Tadasu Takatsu

Hypertrophic nonobstructive cardiomyopathy: A precise assessment of hemodynamic characteristics and clinical implications

A precise assessment of left ventricular function was performed in 20 patients with hypertrophic nonobstructive cardiomyopathy to elucidate the basic pathophysiology, and the data were compared with those in 22 normal subjects. Whereas end-diastolic pressure was high in those with cardiomyopathy, a more accurate index of preload, end-diastolic stress, did not differ from normal value. Afterload was about half the normal value. Both isovolumic indexes [peak positive dP/dt and (dP/dt)/DP40] and ejection phase indexes of contractility (ejection fraction) were in the normal range; however, the end-systolic stress volume ratio was significantly reduced (43% of the normal value). Although the left ventricular minute work index was in the normal range, the unit muscle performance (minute work/mass) was very low (49%). An abnormality of left ventricular relaxation was demonstrated by low peak negative dP/dt (56%) and prolonged time constant T (191%), and a stiff left ventricle was demonstrated by a high diastolic elastic stiffness constant (129%). These observations suggest that the contraction of a unit muscle is inappropriate to produce an adequate contraction of the whole ventricle, and that hypertrophy might be an adaptive process to maintain normal systolic function by increasing mass and reducing afterload.

Biochemical and morphological study of cardiac hypertrophy. Effects of thyroxine on enzyme activities in the rat myocardium

SummaryExperimental hyperthyroidism induced in rats by daily injections of 3,3′,5,5′-tetraiode-l-thyroxine (0.5 mg/kg i.p.) for 14 days resulted in a significant increase in heart weight and heart weight/body weight ratio. Hemodynamic and morphological studies were performed in one group. Thyroxine-treated rats showed a characteristic cardiovascular hyperdynamic state, such as tachycardia and augmented rate of contraction, but no evidence of heart failure such as elevated end-diastolic pressures. The cardiac cells in hyperthyroid rats had a significantly larger diameter and more mitochondria than did those of the control rats. In another group the activities of cardiac enzymes involved in energy utilization and liberation were measured biochemically and compared with those of normal controls. Hyperthyroidism resulted in increased specific activity of cytochrome C oxidase and actomyosin ATPase in the myocardium. The specific activity of long-chain acyl-CoA synthetase, carnitine palmityltransferase, carnitine acetyltransferase, malate dehydrogenase and citrate synthase showed a moderate to marked increment, whereas the specific activity of lactate dehydrogenase and pyruvate kinase remained at the control values. These results suggest that in hyperthyroid rat hearts the functions of both energy liberation and utilization systems are enhanced to meet the added workload. Moreover, the increased activity of the enzymes participating in fatty acid metabolism suggest that in thyroxine-induced hypertrophic and hyperdynamic rat hearts, fatty acids contribute more to the energy supply than do carbohydrates.

A case of idiopathic myocardiopathy with deposits of a peculiar substance in the myocardium; Diagnosis by endomyocardial biopsy☆

Abstract A case of idiopathic myocardiopathy in a 22-year-old man has been described. The diagnosis was made on the basis of physical, extensive graphic, and hemodynamic studies and confirmed by endomyocardial biopsy with Konnos intravascular biopsy catheter, or “bioptome.” The necessity for biopsy specimens for histochemical and electron microscopic studies, and the superiority of Konnos “bioptome” have been discussed briefly. Light and electron microscopic studies on the biopsy specimen from the heart revealed the accumulation of peculiar fine fibrous structures and pigment granules in the sarcoplasm, which suggest some degradation process resulting from abnormal metabolism and functions in the myocardial cells. The histochemical properties of the peculiar substances have also been described. The reduced compliance of both ventricles was probably due mainly to the loss of myofibrils and increased interstitial fibrosis, which was confirmed by histological studies on the biopsy specimen, and which presumably contributed to some of the peculiar physical and hemodynamic features in this case. The patient developed recurrent Stokes-Adams attacks due to A-V block. He is now living a normal life with an implanted pacemaker. Although the etiology could not be determined in this case, the possibility of some type of infection, including virus infection, could not be completely ruled out.

Effects of captopril on arterial and venous pressure, renal function, and humoral factors in severe chronic congestive heart failure

The effects of captopril in several humoral factors were studied to elucidate the role of the renin‐angiotensin (RA) system in arterial and venous pressures and renal function in patients with severe chronic congestive heart failure. A single oral dose of captopril in 20 subjects reduced mean arterial blood pressure from 77 to 67 mm Hg; this decrease correlated with baseline plasma renin activity (PRA). The increase in PRA and the decrease in plasma aldosterone levels after captopril were much greater in subjects with higher PRA. Plasma norepinephrine (NE) levels decreased, while those of epinephrine did not change. Peripheral venous pressure declined from 107 to 77 mm H2O; this decrease correlated with the change in NE levels. During 7‐day captopril therapy, urine volume and sodium excretion increased (1145 to 1136 ml/day and 76 to 94 mEq/day) in 11 subjects in whom renal function was followed. Renal plasma flow (RPF) rose from 237 to 364 ml/min, while glomerular filtration rate did not change; the filtration fraction decreased from 32% to 23%. Simultaneous infusion of aprotinin in six of the subjects did not affect the captopril‐induced increase in RPF, despite the suppression of plasma bradykinin levels. These results suggest that captopril reduces arterial blood pressure in patients with high PRA through inhibition of the RA system and dilates veins by attenuation of sympathetic nervous activity. Increased RPF and urinary sodium excretion induced by captopril might result from inhibition of the RA system; the kallikrein‐kinin system or bradykinin‐mediated prostaglandins do not appear to play a major role.

Effects of converting-enzyme inhibition on cardiorenal hemodynamics in patients with chronic congestive heart failure

The role of the renin-angiotensin system in cardiorenal function in patients with severe chronic congestive heart failure was investigated. A single oral dose of captopril in 16 patients significantly increased cardiac index and reduced arterial blood pressure and total systemic vascular resistance. These changes were significantly greater in subjects with higher baseline plasma renin activity (PRA). During 7-day captopril therapy, renal plasma flow distinctly increased in 10 patients in whom renal function was followed. The increase found in renal plasma flow was greater in subjects with higher PRA. Yet, the reduction in renal vascular resistance was much greater than that of total systemic vascular resistance, even in patients with lower PRA. Simultaneous infusion of aprotinin in eight of these subjects did not affect the captopril-induced increase in renal plasma flow, despite the suppression of plasma bradykinin levels; these responses were the same in both PRA subgroups. The results suggest that captopril reduces total systemic vascular resistance in patients with chronic congestive heart failure through inhibition of the renin-angiotensin system and that the preferential renal vasodilator effect of captopril might be the sole result of this inhibition, with the kallikrein-kinin system or kinin-mediated prostaglandins not playing a major role.

Effects of Captopril on Cardiorenal Hemodynamics in Patients with Severe Chronic Congestive Heart Failure

The effects of captopril on cardiorenal function were studied in patients with chronic congestive heart failure. A single oral dose of captopril in 16 patients significantly increased cardiac indices and decreased total systemic vascular resistance. These changes were greater in subjects with higher baseline plasma renin activity (PRA). The increase in PRA and decrease in plasma aldosterone were also greater in this group. During 7 days of captopril therapy, renal plasma flow distinctly increased in 10 patients in whom renal function was followed. The increase in renal blood flow was greater in subjects with higher PRA. Simultaneous infusion of aprotinin in eight of these subjects did not affect the captopril-induced increase in renal plasma flow: these responses were the same in both PRA subgroups. The results suggest that captopril reduces total systemic vascular resistance in patients with chronic congestive heart failure through the inhibition of the renin-angiotensin system and the preferential renal vasodilating effect of captopril seems exclusively to be the sole result of this inhibition, with the kallikrein-kinin system or kinin-mediated prostaglandins not playing a major role.

Congenital fistula of the right coronary artery-left ventricle--a case report.

While the incidence of right coronary artery-left ventricle fistulae is low, cardiac catheterization, ascending aortogram and selective coronary angiogram led us to suspect the presence of such a fistula in a 10-year old female patient. Arteriorrhaphy with additional ligation was performed and the patient is in good health more than one year after surgery.