Discrepancy between noninvasive and invasive measurements of MVA after BMC.
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Biomedical subjects
Publications and source records attributed to K Miyatake.
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We determined left atrial (LA) volume changes to evaluate LA function, and to correlate the Doppler-determined mitral flow velocity (MFV) pattern. Twenty-four patients with ischemic heart disease who showed 'normal' MFV pattern by pulsed Doppler echocardiography were studied. The patients were divided into 14 patients with left ventricular end diastolic pressure < 18 mmHg (true normals) and 10 patients with > or = 18 mmHg (pseudo normals). The changes in LA volume were determined by echocardiography from apical two- and four-chamber views with modified Simpson's method. The volume measurements were done at the time of mitral valve opening (Vmax), at onset of atrial systole (Va) and at mitral valve closure (Vmin). Then the passive LA emptying volume was calculated by subtracting Va from Vmax, and the active LA emptying volume by subtracting Vmin from Va. The LA ejection fraction was calculated by the formula: [(Va-Vmin)Va] x 100. There was no significant difference in LA ejection fraction in pseudo normal (39+/-6%) and in true normal (41+/-13%) patients. Although the passive LA emptying volume was 16+/-4 ml/beat in true normal and was 11+/-3 ml/beat in pseudo normal (NS), the active LA emptying volume was significantly greater in pseudo normals (22+/-4 m/beat) than in true normals (12+/-2 ml/beat, P<0.001). Thus, the ratio of passive and active LA emptying volume was markedly greater in true normals (1.28+/-0.35) than in pseudo normals (0.52+/-0.19, P<0.001), facilitating the differentiation of these two groups. These results indicate that two-dimensional echocardiographic measurement of LA volume can be valuable in assessing the LA function, providing an alternative method for differentiating pseudo normal from true normal MFV pattern in clinical settings, although several technological shortcomings should be resolved.
This study was designed to examine the impact of coronary artery remodeling, enlargement or shrinkage, on the angiographic disease eccentricity. A total of 82 coronary sites from 73 patients with significant stenosis (>50%) were prospectively analyzed by both quantitative coronary angiography and intravascular ultrasound. By quantitative coronary angiography, the maximal and minimal distances from the center of the stenosis to the outline of the vessel wall were measured, and the eccentricity index was calculated by the formula [(maximal-minimal)/maximal]. By intravascular ultrasound, the maximal and minimal distances from the center of the lumen to the leading edge of the second echogenic zone were measured, and the eccentricity index was calculated by the same formula. For identifying the vessel remodeling, the total vessel area that was determined by tracing the leading edge of the second echogenic zone was measured at the stenotic sites and the adjacent proximal and distal segments. By quantitative coronary angiography, the maximal and minimal distances were 1.76+/-0.6 and 0.97+/-0.3 mm, respectively, yielding an eccentricity index of 0.42+/-0.2. The maximal and minimal distances by intravascular ultrasound were 2.77+/-0.6 mm and 1.46+/-0.4 mm, respectively, yielding an eccentricity index of 0.45+/-0.2 (NS). Although the average eccentricity index was not different between the two methods, there was substantially no correlation between the eccentricity index determined by the two methods (r = 0.38, y = 0.43x+0.22). However, this correlation was significantly improved (r = 0.55, y = 0.73x+0.12, P<0.001) when 44 stenotic segments with remodeling were excluded for comparison. These results indicate that coronary artery remodeling could be a major contributing factor to angiographic misinterpretation of disease eccentricity. We suggest that intravascular ultrasound is a powerful method that can accurately determine diseases eccentricity as well as disease severity.
To clarify the relationship between diabetes mellitus and carbohydrate digestion, the activities of sucrase and isomaltase, which form a complex enzyme (SI complex) on the brush border membranes, were compared in the progression of diabetes mellitus in Otsuka Long-Evans Tokushima fatty (OLETF) rats, a model of human non-insulin-dependent diabetes mellitus with insulin resistance, and Long-Evans Tokushima Otsuka (LETO) rats as non-diabetic controls. Until 40 weeks of age, OLETF rats were obese and had a high plasma glucose level, compared to age-matched LETO rats, but the sucrase and isomaltase activities showed no significant differences between the two strains. Oral glucose tolerance test revealed that during 40-48 weeks of age, NIDDM became very severe with advancing insulin resistance in OLETF rats. In OLETF rats, in contrast to LETO rats, at 48 weeks of age, abnormal increases in the sucrase and isomaltase activities occurred, along with a remarkable decrease in body weight and a further great increase in the plasma glucose level in the non-fasting state. Hyperinsulinemia occurred in 20-week-old OLETF rats; however, at 40 and 48 weeks of age, the plasma insulin level in the non-fasting state in OLETF rats was not significantly different from that in LETO rats. The level of mRNA encoding the SI complex increased abnormally in 48-week-old OLETF rats. These results suggest that the advance of insulin resistance leads to an increase in the expression of the SI complex on the transcriptional level.
BACKGROUND: Nitroglycerin is known to augment vessel wall squeezing at the site with coronary-myocardial bridging (CMB). This study was designed to define the mechanism of nitroglycerin-induced augmentation of CMB in clinical settings. METHODS: We analyzed nitroglycerin reactivity at the site with CMB in 39 patients. Maximal and minimal diameters of CMB during a cardiac cycle were measured by quantitative angiography before and after intracoronary administration of 250 microgram nitroglycerin. In 15 patients, CMB sites were observed by intravascular ultrasound to determine the intimal thickness and the time-serial change in vessel area. RESULTS: Before nitroglycerin, CMB was demonstrated with angiography in 25 patients, and the remaining 14 patients showed CMB after nitroglycerin. The maximal diameter during diastole increased from 1. 4 +/- 0.4 mm to 1.9 +/- 0.4 mm after nitroglycerin, whereas the minimal diameter during systole decreased from 1.0 +/- 0.4 mm to 0.7 +/- 0.4 mm (P <.01). Thus nitroglycerin augmented the percent vessel narrowing during systole from 24% +/- 21% to 65% +/- 16% (P <.01). Under these conditions, intravascular ultrasound showed the reduction of the cross-sectional area of the sites with CMB by -38% +/- 16% (P <.01) during systole, and this phenomenon continued to early diastole (-30% +/- 16%). The intimal thickness was 0.32 +/- 0. 10 mm, which suggests the absence of atherosclerotic disease at CMB sites. CONCLUSIONS: These results indicate that nitroglycerin-induced augmentation of the percent narrowing of CMB can be derived from further systolic compression of the vessel lumen as well as diastolic expansion, probably because of the increase in vessel compliance after nitroglycerin. We suggest that the delayed dilation of coronary lumen during the early diastole may contribute to the occurrence of myocardial ischemia.
BACKGROUND: The aortic valve dysfunction of patients with homozygous familial hypercholesterolemia (FH) suggests that hypercholesterolemia affects not only coronary arteries but also the aortic valve. We studied the aortic root of patients with homozygous FH and those of patients with heterozygous FH to characterize the premature atherosclerotic lesions by using histopathologic specimens. METHODS AND RESULTS: The aortic roots of 10 patients with homozygous FH, age 9 to 58 years, were studied by cardiac catheterization with several angiographies. The aortic roots of 39 patients with heterozygous FH under age 60 years were also examined for aortic and mitral valvular functions by color Doppler echocardiography, and 30 normocholesterolemic patients with coronary artery disease were examined as control subjects. In addition, in 22 patients with FH and 20 control subjects, the internal diameter of the aortic annulus and the aortic ridge in cardiac cycles were measured. Of the 10 homozygotes with FH, 8 patients had aortic regurgitation demonstrated by aortography; 3 of them showed significant transvalvular pressure gradients. Stenotic changes of coronary ostia were observed in 8 of the 10 homozygotes with moderate coronary atherosclerosis. Of the 39 heterozygotes with FH, 10 patients had aortic regurgitation shown by Doppler echocardiography, as did only 1 of the 30 control subjects (P <.05). The average diameter and distensibility of the ascending aorta were significantly reduced in the heterozygotes compared with the control subjects. The surgically resected cusp specimens of aortic valves obtained from 1 homozygous and 1 heterozygous patient showed significant thickening of the cusp with foam cell infiltration. CONCLUSIONS: Premature atherosclerosis in FH had a characteristic distribution, affecting the aortic root dominantly. The involvement of the aortic valve indicating "hypercholesterolemic valvulopathy" was a peculiar feature of FH, especially its homozygous form, but was reminiscent of ubiquitous processes caused by hypercholesterolemia.
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OBJECTIVES: This study sought to investigate the effect of beraprost sodium (BPS), an orally active prostacyclin analogue, on the survival of outpatients with primary pulmonary hypertension (PPH). BACKGROUND: Continuous intravenous administration of epoprostenol (prostacyclin) has been shown to improve survival in PPH. However, the effect of oral BPS on survival in PPH remains unknown. METHODS: Fifty-eight consecutive patients with PPH who could be discharged after the first diagnostic catheterization for PPH were retrospectively divided into two groups: patients treated with BPS (BPS group, n = 24) and those without BPS (conventional group, n = 34). The baseline demographic and hemodynamic data did not significantly differ between the two. RESULTS: Twenty-seven patients died of cardiopulmonary causes in the conventional group during a mean follow-up period of 44 +/- 45 months. In contrast, only 4 patients died of cardiopulmonary causes in the BPS group during a mean follow-up period of 30 +/- 20 months. In a subsample (n = 15) of patients in the BPS group, mean pulmonary arterial pressure and total pulmonary resistance significantly decreased, respectively, by 13% and 25% during a mean follow-up period of 53 days. Among the variables previously known to be associated with the mortality in PPH, the absence of BPS therapy and the reduced cardiac output were independently related to the mortality by a multivariate Cox proportional hazards regression analysis (both p < 0.05). The Kaplan-Meier survival curves demonstrated that the one-, two- and three-year survival rates for the BPS group were 96%, 86% and 76%, respectively, as compared with 77%, 47% and 44%, respectively, in the conventional group (log-rank test, p < 0.05). CONCLUSIONS: The oral administration of BPS may have beneficial effects on the survival of outpatients with PPH as compared with conventional therapy alone.
Although adenosine triphosphate (ATP) is a favorable vasodilator because of its short-acting duration, the agent's effectiveness in facilitating the diagnosis of myocardial ischemia with myocardial contrast echocardiography (MCE) is not fully understood. The goal of this study was to examine the efficacy of intravenous ATP administration (0.15 to 0.30 mg/kg/min for 5 minutes) in diagnosing the flow mismatch with MCE. To achieve this, a critical stenosis was produced in the left circumflex artery in 10 anesthetized dogs. The peak intensity ratio of risk area to control area was reduced by ATP from 0.51 +/- 0.19 to 0.31 +/- 0.12 (P <.05). Systolic wall thickening of the risk area did not change significantly (32.8% +/- 9.8% to 27.5% +/- 12.8%). These changes did not differ from those obtained after dipyridamole. We conclude that MCE with intravenous ATP administration is as useful as the dipyridamole method for diagnosing critical coronary stenosis.
We describe a rare case of Björk-Shiley prosthetic valve obstruction with normal motion of the tilting disk. The cause of obstruction was the annular pannus ingrowth and was well defined by transesophageal echocardiography, but not by cardiac catheterization nor cineradiography.
BACKGROUND: The aim of this study was to investigate the contribution of endothelin-1 (ET-1) to the development of secondary pulmonary hypertension (PH) in patients with left heart failure (HF). METHODS AND RESULTS: The subjects were 40 patients with left HF with (group 1; n = 20) and without (group 2; n = 20) acute exacerbation. Before treatment, the ET-1 level in the pulmonary capillary wedge region was three times greater in patients of group 2 than group 1, although there was no significant difference in mean pulmonary artery pressure (mPAP) or pulmonary vascular resistance index (PVRI) between the two groups. Also, the ET-1 level significantly correlated with mPAP and PVRI for both groups, but with different slopes of the regression lines. After treatment of group 1, the extent of reduction in the ET-1 level significantly correlated with that in mPAP and in PVRI, whereas the ET-1 level itself correlated with mPAP, with the regression lines approximating those of group 2. CONCLUSIONS: Our findings suggest that ET-1 may have differential roles in the development of secondary PH in patients with left HF with or without acute exacerbation.
First, we studied the diagnostic utility of myocardial imaging with 123I-BMIPP (BMIPP), a 3-methyl-branched fatty acid analog, in patients with various types of cardiomyopathy and left ventricular dysfunction (ejection fraction below 40%) by comparing with myocardial flow tracer imaging. The incidence of a dissociation between myocardial BMIPP and 201Tl distributions (BMIPP < 201Tl) as a marker of metabolic abnormality in viable tissue varied considerably among various heart diseases. Patients with ischemic cardiomyopathy and the dilated form of hypertrophic cardiomyopathy had a higher incidence while those with idiopathic dilated, alcoholic and hypertensive cardiomyopathy had a lower incidence. These results suggest that the marked difference between ischemic and idiopathic dilated cardiomyopathies may contribute to the differential diagnosis between these two diseases which are main basic abnormalities in congestive heart failure. Second, we investigated the relationship between myocardial BMIPP uptake and ventricular stress in patients with right ventricular pressure overload due to pulmonary hypertension. Myocardial BMIPP uptake in the right ventricle estimated by referring to uptake in the left ventricle showed a significant correlation with mean pulmonary artery pressure (mPAP) and no significant difference with myocardial 99mTc-sestamibi uptake in the 15-81 mmHg mPAP range. These results suggest that myocardial utilization of free fatty acid may be preserved in the presence of higher ventricular wall stress.
ADP-ribosyl cyclase, which catalyzes the conversion from NAD+ to cyclic adenosine diphosphoribose (cADPR), is proposed to participate in cell cycle regulation in Euglena gracilis. This enzyme, which was found as a membrane-bound protein, was purified almost the homogeneity after solubilization with deoxycholate, and found to be a monomeric protein with a molecular mass of 40 kDa. Its Km value for NAD+ was estimated to be 0.4 mM, and cADPR, a product of the enzyme, inhibited the enzyme competitively with respect to NAD+ whereas another product, nicotinamide, showed noncompetitive (mixed-type) inhibition. In contrast to mammalian CD38 and BST-1, Euglena ADP-ribosyl cyclase lacked cADPR hydrolase activity.
OBJECTIVE: To investigate the value of iodine-123 meta-iodobenzylguanidine (MIBG) myocardial imaging for defining high risk patients with idiopathic dilated cardiomyopathy from among candidates for beta blocker treatment, and for predicting functional improvement of the left ventricle in the early stages of treatment. METHODS: Echocardiographic indices, neurohormonal measurements, and myocardial MIBG distribution were assessed at baseline and after one month and three months of treatment in 27 patients with idiopathic dilated cardiomyopathy. Patients were classified into two groups, based on whether they reached a daily dose of > 20 mg of metoprolol without deterioration of heart failure at three months (group A, n = 20) or not (group B, n = 7). RESULTS: There were no significant differences in the echocardiographic indices or neurohormonal activity at baseline between the two groups, but MIBG uptake was higher, and the washout rate lower, in group A than in group B. After one month, though there were no significant changes in echocardiographic and neurohormonal variables, the heart to mediastinal (H/M) ratio on the delayed image was increased in group A but not in group B. In group A, the degree of increase in the H/M ratio on the delayed image after one month was also correlated with the degree of reduction in plasma concentrations of noradrenaline after three months. CONCLUSIONS: MIBG myocardial imaging may be useful for predicting the outcome of beta blocker treatment for heart failure patients with idiopathic dilated cardiomyopathy.
Serum uric acid (UA), the final product of purine degradation, has been proposed to be a marker for impaired oxidative metabolism and a possible predictor of mortality in patients with chronic heart failure. To elucidate whether serum UA correlates with the severity and the mortality of primary pulmonary hypertension (PPH), serum UA was assessed in 90 patients with PPH together with other clinical variables. Right heart catheterization was performed in all patients. Serum UA was significantly elevated in patients with PPH compared with age-matched control subjects (7.5 +/- 2.5 versus 4.9 +/- 1.2 mg/ml, p < 0.001). Serum UA negatively correlated with cardiac output (r = -0.52, p < 0.001) and positively correlated with total pulmonary resistance (r = 0.57, p < 0.001). Serum UA significantly decreased from 7.1 +/- 1.9 to 5.9 +/- 1.6 mg/dl with vasodilator therapy, associated with a reduction in total pulmonary resistance from 22 +/- 6 to 17 +/- 7 Wood units. During a mean follow-up period of 31 mo, 53 patients died of cardiopulmonary causes. Among noninvasive variables, serum UA was independently related to mortality by a multivariate Cox proportional-hazards analysis. The Kaplan-Meier survival curves according to the median value of serum UA demonstrated that patients with high serum UA had a significantly higher mortality rate than did those with low serum UA (log-rank test, p < 0.01). These results suggest that serum UA increases in proportion to the clinical severity of PPH and has independent association with long-term mortality of patients with PPH.
For objective evaluation in the lung arterial lesions, density histogram revealed by survey thoracic radiographies of fifteen canine filariosis and five normal canine were digitally analyzed, and preparation of pulmonary artery angiogram with inflated-fixed lung, the changes in the histogram and the pulmonary arterial lesion by a soft x-ray examination were compared. In the lung areas affected by filariosis, the density histogram increased the white level and decreased the black level in each part compared to a normal lung. In comparison with the normal parameters, those of the filariosis it were significantly increased in minimum grey level values (Min), maximum grey level values (Max), and the maximum frequency grey level values (Mode) and, it was significantly decreased in maximum frequency values (MaF). The pulmonary arterial lesion of the filariosis showed obvious morphological changes such as in distinction, pruning, angiectasis, and meandering. In the grade of pulmonary arterial lesion, the parameter Min, Max, Mode and MaF were changed significantly. From these results, it was clear that the methods for the lung arterial lesions analysis of x-ray images were confirmed to be highly beneficial in the lung arterial lesions for objective diagnosis.
We analyzed the current state of management of private dental offices in Japan using the 11th Survey of the Current Economy of Medicine and Dentistry conducted in September of 1997. The analysis was mainly performed by comparing the survey in 1997 with the survey conducted in 1989. The results show the medium-term tendencies in dental management. We also compared the data from dental offices with those from private medical offices without facilities for inpatients. The following are the results: the average income from dental practice for a dental office in 1997 was 4,050,000 yen, a decrease of 4.9% (about 210,000 yen) compared with the average income in 1989. The average income from treatment covered by insurance in 1997, which accounted for most of the total income, was 3,540,000 yen, a decrease of 2.8% compared with that in 1989. The average income from non-insured treatment was 490,000 yen, which was also a decrease of 17.4%. The average income from medical practice for a medical office in 1997 was 1,970,000 yen more than the average income from dental practice of the same year. The average medical practice expenses and the average balance in medicine were higher than those in dentistry by 1,360,000 yen and by 600,000 yen respectively. Although the average income from medical practice slightly increased, the average wage costs increased by as much as 42.8%, resulting in a decrease of 21.2% in the average balance. Dental offices attempted to weather the decreased income from dental practice by raising the average fee paid by an insured patient. The analysis in the present study suggested that a decreasing number of patients and increasing dental practice expenses diminished the balance.