The extremely prominent negative U wave occasionally appears during a cardiac attack in variant angina pectoris. The clinical profile of the negative U wave was therefore studied in 80 patients with variant angina pectoris (VA) and 33 controls with resting angina pectoris (RA). The prominent negative U wave appeared in 55 of the patients with VA (68.8% of patients) and in 10 of the patients with RA (30.3%); thus, there was a significant difference in the appearance of the wave between the 2 groups of patients (p<0.001). The leads in which the negative U wave appeared were mostly consistent with those in which the ST segment was elevated. The negative U wave began to appear at about the time when ST-segment elevation began to improve; the wave then gradually became very prominent and then eventually disappeared. The patients with VA and also those with RA on whose ECGs the negative U wave appeared during exercise testing also had negative U waves during spontaneous episodes of angina. An investigation of the frequency of appearance of ST deviation and negative U waves during exercise testing, regardless of the type of angina pectoris, disclosed that the negative U wave appeared in 14 of 20 patients with ST-segment elevation (70% of patients), while the negative U wave appeared in only 52 of 519 patients with either no ST change or ST-segment depression (10.4%); thus, there was a significant difference in the appearance of the negative U wave between these 2 groups (p<0.001). Coronary cinearteriography failed to disclose any apparent difference between the appearance of the negative U wave and the presence of stenosis. The prognosis of VA and RA in patients with negative U waves was less favorable compared to those without negative U waves. In particular, we noted that of the 10 patients with RA associated with negative U waves, 4 died. Although the mechanism of the negative U wave is not yet known, we believe that the above findings contribute to its elucidation.

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Vectorcardiograms of paced and unpaced beats were recorded from 18 patients with implanted pacemakers to investigate the characteristics of post-pacing T inversions. The intraventricular conduction during sinus rhythm of unpaced beats was normal in 13 of 18 patients and abnormal in the other 5 (RBBB in 3, LBBB in 2).
The directions of the maximum QRS vector in paced beats (max QRSp.V) and maximum T vector in unpaced beats (max T unp.V) were studied. In 8 of 13 patients with normal intraventricular conduction (group A) and in 3 patients with right bundle branch block (RBBB), the differences between the directions of max QRSp.V and max T unp.V in both frontal and horizontal planes were less than 30 degrees, and in 5 of 13 patients with normal intraventricular conduction (group B) and 2 patients with left bundle branch block (LBBB), differences exceeded 30 degrees. The direction of max T unp.V tended to be superiorly, posteriorly and to the right regardless of max QRSp.V direction.
The similarity in direction of max QRSp.V and max T unp.V supports the hypothesis by Rosenbaum et al that post-pacing T inversions may be, in part, explained on the basis of 'cardiac memory'. However the absence of correlation between the max QRSp.V and max T unp.V suggests that the post-pacing T inversions may be caused by other unknown mechanisms.

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The myofibrillar ATPase activity and pyrophosphate gel electrophoretic pattern of native myosin of fresh human left ventricular papillary muscles were examined in 52 cases of mitral valve replacement.
The myofibrillar ATPase activity of hypertrophied myocardium did not differ from that of non-hypertrophied myocardium (mean±SD, 36.2±8.7 vs 31.8±8.6nmolPi/mg/min, ns) and there was no significant difference in myofibrillar ATPase activity as a function of left ventricular enddiastolic pressure. Pyrophosphate gel electrophoresis of myosin revealed the presence of two components. It is questionable whether the component of higher electrophoretic mobility (approximately 25-35% in concentration) is identical with rat ventricular myosin VM-1 because an increase in this component seems to correlate with a decrease of myofibrillar ATPase activity, its concentration was significantly higher in the hearts with left ventricular hypertrophy, high enddiastolic pressure, high aortic pressure or low cardiac index.
From these results, it is not necessarily clear whether hemodynamic overload in valvular heart diseases can alter left ventricular myofibrillar ATPase activity, but it can be said that the overload influences the concentration of the two components of native myosin revealed by pyrophosphate gel electrophoresis.

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Right ventricular volume measurements and hemodynamic studies were performed in 20 patients after total correction of tetralogy of Fallot. There were 6 patients with an extracardiac conduit and Hancock xenograft (G-1), 8 with an outflow tract patch (G-2) and 6 without or with a minimal right ventriculotomy and repair of pulmonary valve (G-3). The age at the time of operation was over 3 years in each patient and averaged 5±2 (mean±SD) years. Right ventricular systolic pressure averaged 81±22, 55±22 and 58±30mmHg in G-1, G-2 and G-3, respectively. Right ventriculography showed no contraction of the right ventricular free wall at the anastomosis to the conduit and poor contraction around the anastomosis in G-1. The right ventricular enddiastolic volume index (RVEDVI) was 114±31, 155±57 and 115±28ml/m² in G-1, G-2 and G-3, respectively. The right ventricular ejection fraction (RVEF) was 0.42±0.11 in G-1, 0.53±0.04 in G-2 (p<0.05, vs G-1) and 0.57±0.04 in G-3 (p<0.02, vs G-1). Pulmonary regurgitation was evident in 17 patients, and RVEDVI correlated well with degrees of pulmonary incompetence.
Fourteen patients in G-2 and G-3 were divided into G-A and G-B to evaluate right ventricular function with or without pressure overloading of the right ventricle. G-A consisted of 7 patients with a right ventricular systolic pressure of more than 50mmHg (74±26) and G-B of 7 patients with a value less than 50mmHg (39±4). There was no difference in RVEDVI and RVEF between G-A and G-B. RVEF was significantly lower in G-1 than G-A (p<0.02) and G-B (p<0.05).
These results suggested that an extracardiac conduit with Hancock xenograft reduced the contraction of the right ventricular free wall and induced a depressed right ventricular pump function in patients with a high right ventricular pressure.

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Clinical and pathological findings in 15 autopsy cases, 13 males and 2 females, confirming cardiac free wall rupture after AMI were reported. The incidence is 30.6% of all autopsy cases of AMI in Chinese PLA General Hospital from 1958 to 1979.The ages ranged from 46 to 79 years, 10 being above 60 years. For 73.3% it was the first AMI and 66.7% of the patients had a history of hypertension. Thirteen of the 15 patients died within 5 days after the onset of AMI and another 2 within 7 days. When the cardiac rupture occurred, the ECG generally showed bradycardia, AV-junctional rhythm, III° AV block or isorhythmic ventricular rhythm and cardiac arrest.
Both the gross and microscopic AMI were examined in 13 cases. All of them had a septal infarct, but only 2 had an ECG diagnosis. Of the 6 patients with inferior MI on EGG, 5 had right and left coronary lesions worse than grade III.
The effective prevention of cardiac rupture consists of early diagnosis, control of chest pain and vomiting, prevention or treatment of hypertension or hypotension and 1 to 2 weeks of bed rest after the onset of AMI.

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Blood pressures (BPs) were measured with standardized sphygmomanometers in 434 Japanese boys and girls living in the town of Hisayama. Simultaneously, data on pulse rate, weight and height were obtained. Out of the original 434 subjects, data were obtained repeatedly for 5 years in 280 subjects. BP levels were significantly correlated with weight in those aged 14-15 and also 19-20 years, but correlation coefficients were small. During the 5-year period, the mean systolic and diastolic blood pressure (SBP & DBP) increased significantly in both sexes, but the increments were greater in boys. Both SBP and DBP at 14-15 years of age were significantly correlated with data taken 5 years later for both sexes, and subjects with a higher initial BP (more than 90th percentile of the distribution) tended to have a higher BP after 5 years. SBPs after 5 years were independently correlated with initial SBP levels and changes in QI (D-QI) in both sexes. On the other hand, DBPs after 5 years were independently correlated with initial DBP levels and height for boys, and initial DBP levels and D-QI for girls.

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Red cell sodium (R-Na), potassium (R-K) and sodium to potassium ratio (R-Na/K) were studied in 2, 542 adults participating in periodic medical examinations. The mean values of R-Na and R-Na/K in untreated borderline (n=406) and definite hyper-tensives (n=485) were higher than those in normotensives (n=1, 651), but that of R-K was not different among the groups. The increased R-Na and R-Na/K in the hypertensives were observed only in those under 50 years, but not in those 50 years and over. In the normotensive subjects, age and sex affected the intraerythrocyte cation contents, but a positive family history of hypertension did not. Although a few characteristics correlated with both R-Na and mean blood pressure, and with both R-Na/K and mean blood pressure, multiple regression analyses revealed that R-Na and R-Na/K independently and significantly contributed to the variation in mean blood pressure. It was also indicated that these relations of R-Na and R-Na/K to mean blood pressure were significant in those under 50 years, but not in those 50 years and over. While several characteristics confound the relationships between red cell cation contents and blood pressure, these results suggest that the contributions of R-Na and R-Na/K to the mechanisms of human hypertension still persist in young to middle-aged people.

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As both hormonal and hemodynamic alterations similar to those occurring during exercise can also be produced in humans by hypoglycemia, the present study explored changes in hemodynamic parameters during hypoglycemia and the effects of the al-adrenergic blocker, prazosin, on those responses in hypertensive patients. In the control group, which did not receive prazosin, plasma epinephrine, plasma norepinephrine and plasma renin activity (PRA) all increased along with a rise in blood pressure during hypoglycemia. On the other hand, the blood pressure decreased despite similar increases in plasma catecholamine levels and PRA in the prazosin treated group. The hemodynamic parameters, analyzed using M-mode echocardiography, changed in both the control and prazosin groups during hypoglycemia; stroke volume and cardiac output showed similar increases. However, while the total peripheral resistance did not change significantly in the control group, it decreased in the prazosin group during hypoglycemia. In accord with the changes in total peripheral resistance, the increment in mean-velocity of circumferential fiber shortening (m-Vcf) during hypoglycemia was greater in the prazosin group than in the control. These results suggest that: 1) hypoglycemia stimulates the sympatho-adrenal axis which then releases catecholamines leading to a rise in blood pressure and tachycardia; 2) In contrast, the blood pressure decreases during hypoglycemia in the prazosin group despite an increase in plasma catecholamines, because the α-receptors are blocked by prazosin and the unopposed β-adrenergic effects of the catecholamines are pronounced enough to reduce the total vascular resistance.

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The effects of dopamine and dobutamine on release of norepinephrine from normal and ischemic myocardium were compared in 2 groups of open-chest anesthetized dogs. Both agents were infused intravenously at a rate of 10μg/Kg/min for 2 hours, beginning 40min after snare occlusion of the left anterior descending coronary artery. There were no major differences in hemodynamic responses between the 2 groups. Blood samples were taken simultaneously from the aorta, coronary sinus and the cardiac vein that ran parallel to the left anterior descending coronary artery before and after coronary artery occlusion. Plasma norepinephrine increased 40min after the occlusion, with a net efflux in both coronary sinus and cardiac venous blood. Dopamine caused further increases in plasma norepinephrine. At 20min after the beginning of dopamine infusion the coronary sinus concentration (4.09±1.36ng/ml) was significantly greater than the arterial concentration (2.84±0.87ng/ml). This transcardiac difference disappeared during continuous infusion 2 hours after coronary artery occlusion. Differences in norepinephrine concentration between the arterial and cardiac venous blood, however, were not significant. In contrast, plasma norepinephrine did not increase during dobutamine infusion in either the ischemic or non-ischemic bed. Thus, the results suggest that while these two agents have similar systemic hemodynamic effects, only dopamine increases myocardial release of norepinephrine from either ischemic or normal myocardium during acute myocardial infarction.

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We used standard microelectrode techniques to study the histamine induced or enhanced delayed afterdepolarization (DAD) and triggered activity (TA) of guinea-pig papillary muscle superfused with low-potassium Tyrode's solution. Before histamine, a series of driven action potentials did not induce DAD and TA. Immediately after histamine (10^-5M), DAD was induced and, finally, TA was induced after high rate pacing (150/min to 300/min). The effect of histamine was antagonized by cimetidine (5×10^-6 to 5×10^-5M) but not by diphenhydramine. Also, the amplitude of DAD decreased after verapamil (10^-7 to 3×10^-6M) and lidocaine (4×10^-5 to 8×10^-5M). To investigate indirect evidence of increased cyclic AMP mediation in this histamine induced DAD, we studied the effects of a phosphodiesterase inhibitor (papaverine 10^-5M) or activator (N-methylimidazole 20mM) on the histamine induced or enhanced DAD. The former enhanced and the latter depressed the histamine-induced (or enhanced) DAD. Thus, histamine may induce or enhance the DAD and TA by increasing the slow inward current. This mechanism may be mediated by histamine H₂-receptors and the adenylate cyclase system in the cardiac ventricular muscle.

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We studied the mechanisms of ST segment displacement in the ECG recorded from the epi- and subendocardium of ischemic ventricles in the isolated and perfused canine heart. ST segment changes were observed in association with a relatively large area of ischemia produced by occlusion of the left anterior descending and septal arteries (LAD+Sept.) or of the left circumflex artery (LCx).Contrary to previous reports, we found that the amount of subendocardial ST elevation was not always greater than that in the epicardial ECG recorded at the center of ischemia. Also, in the non-ischemic area, the degree of the ST depression in the subendocardial record was nearly the same as the epicardial record. On the other hand, the degree of the epicardial ST elevation on the border zone was always smaller than that at the ischemic center, which seemed to be due to the broadness of the border zone. The amplitude of the ST depression in the non-ischemic area was greater when the recording electrode was near the ischemic border, which supports the solid angle theory. The degrees of both ischemic ST elevation and reciprocal ST depression in the LCx perfused area were always greater than in the LAD+Sept. perfused area. These results strongly suggest that ST segment displacement depends on the relative position of the recording electrode to the electric double layer which exists at the border between the ischemic and non-ischemic area.

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The efficacies of MDL 17043 and MDL 19205 in ameliorating heart failure were assessed in dog heart-lung preparations in which cardiac function had been severely depressed by pentobarbital. Six preparations were used for each drug. Both drugs in doses of 1-30μmol similarly improved cardiac function in adose-dependent manner and at 30μmol improved it beyond control values. AV conduction impaired by pentobarbital was restored by 30μmol of the 2 drugs. In these doses, however, neither of the drugs produced a significant increase in heart rate or arrhythmias. These results indicate that the 2 drugs would be of use in the treatment of heart failure.

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To elucidate the mechanisms of the beneficial hemodynamic action of nifedipine in congestive heart failure, the systolic and diastolic hemodynamic parameters were evaluated for 30min after sublingual administration of 20mg of nifedipine in 12 dogs with acute mitral regurgitation (group 1) and in 5 dogs without mitral regurgitation (group 2, sham operation group). An additional 6 dogs with mitral regurgitation were followed for 30min without nifedipine (group 3).
Nifedipine lowered both arterial pressure and systemic vascular resistance, increased coronary blood flow and stroke volume significantly in both groups 1 and 2. The left ventricular developed tension was increased by nifedipine only in group 1, probably due to the geometric changes in the expanded left ventricle in failure, secondary to left ventricular preload and afterload reduction. Nifedipine had no effects on ventricular relaxation properties in this study.

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Regional myocardial blood flow during exercise was determined using the thermodilution technique in 2 patients suffering from both spontaneous and exertional chest pain.
In both cases we observed that effort-related anginal attacks were due to coronary spasm with sudden reduction of regional left ventricular blood flow. In 1 patient the exercise-induced ST-segment elevation in the anterior leads was accompanied by a reduction of flow in the great cardiac vein. In the second patient the exercise-induced ST-segment depression in the lateral leads was accompanied by a reduction of coronary flow in the area supplied by the circumflex artery. In 1 patient, nifedipine was effective in prolonging exercise tolerance by preventing the occurrence of coronary spasm and by increasing blood supply to the ischemic region during exercise.

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Rapid cyclic fluctuations of blood pressure in patients with a pheochromocytoma have rarely been reported. The suitable conditions to induce this phenomenon are not adequately known. We report here a patient with an adrenal pheochromocytoma who showed this phenomenon after oral administration of labetalol.

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A patient with the Marfan syndrome and echocardiographic and angiocardiographic evidence of hypertrophic cardiomyopathy is presented. Endomyocardial biopsy was performed. Histologic abnormalities of the endomyocardium noted in this patient were considered to be related to the basic generalized connective tissue abnormality, and the patient subsequently developed myocardial disease compatible with hypertrophic non-obstructive cardiomyopathy. We believe that this case emphasizes the possible coexistance of subclinical myocardial disease in patients with the Marfan syndrome.

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