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Biomedical subjects

T Yamakado

Publications and source records attributed to T Yamakado.

At least 19 recordsLinked to original sources
PubMed1994

Regression of left ventricular hypertrophy with long-term treatment of nifedipine in systemic hypertension.

We investigated the regression of left ventricular (LV) hypertrophy with long-term treatment of nifedipine in patients with systemic hypertension. Echocardiograms of the LV were obtained in nine patients before and at a mean of 50 months (13-105 months) after nifedipine monotherapy (30-60 mg/day). Nifedipine significantly reduced both systolic and diastolic blood pressures (BP) by a mean of -46 mmHg and -21 mmHg, respectively. With systemic BP reduction, LV mass was significantly reduced by a mean of -15%, associated with a decrease in LV posterior wall thickness and end-diastolic dimension. There was no significant change in LV fractional shortening. We conclude that nifedipine may cause regression of LV hypertrophy in systemic hypertension, and that reversal of the increase in LV mass could be maintained during long-term nifedipine treatment.

Adult↗
PubMed1994

Left ventricular diastolic pulsus alternans in hypertrophic cardiomyopathy.

We examined left ventricular (LV) diastolic pulsus alternans associated with systolic pulsus alternans in a patient with hypertrophic cardiomyopathy. Alternation in abnormal LV diastolic pressure waveforms persistently declining into mid-diastole (incomplete relaxation) and normal diastolic pressure were noted. Diastolic pulsus alternans was not corrected by isoproterenol and may possibly be independent of systolic pulsus alternans.

Cardiac Catheterization↗
PubMed1993

Development of acute myocardial infarction associated with coronary collateral regression after reperfusion by percutaneous transluminal coronary angioplasty.

Clinical and experimental observations have suggested that newly developed collaterals usually remain even after successful revascularization. We present a patient in whom coronary collateral regression was angiographically demonstrated within about 1 month after percutaneous transluminal coronary angioplasty, which led to the development of acute myocardial infarction. This case suggests that there may be a possibility of unexplained clinically important anatomical or functional regression of collaterals after reperfusion.

Adult↗
PubMed1992

Effects of sublingually administered nifedipine on left ventricular isovolumic relaxation, diastolic filling, and distensibility in patients with chronic coronary artery disease.

The acute effects of nifedipine (20 mg) on left ventricular diastolic function were investigated in 16 patients with chronic coronary artery disease by measuring left ventricular pressure with a manometer-tipped catheter and by measuring volume with cineangiography. Heart rates were maintained by right atrial pacing. Left ventricular peak systolic pressure (-15%; p less than 0.01 vs control) decreased significantly. With afterload reduction, left ventricular ejection fraction (+11%; p less than 0.01) increased. There was no significant change in left ventricular end-diastolic pressure. The diastolic peak filling rate of left ventricular volume significantly increased (+36%; p less than 0.05), whereas the time from end-systole to the peak filling rate remained unchanged. Administration of nifedipine did not improve left ventricular relaxation as assessed by the isovolumic pressure decay. There was also no significant change in the left ventricular diastolic pressure-volume relationship. We conclude that nifedipine improves left ventricular systolic function with afterload reduction but has little or no effect on left ventricular diastolic properties in patients with chronic coronary artery disease.

Administration, Sublingual↗
PubMed1992

[Left ventricular diastolic function in apical hypertrophic cardiomyopathy].

To investigate left ventricular (LV) diastolic function in patients with apical hypertrophic cardiomyopathy (AHCM), we analyzed the LV cineangiograms (RAO 30 degrees) and pressures (tip manometer) in 11 patients with AHCM who had giant negative T waves on their electrocardiograms and "ace of spades" configurations on the LV angiograms. Ten patients with non-obstructive HCM (HNCM) and 10 normal subjects served as controls. LV volumes and instantaneous rates of LV volume changes were derived from frame-by-frame analyses of their LV angiograms. LV isovolumic relaxation was assessed according to the time constant (T) of LV pressure decay. LV diastolic distensibility was evaluated by plotting diastolic pressure-volume curves. There was no significant change in the LV systolic functions among these 3 groups. Compared with normals, LV end-diastolic pressure was equally elevated in AHCM and HNCM. The T of isovolumic pressure decay was significantly prolonged in AHCM and HNCM. LV early diastolic filling was maintained at the normal level in AHCM as assessed by the peak filling rate (PFR) during the rapid filling period and the time from end-systole to PFR. The LV diastolic pressure-volume relation shifted upwards in both AHCM and HNCM. In conclusion, impaired LV isovolumic relaxation and decreased diastolic distensibility, which are associated with HNCM, may also be present in AHCM.

Adult↗
PubMed1992

[The effect of heart rate on the time constant of isovolumic relaxation of the left ventricle].

A time constant (T) of the left ventricular isovolumic relaxation, which expresses the relaxation rate of the left ventricle, may be affected by change of the heart rate. There are few clinical reports concerning the relationship between T and heart rate. We studied the relationship between T and heart rate in 10 patients with normal coronary arteries and left ventricular function. Left ventricular pressure was measured using a catheter-tip manometer during right atrial pacing, which was performed at the rate of 10, 20, 40 beats/min in addition to the baseline rate, and finished at 140 or 150 beats/min. Two measurements were made for T.1) Tw from the slope of In (pressure) against time, and 2) Tb by exponential analysis which also estimated the asymptote. As the heart rate increased, both Tw and Tb gradually shortened (Tw: from 38.5 +/- 4.9 msec at the control heart rate to 28.9 +/- 5.6 msec at 140 or 150 beats/min; Tb: from 54.7 +/- 11.4 msec at the control heart rate to 34.9 +/- 5.7 msec at 140 or 150 beats/min). These findings suggest that left ventricular isovolumic relaxation is strongly affected by change of the heart rate in man.

Adult↗
PubMed1992

[A case of congenital long QT syndrome associated with T wave alternans].

A case was presented in which a rare T wave alternans occurred in association with congenital long QT syndrome. A 71-year-old woman, who had experienced several syncopal attacks per year for the previous forty years, was admitted for further evaluation of the syncope. She had a family history of sudden death (sister) and QT prolongation (son). Electrocardiogram showed a corrected QT interval of 0.68 seconds. Treadmill exercise-tolerance test revealed both T wave alternans immediately after exercise and torsades de pointes 150 seconds after exercise. The syncope was induced by the mental excitation. A prolonged corrected QT interval reduced from 0.70 seconds to 0.58 seconds by the correction of her serum potassium and magnesium. The effect of propranolol, verapamil, phenytoin or mexiletine on T wave alternans and ventricular arrhythmia was evaluated by the treadmill exercise-tolerance test. The treatment with propranolol was most effective.

Adrenergic beta-Antagonists↗
PubMed1991

The calcium binding protein tropomyosin in human platelets and cardiac tissue: elevation in hypertensive cardiac hypertrophy.

Intracellular calcium transients play a major role in the control of cellular contraction and act through binding to target proteins and inducing subsequent conformational changes and activation of enzymes. Abnormalities of intracellular calcium handling are involved in the pathophysiology of essential hypertension and cardiac hypertrophy. In this study we report on the isolation, purification and calcium binding of a 33 kDa protein from human platelets and of a 38 kDa protein from cardiac tissue, both of which are identified as tropomyosin. The calcium binding properties of these human tropomyosin isoforms indicate a putative role for these proteins in the fine tuning of the cellular contraction. Elevated tropomyosin level is demonstrated in platelets from untreated essential hypertensive patients with left ventricular hypertrophy (tropomyosin/actin: 45.1 +/- 3.5, n = 12) relative to essential hypertensive patients without cardiac hypertrophy (tropomyosin/actin: 33.8 +/- 2.3). These findings suggest an association between the enhanced expression of tropomyosin in platelets and the development of cardiac hypertrophy which may relate to the cellular calcium overload of this disease.

Amino Acid Sequence↗
PubMed1991

[Analysis of left ventricular pulsus alternans in hypertrophic cardiomyopathy].

We analyzed left ventricular (LV) pulsus alternans in 49 patients with hypertrophic cardiomyopathy during cardiac catheterization. LV pulsus alternans was noted in 6 of 17 patients with hypertrophic obstructive cardiomyopathy, 5 of whom already showed intraventricular pressure gradient at rest. No patient with hypertrophic non-obstructive cardiomyopathy had LV pulsus alternans. Pulsus alternans was neither observed in the right ventricle nor in the pulmonary artery. There was little, if any, pulsus alternans in a low pressure LV chamber (subaortic portion) and peripheral artery during LV pulsus alternans in a high pressure chamber. LV end-diastolic pressure also remained unchanged during LV pulsus alternans, except in one case. It is suggested that LV pulsus alternans in hypertrophic obstructive cardiomyopathy may imply LV dysfunction associated with increased afterload.

Adult↗
PubMed1991

[Exercise-induced ST segment shift in vasospastic angina with special reference to comparisons between treadmill and bicycle ergometer exercise testings].

To assess the difference between cardiovascular responses to treadmill exercise (TM) and those to bicycle ergometer exercise (EM) in provoking coronary spasm, we compared the ST segment shifts (elevation or depression) during TM and EM in 67 patients with vasospastic angina. Coronary artery spasm was demonstrated on angiography. Both TM and EM were performed on the same day during a medication-free period. For both tests, multistage, symptom-limited exercise protocols were used; EM in the morning and TM in the afternoon. The results obtained were as follows: 1. Rate-pressure products at peak exercise during TM and EM were similar. Systolic blood pressure levels at peak exercise were higher during EM than during TM (p < 0.01). The patients' heart rates at peak exercise were higher during TM than during EM (p < 0.01). Diastolic blood pressure levels at peak exercise were higher during EM than during TM (p < 0.05). 2. Exercise-induced ST elevation occurred more frequently with TM than with EM (19% vs 9%, p < 0.05). 3. Exercise-induced ST depression was provided in 27 patients during TM and in 13 during EM (40% vs 19%, p < 0.01). Among 45 patients without significant lesions, ST depression occurred in 19 during TM, but in only 7 during EM (42% vs 16%, p < 0.01). In conclusion, coronary spasm seemed to occur more frequently with TM than with EM. The mechanism causing such difference remains to be elucidated, however, we speculate that the difference between TM and EM as to enhanced autonomous nervous system activity and coronary perfusion exercise may be related to the difference in the incidence of coronary spasm.

Aged↗
PubMed1991

[Relaxation and diastolic filling precisely evaluated in patients with left ventricular dysfunction].

To assess left ventricular (LV) diastolic function in patients with LV dysfunction, LV pressures (manometer tip) and biplane angiograms were analyzed for 27 patients with LV systolic dysfunction (EF < or = 0.45) (dilated cardiomyopathy or coronary artery disease) and 18 normal controls. LV volumes were obtained from frame-by-frame analyses of angiograms. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV relaxation was impaired in patients with LV dysfunction, however, early diastolic filling assessed by the peak filling rate (PFR) and mean filling rate (MFR) during the rapid filling phase was maintained. Compared to the control group, early diastolic filling was significantly decreased in patients with LV dysfunction without mitral regurgitation (MR), but not in those with LV dysfunction with MR. In conclusion, although diastolic filling may be modified by MR, LV relaxation and early diastolic filling are essentially impaired in patients with LV dysfunction.

Adolescent↗
PubMed1990

Effects of nifedipine on left ventricular diastolic function in patients with asymptomatic or minimally symptomatic hypertrophic cardiomyopathy.

We investigated the effects of nifedipine on left ventricular diastolic function in 17 asymptomatic or minimally symptomatic patients with hypertrophic cardiomyopathy by simultaneously measuring left ventricular pressure and volume with a catheter-tipped manometer and biplane cineangiography. Studies were performed before and 20 minutes after sublingual administration of nifedipine (20 mg). Heart rates were held constant (79 +/- 12 beats/min, mean +/- SD) by right atrial pacing. Left ventricular volumes and instantaneous rates of left ventricular volume were derived from frame-by-frame (20-msec) analyses of left ventricular biplane angiograms. Left ventricular peak systolic pressure (from 122 +/- 21 to 108 +/- 13 mm Hg, p less than 0.01 vs. control) and mean aortic pressure (from 96 +/- 15 to 87 +/- 11 mm Hg, p less than 0.01) decreased significantly with nifedipine. With afterload reduction, left ventricular ejection fraction (from 0.69 +/- 0.12 to 0.74 +/- 0.08, p less than 0.01) and cardiac output (from 6.4 +/- 2.0 to 7.2 +/- 2.2 l/mm, p less than 0.05) increased significantly. However, there was a slight but significant increase in left ventricular end-diastolic pressure (from 15 +/- 8 to 18 +/- 8 mm Hg, p less than 0.05). Nifedipine did not improve left ventricular relaxation as assessed by the time constants of isovolumic pressure decay (t1/2, from 39.8 +/- 6.6 to 39.4 +/- 7.7 msec, NS; t1/e, from 53.8 +/- 9.0 to 54.4 +/- 10.7 msec, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1990

Left ventricular systolic and diastolic function in the hypertrophied ventricle.

To investigate left ventricular (LV) systolic and diastolic function in cardiac hypertrophy, we analysed LV pressure (catheter tip-manometer) and simultaneously performed cineangiography in 24 patients with systemic hypertension (HT), 25 patients with hypertrophic cardiomyopathy (HCM) and 25 normal subjects. We digitized LV cineangiograms frame by frame and computed volume and its derivatives, wall thickness and circumferential wall stress. LV systolic pump function was normal or supernormal in HT and HCM. However, myocardial contractility assessed by end-systolic wall stress-volume relation was depressed in HCM whereas it is normally maintained in HT. LV diastolic function was also impaired in HCM and even in HT despite normal systolic function. The LV hypertrophy group showed significantly prolonged time constant of isovolumic relaxation, increased time from end-systole to the peak filling rate, and upward shift of the diastolic pressure-volume relationship. The characteristic findings of LV diastolic function in LV hypertrophy, therefore, can be summarized as impaired isovolumic relaxation, delayed early diastolic filling and decreased diastolic distensibility. The mechanisms of abnormal systolic and diastolic function may include myocardial ischemia and/or calcium overload in hypertrophied myocardium, but further study will be needed to clarify these problems.

Adult↗