Clinical, hemodynamic, coronary arteriographic, and ventriculographic findings of 94 patients (pts) with coronary artery disease (CAD) and old myocardial infarction (MI) have been described and compared with those of 79pts with CAD and no previous MI.
Pts with old MI presented a more compromised functional and hemodynamic status, with a higher incidence of NYHA class III-IV pts (40%), symptoms of left ventricular (LV) failure (31%), cardiomegaly (70%), higher left ventricular end-diastolic pressure (LVEDP) (19.6±9.6mmHg; p<0.05), compared with 32%, 22%, 54% and 16.0±6.8mmHg respectively in CAD pts with no MI.
MI pts presented more severe CAD, higher incidences of three vessel disease (56%, p<.005) and of left anterior descending (LAD) (34%) and right coronary artery (RCA) (36%) occlusions, compared with 34%, 6%, and 9% respectively in pts with no MI.
Furthermore, pts with old MI showed more diffuse and severe LV segmental wall contraction abnormalities, with higher frequencies of LV aneurysm (31%) and of pts with asynergy of more than 2LV segments (26%), compared with 1% and 3% respectively in pts with no MI.
Within the group with old MI, LVEDP was higher in pts with anterior (A) (22.0±11mmHg, p<.02)and anterior+diaphragmatic (A+D) (21.5±7.9mmHg, p<.05) MI, compared with pts with diaphragmatic (D) MI (16.6±7.1mmHg); furthermore, LVEDP increase was significantly correlated with the severity and the extent of LV asynergy.
In A and D MI, LAD and RCA stenoses or occlusions were prevalent respectively; pts with A+D MI showed larger numbers of coronary stenosis (3.05) and occlusion (1.05) per patient. The coronary artery supplying the infarcted area showed stenosis (≥75%) in 95.6% and was normal in 2.2% of cases.
Thus, pts with CAD and old MI, and particularly of A+D and A MI, show a more compromised hemodynamic status and more severe degrees of CAD and of LV segmental wall contraction abnormality, which are responsible for their poor prognosis, compared to pts with CAD but no old MI.

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To assess whether echocardiography may represent a useful mean to evaluate the degree of mitral regurgitation (DR), left ventricular diastolic internal dimension (LVIDd), left atrial dimension (LAD), and velocity of circumferential fiber shortening (Vcf) were compared to DR assessed by left ventriculography in 48 patients with primary (n=21) and cardiomyopathic (n=27) valvular incompetence.
In patients with good left ventricular contractility, i.e. with Vcf values above 1.02, a significant positive linear correlation was found between LVIDd and DR (LVIDd=5.38+0.45DR; r=0.72; p<0.001). In contrast, in patients with depressed left ventricular function, i.e. with Vcf values below 1.02, LVIDd did not correlate to DR. In either group LAD and Vcf did not correlate to DR.
Thus, echocardiography may provide useful semiquantitative information concerning DR only in patients with preserved left ventricular performance.

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Pulsed Doppler echocardiography (PDE) was performed in 10 patients with Ebstein's anomaly and 10 cases of tricuspid regurgitation secondary to mitral stenosis.
Distal atrialized right ventricle (ATRV): In all patients with Ebstein's anomaly, tricuspid regurgitant flow was recognized by PDE. In this lesion with moderate tricuspid regurgitation, a widely dispersed dot pattern was recorded during systole. However, in the cases with severe tricuspid regurgitation a relatively smooth dot pattern was recognized. In the cases with marked delay in pressure rise in the right ventricle, PDE showed a bimodal regurgitant flow pattern. The interval between the onset of QRS and that of tricuspid regurgitant flow with right ventricular pressure rise was measured. The interval corrected for heart rate ranged from 0.10 to 0.35 with an average of 0.19±0.08 sec. In the subjects with secondary tricuspid regurgitation, it ranged from 0.07 to 0.11 sec. This interval was significantly prolonged in Ebstein's anomaly as compared to that in secondary tricuspid regurgitation (p<0.001).
Proximal ATRV: Tricuspid regurgitant flow was detected in 6 of 10 patients with Ebstein's anomaly. The disturbed flow was less apparent in the proximal ATRV than in the distal ATRV.

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A phonocardiographic study in a medium frequency range was made over various areas of the precordium in 27 cases of right bundle branch block (RBBB), 28 cases of left bundle branch block (LBBB), and 30 normal subjects of the same age. The various components of the first heart sound plus the pulses at the suprasternal notch and the right carotid artery were studied in regard to timing, relationship with the ECG and the arterial pulses, intervals between components, and amplitude.
The timing and intervals of the three components of the first sound were found normal in RBBB and so were the arterial pulses; apparent wide splitting was occasionally noted, due to recording of the first (a) and third (c) components, the latter being larger, as frequently observed in old age. All three components of the first sound were found small and delayed in LBBB; a delay of the arterial pulses was also noted. No additional component that might be attributed to the right heart preceded the delayed first sound.

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Systolic time intervals (STI) were measured non-invasively in 12 controls and 10 cases each with fever due to acute malaria, acute viral infection, typhoid fever, and fever induced by T.A.B. vaccine. Apart from tachycardia, no clinical feature of impaired cardiovascular function was present in any of the febrile cases. Abnormalities of STI were found in all febrile groups. Of the total 40 cases, only 18 showed normal STI, 2 cases showed decreased PEP/LVET indicative of hyperdynamic circulatory state, and 20 cases showed increased PEF/LVET suggesting the presence of subclinical impairment of myocardial function.

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In 30 patients with old anterior myocardial infarction, body surface isopotential maps were correlatively studied with left ventriculographic findings.
In 25 patients with ventricular asynergy restricted to the anterior segments, surface potential abnormalities due to infarction were observed during specific phases of QRS and in specific portions of the chest surface depending on the location and extent of severe ventricular asynergy (akinesis and dyskinesis). However, the remaining 5 patients with coexisting severe asynergy in the inferoposterior segment, showed body surface potential maps quite different from those of the above 25 patients.
It was suggested that body surface isopotential maps were useful in detecting the location and extent of ventricular severe asynergy in patients with old anterior myocardial infarction.

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To evaluate clinically the effects of coronary vasodilating drugs, isosorbide dinitrate (ISDN), dilazep (DL), and dipyridamole (DP), on the myocardial perfusion, quantitative analysis of Thallium-201 myocardial imagings was performed before and after their sublingual or oral administration in 17 patients with ischemic heart disease (IHD) and 9 normal volunteers.
The ratio of total myocardial blood flow to cardiac output (TMBF/CO) and the ratio of ischemic regional myocardial blood flow to cardiac output (RMBF/CO) were calculated according to the indicator fractionation principle. The ratio of radio-activity of infarcted region to total myocardium (R/T) was also calculated to judge the degree of scintigraphic defect objectively.
There were increases in TMBF/CO in 7 of 9 patients after ISDN, 4 of 5 patients after DL, and 2 of 6 patients after DP. Increases in RMBF/CO were observed in all patients studied after ISDN and DL, whereas in 2 of 6 patients after dipyridamole. Decreases both in RMBF/CO and R/T which suggest coronary steal phenomenon were observed in 4 of 6 patients after DP.
The myocardial imaging technic is a useful noninvasive method for clinical evaluation of coronary vasodilating drug.

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Fibrinolytic activity and plasmin inhibitor activity were determined by Blue Dextran-fibrin method in patients with acute myocardial infarction. The normal values of fibrinolytic activity and plasmin inhibitor activity were 3.34±0.74 units and 10.10±2.39 units (means±SD), respectively. The fibrinolytic activity in normal women (3.63±0.99 units) was slightly higher than that in normal men (3.17±0.79 units), but the plasmin inhibitor activity was not significantly different in the two sexes statistically. Neither activity varied significantly with age. The blood fibrinolytic activity was depressed in the first week after acute myocardial infarction, the decrease being maximal 3 to 4 days after the event (1.73±0.31 units). The mean plasmin inhibitor activity remained normal after acute myocardial infarction, but it was increased in 3, and decreased in 4 of the 7 patients in whom it was measured 3 to 4 days after the event.

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The surface morphology of the infundibular muscles obtained from open heart surgery was investigated in 10 patients with tetralogy of Fallot. Various degrees of abnormal surface morphological changes were observed from the endocardium to the myocardium. In the endocardium striking proliferation of the endothelial cells was usually accompanied by focal loss of the endothelium with fibrotic change. Based on the characteristic alterations of the surface morphology 4 different groups of myocardial cells could be identified: normal myocytes, defective myocytes, sclerotic myocytes, and necrotic myocytes. Because intact surface morphology is responsible for integrated cellular function these pathological findings observed on the surface morphology of the endocardium and myocardium can provide a valuable reference to further understanding of functional disorders of the infundibular muscle in patients with tetralogy of Fallot.

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The 26 year history of echocardiographic detection of pericardial effusion ideally demonstrates the scientific method. The initial observations by Edler and Hertz in 1954 lead to animal experiments by Feigenbaum and Soulen many years later. Human applications were confirmed again and again with cardiac catheterization, surgery, autopsy and radiologic procedures. Older methods of effusion detection were compared to this new and noninvasive method and found lacking. Echocardiography has been a safe, reliable and accurate method to establish the presence of pericardial effusion in the symtomatic and asymtomatic patient. It has been used as the diagnostic standard for other detection methods. Investigators and clinicians are now utilizing echocardiography to explain cardiac physiology when pericardial effusion is present; and to follow the effects of their therapeutic interventions. While the presence of pericardial effusion has proven to be more prevalent than expected, the pathologic and hemodynamic significance of unsuspected effusion has not yet been established. Experimental and clinical studies are continuing with the aid of computerized technology for data retrieval and analysis. Thousands of patients are examined yearly with echocardiography and their statistics roll from the pages of scientific and clinical publications. The world's literature is at one's fingertips. But-the echocardiogram and its derived data are only as good as the knowledge and skill of the examiner, technologist and physician alike who "… must understand the physics of ultrasound, the operation of a complex electronic instrument, the nature of intracardiac anatomy, and clinical cardiology as well as echographic manifestations of normal and disease conditions. Information can seldom be extracted retrospectively from the echocardiogram that was not deliberately depicted at the time of the examination.
More than a quarter of a century has honed present day skills to record and interpret echocardiographic tracings of pericardial effusion. Yet, it is sobering to consider how primitive our best efforts are compared to methods still unknown which will be used by technologists and physicians fifty years from now.

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This study was performed to investigate the prophylactic effect of disopyramide phosphate on ventricular fibrillation in acute myocardial infarction. Lidocaine and disopyramide phosphate were compared in terms of their effects on the lowered ventricular fibrillation threshold in experimental myocardial infarction produced by coronary ligation in dogs. The following results were obtained:
1) The effect of lidocaine i.v.+infusion appeared promptly and the ventricular fibrillation threshold exceeded control levels from 45min onwards (p<0.01).
2) The i.m. injection of lidocaine was effective in a dose of 10mg/Kg. The minimally effective blood level was 1.7mcg/ml.
3) Disopyramide phosphate 5mg/Kg i.v. produced a tendency towards recovery from 15min onwards. After 30min, the ventricular fibrillation threshold was significantly higher than control (p<0.01).
4) Disopyramide phosphate 5mg/Kg i.m. was initially effective after 45min. The effect was significant from 1 hour and 30min onwards, compared with control (p<0.01). The minimally effective blood level was 2.4mcg/ml.
5) Disopyramide phosphate 2mg/Kg i.m. produced a tendency towards recovery but the difference from the control was not significant.
6) In equivalent i.m. doses, disopyramide phosphate tended to be more potent than lidocaine in increasing the ventricular fibrillation threshold.
7) In the aforementioned doses, disopyramide phosphate did not cause any marked changes in PQ interval or QT time in ECG.
These results suggest that the intramuscular injection of disopyramide phosphate is a hopeful clinical treatment to prevent ventricular fibrillation in the very early stages of acute myocardial infarction.

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Acute ligation of the left coronary artery of rats produced abnormal Q-wave in the electrocardiogram, tachycardia and frequent ventricular fibrillation. Serum CPK level was elevated, reaching a maximum at 3 to 5 hours after ligation and returning to near the pre-ligation level 24 hours later, when CPK activity in the left ventricle markedly decreased. Pretreatment with bucumolol at 2.5mg/Kg s.c. and 5mg/Kg s.c. lessened these changes and increased the survival rate in a dose related manner. d-Bucumolol at 5mg/Kg, on the other hand, increased survival rate primarily by suppressing ventricular fibrillation without any significant effect on other parameters. These results suggest that the membrane stabilizing action does not contribute to protective actions of bucumolol against myocardial ischemia.

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The effects of prednisolone and anti-macrophage serum (AMS) on the development of cardiac and articular lesions were compared in experimentally infected mice with group A hemolytic streptococci. The predonine^®-treated mice had a higher mortality rate and greater abscess formation than in the AMS-treated mice. The predonine^®-treated group had a higher incidence of cardiac lesions due to chronic pericarditis and chronic myocarditis, and the former was particularly frequent. Pathologic findings seen in the AMS-treated mice were those of acute pancarditis. The AMS-treated animals also had lesions of subacute or chronic arthritis, whereas articular lesions encountered in the Predonine^®-administered group were frequently those of chronic periarthritis and, in no instance, synovitis. These data indicated that treatment with AMS is more effective than that with prednisolone to experimentally induced rheumatic fever in laboratory animals.

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Comparative effects of heart rate and aortic blood pressure on myocardial oxygen consumption (MVO₂) were studied in anesthetized openchest dogs. The left coronary artery was perfused through the external shunt with blood from the left common carotid artery. Heart rate was changed with the left atrial pacing and the constriction of the descending thoracic aorta was utilized to elevate the proximal aortic blood pressure (BP). The left ventricular enddiastolic pressure was insignificantly changed with the atrial pacing and with the aortic constriction. With the constant BP (100±5mmHg), an unit increase in heart rate per minute augmented MVO₂, by 0.027ml/min/100Gm of left ventricular muscle, while one mmHg elevation of BP caused 0.15ml increment in MVO₂ per minute per 100Gm of left ventricular muscle under the conscant heart rate (115±5beats/min). Therefore an unit change in BP caused five-to six-fold greater increase in MVO₂ compared with that in heart rate, indicating extremely important roles of BP in MVO₂.

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Effect of sodium intake on angiotensin-converting enzyme activity was studied in five areas of the brain (cerebral cortex, midbrain, striatum, thalamus and hypothalamus) and in subcellular fractions of the aorta (homogenate, mitochondria, microsomes and supernatant) in normotensive, spontaneously hypertensive, and stroke-prone spontaneously hypertensive rats. Angiotensin-converting enzyme activity was significantly higher in the hypothalamic area than in the other areas of the brain in spontaneously hypertensive rat. The enzyme activity of subcellular fractions of the aorta showed an extremely high value in the supernatant in normotensive, spontaneously hypertensive, and stroke-prone spontaneously hypertensive rats. Sodium intake resulted in a marked decrease in the aortic converting enzyme activity, while it did in a significant rise of the enzyme activity in the midbrain area in spontaneously hypertensive rat, and in the midbrain and striatum areas in stroke-prone spontaneously hypertensive rat. It is likely therefore that sodium intake lowers the converting enzyme activity of the aorta. Increased converting enzyme activity of the brain in spontaneously hypertensive rats may play a possible role in hypertension induced by sodium intake.

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Lipids from erythrocyte membranes of normal and cholesterol fed animals were isolated and the various fractions were analyzed quantitatively. Erythrocyte membrane lipid composition of animals fed with an atherogenic diet for 2 months revealed marked elevations in cholesterol followed by significant alterations in phospholipids, free fatty acids and triglycerides. These findngs were discussed from the point of view of the role of membrane lipids in the maintenance of cell integrity, shape, and homeostasis.

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We report a case of recurrent pulmonary thromboembolism with echocardiographic findings, documenting the occurrence, resolution and recurrence of pulmonary hypertension with right ventricular pressure and volume overload.

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Triphasic dove-coo murmur in a patient with aortic regurgitation was studied as to the mechanism of its generation using simultaneous recording phonocardiography and dual echocardiography. The murmur arose coincident with the coarse regular fluttering of aortic posterior wall during the opening of mitral valve and decreased coincident with the protrusion of mitral valve anterior leaflet into the left ventricular outflow tract. Thus the murmur might occur, provided that normal mitral valve opening and closure was maintained. It may well explain why the murmur hardly occurs in aortic regurgitation of rheumatic origin in which rheumatic lesion often is thought to involve mitral valve, restricting mitral opening during diastole and thereby inhibits aortic root vibrations.

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