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Biomedical subjects

H Toshima

Publications and source records attributed to H Toshima.

At least 91 records · Page 5Linked to original sources
PubMed1990

Physical training in patients with valvular heart disease after surgery.

The necessity, the methodology and clinical benefit of physical training were evaluated in 85 patients with valvular heart surgery. In 21 patients who had undergone the exercise stress test before surgery, corrective valvular surgery increased maximal oxygen uptake (max.VO2) from 15.4 before to 18.9 ml/min/kg, while 11 (52%) of them failed to increase exercise capacity over 5 METs. Of the total 85 patients, 41 (58%) again showed reduced exercise capacity in the initial postoperative stress test, suggesting that a return to work might be difficult without rehabilitation in these patients. We then compared two training programs: program A of short duration and frequent exercise and program B of longer duration and less frequent exercise, both using a bicycle exercise set at an intensity of 70% of the max.VO2. Both programs similarly increased max.VO2, while patients preferred program A, suggesting that exercise of longer duration could not be tolerated because of deconditioning. Program A was then prescribed to 62 patients, and it increased max.VO2 from 18.2 to 20.7 ml/min/kg after 4 weeks training without any complication. In 9 patients who served as controls undergoing no physical training, no spontaneous improvement in exercise capacity was observed. Of the 76 patients who received either program A or B, 28 patients failed to increase the max.VO2 by 10% or more. These patients presented atrial fibrillation, a cardiothoracic ratio greater than or equal to 60% or exercise-induced ST depression more frequently, suggesting that residual cardiac dysfunction might inhibit the training effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Relationship between coronary risk factor and arteriographic feature of coronary atherosclerosis.

Coronary arteriography was performed in 1,029 consecutive patients with ischemic heart disease and the relationship between the arteriographic features of coronary atherosclerosis and coronary risk factors was analyzed by case control studies. Patients were divided into four groups according to coronary arteriographic findings. Patients with normal or near normal coronary arteriograms (Group I) showed a high prevalence of smoking habit and a higher value of serum uric acid compared with the control group, so smoking and hyperuricemia were considered to be the risk factors for coronary atherosclerosis in patients of group. Four selected variables: smoking, hyperuricemia, hypertension and hyperlipidemia, were identified to be risk factors for the patients with minor plaques in the coronary arteries (Group II). As in Group I, smoking and hyperuricemia had a close relationship to solitary tight plaque in a branch of the coronary artery (Group III). Multiple tight stenoses in the coronary arteries (Group IV) correlated closely with smoking, hyperuricemia, hypertension, hyperlipidemia and diabetes mellitus. Thus, there were many strong risk factors for patients with diffuse, extended coronary atherosclerosis (Group II and Group IV), while only two factors, smoking and hyperuricemia, were considered to be risk factors for the patients with near normal coronary arteries ies or a solitary plaque in a branch of the coronary artery. These findings suggest that the role of the coronary risk factors on the pathogenesis of coronary atherosclerosis is not uniform but variable depending on the morphologic variability of the coronary atherosclerosis and on the pathophysiology of the ischemic heart disease.

Adult↗
PubMed1990

Increased cardiovascular responses to norepinephrine in patients with hypertrophic cardiomyopathy.

Sympathetic nerve-adrenergic receptor systems have been implicated in the pathogenesis of hypertrophic cardiomyopathy (HCM). We studied plasma norepinephrine (NE) levels during exercise and cardiovascular responses to NE in 26 patients with nonobstructive HCM and 26 age- and sex-matched controls. There were no differences in the plasma NE levels at rest (201 +/- 84 vs 233 +/- 100 pg/ml) or in the slope of the log NE-heart rate relationship during exercise between the HCM patient and control groups. When NE was infused intravenously, with increasing doses to 0.20 microgram/kg/min, HCM patients displayed significantly greater increases in mean blood pressure (29 +/- 7 vs 14 +/- 5%, p less than 0.001) and peripheral vascular resistance (39 +/- 7 vs 26 +/- 7%, p less than 0.001) than controls. Although the fractional shortening decreased during NE infusion in controls, it was unaffected in HCM patients, despite a greater elevation of systolic pressure. The responses of left ventricular contractility, estimated by a ratio of systolic blood pressure to end-systolic dimension, were significantly greater in patients with HCM (31 +/- 7 vs 13 +/- 6%, p less than 0.001). These observations indicate that vasoconstrictive responses of the peripheral arteries and inotropic responses of the left ventricular muscle to NE were augmented in patients with HCM, while sympathetic nervous activity remained unchanged. Accordingly, we propose that increased activity of the cardiovascular adrenergic receptor systems, rather than enhanced sympathetic nervous function, may be related to the development of abnormal hypertrophy in HCM.

Adult↗
PubMed1990

The effects of pacing-induced left bundle branch block on left ventricular systolic and diastolic performances.

To assess the effects of pacing-induced left bundle branch block on left ventricular (LV) systolic and diastolic performance, we performed digital subtraction ventriculography while simultaneously measuring LV pressure with a catheter tip micromanometer. The subjects included 10 patients with a sinus rhythm, a normal QRS duration and PR interval within 0.22 sec. LV performance was assessed during both right atrial pacing (AP) and atrioventricular sequential pacing (AVP) at the same pacing rate. The atrioventricular pacing interval during AVP was adjusted to be the maximal interval that showed the QRS configuration seen during complete right ventricular pacing. LV end-diastolic pressure and volume during AVP did not differ from those during AP. Peak positive and negative dp/dt during AVP were significantly lower than those during AP. Time constants were also significantly longer during AVP. The QRS duration during AVP significantly correlated with end-systolic volume and time constants, and inversely correlated with ejection fraction and +dp/dt. These observations indicated that conduction disturbance per se, induced by AVP, could not only impair LV systolic performance but also diastolic performance, possibly due to asynchronous contraction and relaxation of the left ventricle.

Adult↗
PubMed1990

The role of cigarette smoking and drinking in the development of liver cancer: 28 years of observations on male cohort members in a farming and fishing area.

Cohort studies of 639 males in a farming area (Cohort I) and 677 males in a fishing area (Cohort II) in Kyushu, Japan, had been conducted to assess the involvement of smoking and drinking in the development of liver cancer. An observed-to-expected (O/E) ratio of liver cancer was 1.3 in Cohort I and 3.1 (p less than 0.01) in Cohort II. A significant excess in deaths was found in Cohort II. No significant risk elevation was observed for smokers and drinkers in Cohort I. Although the odds ratio (OR) of 3.6 (0.6 to 22.3) suggested an elevated risk among cigarette smokers in Cohort II, no clear linear trend of ORs was observed. In contrast, a significant elevation of OR (7.0) was noted among shochu drinkers in this cohort. The respective ORs were 5.0 (1.3 to 19.7), 8.6 (2.1 to 36.1), 14.1 (3.6 to 55.9) for shochu drinkers of less than 1, 1 to 2, and 2+ units (approximately 180 ml in volume), and a highly significant dose-response relationship was observed (chi 2 = 12.1; p less than 0.001). Multiple logistic regression analysis indicated an insignificant effect of smoking and a major contribution of drinking to the development of liver cancer. Shochu drinking (or probably high alcohol intake) seems to have a significant involvement in the etiology of liver cancer, at least in Cohort II.

Aged↗
PubMed1989

Role of adrenergic receptor systems in canine left ventricular hypertrophy.

Although the sympathetic nervous system and catecholamines have been postulated to play an important role in the development of myocardial hypertrophy, the precise mechanism is still ill-defined. We therefore investigated myocardial norepinephrine and the adrenergic receptor systems in two experimental canine models for cardiac hypertrophy; in 12 dogs with surgical cardiac denervation, and in 12 dogs with chronic infusion of a subhypertensive dose of norepinephrine at a rate of 0.04 mg/kg/day. After two months both models induced myocardial hypertrophy, indicated by significant increases in the heart weight, left ventricular wall thickness and cell diameter, as compared with 14 sham-operated control dogs. Cardiac denervation remarkably depleted myocardial norepinephrine while plasma norepinephrine remained unchanged. Both alpha 1- and beta-receptors were up-regulated, with Bmax increasing by 124% and 49%, respectively. The decrease in myocardial cyclic AMP content was relatively small as compared with the marked depletion in myocardial norepinephrine, probably compensated by augmentation of beta-receptor system activity. Chronic norepinephrine infusion also reduced myocardial norepinephrine content possibly due to stimulation of presynaptic alpha 2-receptor inhibiting norepinephrine synthesis and release. The number of alpha 1- and beta-receptors also increased by 97% and 30%, respectively, while myocardial cyclic AMP content remained unchanged. These observations indicate that neither direct stimulation of norepinephrine on the myocardial cell nor increased cyclic AMP is the mechanism for cardiac hypertrophy. A greater increase in the alpha 1-receptor, rather than in the beta-receptors, in both models implies that a disproportional augmentation of the alpha 1-receptor system may play an important role in the development of myocardial hypertrophy.

Animals↗
PubMed1989

Assessment of cardiopulmonary baroreflex function in hypertensive and normotensive subjects with or without hypertensive relatives.

1. To investigate whether cardiopulmonary baroreflex control contributes to the pathogenesis and progression of hypertension, we have evaluated the function of the cardiopulmonary baroreflex in 22 patients with essential hypertension and in 17 volunteers with normotension. The normotensive group consisted of 8 subjects with a family history of hypertension and nine with no family history. 2. Forearm vascular resistance (FVR) and central venous pressure (CVP) were measured under control conditions when -10 mmHg lower body negative pressure was applied; the cardiopulmonary slope (CPS = delta FVR/delta CVP) was calculated as an index of the cardiopulmonary baroreflex function. 3. CPS was significantly higher in hypertensives (6.0 +/- 3.93 [s.d.], P less than 0.01) and also tended to be higher in normotensives with a family history of hypertension (3.9 +/- 3.53, P less than 0.05), compared with normotensives without a family history of hypertension (1.7 +/- 0.88). 4. When the hypertensives were divided into two groups, depending on whether CPS was greater or less than 6.0 units, cardiac wall thickness (20 +/- 1.6 mm vs 23 +/- 3.2 mm, P less than 0.05) and the renal vascular resistance (20.9 +/- 6.52 units vs 28.9 +/- 7.32 units, P less than 0.05) were both significantly higher in the Low CPS group. 5. These findings suggest that cardiopulmonary baroreflex function was augmented even in normotensive subjects with hypertensive relatives, as compared with those without hypertensive subjects. Furthermore, cardiopulmonary baroreflex function was augmented in the early stages of hypertension and diminished further with increasing severity.

Adult↗
PubMed1989

Electrophysiological properties of cultured dog myocytes obtained by endomyocardial biopsy.

Right ventricular cardiac tissue (10-20 mg wet weight) was obtained from anesthetized adult dogs by endomyocardial biopsy. The biopsy could be repeated in one dog every 2 weeks for up to 3 months. Fifty to 200 cardiomyocytes, dispersed with collagenase and trypsin, were collected by centrifugation of the cells with 50% polysucrose-sodium diatrizoate solution (Ficoll-Paque). Single cardiomyocytes were suspended in a minimum essential medium containing 20% fetal bovine serum and 8-bromoadenosine 3': 5'-cyclic monophosphate (0.1 mM) for up to 3 weeks. Approximately 70-80% of the cultured cardiomyocytes were rod shaped after 24 hours (10-20% after 7 days). Cytoplasmic organelles of the cultured cells, examined with a transmission electron microscope, were within the normal range of canine heart morphology in vivo. Resting membrane potential of the cells was about -80 mV when superfused with a Krebs' solution containing 4.7 mM potassium ions. The action potential lasted for 300 msec and had a peak amplitude of about 120 mV. Voltage-clamp experiments demonstrated the presence of an inward calcium current (congruent to 0.9 nA at +9 mV), which was facilitated by isoproterenol (0.1-1 microMs). The background potassium current showed typical inward rectification at potentials more negative than -80 mV. The results indicate that morphological, electrophysiological, and pharmacological properties of the cultured cardiomyocytes were intact. We propose that the culture techniques we have developed can be useful for repeated investigation on functional aspects of cardiac muscles in myocardial disease.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Sudden death in hypertrophic and dilated cardiomyopathy.

The long-term prognosis for 314 patients with hypertrophic cardiomyopathy (HCM) and 82 with dilated cardiomyopathy (DCM) was investigated in an attempt to elucidate clinical variables predicting sudden death (SD). In the patients with HCM, 68% of cardiac deaths occurred suddenly and unexpectedly. Variables associated with an increased risk to SD were young age (less than 30 years), reduced fractional shortening (less than 35%) and elevated left ventricular end-diastolic pressure (greater than or equal to 20 mmHg). Eight of the 10 patients who died suddenly during or immediately after strenuous exercise were less than 30 years old, and the collapse tended to be associated with exercise-induced ST-depression. In contrast, SD occurring during mild activities, resting or sleep was mainly observed in those aged 30 years or more. Ventricular tachycardia was observed on electrocardiographic monitoring in 24% of those 30 years or more, while it was rare in those under 30 years (5%). On the other hand, no SD was found in patients with apical hypertrophy nor in those 50 years or more. These observations suggest that HCM patients at a young age, with impaired left ventricular systolic and diastolic function, have an increased risk to SD. Since exercise-induced myocardial ischemia rather than ventricular arrhythmias appears to be the more likely mechanism for SD for those under 30 years old, restriction of strenuous exercise should be strongly advised for these patients. For those aged from 30 to 50 years, ventricular tachycardia should be controlled by antiarrhythmic agents for the prevention of SD. In patients with DCM, 24% of all cardiac deaths were attributed to SD. Although no variables reliably predicted SD, it was of note that only one patient out of 26 with SV1 + RV5 greater than or equal to 35 mm died suddenly. Whereas ventricular arrhythmias are known to be a contributing cause for SD, the prognostic significance of ventricular tachycardia on electrocardiographic monitoring in predicting SD has not yet been established. In addition, antiarrhythmic agents often precipitate hemodynamic deterioration. It therefore appears that use of antiarrhythmic agents is not a therapy of first choice and that primary treatment should be focused upon improvement in ventricular function in order to prevent SD in patients with DCM.

Adult↗
PubMed1989

Lymphocyte subsets in patients with acute myopericarditis, arrhythmias and dilated cardiomyopathy.

To investigate the role of immunoregulatory function in determining the clinical course of acute myopericarditis, lymphocyte subsets were analysed by laser flow cytometry in 20 patients with acute myopericarditis, 30 with various arrhythmias or atrio-ventricular block and 31 with dilated cardiomyopathy. During the healing stage of acute myopericarditis, patients with residual electrocardiographic or left ventricular wall motion abnormalities presented altered frequencies of lymphocyte subsets, increased B 1 and reduced OKT 8 positive cells with an elevated OKT 4/8 ratio. The abnormal pattern was not evident in patients with acute pericarditis nor in those with acute myocarditis who recovered completely without residual abnormalities. This observation suggested that an imbalance of helper/suppressor T cells could modulate the clinical course of acute myopericarditis, either by producing extensive and irreversible myocardial damage during acute illness or by inducing chronic smoulding myocardial inflammation. Patients with ventricular arrhythmias and left ventricular wall motion abnormalities also presented reduced suppressor/cytotoxic T cells, implying that they had been suffering from chronic smoulding myocarditis mediated by immunoregulatory dysfunction. However, we could not determine whether the imbalance of helper/suppressor T cells could mediate the progression from myocarditis to dilated cardiomyopathy, since no association was demonstrated between the abnormal lymphocyte subsets and mononuclear cell infiltration in endomyocardial biopsy sample from patients with dilated cardiomyopathy.

Acute Disease↗
PubMed1989

[Concentric left ventricular hypertrophy in patients with aortic regurgitation].

Chronic aortic regurgitation (AR) is a disease incorporating volume overload of the left ventricle (LV) which is characterized by hyperactive left ventricular dilatation (LVD). However, we have encountered several patients who had concentric LV hypertrophy (LVH) instead of LVD. We therefore studied 50 consecutive patients with isolated AR but without aortic stenosis and found seven patients with concentric LVH having LV wall thickness (determined by summing ventricular septal and posterior wall thicknesses) exceeding 30 mm and LV diastolic diameters of less than 60 mm. These seven patients with AR and LVH were older (55 +/- 27 vs 42 +/- 11 years) and tended to have milder degree of AR, compared with the remaining 43 patients having AR and LVD. However, patients with AR and LVH did not differ from AR and LVD as to the cardiothoracic ratio, SV1 + RV5, T-waves, ejection fraction, operative findings of valvular morphology and underlying etiologies. In contrast, patients with AR and LVH presented higher systolic (196 +/- 41 vs 149 +/- 26 mmHg, p less than 0.01) and diastolic pressures (74 +/- 14 vs 51 +/- 13 mmHg, p less than 0.01) and higher systemic vascular resistance (1,854 +/- 399 vs 1,388 +/- 352 dyne.sec.cm-5, p less than 0.05) during catheterization than did those with AR and LVD. However, blood pressure at the time of admission was not different in the two groups. These observations indicate that concentric LVH is not rare among patients with AR, and that an association of pressure overload with volume overload of the LV, particularly during exercise or stress, may lead to concentric LVH, even in patients with chronic AR.

Adult↗
PubMed1988

Impaired myocardial perfusion in patients with hypertrophic cardiomyopathy: assessment with digital subtraction coronary arteriography.

To study the clinical significance of abnormal myocardial perfusion in patients with hypertrophic cardiomyopathy (HCM), we performed a computerized washout analysis of digital subtraction coronary arteriograms in 28 patients with HCM and 16 control subjects. The contrast disappearance half-life (T1/2) was calculated from a time-density curve generated in the four sectors of the myocardium perfused by the left anterior descending coronary artery and the mean T1/2 was calculated by averaging T1/2 values for these four sectors. Patients with HCM demonstrated longer T1/2 in the ventricular septal region than control subjects. Thirteen (46%) of the patients with HCM presented abnormally longer mean T1/2 values, suggesting impaired myocardial perfusion. Family histories of HCM were more frequent in patients with abnormal mean T1/2 values (92% vs 47%; p less than 0.05). On the exercise stress test, patients with abnormal T1/2 values presented significantly lower exercise tolerance with more frequent exercise-induced ST segment depression (62% vs 13%; p less than 0.05). However, there were no significant differences between the two groups with regard to ventricular wall thickness, left ventricular end-diastolic pressure, or the severity of systolic narrowing of the coronary arteries. These findings suggest that 13 (46%) of the patients with HCM have impaired myocardial perfusion, which may be a manifestation of intramural coronary artery disease in addition to left ventricular hypertrophy, elevated left ventricular end-diastolic pressure, or systolic narrowing of the coronary arteries. Additionally, significant association of the prolonged T1/2 with a familial occurrence of HCM and depressed exercise tolerance with ST segment depression imply that impaired myocardial perfusion could be an important inherent pathophysiological state leading to myocardial ischemia during exercise.

Adolescent↗
PubMed1988

[Four cases of Fabry's disease mimicking hypertrophic cardiomyopathy].

Four patients with Fabry's disease diagnosed by right ventricular endomyocardial biopsy had cardiac manifestations simulating hypertrophic cardiomyopathy (HCM). Case 1: A 51-year-old woman, whose elder sister had congestive heart failure, was hospitalized for exertional dyspnea and cardiomegaly. Her electrocardiogram (ECG) showed a short PQ interval (0.10 sec) and left ventricular hypertrophy. Her echocardiogram (Echo) showed moderate symmetrical hypertrophy of the left ventricle (IVST/PWT = 18 mm/17 mm). Case 2: A 32-year-old woman, whose elder sister had an abnormal ECG, was hospitalized for the ECG abnormalities consisting of a short PQ interval (0.10 sec) and ST-T changes in the left precordial leads. The Echo revealed mild symmetrical hypertrophy of the left ventricle (IVST = 13 mm, PWT = 13 mm). Case 3: A 44-year-old man was hospitalized for his ECG suggestive of left ventricular hypertrophy, and his Echo showed asymmetrical septal hypertrophy (ASH; IVST = 22 mm). Case 4: A 51-year-old man was hospitalized for his ECG showing high voltage in the left precordial leads, and his Echo showed ASH (IVST = 20 mm). The cardiac histopathological findings of these cases included cytoplasmic vacuolization by light microscopy, and electron-dense deposits consisting of parallel or concentric lamellae with periodic spacing, suggesting Fabry's disease. The urinary glycolipids of Case 1 were increased biochemically; then the diagnosis of Fabry's disease was confirmed. Cardiac hypertrophy in Fabry's disease has many aspects, because the histopathological changes and clinical manifestations are determined by genetic factors. It was concluded that Fabry's disease may be concealed in some patients with the clinical diagnosis of HCM.

Adult↗