused by loss of cell membrane integrity. Our results indicate that, during naturally occurring cell deterioration, loss of [Ca²⁺]_i control at the membrane of the sarcoplasmic reticulum precedes contracture and catastrophic increase in [Ca²⁺]_i.

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In vitro filtration was used to characterize and compare the function of two types of LDL apheresis module: membrane filtration (module M: pore diameter, 0.04μm; effective surface area. 0.1m²) and LDL adsorption (module A: a column containing 20ml of polyvinyl alcohol gels fixed with polyacrylic acid). Module A had better selectivity of LDL removal, while module M could rapidly remove a larger amount of LDL. The effect of repetitive LDL apheresis with module 'A on the plasma cholesterol level and on the development of aortic atherosclerosis was examined in 6 heterozygous WHHL rabbits (5 to 10 months old; mean plasma total cholesterol level, 270±39mg/dl), treated with LDL apheresis at weekly intervals for 2 months. Plasma total and LDL cholesterols were lowered approximately 40% by a signal procedure. The LDL cholesterol level tended to de-crease as treatment progressed. while the HDL cholesterol level was unchanged or rose above the baseline value in a week after LDL apheresis. The ratio of atherosclerotic lesion area to whole aortic area was relatively low in treated rabbits (6.5±1.9%) in comparison with that in 5 untreated heterozygous WHHL rabbits (18.3±7.7%). The mean cholesterol content in the thoracic aorta was 4.9±1.3mg/g wet tissue in treated rabbits vs 13.3±6.1mg/g wet tissue in untreated rabbits. These results suggest that repetitive LDL apheresis might be effective in maintaining a lower level of LDL cholesterol and retarding the atherosclerotic process in vivo.

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Interaction between adenosine and isoproterenol (ISP) on myocardial inotropic action was studied in open-chest dog hearts. The local myocardial force and the left ventricular (LV) dP/dt were measured as indices of myocardial contractility. Isoproterenol [ISP, 9.47 μM (2μg/ml)] was infused into the left circumflex coronary artery at rates of 0.05ml/min (low dose ISP) or 0.2ml/min (high dose ISP). Two mM adenosine or 0.5mM N⁶-phenylisopropyl-adenosine (PIA) were infused into the coronary artery at rates of 0.2 (4×10^-7 mol/min.), 0.5 (1×10^-6 mol/min) and 10ml/min (2×10<-5> mol/min) In the presence of either a low or a high dose of ISP. Adenosine infusion at a rate of 0.2ml/min did not modify myocardial contractility in the presence of the both doses of ISP. The larger doses of adenosine. 0.5ml/min and 10ml/min, decreased myocardial-developed tension and LVmax dP/dt dose-dependently. However, the dose of adenosine which affected myocardial contractility was inphysiologically high in comparison with the concentration in the ischemic myocardium. PIA, a potent agonist of adenosine A1-receptor, attenuated an increase in myocardial contractility in a dose-dependent manner which was caused by intracoronary ISP infusion. This indicates that A1-adenosine receptors exist, but a functional adenosine-catecholamine antagonism does not play a significant role in the canine left ventricle.

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