Short axis views of the left ventricle were studied in 68 patients with hypertrophic cardiomyopathy (HCM) and 20 healthy persons using crosssectional echocardiography.
Configurations of the short axis view of the left ventricular cavity at the level of the papillary muscles in HCM were classified into 2 types, dumbbell and mushroom, which were formed by the position of papillary muscles. Anterior dislocation of the papillary muscles was seen in the dumbbell type, and marked hypertrophy of the papillary muscles in the proper position was seen in the mushroom type. Dumbbell shape (50 patients) was observed in the patients with marked hypertrophy in the basal portion of interventricular septum. Mushroom shape (18 patients) was seen in the patients with hypertrophy around the apex of the heart except for in a few patients.
Areas of the papillary muscles (AP) and the left ventricular cavity (ALV) were measured and AP/ALV+AP ratio was calculated. The AP/ALV+AP ratio in HCM was significantly larger than that in the healthy persons, but no difference was seen between these 2 groups of HCM.
It should be noted that the position of the hypertrophied papillary muscles is closely related to the distribution of hypertrophy in HCM.

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Six patients aged between 1 to 11 years (4 females and 2 males) developed Stokes-Adams attacks with complete heart block due to acute nonspecific myocarditis. Transvenous pacing was instituted in 2 patients, but in the other 4 patients the ECG returned to normal by isoproterenol. All ECGs in complete heart block showed QRS complexes of right bundle branch block with left posterior hemiblock pattern, except for 1 which showed QRS complexes of complete left bundle branch block pattern. The ECG improved sequentially in order and left anterior hemiblock pattern of QRS complexes remained to the last during the convalescent period. Normal atrioventricular conduction returned by 2 to 24 hours in all but 1 patient who was dead and 1 of the 2 patients with shock. In another patient bifascicular block has persisted.

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Five children with idiopathic hypertrophic subaortic stenosis (IHSS) were operated upon during the past 7 years and all survived. Their ages ranged from 4 years and 5 months to 14 years (mean 8 years and 5 months). The operations performed were 1 right ventricular myectomy and 4 transaortic left ventricular myotomies. Whether surgery perfomed in childhood would change the natural history or not is still unknown, however, according to our results and many available reports, we have so far reached the following conclusions;
1. Transaortic left ventricular myotomy or myectomy is a safe and effective operation for localized muscular subaortic stenosis in children.
2. Because the disease is progressive, operation in childhood may be worth to be considered, when the resting or provocative pressure gradient is excessive.
3. For those who have a marked increase in left ventricular outflow pressure gradient by the provocation, operation would be considered even though the gradient at rest is less than 50mmHg.

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Twenty post-open heart surgery patients with low output syndrome were given dopamine, sodium nitroprusside (SNP) alone and in combination. Dopamine alone (3-4mcg/Kg/min) caused an increase of cardiac output (CO) from 3.2 to 4.6L/min/M² (p<0.001), SNP (1-1.5mcg/Kg/min) raised the CO to 3.7L/min/M² (p<0.005). While the combination of the 2 drugs elevated the CO to 5L/min/M² (p<0.001). The mean pulmonary artery wedge pressure dropped moderately with dopamine and significantly with SNP and combined drugs. The diastolic pulmonary artery pressure fell significantly with either drug and in combination. The stroke index increased significantly with dopamine and combined therapy. All patients survivied.
It is concluded that in post-open heart surgery patients with low output syndrome substantial hemodynamic improvement results with the combined use of dopamine and SNP more than with either agent alone.

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Previous reports from this laboratory have shown that penicillamine effectively reduces serum digoxin levels and is a clinically useful drug in correcting digoxin intoxication. To elucidate further the antidigitalis effects of penicillamine a prospective study was undertaken in 10 children aged 4-14 years with congestive heart failure. Plasma and intracellular erythrocyte concentrations of sodium, potassium, calcium as well as Na⁺/K⁺ and Na⁺/Ca⁺⁺ ratios were measured before digitalization, 6 days after full digitalization while the patients were on maintenance doses of digoxin (0.02mg/Kg/day, po, maximum 0.25mg/day) and 6 hours after 1Gm of oral penicillamine.
After digitalization RBC Na⁺, Ca⁺⁺, Na⁺/K⁺, and Na⁺/Ca⁺⁺ increased, whereas RBC K⁺ levels decreased significantly. Administration of penicillamine not only reduced serum digoxin levels, but it also caused significant alterations in RBC electrolyte concentrations, toward predigoxin values. All values were significantly changed after penicillamine. Plasma and RBC magnesium levels were not altered significantly, neither after digitalization nor after penicillamine. It is concluded that in addition to RBC Na⁺ and K⁺ levels, intra-erythrocyte levels of calcium are sensitive indicators of digoxin effect; and that penicillamine reverses digoxin-induced RBC electrolyte alterations towards pre-digitalization values.

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We measured the concentration of digoxin in sera of 136 patients by a radioimmunoassay during maintenance digoxin therapy. The serum digoxin concentration in patients with 0.25mg of tablet was compared with that with 0.25mg of powder produced by the same manufacturer to study the effect of digoxin form on serum digoxin concentration. Mean serum digoxin concentration in patients with 0.25mg of tablet per day was 1.34ng/ml, while in patients with 0.25mg of powder per day was 2.11ng/ml. Mean serum concentration was 1.23ng/ml in both preparations, if toxic patients were omitted. Mean serum digoxin concentration in 8 patients with a definite digoxin intoxication was 3.16ng/ml. Mean serum digoxin concentration in patients with 30mg/100ml or more of BUN was significantly higher than those with 20mg/100ml or less of BUN (p<0.001), but there was no significant difference in serum digoxin concentration between patients with and without high creatinine level. There was a significant negative correlation between the creatinine clearance and serum digoxin concentration. Mean serum digoxin concentration was significantly higher in patients with both digoxin and furosemide than those with digoxin only (p<0.01), and in patients with digoxin, furosemide, and spironolactone than in those with only digoxin (p<0.001). Serum digoxin concentration was elevated with advance of cardiac failure. There was no significant difference between the elderly (60 years or more) and the adult (less than 60 years old) groups in mean serum digoxin concentration. There was no difference between the 2 groups in prevalence of digoxin intoxication.

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Twenty-one patients with essential hypertension received a constant infusion of angiotensin II and des-aspartyl1-angiotensin II for 45min on 2 consecutive days during normal sodium intake. Des-aspartyl1-angiotensin II increased mean blood pressure from 127.5±17.7 to 142.3±18.8mmHg and plasma aldosterone concentration from 12.1±7.8 to 18.8±11.4ng/100ml. Although plasma aldosterone concentration elevation was positively correlated with pre-infusion levels of plasma renin activity (r=0.862, p<0.001), mean blood pressure elevation was inversely correlated with the values of renin activity (r=-0.599, p<0.01). In contrast, elevations of both plasma aldosterone concentration and mean blood pressure were inversely correlated with pre-infusion levels of plasma renin activity in angiotensin II infusion. Des-aspartyl1-angiotensin II and angiotensin II were equally effective in suppressing renin release. These data demonstrate that des-aspartyl¹-angiotensin II rather than angiotensin II plays an important role in aldosterone production in essential hypertension.

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The concentration of heparin in plasma was measured using a chromogenic substrate. It appeared that the measurement of heparin concentration in plasma was important in therapeutic control and evaluation of heparin. There was a correlation between the activated partial thromboplastin time (APTT) and heparin concentration in plasma, but since the gradients of regression line differed in each of the cases, measurement of APTT alone would give a different estimate of heparin concentration in each case. Fibrinopeptide A (FPA) is considered as the best indicator for evaluation of therapeutic effects of heparin. Therapeutic heparin concentrations were defined as ranging from 0.2 to 1.2IU/ml because the normalization of FPA was observed and there happened no hemorrhagic accidents in that range.

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Responses of the left ventricle to changes in afterload were tested in 11 open-chest dogs of which left atrial pressure was controlled arbitrarily. Maximal left ventricular dP/dt remained unchanged statistically against changes in afterload when left atrial pressure was kept constant, while it was changed with alteration of preload and by deterioration of left ventricular contractility induced by coronary ligation. Peak aortic flow velocity showed negative linear relationship against diastolic aortic pressure when left atrial pressure and left ventricular contractility were constant. This linear relation shifted downwards not only by reduction of contractility but also by lowering preload. Stroke volume also showed similar relationship, but abrupt decrease in stroke volume in higher range of aortic pressure. Effects of extracardiac factors on stroke volume which was ejected by constant ventricular contractility were considered to be complex.
Peak aortic flow velocity at 50mmHg of aortic diastolic pressure under the constant state of preload could be one of the indexes of ventricular function.

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Effects of temperature on atrial contractility were investigated on isolated, blood-perfused canine atrial preparations which were spontaneously beating or constantly paced at 2Hz and 2.5Hz. The contractility was increased by cooling from 37°C to 27°C in spontaneously beating hearts (the rate decreased from 100 to 56 beats/min) but in the paced atrium the increase of contactile force was followed by a slight decrease under 29°C usually with pulsus alternans. The durations of shortening and relaxation of the developed tension were increased in parallel with cooling of temperature. The rate of shortening was slightly increased by cooling in both spontaneous rate and constant rate. On the other hand, the rate of relaxation was not so influenced in spontaneously beating hearts but slightly increased in paced atria but not significantly.
The frequency-force relationship showed the positive staircase phenomenon (2 to 3.5Hz) at 37°C. However, at lower temperature the positive staircase was not clear and rather negative staircase appeared (1-3Hz).

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Because the mechanism of adverse reactions to abrupt cessation of propranolol in patients with coronary heart disease was an enigma, we studied the effect of cessation of propranolol on beta-adrenergic receptor reactivity to catecholamine stimulation. The cyclic AMP concentrations in plasma and left ventricular muscle after the administration of isoproterenol (5mg/Kg) were measured in rats before, during, 2 days after, and 4 days after of the administration of propranolol (5mg/Kg). Two days after withdrawal from propranolol, the cyclic AMP concentrations in plasma and left ventricular muscle were significantly increased (p<0.005, p<0.01). Four days after withdrawal from propranolol, the cyclic AMP concentration in plasma was significantly increased (p<0.001). On the other hand, that of left ventricular muscle showed a tendency to have higher value, although, this was statistically not significant. From these results, this study supports that there is a hypersensitivity to adrenergic stimulation after abrupt cessation of long-term propranolol treatment. The explanation of propranolol withdrawal phenomenon most likely lies in the nature of beta adrenergic receptors that become activated during long-term blockade.

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A rare type of congenital fistula between the right coronary artery and the right atrium, where fistula was draining just above the inferior vena caval orifice, is presented. Patient was operated on utilizing cardiopulmonary bypass and the fistulous opening into the right atrium was closed by interrupted ti-cron sutures supported with teflon pledgets. The benefits of using cardiopulmonary bypass in these operations or at least having it stand-by in the operating room are emphasized for safer closure of the fistula when needed.

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There have been a few reports of cardiac involvement in the Kugelberg-Welander syndrome. We presented a case of this syndrome complicated with cardiomegaly and conduction disturbance. The patient, a 21-year-old woman, had atrial standstill and A-V junctional rhythm. The chest X-ray film showed marked cardiomegaly. The His bundle electrogram revealed that H-V interval was 40 msec. She was treated with implantation of cardiac pacemaker.

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Primary aldosteronism usually shows mild hypertension and is characterized by suppression of plasma renin activity (PRA) and elevation of plasma aldosterone concentration (PAC). Almost all previously reported cases of malignant hypertension associated with primary aldosteronism showed low PRA.^3)-6) However, only I case which showed high PRA was reported by Baglin et al in 1973.²⁾ The patient reported below is the second case of primary aldosteronism with high PRA.
A 34-year-old man was admitted to our clinic because of severe hypertension, renal insufficiency, and papilledema. Both PRA and PAC were abnormally high, 4.6ng/ml/hr and 23.0ng/100ml, respectively. Serum cortisol levels and urinary catecholamine excretion were within normal ranges. Serum K was normal ranging from 3.6 to 4.9mEq/L. In spite of strong anti-hypertensive drugs, peritoneal, and hemodialysis, the patient died of pulmonaly infection about 3 months later.
Postmortem examination revealed a right adrenocortical tumor of 8mm in diameter. Histologically, the tumor consisted of large clear cells; that was adenomatous hyperplasia characteristic in primary aldosteronism. Neither juxtaglomerular tumor nor renal artery stenosis was found.
We thought that PRA in primary aldosteronism could rise with progress of renal involvement as secondary changes due to long-standing and untreated hypertension. Normal serum K could be explained by the fact that retention of potassium due to severely disturbed renal function exceeded its loss through aldosterone action. It must be kept in mind that normokalemia and elevated PRA can be encountered under these circumstances.

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A Björk-Shiley mitral valve prosthesis had to be replaced 4 years after implantation because of disc entrapment by an over-grown fibrous tissue on its sewing cuff. This abnormal fibrous tissue was found out to be an organizing platelet-fibrin deposit, of which luminal surface was only incompletely endothelialized. It is indicated that the heart valve prosthesis generally remains non-endothelialized for a prolonged period of time after implantation in man. Anticoagulation therapy should thus be given throughout the postoperative period for patients with the heart valve prosthesis.

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A case of a 3-month-old male infant with myocardial infarction due to left coronary ostial stenosis is presented. Clinically it was quite similar to anomalous origin of the left coronary artery. Aortogram demonstrated hypoplastic left coronary artery. Postmortem examination revealed quite narrow left coronary ostium and myocardial infarction with aneurysm of the left ventricular apex.

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An autopsy case of interruption of the aortic arch with distal type of aorticopulmonary septal defect which is located between the left posterolateral wall of the ascending aorta and the junctional portion between the right pulmonary artery and the pulmonary trunk was reported.

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