Autopsy study of 60 cases of rheumatic heart disease is presented, demonstrating an increased incidence of panvalvulitis in our series. The presence of Aschoff bodies is correlated with the clinical and laboratory parameters of activity and their significance is discussed.

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Histo-morphological changes of the coronary vessels in cases of rheumatic heart disease (RHD) have been studied in 60 cases.
Involvement of intramyocardial branches of coronary vessels in the form of active rheumatic vasculitis or inactive lesions characterized by medial hypertrophy and replacement fibrosis was seen in 15 of 60 cases. These lesions may affect myocardial function. Atherosclerosis of the pulmonary trunk and its branches was frequently seen in these hearts, indicating that this may be an important index of pulmonary hypertension. An unusual association of bicuspid aortic stenosis and RHD was seen in one case. Another case showed acute myocardial infarction due to coronary embolism from bacterial vegetation of bacterial endocarditis.

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In order to clarify the clinical significance of a persistent negative U wave in patients with myocardial infarction, the clinical features and prognosis of a group of such patients were compared with a group without negative U waves. The persistent negative U wave was defined as the presence of a negative U wave at the time of discharge. The subjects were classified into 2 groups: group A-55 patients (50 males and 5 females, 59±10 years) with negative U waves; group B-70 patients (55 males and 15 females, 61±9 years) without negative U waves. The average follow-up periods were 49±21 months in group A and 42±18 months in group B. Negative U waves appeared in leads where r or R waves were present, but were not observed in leads with a QS pattern. The incidences of a diseased left anterior descending artery, multi-vessel disease, left ventricular wall motion abnormality and left ventricular ejection fraction below 50% were higher in group A than in group B. The recurrence of myocardial infarction was 18.2% in group A and 7.1% in group B, and the number of patients treated with antianginal drugs was higher in group A than in group B. The rate of recurrence of myocardial infarction at 1, 3 and 5 years was 6%, 17% and 26%, respectively in group A and 6%, 8% and 11%, respectively in group B. Thus, it was concluded that patients in group A require more active treatment than those in group B.

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The effects of mild aerobic exercise on serum lipids, apolipoproteins and lecithin-cholesterol acyltransferase (LCAT) activity were examined in 11 male patients with coronary artery disease and 4 healthy male controls. The mild aerobic exercise program involved exercise intensity at 50% of maximal oxygen uptake, as determined from the blood lactate threshold, for 60min periods 3 times per week for 10 weeks. Following mild aerobic exercise, serum levels of high density lipoprotein cholesterol (HDL-C) were increased significantly from 50±7mg/dl to 59±11mg/dl (p<0.05) with a simultaneous increase in apolipoprotein A-I (apo A-I) in normal controls. The LCAT activity was significantly increased from 65±22nmol/ml/hr to 99±30nmol/ml/hr in normal controls (p<0.05). Furthermore, maximal oxygen uptake (VO₂max) was significantly increased in normal controls. In contrast, no significant changes were found in HDL-C, apo A-I, apo B, VO₂max and body weight in patients with coronary artery disease. There was significant correlation between the initial HDL-C level and the change in HDL-C level following the exercise program in the combined group of normal controls and patients with coronary artery disease.

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Left ventricular (LV) functions as reflected in systolic time intervals (STIs) were studied in 28 patients with chronic renal failure (CRF) and in an equal number of age and sex matched normal controls. Measurement of STIs revealed that mean total electromechanical systole (QS₂) and left ventricular ejection time (LVET) were significantly decreased, whereas isovolumic contraction time (IVCT) was significantly increased in patients with CRF as compared to controls. Mean PEP/LVET ratio did not show any significant change. Eleven cases of CRF had congestive heart failure, and in 9 of them the PEP/LVET ratio was normal. Seven cases of CRF had evidence of left ventricular dysfunction (PEP/LVET>0.4). In 6 cases, STIs were also recorded following dialysis, and revealed an increase in PEP, IVCT and PEP/LVET and a decrease in QS₂ and LVET, but none of these changes were statistically significant. It is concluded that only a small percentage of cases of renal failure show LV dysfunction. However, signs of congestion are seen in a greater number of cases. These are not necessarily indicative of LV dysfunction but may be due to fluid and electrolyte overloading.

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The physiological mechanism regulating secretion of human atrial natriuretic polypeptide (hANP) was examined by measuring plasma hANP by a specific radioimmunoassay during head-out total body water immersion (WI) and saline infusion in normal men. Seven healthy men were immersed in water for 1 hour, 6 normal men and women were given an infusion of 1 liter of normal saline over 1 hour and 8 normal men were given a similar infusion over 2 hours. During WI, the urinary volume (UV) and urinary Na excretion (UNaV) increased significantly, and the plasma hANP level increased significantly from 246±12 (mean±SE) pg/ml to 392±32 pg/ml after 35±5min, but returned to the basal level after 90min. The increase in hANP level was correlated with an increased UNaV between 30 to 60min during WI. The plasma norepinephrine, renin activity, aldosterone and cortisol levels also decreased during WI. Saline infusion caused variable increases in the hANP level: the mean peak values of hANP and times of the peaks from the start of saline infusion were respectively 305±30 pg/ml after 30±3min of infusion at a rate of 1L/1 hr and 285±25 pg/ml after 69±15min of infusion at a rate of 1L/2 hrs. The time of the peak of plasma hANP during infusion at lL/2 hrs was significantly longer than the peaks for WI or an infusion of saline at 1L/1 hr. Moreover, the peak hANP level was significantly smaller during either condition of saline infusion than during water immersion. These results indicate that i) acute central hypervolemia caused by WI increases hANP secretion, and this increase may participate in natriuresis during WI, and ii) saline infusion causes an increase in plasma hANP of variable magnitude, the increase being more rapid for a more rapid infusion of saline. This suggests that hANP is released into the circulation by acute volume expansion and plays a physiologically important role in maintaining blood volume homeostasis in man.

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To investigate the mechanisms of polyuria associated with tachycardia, we measured plasma concentrations of α-human atrial natriuretic polypeptide (α-hANP) and cGMP in 6 patients with paroxysmal tachycardia. Plasma concentrations of immunoreactive α-hANP and cGMP increased by +69% (p<0.05) and +100% (p<0.05), respectively, during both paroxysmal atrial tachycardia and atrial fibrillation. To examine whether tachycardia per se raises the secretion of α-hANP, we also determined plasma concentrations of α-hANP and cGMP in 5 patients during rapid atrial pacing. The pacing-induced tachycardia also increased both of the plasma concentrations. Further, the examinations of cardiac and renal functions in patients with complete atrioventricular block during rapid pacing revealed that each of the increases in atrial pressures, urinary sodium excretion and creatinine clearance were in parallel with the change in plasma concentration of α-hANP. These results suggest that an increase in plasma concentration of α-hANP during paroxysmal tachycardia is mainly due to elevation of atrial pressure and that this increase in α-hANP contributes to tachycardia polyuria.

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The analgesic, hemodynamic and respiratory effects of buprenorphine (0.3mg i.v.) were monitored in 15 coronary care unitadmitted patients presenting with myocardial infarction who were in functional class I according to the Killip classification. At the time of the study, 8 of them had unequivocal precordial pain (group 1); the remaining 7 were painfree (group 2). The agent showed a prompt and potent analgesic action. It also induced a slight decrease in mean aortic pressure associated with a reduction in systemic vascular resistance and an increase in cardiac index, a rise in the pulmonary arterial pressure and arteriolar resistance and right atrial pressure, a reduction in arterial pO₂, and pH and an increase in pCO₂. Tension-time-indices of the left and right ventricles varied in parallel with variations in aortic and pulmonary artery pressure, respectively. These responses were probably unrelated to analgesia since they were similar in groups 1 and 2. Changes in systemic circulation were such as to possibly decrease the contractile effort and the oxygen need of the left ventricle and the size of infarction. On the contrary, the rise in pulmonary arterial pressure imposes a hemodynamic burden on the right ventricle that, depending on the patient's condition, may assume clinical importance. It is felt that the use of buprenorphine in myocardial infarction should be restricted to uncomplicated and selected cases.

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Changes in hemodynamic variables regulating systolic function were examined by M-mode echocardiography in 14 patients with long-duration primary uncomplicated hypertension treated with nitrendipine once daily (20mg). At the end of treatment (8th week) blood pressure and peripheral resistance were greatly reduced (p<0.0001), while the indices of cardiac function (ejection fraction and cardiac index) showed significant increases (p<0.01). The variations in ejection fraction were analyzed by multiple linear regression and were mainly influenced by the decrease in end-systolic stress (contribution: 60%). At baseline, despite no radiographic or clinical signs of heart failure, 6 of the studied patients showed impaired systolic function, likely due to the strength of other variables (age, risk factors); in those patients, systolic function was clearly enhanced at the end of treatment, while no change was found in patients with initial normal pump function. Changes in cardiac output were due toasignificant increase in heart rate in patients with normal pump function and to improved stroke volume in the others. Left ventricular mass index was slightly reduced (p<0.005), primarily because of the reduction in end-diastolic volume (p<0.01). When analyzed by the 2 subgroups (with or without impaired systolic function), the left ventricular mass index appeared to be significantly reduced only in those patients with normal basal pump function. This difference was most likely due to the different effects of treatment on enddiastolic volume.

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The enzyme level profiles of some regulatory enzymes and the isozyme patterns of some marker enzymes in bovine adult specialized, adult ordinary and fetal ordinary heart muscles were examined in order to biochemically characterize specialized heart muscle.
The activities of hexokinase, phosphofructokinase and glucose-6-phosphate dehydrogenase in adult specialized heart muscle were significantly higher than those in adult ordinary heart muscle, but were similar to those in fetal ordinary heart muscle. The carnitine content and carnitine acetyltransferase activity in adult specialized heart muscle were lower than those in adult ordinary heart muscle. The isozyme patterns of creatine kinase, fructose-bisphosphate aldolase and pyruvate kinase in adult specialized heart muscle resembled those in fetal ordinary heart muscle. These results indicate that adult specialized heart muscle has the biochemical characteristics of fetal ordinary heart muscle.

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Vitamin E (E) and selenium (Se) are important antioxidant nutrients, preventing membrane damage by lipid hydroperoxides. In a previous study on E+Se deficient rats it was shown that plasma levels of lipoproteins increase dramatically. In continuation of this study a quantitative microscopic study was undertaken to determine the behavior of myocardial interstitial tissue space (ITS) in E+Se deficient rats as compared to control rats. Four rats fed on normal laboratory chow and 8 rats fed on basal diet supplemented with adequate E+Se served as control. Eight rats were fed on E+Se deficient diet. The animals were sacrificed after 13 to 20 weeks. Qualitative microscopic study showed patchy areas of hemorrhage, edema, infiltration of macrophages and myocardial damage consisting of pyknosis and coagulation necrosis in the deficient rats. Quantitative microscopic study of the apparently normal areas of myocardium of deficient rats showed a shrinkage of ITS (21.0±1.29% vs 16.51±4.62%, α=0.01), whereas the ITS of normal laboratory chow and E+Se supplemented groups were similar. The myocardial fiber diameter was unchanged. Using Starling's hypothesis regarding fluid movement across capillary walls, several mechanisms could be advanced to explain this apparently paradoxical phenomenon. We contend that the interstitial fluid of normal areas of the myocardium is either absorbed by the adjacent damaged areas, or before extravasation of the intravascular proteins and swelling of ITS, the interstitial fluid is first absorbed by the intravascular compartment, due to capillary membrane damage.

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The intravenous administration of verapamil to 2 patients with paroxysmal supraventricular tachycardia (PSVT) resulted in an induction of PSVT during a programmed electrophysiological stimulation study. Each patient had a documented episode of PSVT. Baseline programmed stimulation studies revealed neither induction of PSVT nor an atrial echo; however, PSVT was induced immediately after injecting verapamil (0.15mg/kg) intravenously in both patients. In 1 patient, the study was repeated 2 days later and similar results were obtained. The serum concentration of verapamil when PSVT was induced was about 80ng/ml in both cases. Clinicians using verapamil should note that this antiarrhythmic drug may aggravate PSVT, depending on critical changes in AV nodal conduction and refractoriness.

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Hypertrophic cardiomyopathy (HCM) is most probably a genetically transmitted disease with different clinical and hemodynamic features. In hypertrophic obstructive cardiomyopathy (HOCM) the obstruction is predominantly in the left ventricular outflow tract (IHSS). In a minority of cases the obstruction is strictly located in midventricle (midventricular obstruction, MO). Hypertrophic nonobstructive cardiomyopathy (HNCM) includes asymmetric septal hypertrophy (ASH) and apical hypertrophy (AH). Right ventricular hypertrophic obstruction (RVHO) is an uncommon type of HCM and is almost always combined with other types of left ventricular HCM.
We describe in the present report 1 case of RVHO with IHSS, 2 cases with MO and, to our knowledge, the first case with AH.

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A 12-year-old boy with rheumatic fever associated with myocardial infarction is presented. As sequelae, left ventricular aneurysm and diffuse narrowing of the anterior descending branch of the left coronary artery were demonstrated by angiography. Given the high incidence of coronary arteritis in rheumatic fever, it is likely that arteritis contributed to the infarction.

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