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Purpose Because the posterior wall of the aorta and left atrium are interlocked, the amplitude of motion of the aortic wall (AMAW) may reflect cardiac and vessel functions. This study examined the relationship between cardiac and vessel functions and AMAW. Methods Patients with cardiovascular diseases or patients undergoing health examinations who visited a participating hospital and underwent echocardiography and brachial–ankle pulse-wave velocity (baPWV) examinations were registered. The correlations between echocardiographic indices, ankle–brachial index, and baPWV and AMAW on M-mode echocardiography were analyzed. Results Overall, 184 patients were enrolled. Heart rate (r = − 0.1587), ejection fraction (EF; r = 0.3240), wall thickness (r = − 0.1598), peak early diastolic mitral annular velocity (E) to peak early diastolic mitral annular velocity ratio (e’; r = − 0.2463), and baPWV (r = − 0.1928) significantly correlated with AMAW. In the stratified multiple regression analysis, E/e’ (standardized partial regression coefficients = − 0.1863) and mean baPWV (standardized partial regression coefficients = − 0.1917) in patients with an EF of ≥ 60% (n = 114) significantly correlated with AMAW. In patients with an EF of n = 70), E/e’ (standardized partial regression coefficients = − 0.2443) significantly correlated with AMAW. Conclusion Because E/e’ correlated with AMAW in patients with an EF of

The aim of this study was to demonstrate the safety and efficacy of H2-saline infusion for treatment of rheumatoid arthritis (RA). We conducted a randomized, double-blind, placebo-controlled investigation of the infusion of 1 ppm H2-dissolved saline (H2-saline) in 24 RA patients. Patients were randomized 1:1 to receive 500 ml of either H2-saline or placebo-saline, which was drop infused intravenously (DIV) daily for 5 days. The disease activity score in 28 joints (DAS28) was measured at baseline, immediately post infusion, and after 4 weeks. Therapeutic effects of H2-saline on joint inflammation were estimated by measuring serum biomarkers for RA, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6), matrix metalloproteinase-3 (MMP-3), and urinary 8-hydroxydeoxyguanosine (8-OHdG). In the H2-infused group, average DAS28 decreased from 5.18 ± 1.16 to 4.02 ± 1.25 immediately post infusion and reached 3.74 ± 1.22 after 4 weeks. No significant decrease in DAS28 was observed in the placebo group throughout the study. IL-6 levels in the H2 group significantly decreased in 4 weeks by 37.3 ± 62.0% compared to baseline, whereas it increased by 33.6 ± 34.4% in the placebo group. TNFα levels did not change remarkably in the H2 or placebo groups in 4 weeks post-infusion compared to baseline. The relative ratio of 8-OHdG in the H2 group also significantly decreased by 4.7%. After 4 weeks, MMP3 was significantly reduced by 19.2% ± 24.6% in the H2 group, and increased by 16.9% ± 50.2% in the placebo group. Drop infusion of H2 safely and effectively reduced RA disease activity.

BACKGROUND: Hypertension is an important risk factor of coronary heart disease. A new guidelines for hypertension prevention and management in The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure in the United States recommended lifestyle modification or medical treatment for subjects with prehypertension. However, whether prehypertension increases the risk of coronary atherosclerosis in the Japanese population is still unknown. METHODS: A cross-sectional study in a clinical setting was conducted. The subjects were 705 patients (417 males and 288 females) aged 30 years and older who underwent a first-time coronary angiography for suspected or known coronary heart disease at 5 major cardiology departments in the Fukuoka metropolitan area between September 1996 and August 1997. RESULTS: Compared to subjects with normal blood pressure, those with prehypertension had an increased risk of coronary atherosclerosis even after adjusting for other factors. CONCLUSION: Prehypertension may be an important clinical entity which requires treatment in the Japanese population.

Postprandial increase in remnant lipoprotein concentrations has been suggested as an important atherogenic factor. However, the influence of these remnants on the development of restenosis after percutaneous coronary intervention (PCI) remains to be examined. The present study was designed to address this point. In 60 consecutive patients with successful PCI, the influences of possible risk factors on the development of restenosis, including remnant-like particles (RLP) cholesterol (RLP-C) and triglyceride (RLP-TG), were examined. While mean concentrations of RLP-C and RLP-TG were normal in fasting state, postprandial change in RLP-C concentrations was a significant and independent risk factor for restenosis after PCI. The calculated cut-off index (COI) for the change was +64%. When the patients were divided into 2 groups according to this COI, minimal lumen diameter (MLD) and reference coronary diameter were comparable before and immediately after PCI between the high- (COI < 64%) and the low- (COI < 64%) responders. However, follow-up coronary angiography 3 to 6 months after PCI demonstrated that MLD, late loss, and loss index were all worse in the high responders compared with the low responders. These results indicate that post-prandial increase in RLP-C concentrations is an independent risk factor for restenosis after successful PCI, even in patients with normal fasting RLP-C levels.

This study examined the relation of Type A behavior pattern and its components to angiographically documented coronary atherosclerosis in 198 Japanese women. A questionnaire-based interview elicited psychosocial and other factors. Type A behavior pattern was measured by 12 questions. Significant coronary stenosis was defined when a 75% or greater luminal narrowing occurred at one or more major coronary arteries or 50% or greater narrowing occurred at the left main artery. Gensini's score also was calculated. Logistic regression analysis was used to calculate odds ratios and 95% confidence intervals with adjustment for traditional coronary risk factors and the presence of a job. Global Type A behavior pattern showed no material association with the severity of coronary atherosclerosis assessed by both Gensini's score and the presence of significant coronary stenosis. However, its subcomponents, enthusiasm and competitiveness, were positively related to the severity of coronary atherosclerosis, whereas self-confidence and perfectionism were negatively related. These findings suggest overall a null association between global Type A and coronary atherosclerosis as well as the presence of toxic or beneficial components of Type A behaviors in Japanese women.

Objectives This study investigated the effect of reducing serum lipids on carotid artery intima-media thickness (IMT) in asymptomatic patients with hypercholesterolemia from Fukuoka, Japan. Background Carotid atherosclerosis is a strong, independent predictor of morbidity and mortality in patients with coronary heart disease (CHD). Methods A total of 246 asymptomatic hypercholesterolemic patients (mean age 66 years) were randomized to receive either probucol (500 mg/day, n = 82) or pravastatin (10 mg/day, n = 83) or to enter a control group (diet alone, n = 81); they were followed for two years. The change in IMT in the common carotid artery was the primary end point measure, and the incidence of major cardiovascular events was the secondary measure. Results Over the two-year period, serum low-density lipoprotein (LDL) cholesterol was significantly reduced in the pravastatin group (36%), the probucol group (29%) and the control group (12%) (p Conclusions Probucol reduced cholesterol levels and stabilized plaque, leading to a lower incidence of cardiac events in these hypercholesterolemic patients.

Discordance between the (123)I-labelled 15-iodophenyl-3-R, S-methyl pentadecanoic acid (BMIPP) and (201)Tl findings may indicate myocardial viability (MV). This study compared dobutamine stress echocardiography (DSE) and single-photon emission computed tomography (SPECT) using the dual tracers for assessment of MV and prediction of functional recovery after acute myocardial infarction (AMI). DSE and dual SPECT were studied in 35 patients after AMI, of whom 28 underwent percutaneous coronary intervention in the acute stage. Dual SPECT was performed to compare the defect score of BMIPP and (201)Tl. The left ventricular wall motion score (WMS) was estimated during DSE and 6 months later to assess functional recovery of the infarct area. The rate of agreement of MV between dual SPECT and DSE was 89% (p

Although previous studies have demonstrated that even quantitative coronary angiography (QCA) can not provide accurate disease morphology, there has not been a systematic comparison of disease morphology determined by QCA and intravascular ultrasound (IVUS), particularly in Japanese patients. Therefore, the present study prospectively examined patients in a multicenter cooperative study. A total of 491 coronary sites from 562 patients (446 men, 116 women; mean age, 64+/-11 years) who underwent coronary interventions were enrolled. The target lesions (>50% diameter stenosis) were evaluated pre-operatively by both QCA and IVUS operating at 30-40 MHz and the percent area stenosis, eccentricity index (EI) and lesion length were determined. The minimal (min) and maximal (max) distances from the center of the stenotic lesion to the outline of the vessel wall were measured, and the EI was calculated by the formula: [(max - min)/max]. By QCA, lesion length was determined by measuring the distance between the proximal and distal shoulders of the lesion. When the lesions were observed by IVUS with a motorized pull-back system, the length was calculated by multiplying the time for observation of the disease and 0.5 or 1 mm/s. Although the severity of the stenosis determined by QCA (86+/-10%, mean +/- SD) did not differ from that by IVUS (83+/-13%), there was no correlation between them (r=0.32, y=0.25x+65) and the correlation did not improve when lesions with remodeling, enlargement (n=176) or shrinkage (n=79) were omitted from the calculation. The EIs by QCA and IVUS were 0.51+/-0.26 and 0.52+/-0.22, respectively (NS), and there was no correlation between them (r=0.30, y=0.36x+33). However, when the lesions with remodeling were excluded, the correlation greatly improved (r=0.80, y=0.84x+10.6, p

Takaaki Sakai,1 Bunpei Sato,2 Koji Hara,3 Yuichi Hara,3 Yuji Naritomi,3 Samon Koyanagi,1 Hiroshi Hara,3 Tetsuhiko Nagao,4 Toru Ishibashi51Department of Cardiology, Haradoi Hospital, Fukuoka, Japan; 2MiZ Company Limited, Fujisawa, Kanagawa, Japan; 3Department of Internal Medicine, Haradoi Hospital, Fukuoka, Japan; 4Midorino Clinic, Aoba, Higashi-ku, Fukuoka, Japan; 5Department of Rheumatology and Orthopedic Surgery, Haradoi Hospital, Fukuoka, Japan Background: The redox imbalance between nitric oxide and superoxide generated in the endothelium is thought to play a pivotal role in the development of endothelial dysfunction. A third reactive oxygen species (ROS), H2O2, is known to have both beneficial and detrimental effects on the vasculature. Nonetheless, the influence of the hydroxyl radical, a byproduct of H2O2 decay, is unclear, and there is no direct evidence that the hydroxyl radical impairs endothelial function in conduit arteries. Molecular hydrogen (H2) neutralizes detrimental ROS, especially the hydroxyl radical. Objectives: To assess the influence of the hydroxyl radical on the endothelium and to confirm that a gaseous antioxidant, H2, can be a useful modulator of blood vessel function. Methods: The efficacy of water containing a high concentration of H2 was tested by measuring flow-mediated dilation (FMD) of the brachial artery (BA). The subjects were randomly divided into two groups: the high-H2 group, who drank high-H2 water containing 7 ppm H2 (3.5 mg H2 in 500 mL water); and the placebo group. Endothelial function was evaluated by measuring the FMD of the BA. After measurement of diameter of the BA and FMD at baseline, volunteers drank the high-H2 water or placebo water immediately and with a 30-minute interval; FMD was compared to baseline. Results: FMD increased in the high-H2 group (eight males; eight females) from 6.80%±1.96% to 7.64%±1.68% (mean ± standard deviation) and decreased from 8.07%±2.41% to 6.87%±2.94% in the placebo group (ten males; eight females). The ratio to the baseline in the changes of FMD showed significant improvement (P

Psoriasis, a chronic inflammatory skin disease, is caused by infiltrating lymphocytes and associated cytokines, including tumor necrosis factor (TNF)α, interleukin (IL)-6, and IL-17. Effective treatments, including pathogenesis-based biological agents against psoriasis, are currently under development. Although the role of reactive oxygen species (ROS) in the pathogenesis of psoriasis has been investigated, it remains to be fully elucidated; ROS-targeted therapeutic strategies are also lacking at present. Therefore, the objective of the present study was to assess whether H2, a ROS scavenger, has a therapeutic effect on psoriasis-associated inflammation by reducing hydroxyl radicals or peroxynitrite in the immunogenic psoriasis cascade. Three methods were used to administer H2: Drop infusion of saline containing 1 ppm H2 (H2-saline), inhalation of 3% H2 gas, and drinking of water containing a high concentration (5-7-ppm) of H2 (high-H2 water). Treatment efficacy was estimated using the disease activity score 28 (DAS28) system, based on C-reactive protein levels, and the psoriasis area and severity index (PASI) score, determined at baseline and following each H2 treatment. Furthermore, levels of TNFα, IL-6, and IL-17 were analyzed. The DAS28 and PASI score of the three patients decreased during H2 treatment, regardless of the administration method. The psoriatic skin lesions almost disappeared at the end of the treatment. IL-6 levels decreased during H2 treatment in Case 1 and 2. IL-17, whose concentration was high in Case 1, was reduced following H2 treatment, and TNFα also decreased in Case 1. In conclusion, H2 administration reduced inflammation associated with psoriasis in the three cases examined and it may therefore be considered as a treatment strategy for psoriasis-associated skin lesions and arthritis.

The present study evaluated the effect of hypertension (HT), dyslipidemia and diabetes mellitus (DM) on the development of coronary atherosclerosis in the Japanese population, using a cross-sectional study of 433 patients (254 men and 179 women) aged 30 years or older who underwent coronary angiography for suspected or known coronary heart disease angina at 5 cardiology departments in the Fukuoka area between September 1996 and August 1997. Patients with a disease duration of 6 months or more were excluded. The main outcome measure was angiographically defined coronary artery stenosis and was found to a significant degree in 146 patients (33.7%). HT, DM, low levels of high-density lipoprotein cholesterol (HDL-C) and hypertriglyceridemia remained as significant coronary artery disease (CAD) risk factors even after controlling for age, sex, hospital, smoking, alcohol use, body mass index and leisure time physical activity. However, hypercholesterolemia was not a significant risk factor after adjusting for these variables. After controlling for these variables, DM, low HDL-C and hypertriglyceridemia were significant CAD risk factors for men, but only DM was a significant CAD risk factor in women. These results indicate that in Japan DM, low HDL-C and hypertriglyceridemia may be more important CAD risk factors than hypercholesterolemia.

Resting iodine 123—labeled metaiodobenzylguanidine ( 125 I-MIGB) scintigraphy was performed in 19 patients with unstable angina to determine if it can detect myocardial ischemia and identity the angina-provoking coronary artery. Visual assessment of 123 I-MIBG single-photon-emission computed tomograms was related to coronary vessel stenoses revealed by artariography at each vascular territory. Fourteen (74%) of 19 patients had regional 123 I-MIBG—identified defects at areas with preserved thallium-201 perfusion. 123 I-MIBG defects were highly positive at areas supplied by angina-provoking coronary arteries. The sensitivity and specificity of 123 I-MIBG defects for identifying the angina-provoking coronary vessel were 71% and 78%, respectively. The interval between the most recent angina attack and imaging was shorter and the angina occurred more commonly after admission in patients with 123 I-MIBG defects than in those without defects. These data suggest that repetitive myocardial ischemia impairs regional 123 I-MIBG uptake and that this impairment persists for several days after perfusion has been restored. Thus resting 123 I-MIBG scintigraphy is a useful noninvasive method to detect coronary stenoses provoking repetitive ischemia in patients with unstable angina in its acute phase.

The purpose of this study was to assess the factors involved in the development of the right-to-left (R-L) shunt in patients with atrial septal defect (ASD), especially the role of tricuspid regurgitation (TR). Thirty-one consecutive patients with ASD underwent transesophageal Doppler echocardiography to determine the size of ASD, the shunt flow, and the TR flow, and they were compared with hemodynamics examined by cardiac catheterization. Sixteen patients with the R-L shunt were older (53 +/- 11 vs 34 +/- 9 years; p0.001) and had higher pulmonary arterial pressure (36 +/- 17 vs 25 +/- 5 mmHg; p0.05) and a greater Qp/Qs (3.6 +/- 1.2 vs 2.4 +/- 0.9 L/min; p0.01) as compared with 15 patients with the pure left-to-right shunt. In six of 21 patients with TR, the regurgitant flow oriented toward ASD and blew into the left atrium through the defect. Besides the deviation of TR flow, the prevalences of the maximum diameter of ASD2.5 cm and the maximal TR flow area4 cm2 were significantly higher in the six patients as compared with patients with TR not related to the R-L shunt (p0.05 and p0.05), despite the pulmonary arterial pressure being similar in the two groups. Reversal of pressure gradient between the left and right atrium was not observed during the cardiac cycle in all patients. In conclusion, TR is a determinant of the R-L shunt in patients with ASD even in the absence of the reversal of pressure gradient between the left and right atrium.

The objective of this study was to examine the prevalence and pathogenesis of silent myocardial ischemia during exercise following myocardial infarction. Exercise-induced myocardial ischemia was assessed by 201Tl-SPECT (single photon emission computed tomography) 4.5 weeks after acute myocardial infarction in 229 patients. Exercise-induced myocardial ischemia occurred in 109 patients (48%), and 72 (32%) had silent ischemia. Although the prevalence of multivessel coronary artery disease was similar between patients with silent and symptomatic ischemia, the size of reversible myocardial ischemia was larger in patients with symptomatic ischemia than in those with silent ischemia (21.3 +/- 3.0% vs 13.2 +/- 1.9% of LV, p0.05). The incidence of reversible ischemia remote from the infarct area was higher in patients with symptomatic ischemia than in those with silent ischemia (30% vs 17%, p0.10). The cause of silent ischemia after myocardial infarction may be closely related to the smaller size of reversible myocardial ischemia. Ischemia remote from, or adjacent to, the infarct area could be a factor in determining the presence or absence of pain.

The role of coronary vasospasm in the pathogenesis of myocardial infarction is unclarified. Among 212 patients with myocardial infarction in whom percutaneous transluminal coronary angioplasty (PTCA) or coronary thrombolysis was not performed at the acute stage, 21 patients (10%) showed no significant coronary stenosis (the degree of stenosis was less than 50% of the luminal diameter) by coronary angiography 4 weeks after myocardial infarction. Among them, 11 (52%) had preinfarction angina at rest, including two with variant angina, and nine (43%) had postinfarction angina at rest. Intracoronary ergonovine maleate induced coronary vasospasm in 12 (75%) of 16 patients examined. Coronary vasospasm occurred in the infarct-related coronary arteries in all patients, and importantly, multivessel coronary vasospasm occurred in 11 patients (69%). The infarct size was relatively small in these patients: (1) seven patients (33%) had Q wave myocardial infarction while 14 patients (67%) had non-Q wave myocardial infarction; (2) peak creatine phosphokinase (CPK) was lower than 1000 IU/ml in all patients; and (3) thallium-201 (TI-201) scintigraphic study showed no perfusion defect in 8 of 18 patients. There was only one patient with congestive heart failure and no patient died. These results suggest that coronary vasospasm may play an important role in the pathogenesis of myocardial infarction in patients without significant coronary stenosis. The relatively small infarct size suggests that coronary reperfusion occurred in the early stages of myocardial infarction.

To elucidate the pathogenesis of mitral regurgitation (MR) after myocardial infarction (MI), the incidence of papillary muscle dysfunction (PMD), mitral annular size, and the extent of wall-motion abnormalities were examined in 81 patients with previous MI by two-dimensional echocardiography and real-time two-dimensional Doppler flow imaging. The prevalence of pathological MR was lower in patients with anterior MI (36%) than in those with inferior (65%) or anterior and inferior MI (88%) (P < 0.01 vs anterior MI group). The incidence of PMD in patients with MR in the anterior MI group (15%) was lower than that in the inferior (50%, P < 0.01) or anterior and inferior MI group (43%, P < 0.05). The mitral annular dimension in patients with MR was significantly greater than in those without MR, but it was similar among the three groups. The extent of wall-motion abnormality correlated significantly with the area of MR jet in the anterior MI group (y = 3.1x + 15.5, r = 0.52, P < 0.01) and in the inferior MI group (y = 8.3x + 32.7, r = 0.57, P < 0.01). However, the slope of this relationship was significantly steeper in the inferior MI group than in the anterior MI group (P < 0.05). These results indicated that the degree of MR with inferior MI was greater than with anterior MI for a given MI area. PMD may play an important role in the higher prevalence and greater degree of MR in inferior MI.

To determine the factors influencing the spontaneous remission of variant angina, clinical characteristics were examined in 75 Japanese patients with variant angina. Spontaneous remission was defined as an absence of angina at rest for at least 3 months after withdrawal of treatment with calcium antagonists. This remission occurred in 12 patients (16%) (remission group), while angina persisted despite treatment with calcium antagonists and nitrates in 33 patients (44%) (persistent angina group). The remaining 30 patients (40%) were angina-free under treatment with calcium antagonists and/or nitrates (angina-free on treatment group). The prevalence of significant coronary artery stenosis (> 75%) was significantly higher in the remission group than in the persistent angina group (44% vs 7%, p < 0.05). The prevalence of cessation of smoking was significantly higher in the remission group than in the persistent angina group (92% vs 39%, p < 0.01). Age, gender, other coronary risk factors, disease activity of variant angina and site of myocardial ischemia during anginal attacks were not statistically different among the 3 groups. There data indicate that remission of variant angina occurs more frequently in patients with than in those without significant coronary artery stenosis and that cessation of smoking is an important factor for remission of variant angina.

BACKGROUND It has been shown that atrial natriuretic peptide (ANP), an endogenous vasodilator, dilates coronary arteries and decreases coronary vascular resistance. The purpose of this study was to determine whether an intravenous administration of ANP attenuated exercise-induced myocardial ischemia in 14 patients with stable effort angina pectoris. METHODS AND RESULTS The first 12 patients (patients 1-12) who had exercise-induced ST segment depression underwent treadmill exercise testing and the last seven patients (patients 8-14) underwent the exercise 201Tl-single-photon emission computed tomography (SPECT) study while synthetic 28-amino acid alpha-human ANP (0.1 micrograms/kg per minute) or saline was intravenously infused in a double-blind, cross-over manner. The duration of exercise testing was the same during ANP and saline infusion, which was determined in preliminary exercise testings in each patient to cause a transient perfusion defect and/or ischemic ST segment depression. During saline infusion, all 12 patients developed exercise-induced ischemic ST segment depression, whereas no significant ST segment depression appeared during ANP infusion. Average ST segment depression during ANP infusion was significantly less (p < 0.01) than that during saline infusion (0.0 +/- 0.0 versus 0.2 +/- 0.1 mV, mean +/- SD). The averaged extent and severity scores assessed by 201Tl-SPECT were smaller (p < 0.05) during ANP infusion than during saline infusion (extent score: 0.22 +/- 0.20 versus 0.42 +/- 0.20; severity score: 18.77 +/- 23.45 versus 38.24 +/- 24.04, respectively). ANP decreased resting systolic blood pressure from 125 +/- 15 to 110 +/- 15 mm Hg (p < 0.01) but did not alter resting heart rate. At peak exercise, systolic blood pressure, heart rate, and the rate-pressure products did not differ during ANP and saline infusion. At peak exercise, plasma ANP increased from 98 +/- 45 to 4,383 +/- 2,782 pg/ml and cGMP increased from 3.6 +/- 1.7 to 34.5 +/- 16.1 pmol/ml during ANP infusion; values were significantly higher than those during saline infusion (from 96 +/- 42 to 133 +/- 66 pg/ml and from 3.4 +/- 1.8 to 4.6 +/- 1.8 pmol/ml, respectively). CONCLUSIONS An intravenous administration of ANP attenuated exercise-induced myocardial ischemia in patients with stable effort angina pectoris. Although the mechanism by which ANP attenuated myocardial ischemia was not defined, increased myocardial perfusion to the ischemic region might be an important factor.

The incidence of and the Doppler color-flow echocardiographic characteristics of aortic valve prolapse with nonrheumatic aortic regurgitation were examined. Aortic valve prolapse was observed in 21 of 243 patients (15 men and 6 women) with aortic regurgitation as detected by Doppler color-flow echocardiography (rheumatic, 112; nonrheumatic, 131) in 1247 consecutive patients. Patients with aortic valve prolapse included three patients with essential hypertension and one with annuloaortic ectasia. The remaining 17 patients (7% of those with aortic regurgitation) had no other associated cardiovascular disease (idiopathic aortic valve prolapse). Prolapse of the mitral or the tricuspid valve or both was associated with aortic valve prolapse in seven patients. Aortic regurgitation jet was markedly deviated from the axis of left ventricular outflow tract toward the anterior mitral leaflet or the interventricular septum in 17 of 21 (81%) patients with aortic valve prolapse, whereas 28 of 110 (25%) patients with nonrheumatic aortic regurgitation without prolapse and 17 of 112 (15%) patients with rheumatic aortic regurgitation without prolapse showed the deviation of regurgitant jet (p < 0.001). In conclusion, idiopathic aortic valve prolapse is one of the significant causes of aortic regurgitation, and a marked deviation of regurgitant jet is a characteristic Doppler color-flow echocardiographic finding of aortic regurgitation that results from aortic valve prolapse.

A noninfarcted, entirely collateral-dependent myocardial region provides an opportunity to assess the effect of nitroglycerin on coronary collateral function during exercise. Stress thallium-201 computed tomography was performed in seven patients with effort angina and no history of myocardial infarction, both before and after nitroglycerin (0.3 mg). All patients had single-vessel disease with total or subtotal (99% with delay) occlusion of proximal left anterior descending coronary artery and well-developed collaterals. The pressure-rate product, mean blood pressure, and heart rate at peak exercise did not differ before and after nitroglycerin. The size of the perfusion defect and the severity of ischemia during exercise estimated by quantitative analysis of thallium-201 single photon emission computed tomography were significantly less after nitroglycerin administration (extent score: 23 +/- 17 vs 7 +/- 9, p less than 0.01; severity score: 20 +/- 22 vs 3 +/- 4, p less than 0.05). The pressure-rate products at peak exercise did not differ before and after nitroglycerin, which suggested that the reduction in perfusion defect size was unlikely to be the result of decreased myocardial oxygen consumption. These results suggest that nitroglycerin improved coronary collateral function during exercise and thus prevented exercise-induced myocardial ischemia.

We report a case of a 40-year-old man who had a quadricuspid aortic valve associated with aortic regurgitation. The anomaly was revealed by transesophageal echocardiography (TEE), and confirmed by cardiac surgery. TEE is a useful noninvasive method for identifying the quadricuspid aortic valve.

Chronic arterial hypertension (HT) and left ventricular hypertrophy (LVH) increase the morbidity and mortality of acute myocardial infarction in patients. In this article, we discuss earlier studies from Koyanagi et al. in our laboratory that showed that when animals with chronic HT and LVH (HT-LVH) were subjected to acute coronary artery occlusion (CAO), there was a 3.5-fold increase in mortality and a 35% increase in infarct size expressed as a percent of the area at risk. We subsequently determined the effect of HT-LVH on the wavefront of myocardial infarction. Dogs were made hypertensive using a single-kidney, single-clip model of renovascular hypertension that produced mean arterial blood pressure (BP) = 141 +/- 3 mm Hg and left ventricular:body weight = 5.8 +/- 0.1 g/kg (p less than 0.05 vs. control animals). Conscious animals with HT-LVH and control animals were subjected to 1 or 3 h of CAO. Infarct and risk areas were measured using triphenyltetrazolium chloride (TTC) stain and barium angiography, respectively. The results suggested that the wavefront of infarction was accelerated in animals with HT-LVH. Further studies suggested that the wavefront of myocardial infarction could be markedly retarded by normalizing blood pressure (nitroprusside) 1 h following CAO. Recent studies in an animal model of HT-LVH suggested that electrophysiological abnormalities occur when these animals were subjected to CAO. Sixty-five percent of animals with HT-LVH had sudden death during CAO compared to 27% of the control group. We studied whether chronic beta-adrenergic blockade would reduce mortality associated with CAO in animals with HT-LVH.(ABSTRACT TRUNCATED AT 250 WORDS)

To clarify the incidence and clinical characteristics of exercise-induced myocardial ischemia in patients with vasospastic angina, we performed exercise thallium computed tomography in 25 patients who had no significant coronary artery stenosis greater than 70%. Coronary artery spasm was documented by coronary angiography in all patients. Eleven patients (44%) developed exercise-induced perfusion defects, but only four of them had anginal pain (36%). Diltiazem (90 mg, administered orally) prevented the development of exercise-induced perfusion defects in all patients. Multivessel coronary spasm was documented by coronary angiography in 11 patients, and nine of them (82%) showed exercise-induced perfusion defects (p less than 0.05).(1) Exercise-induced myocardial ischemia was demonstrated in 44% of patients who had vasospastic angina without fixed coronary stenosis, and 64% of them were asymptomatic. (2) Patients with multivessel spasm had a greater prevalence of exercise-induced myocardial ischemia than those with single-vessel spasm.

Although previous studies have demonstrated that even quantitative coronary angiography (QCA) can not provide accurate disease morphology, there has not been a systematic comparison of disease morphology determined by QCA and intravascular ultrasound (IVUS), particularly in Japanese patients. Therefore, the present study prospectively examined patients in a multicenter cooperative study. A total of 491 coronary sites from 562 patients (446 men, 116 women; mean age, 64+/-11 years) who underwent coronary interventions were enrolled. The target lesions (50% diameter stenosis) were evaluated pre-operatively by both QCA and IVUS operating at 30-40 MHz and the percent area stenosis, eccentricity index (EI) and lesion length were determined. The minimal (min) and maximal (max) distances from the center of the stenotic lesion to the outline of the vessel wall were measured, and the EI was calculated by the formula: [(max - min)/max]. By QCA, lesion length was determined by measuring the distance between the proximal and distal shoulders of the lesion. When the lesions were observed by IVUS with a motorized pull-back system, the length was calculated by multiplying the time for observation of the disease and 0.5 or 1 mm/s. Although the severity of the stenosis determined by QCA (86+/-10%, mean +/- SD) did not differ from that by IVUS (83+/-13%), there was no correlation between them (r=0.32, y=0.25x+65) and the correlation did not improve when lesions with remodeling, enlargement (n=176) or shrinkage (n=79) were omitted from the calculation. The EIs by QCA and IVUS were 0.51+/-0.26 and 0.52+/-0.22, respectively (NS), and there was no correlation between them (r=0.30, y=0.36x+33). However, when the lesions with remodeling were excluded, the correlation greatly improved (r=0.80, y=0.84x+10.6, p0.05). Lesion length determined by QCA (12.4+/-6.1 mm) was significantly shorter than that by IVUS (16.3+/-8.9 mm, p0.01). These results demonstrate that coronary angiography significantly misinterprets disease morphology in terms of severity, eccentricity and length, in part because of vessel remodeling that can be accurately determined only by IVUS.

The relation of alcohol consumption to the severity of coronary atherosclerosis was examined among 323 men and 220 women who underwent coronary arteriography. Severity of coronary atherosclerosis was assessed by the number of vessels obstructed ≥75% in diameter and Gensini's severity score. Alcohol consumption was divided into 5 categories in men (never, past, 1–24, 25–49, and ≥50 ml per day) and 3 categories in women (never, past, and current). Among men, odds ratios of severe stenosis (multiple-vessel disease or Gensini's score >15) decreased substantially and significantly in all current drinking categories but without dose-response effect. There was a weak, inverse association of current alcohol consumption with one-vessel disease, but not with moderate stenosis in terms of Gensini's score (≤15). Past drinkers showed a fairly large, but statistically nonsignificant, decrease in the odds ratios of not only severe stenosis but also of moderate stenosis. Among women, current drinkers showed a small, statistically nonsignificant decrease in the risk of severe stenosis in terms of Gensini's score. These associations with alcohol use did not change after adjustment for known coronary risk factors. The present findings add to evidence that alcohol drinking confers protection against coronary atherosclerosis.

Objective : To examine the relation of type A behavior pattern and job strain to angiographically documented coronary stenosis. Methods : Subjects were 197 male Japanese patients with a full-time job. A questionnaire-based interview elicited psychosocial and other factors. Type A behavior pattern was measured by 12 questions, and job strain by the method of Karasek. Significant coronary stenosis was defined when a 75% or greater luminal narrowing occurred at one or more major coronary arteries or when a 50% or greater narrowing occurred at the left main artery. Logistic regression analysis was used to calculate odds ratio (OR) and 95% confidence interval (CI) with adjustment for traditional coronary risk factors and job type Results : Type A behavior pattern was related to a statistically non-significant lower prevalence of the coronary stenosis especially in the absence of job strain (adjusted OR 0.6, 95% CI 0.3–1.2). Job strain was non-significantly associated with a modestly increased prevalence of coronary stenosis (OR 1.7, 95% CI 0.6–5.2) Conclusion : These findings suggest that both the behavioral pattern and psychosocial work environment may be related to coronary artery stenosis.

PURPOSE: To examine the relation between green tea consumption and arteriographically determined coronary atherosclerosis. METHODS: Study subjects were 512 patients (302 men and 210 women) aged 30 years or older who underwent coronary arteriography for the first time at four hospitals in Fukuoka City or one hospital in an adjacent city between September 1996 and August 1997. Lifestyle characteristics including green tea consumption were ascertained before arteriography by a questionnaire supported with interview. RESULTS: 117 men (38.7%) and 50 women (23.8%) had significant stenosis of one or more coronary arteries. Green tea consumption tended to be inversely associated with coronary atherosclerosis in men, but not in women. An evident, protective association between green tea and coronary atherosclerosis was observed in a subgroup of 262 men excluding those under dietary or drug treatment for diabetes mellitus. In this subgroup, after adjustment for traditional coronary risk factors and coffee, odds ratios of significant stenosis for consumption of 2–3 cups and 4 or more cups per day were 0.5 (95% confidence interval 0.2–1.2) and 0.4 (0.2–0.9), respectively, as compared with a consumption of one cup per day or less. CONCLUSIONS: The results indicate that green tea may be protective against coronary atherosclerosis at least in men.

The purpose of this study was to determine whether the early stages of arterial atherosclerosis could be evaluated by the vascular response to nitroglycerin (NTG). The vascular elasticity of the common carotid artery (CCA) was evaluated at sites without atheromatous plaque using high-resolution ultrasonography before and after sublingular NTG administration. The vascular elasticity was expressed by vascular strain (VS) and pressure-strain elastic modulus (Ep). The study was performed in 9 normal young males (group N) and 52 patients who were suspected to have coronary artery disease (CAD). In group N, VS of the CCA increased from 9+/-2 to 13+/-4%, Ep decreased from 80+/-18 to 42+/-14 kPa (p

The severity of mitral regurgitation (MR) was assessed by transesophageal Doppler flow echocardiography (TEE) using new criteria in 87 patients. The severity of MR assessed by TEE (TEE-MR) was compared with that obtained by left ventriculography (LVG-MR). Although the severity of TEE-MR has been evaluated by MR jet area, it is often difficult because the MR jet extends beyond a single frame image in severe MR. We found that (1) when the MR area was larger than 3 cm2, the severity of MR was more than second-degree by LVG; (2) there was systolic turning flow (STF) of the MR jet within the left atrial cavity in 27 of 30 patients with third- and fourth-degree LVG-MR; and (3) there was late systolic backward flow (SBF) in the pulmonary veins in 9 of 10 patients with fourth-degree LVG-MR. A new grading of the severity of MR by TEE was proposed, which combined the findings of STF, SBF, and the MR area. These new criteria of the severity of TEE-MR excellently correlated with that by LVG (y = 0.94x + 0.08; r = 0.95, p less than 0.01). The criteria for MR by TEE were also useful for assessment of MR in patients with prosthetic mitral valve dysfunction (y = 0.96x + 0.04; r = 0.97, p less than 0.01). We conclude from this study that the severity of MR can be accurately assessed with TEE by measuring the MR area and the specific flow patterns in the left atrium and pulmonary veins.

Two siblings presented with symptoms of left ventricular dysfunction and ventricular arrhythmias. Echocardiography and left ventriculography revealed dilatation, diffuse hypokinesis and apical aneurysm of the left ventricle in both cases. Myocardial infarction was unlikely by history and examinations. We diagnosed them as cases of familial dilated cardiomyopathy complicated by left ventricular aneurysm.

Of 383 patients with vasospastic angina who were followed for a period of 3.2 +/- 0.1 years, 9 (2%) died suddenly from cardiac causes. Calcium antagonists had been given to 98% of our patients. Only one patient who died suddenly had a fixed coronary stenosis of 75% or greater. Eight of the 9 patients showed ST segment elevation during anginal attack at rest, and 3 patients showed ST segment elevation at both anterior and inferior leads. Sudden death occurred in 6 of 41 patients (12.5%) who were documented to have multivessel coronary spasm, but in only 3 of 342 patients (1%) who had single vessel spasm (p less than 0.01). Serious arrhythmia occurred during anginal episode in 3 of 9 patients who died suddenly (53%) and in 52 of 374 who did not (14%). These results suggest that the frequency of sudden cardiac death was rather low in Japanese patients with vasospastic angina. The risk of sudden death was increased in patients with multivessel spasm and serious arrhythmia during anginal attacks but not these with fixed coronary stenosis.

To test the hypothesis that the relationship between infarct area (IA) and area at risk (AR) varies in different layers of the left ventricle (LV), we occluded the circumflex coronary artery for 48 h in 20 conscious dogs. AR was determined by postmortem coronary stereoarteriography, and infarct area by pathological examination. Both AR and IA were divided into four layers: posterior papillary muscle (PPM), subendocardium (Endo), midwall, and subepicardium (Epi) and quantified with planimetry. Hemodynamics and regional myocardial flow with tracer microspheres (7-10 micrometers diam) were measured before and after coronary occlusion. IA was closely correlated with AR for PPM (r = 0.96), Endo (r = 0.97), and Epi (r = 0.92). However, the slope of IA/AR for Endo (1.30 +/- 0.08) was significantly steeper (P less than 0.05) than that for Epi (0.89 +/- 0.11); furthermore, the intercepts at zero infarction for PPM (0.5 +/- 0.1% of LV), Endo (4.2 +/- 0.4%), and Epi (0.1 +/- 0.7%) were significantly different from each other. Regional blood flow measurements indicate that the differences in IA/AR in various layers reflected earlier and greater total collateral flow to the noninfarcted AR in the epicardium. Thus IA/AR for the entire LV is a composite representing separate IA/AR specific to various transmural layers of the LV. In addition, this study demonstrates that the lateral border zone between the IA and the AR is minimal (less than 3-5 mm) in the subendocardium and midwall layers of the left ventricle.

We have shown that there was a 50% increase in infarct size and a threefold increase in the incidence of sudden death following coronary occlusion in dogs with hypertension and left ventricular hypertrophy (LVH). To further investigate this problem, we separated the effects of hypertension from those of LVH by decreasing arterial pressure either by renal anastomosis or intravenous administration of nitroprusside in dogs with chronic renal hypertension and LVH. In 123 conscious dogs, the circumflex coronary artery was acutely occluded. Hemodynamics were monitored, myocardial perfusion was measured with labeled microspheres, the risk area was defined by postmortem angiography, and infarct size was determined pathologically 48 h after occlusion. The incidence of sudden death following acute coronary occlusion decreased dramatically in dogs with LVH if the arterial pressure was decreased with either nitroprusside or renal anastomosis. In addition, if arterial pressure was decreased with nitroprusside or renal anastomosis, infarct size in dogs with LVH was not augmented. In conclusion, normotension induced by renal anastomosis or nitroprusside returned infarct size and the incidence of sudden death in dogs with chronic hypertension and LVH toward control values. Thus it is likely that hypertension, as opposed to LVH, is the critical factor responsible for the increase in infarct size and the high incidence of sudden death observed in dogs with hypertension and LVH following sudden coronary occlusion.

A 37-year-old woman was admitted with an acute anterior myocardial infarction. Coronary arteriography revealed a dissecting aneurysm of the left main coronary artery. The patient died from perioperative myocardial infarction following aortocoronary bypass surgery on the 102nd hospital day. Histologic sections of the aneurysm revealed that granulation tissue had replaced the aneurysm, suggesting spontaneous healing of the dissecting aneurysm.

It is not known whether coronary vasospasm is associated with coronary thrombosis. In this study, plasma levels of fibrinopeptide A during anginal attacks in 24 patients with variant angina were examined. A hyperventilation test was used to induce angina. Hyperventilation induced angina and ST segment elevation (AST: 0.32 +/- 0.14 mV, p less than 0.01) in eight patients with variant angina. Fibrinopeptide A increased from 0.75 +/- 0.27 at control to 7.8 +/- 4.4 ng/ml (p less than 0.01) during anginal attacks in these eight patients. In addition, four patients had spontaneous attacks of angina; they also had elevated levels of fibrinopeptide A during attacks (from 2.0 +/- 1.2 at control to 21.9 +/- 18.0 ng/ml [p less than 0.01] during attacks). Hyperventilation did not induce either angina or ST segment elevation in 12 of the patients with variant angina. Fibrinopeptide A levels did not change with hyperventilation in these patients. To determine whether elevated plasma levels of fibrinopeptide A were associated with angina, the plasma levels of fibrinopeptide A were examined during exercise-induced angina in seven additional patients with stable effort angina. They all developed angina with treadmill exercise; however, plasma fibrinopeptide A did not change. Therefore, only the patients with variant angina demonstrated elevated levels of fibrinopeptide A during anginal attacks. These findings suggest that coronary vasospasm associated with myocardial ischemia may induce stasis of blood, resulting in fibrinogen-fibrin conversion in the coronary vessels.

Echocardiographic studies of a 19-year-old female with Ebstein's anomaly and type B Wolff-Parkinson-White syndrome showed an earlier closure of the anterior tricuspid leaflet (ATL) than of the anterior mitral leaflet (AML), contrary to the previous reports. The interval between the closure of the ATL and the AML was 20 msec and 30 msec, respectively, before and after administration of edrophonium chloride. However, closure of the AML preceded that of the ATL after administration of atropine sulfate and during supraventricular tachycardia by 10 msec and 60 msec, respectively, concomitant with the shortening of the duration of the QRS complex. We conclude that early closure of the ATL may depend on preexcitation of the right ventricle.

The relationship between coronary perfusion pressure and regional myocardial performance of the right ventricular free wall was studied, in the presence or absence of right ventricular hypertension in 13 open-chest dogs. The right coronary artery was perfused through a shunt from a carotid artery. Regional systolic shortening of the right ventricular free wall was measured by means of a sonomicrometric technique at various levels of coronary perfusion pressure. Regional shortening was insensitive to coronary perfusion pressure or flow when it was above 31 mm Hg or 0.27 ml/min per g. Once coronary perfusion was below this critical level, regional shortening in both base to apex and circumferential orientations decreased linearly, depending on the degree of perfusion pressure. Despite the presence of a monoexponential relationship between coronary perfusion pressure or flow and regional shortening, a direct linear relation between perfusion pressure and flow was consistently noted, with or without pulmonary artery banding, suggesting that there is limited autoregulation of right coronary flow. The critical perfusion pressure for maintaining regional myocardial function of the right ventricle was highly dependent on the level of right ventricular systolic pressure (r = 0.64 - 0.72, P less than 0.05). Thus, right ventricular systolic pressure was one of the important determinants of regional wall motion during coronary underperfusion.

The evolution of myocardial infarction 24 hours after ligating both the right coronary artery and the obtuse marginal branch of the left circumflex coronary artery was examined in 33 anesthetized dogs. Postmortem coronary angiography and a tracer microsphere technique were used to determine risk areas and their collateral blood flows, respectively. The mean weight of the risk areas was 11.3 +/- 0.5 g (mean +/- SEM) in the right ventricle and 10.5 +/- 0.9 g in the left ventricle (NS). The weight of infarcted tissue was 5.7 +/- 0.7 g in the right ventricle and 5.2 +/- 0.9 g in the left ventricle (NS). In both ventricles, infarct weight was linearly related to risk area size, and the percent of risk area necrosis was inversely correlated with the extent of collateral flow at 24 hours of coronary ligation, defined as the mean myocardial blood flow inside the central risk area. Ratios of infarct to risk area between the subendocardial and subepicardial layers were 0.76 +/- 0.06 and 0.28 +/- 0.05 in the right and left ventricles, respectively (p less than 0.01, between ventricles, n = 31), which coincided well with subendocardial-to-subepicardial-flow ratios at 24 hours, ie, 0.86 +/- 0.04 in the right ventricle and 0.32 +/- 0.06 in the left ventricle (p less than 0.01). The regional distribution of myocardial infarction correlated well with flow distribution inside the risk area; the slope of these relations was similar between the subendocardium and subepicardium in the right ventricle, whereas in the left ventricle it was larger in the subendocardium than in the subepicardium. Thus, in the dog, the inherent change in the regional distribution of coronary collateral blood flow is an important modifier in the evolution of myocardial infarction, especially in the left ventricle.

Relationship of coronary perfusion pressure with total and regional myocardial blood flow in right ventricular free wall was studied in 10 anaesthetised open chest dogs. The right coronary artery was perfused by an autoperfusion system from the carotid artery. Total coronary blood flow into the perfused area was measured by an extracorporeal electromagnetic flow probe. Critical perfusion pressure of the right coronary artery, defined as the lowest pressure level below which the regional wall motion deteriorated, was 39(SEM1) mm Hg. Reactive hyperaemia was noted at 60(2) mm Hg, a level well above the critical perfusion pressure. There was an inverse linear relation between the level of reactive hyperaemia and perfusion pressure. Regional myocardial blood flow was measured by a tracer microsphere technique at control condition, just above and below the critical perfusion pressures and during coronary occlusion. This correlated closely with values obtained by an electromagnetic flow probe (r = 0.94, p less than 0.001) and both values were dependent on the level of perfusion pressure. Endocardial to epicardial flow ratio remained at unity at any level of coronary perfusion pressure. Thus the level of coronary perfusion pressure was a major determinant of the regional myocardial blood flow into the right coronary artery, and autoregulation of the regional myocardial blood flow was not apparent across the wall, despite the presence of a reactive hyperaemia.