Search

Although the renin-angiotensin system (RAS) is counter-balanced by a salt-sensitive mechanism in the hypertensive state, both are reported to be up-regulated in chronic kidney disease (CKD) patients. We conducted this study to evaluate the associations among the RAS, renal function, hypertension, and atherosclerosis, as well as to identify markers for salt-sensitivity. A total of 213 pre-dialysis CKD patients with preserved cardiac function (EF >50 %) were enrolled. Their renal and cardiac biochemical markers and plasma renin activity (PRA) were measured, and echocardiography and carotid artery ultrasound were performed. Their salt intake was estimated by the NaCl excretion from a 24-h collected urine sample. The PRA was higher in patients with hypertension (p = 0.018), and had a significant negative correlation with the eGFR (r = -0.23, p = 0.0067). Importantly, the PRA had a strong negative correlation with the brain natriuretic peptide (BNP) level (r = -0.28, p = 0.017) regardless of whether the patients were being treated with RAS inhibitors. The BNP level was related to the renal functions (eGFR: p = 0.001, ACR: p = 0.009). There was a significant positive correlation between the BNP level and carotid intima-media thickness (p

New oral anticoagulants (NOACs) are now clinically available. However, few studies have demonstrated which patients with non-valvular atrial fibrillation (NVAF) actually receive NOACs in a clinical setting. We analyzed 182 NVAF patients who received oral anticoagulants. Clinical backgrounds and the risk of stroke, systemic embolism, and bleeding associated with oral anticoagulants were investigated. Seventy-three (40 %) patients were treated with NOACs and 109 (60 %) patients were treated with warfarin. A significantly lower mean number of bleeding risk factors was observed among the patients treated with NOACs than among those treated with warfarin (P = 0.010). Of the bleeding risk factors, NOACs were significantly less frequently prescribed in patients with a bleeding history and elderly subjects (>65 years) than in those who received warfarin (P

Hypertrophic cardiomyopathy (HCM) has various morphological and clinical features. A decade has passed since the previous survey of the epidemiological and clinical characteristics of Japanese HCM patients. The Aichi Hypertrophic Cardiomyopathy (AHC) Registry is based on a prospective multicenter observational study of HCM patients. The clinical characteristics of 42 ambulant HCM patients followed up for up to 5 years were investigated. The primary endpoint was major adverse cardiac events (MACE), defined as death, non-fatal stroke, admission due to congestive heart failure (CHF), or episodes of sustained ventricular tachycardia/fibrillation. The MACE-free survival during the 5-year follow-up period was 76% according to Kaplan-Meier analysis. HCM-related death occurred in 3 (7%) patients and SCD occurred in 2 (5%) patients. Additionally, 3 (7%) patients were admitted to the hospital due to CHF. Meanwhile, sustained VT was detected in one (2%) of the patients who received ICD implantation and subsequently terminated with antitachycardia pacing using an ICD. The patients with HCM exhibiting left ventricular outflow obstruction (HOCM) had a slightly lower MACE-free survival rate than those with neither HOCM nor dilated-HCM (dHCM) (71% versus 81%, log-rank P = 0.581). Furthermore, the patients with dHCM demonstrated a significantly lower MACE-free survival rate than those with neither HOCM nor dHCM (33% versus 81%, log-rank P = 0.029). In the AHC Registry targeting current Japanese HCM patients, we demonstrated that many HCM patients continue to suffer from MACE despite the development of various treatments for HCM.

Takotsubo cardiomyopathy is a disorder characterized by left ventricular apical ballooning with preceding emotional and/or physical stressors. This condition is also an important differential diagnosis of acute coronary syndrome. We herein describe a case of Takotsubo cardiomyopathy, a significant clinical phenomenon, triggered by delayed-onset rhabdomyolysis following the administration of long-term statin treatment, without any preceding stressors or changes in the patient's medical condition, in association with complaints of non-specific muscle-related symptoms. Although an electrocardiogram showed remarkable ST-segment elevation, a careful reading of the electrocardiogram findings revealed the features of Takotsubo cardiomyopathy. Withdrawing the statin therapy improved the patient's cardiac function.

The number of elderly patients with hypertension has been steadily increasing. However, there are limited data on the safety and efficacy of the new angiotensin type 1 receptor blocker (ARB) azilsartan in elderly patients with hypertension. We investigated the clinical efficacy and safety of azilsartan in this population.The study population comprised 56 ambulatory patients with essential hypertension. We evaluated the reduction in blood pressure and safety after 12 weeks of treatment with azilsartan in 29 hypertensive patients ≥65 years of age (aged group) in comparison with the findings in 27 patients65 years of age (non-aged group).Systolic blood pressure in the aged group declined significantly from 155 ± 18 mmHg at baseline to 138 ± 11 mmHg after 12 weeks of treatment with azilsartan, and that in the non-aged group also declined significantly from 152 ± 20 mmHg at baseline to 142 ± 13 mmHg after 12 weeks of treatment with azilsartan. There were no significant differences in the magnitude of change in blood pressures from pre-treatment to post-treatment with azilsartan between the non-aged and aged groups. There were no changes in clinical laboratory findings, including serum levels of creatinine, potassium, lipids, and other metabolic variables, after 12 weeks of treatment with azilsartan in both groups.Our findings suggest that azilsartan is effective in lowering blood pressure in elderly patients and may be safe. Therefore, azilsartan could be a valuable option for treating hypertension in elderly and non-elderly patients.

Previous studies have shown highly effective lowering of blood pressure with thiazide diuretics in combination with angiotensin receptor blockers. However, thiazide diuretics may cause the development of diabetes and abnormal lipid metabolism. Little is known as to whether dysmetabolic potential of thiazide diuretics could be neutralized when adding angiotensin receptor blockers. This study consisted of 26 patients with essential hypertension. Patients were randomized to 24 weeks of treatment with either candesartan, 12 mg monotherapy (n = 13, group A), or hydrochlorothiazide (HCTZ), 6.25 mg in combination with candesartan, 8 mg (n = 13, group B). Before and after treatment, we assessed glucose and lipid profiles including adiponectin, resistin, and active glucagon-like peptide-1 (GLP-1) levels. At baseline, there were no differences in age, body mass index, systolic blood pressure (SBP), and diastolic blood pressure (DBP), as well as plasma levels of hemoglobin A1c, insulin, low-density lipoprotein cholesterol, triglycerides, adiponectin, resistin, and active GLP-1 between the two groups. There were significant reductions in SBP (from 152 ± 10 mmHg at baseline to 134 ± 12 mmHg after treatment) and DBP (from 84 ± 5 mmHg at baseline to 71 ± 8 mmHg after treatment) in group A. There were also significant reductions in SBP (from 148 ± 10 at baseline to 128 ± 7 mmHg after treatment) and DBP (from 90 ± 9 at baseline to 74 ± 12 mmHg after treatment) in group B. There were no differences in reduction of SBP or DBP after 24 weeks of treatment between the two groups. There were no changes of the glucose and lipid profiles, including adiponectin, resistin, insulin, and active GLP-1 levels after 24 weeks of treatment in both groups. A low dose of HCTZ in combination with candesartan reduces blood pressure effectively without adverse effects on the glucose and lipid profiles. Therefore, the combination of thiazide diuretics and angiotensin receptor blockers could assist patients in achieving long-term control of blood pressure with good tolerability.

Hypertrophic cardiomyopathy (HCM) has various morphological and clinical features. A decade has passed since the previous survey of the epidemiological and clinical characteristics of Japanese HCM patients. The Aichi Hypertrophic Cardiomyopathy (AHC) Registry is based on a prospective multicenter observational study of HCM patients. The clinical characteristics of 42 ambulant HCM patients followed up for up to 5 years were investigated. The primary endpoint was major adverse cardiac events (MACE), defined as death, non-fatal stroke, admission due to congestive heart failure (CHF), or episodes of sustained ventricular tachycardia/fibrillation. The MACE-free survival during the 5-year follow-up period was 76% according to Kaplan-Meier analysis. HCM-related death occurred in 3 (7%) patients and SCD occurred in 2 (5%) patients. Additionally, 3 (7%) patients were admitted to the hospital due to CHF. Meanwhile, sustained VT was detected in one (2%) of the patients who received ICD implantation and subsequently terminated with antitachycardia pacing using an ICD. The patients with HCM exhibiting left ventricular outflow obstruction (HOCM) had a slightly lower MACE-free survival rate than those with neither HOCM nor dilated-HCM (dHCM) (71% versus 81%, log-rank P = 0.581). Furthermore, the patients with dHCM demonstrated a significantly lower MACE-free survival rate than those with neither HOCM nor dHCM (33% versus 81%, log-rank P = 0.029). In the AHC Registry targeting current Japanese HCM patients, we demonstrated that many HCM patients continue to suffer from MACE despite the development of various treatments for HCM.

冠攣縮性狭心症 (VAP) において血管痙攣のない時期に, 体表面でのActivation Recovery Interval (ARI) Mapの空間分布を評価することによってVAPの診断および攣縮冠動脈枝の検出が可能か否か検討した, 非発作時に正常な標準12誘導心電図を示すVAP22例を対象にした, 対照は心疾患のない41例とした.体表面ARl mapは, 多目的心電計 (VCM3000, フクダ電子社製) にて87誘導点方法で冠攣縮のない時期に記録した.ARIは, QRS波の最小一次微分値の時点からT波の最大一次微分値の時点までの時間として各誘導点ごとに測定し, 等しいARIを結んでARI mapを作成した.ARI値は心拍数により変動するので, Bazettの式で補正してARIcを用いた.ARIc map記録は発作直後, 2週間, 1カ月, 6カ月後に記録した.攣縮冠動脈が右冠動脈であれば右前胸部下方に, 左冠動脈であれば前胸部中央やや左寄りにARIcの短縮領域が出現し, 虚血領域に対応する結果が得られた.VAPでは, 正常群に比し最小ARIc値が短縮していた.最小ARIc値の平均値はそれぞれVAP=160±28.8msec, 正常群: 196±14.8msecであった (p

Background Recently, long-term constriction of the vessel has been suggested as an alternative mechanism of restenosis after coronary angioplasty. Methods and Results To understand remodeling of human coronary arteries undergoing coronary angioplasty or atherectomy, serial intravascular ultrasonographic examinations were performed at preintervention and postintervention examinations and at 24 hours, 1 month, and 6 months. Complete serial data were obtained in 61 lesions (balloon angioplasty, 35 lesions; directional atherectomy, 26 lesions). Lumen area improved from 6.81±2.24 mm 2 after intervention to 8.22±2.79 mm 2 at 1 month ( P =.0001) and decreased to 4.88±2.86 mm 2 at 6 months ( P =.0001). Vessel area enlarged from 17.32±5.35 mm 2 after intervention to 19.39±5.33 mm 2 at 1 month ( P =.0001) and decreased to 16.33±5.54 mm 2 at 6 months ( P =.0001). Plaque+media area increased significantly from postintervention examination to 24 hours (10.51±4.38 versus 10.96±4.49 mm 2 , P =.0008) and from 24 hours to 6 months (10.96±4.49 versus 11.45±4.45 mm 2 , P =.03). Changes in lumen area in each study interval correlated more closely with changes in vessel area than with changes in plaque+media area. Restenotic lesions compared with nonrestenotic lesions had a greater decrease in the vessel area between 1 month and 6 months (−4.33±2.73 versus −2.49±2.15 mm 2 , P =.006) and greater increase in the plaque+media area both within 24 hours (0.84±1.22 versus 0.27±0.38 mm 2 , P =.04) and between 24 hours and 6 months (1.19±2.19 versus 0.18±1.46 mm 2 , P =.04). Conclusions Remodeling after coronary angioplasty or atherectomy was characterized by early adaptive enlargement and late constriction of the vessel.

This serial follow-up study was designed to identify the time course of reocclusion and/or restenosis after direct angioplasty for acute myocardial infarction. Direct angioplasty for acute myocardial infarction was attempted in 160 patients. Of the 141 patients who underwent successful reperfusion and were discharged, 137 (97%) were enrolled in this study. At the 3-week follow-up study (100% eligible), angiographic restenosis of the infarct-related artery was documented in 21 patients (16%), 9 (43%) of which were reocclusions. At 4 months in 100 patients (92% of those eligible), restenosis was newly documented in 28 infarct-related arteries (28%), 3 of which were reocclusions (11%). At 1 year in 64 patient (89% of those eligible), restenosis was newly documented in 5 infarct-related arteries (7.8%), with no reocclusions. The cumulative restenosis rate was 20% at 3 weeks, 43% at 4 months, and 47% at 1 year; when divided into occlusive and nonocclusive types, restenosis rates were 12% and 8.8% at 3 weeks and 14% and 29% at 4 months, respectively. Restenosis was most prevalent within the first 4 months and rarely occurred after that. When restenosis is manifested as reocclusion, it occurs earlier than in nonocclusive restenosis, often within 3 weeks.

Coronary-artery stents are known to reduce rates of restenosis after coronary angioplasty, but it is uncertain how long this benefit is maintained.We evaluated clinical and angiographic follow-up information for up to three years after the implantation of Palmaz-Schatz metallic coronary-artery stents in 143 patients with 147 lesions of native coronary arteries.The rate of survival free of myocardial infarction, bypass surgery, and repeated coronary angioplasty for stented lesions was 74.6 percent at three years. After 14 months, revascularization of the stented lesion was necessary in only three patients (2.1 percent). In contrast, coronary angioplasty for a new lesion was required in 11 patients (7.7 percent). Follow-up coronary angiography of 137 lesions at six months, 114 lesions at one year, and 72 lesions at three years revealed a decrease in minimal luminal diameter from 2.54 +/- 0.44 mm immediately after stent implantation to 1.87 +/- 0.56 mm at six months, but no further decrease in diameter at one year (in patients with paired angiograms, 1.95 +/- 0.49 mm at both six months and one year). Significant late improvement in luminal diameter was observed at three years (in patients with paired angiograms, 1.94 +/- 0.48 mm at six months and 2.09 +/- 0.48 mm at three years; P0.001).Clinical and angiographic outcomes up to three years after coronary-artery stenting were favorable, with a low rate of revascularization of the stented lesions. Late improvement in luminal diameter appears to occur between six months and three years.

BackgroundMechanisms of the pseudonormalization (PN) of the transmitral flow (TMF) velocity pattern have been mainly attributed to left ventricular diastolic function.PurposeTo assess the influence of left atrial (LA) function on the PN with two-dimensional tissue tracking technique.MethodsThe subjects consisted of 21 healthy volunteers and 70 patients with various cardiac diseases. Images of one cardiac cycle in the apical four-chamber view were stored by the HIVISION 900 (Hitachi Medico, Chiba, Japan). The LA volume (LAV) loop was created using two-dimensional tissue tracking technique and LAV index (LAVI) at a given cardiac phase was calculated. A preload of 90mmHg was applied using a customized lower body positive pressure (LBPP) system. Patients were divided into the PN group (n=18) with their early diastolic TMF velocity (E) increased and late diastolic TMF velocity (A) decreased, and the non-(N)-PN group (n=52) with both E and A wave velocities increased by LBPP.Results(1) During LBPP, the LAVImax in both the groups increased significantly. (2) In the N-PN group, the LAVIpass (p

Coronary artery spasm plays an important role in acute ischemic events, and it has a close relationship with coronary atherosclerosis. Thus we attempted to determine the most significant risk factor for coronary artery spasm. Among 3000 consecutive patients who underwent coronary cineangiography with ergonovine maleate testing, 330 with typical angina pectoris (group 1) and 294 with old myocardial infarction (group 2) were studied. We divided each group into three or four subgroups according to the presence of fixed organic stenosis (FOS+) or a positive reaction to ergonovine maleate (coronary artery spasm [CAS]+). We examined the relationship between coronary artery spasm and eight coronary risk factors: age, sex, hypertension, diabetes mellitus, smoking, and serum cholesterol, uric acid, and high-density lipoprotein cholesterol levels. The proportion of smokers in the subgroups with CAS(+) was significantly higher than in the subgroups with CAS(-)(p less than 0.01). There was no correlation between smoking and fixed organic stenosis. According to the results of multiple regression analysis, there was a positive correlation between smoking and CAS(+) and between serum high-density lipoprotein cholesterol levels and CAS(+)(p less than 0.01). Thus we concluded that smoking is the most significant risk factor in discriminating between patients with and without coronary artery spasm.

Histopathologic examination was performed in 20 patients undergoing antemortem coronary angioplasty. Thirty-four lesions were dilated and the interval between coronary angioplasty and death ranged from several hours to 4 years. Intimai proliferation of smooth muscle cells, as a major cause of restenosis, was observed in 83% to 100% of 28 lesions examined 11 days to 2 years after coronary angioplasty. In 20 lesions examined within 6 months, proliferating smooth muscle cells were predominantly of the synthetic type and there was abundant extracellular matrix substance chiefly composed of proteoglycans. In eight lesions examined between 6 months and 2 years, contractile type smooth muscle cells were dominant and extracellular matrix was composed chiefly of collagen. In three lesions examined after 2 years, evidence of antemortem coronary angioplasty was hardly identifiable and these lesions were almost indistinguishable from conventional atherosclerotic plaque. These temporal changes in histologic pattern provide a pathologic background for clinical reports that restenosis is predominantly found within 6 months after coronary angioplasty. Morphometry analysis revealed that the extent of intimai proliferation was significantly greater in lesions with evidence of medial or adventitial tears than in lesions with no or only intimai tears.

The diagnostic accuracy of using electrocardiographic findings to identify affected vessels in cases of myocardial infarction and angina pectoris treated by percutaneous transluminal coronary angioplasty was assessed. From the anterior wall leads, ST segment elevation in leads I and aV(L) showed diagnostic accuracy (sensitivity, specificity and positive predictive value) in identifying proximal lesions of the left anterior descending coronary artery of 89%, 58% and 62%, and the diagnostic accuracy of the QS wave in V(1) was 62%, 83% and 72%, respectively. For the posterior wall leads, the corresponding values for the diagnosis of affected vessels based on R/S>1 in V(1) for the left circumflex coronary artery were 50%, 89% and 60%, respectively. The inferior wall leads with ST segment elevation in leads II, III and aV(F), and ST segment depression in aV(L), showed diagnostic accuracy for the right coronary artery of 90%, 90% and 92%, respectively. Bifurcation of the first diagonal branch, dominance of the posterior descending branch, the normal subtypes of the coronary artery and the occurrence of spontaneous recanalization may have influenced the accuracy of diagnosis. Adding a high lateral wall lead one intercostal space above V(4) and a posterior wall lead located one intercostal space below V(6) appeared to increase the diagnostic accuracy of detecting the coronary artery lesions responsible for myocardial ischemia.

To determine whether the departure parameters derived from a "departure loop" of a vectorcardiogram are more accurate than conventional spatial parameters in evaluating myocardial infarct size, 74 patients with first-onset myocardial infarction (MI) were studied. The correlation between the departure parameters (amplitudes in scalar leads of the departure loop) and the percent defect volume of thallium myocardial scintigrams (%DV) was compared with that of the spatial parameters (magnitude, azimuth, and elevation of the original QRS loop). In anteroseptal MI, the amplitude of a 20-msec vector in the z-axis and the azimuth of a 30-msec vector (H30) were significantly correlated with %DV (r=0.783, p

A total of 239 patients undergoing serial coronary angiography with a concomitant ergonovine provocation test were studied between July 1974 and June 1987. The progression of coronary artery disease was evaluated in relation to risk factors, especially coronary artery spasm. Patients were classified into three groups: 1) new myocardial infarction group (39 patients); 2) progression without infarction group (90 patients); and 3) nonprogression group (110 patients).To assess how risk factors and coronary spasm are related to the occurrence of new myocardial infarction and progression without infarction, 11 variables in the three groups were examined: age, gender, the time interval between the studies, fasting blood sugar, systolic blood pressure, diastolic blood pressure, smoking, serum cholesterol, triglyceride, uric acid and a positive response to the ergonovine provocation test. Multiple regression analysis selected three independent predictors of progression without infarction: cholesterol (p < 0.01), systolic blood pressure (p < 0.05) and a positive response to the ergonovine provocation test (p < 0.001). Multiple regression analysis also selected three independent predictors of the occurrence of new myocardial infarction: fasting blood sugar (p < 0.01), systolic blood pressure (p < 0.05) and a positive response to the ergonovine provocation test (p < 0.001). A positive response to the ergonovine provocation test was the strongest factor for occurrence of both new myocardial infarction and progression without infarction.To evaluate segmental arterial changes, 3,275 coronary artery segments were analyzed in the 239 patients. Both new myocardial infarction and progression without infarction frequently occurred in the proximal segments of the right coronary artery, the proximal and middle segments of the left anterior descending artery and the middle segments of the circumflex coronary artery. Although occurrence of both new myocardial infarction and progression without infarction were often evident in coronary artery segments with severe narrowing, >50% of new myocardial infarctions occurred in relation to segments narrowed

There has been no report on T wave alternans (TWA) in patients with cardiac sarcoidosis. In this study, we investigated TWA in patients with cardiac sarcoidosis. Electrocardiographic recording for TWA was performed in 6 patients, using the CH2000 (Cambridge Heart). TWA was defined as positive in cases where alternans voltage of >1.9 μV and alternans ratio of >3.0 persisted more than 1 minute during exercise with ergometer with heart rate above 105 beats/min. TWA was positive in 3 patients, negative in 2 patients, and not determined in 1 patient. Arrhythmia was noted on Holter electrocardiogram in all 3 patients with positive TWA: sustained ventricular tachycardia in 1 patient and nonsustained ventricular tachycardia in 2 patients. Mean left ventricular ejection fraction in the 3 patients with positive TWA was 39.0%, whereas in the 2 patients with negative TWA it was 58.5%. A close relationship was suggested between TWA and severity of cardiac sarcoidosis.

To further understand the temporal mode and mechanisms of coronary restenosis, 229 patients were studied by prospective angiographic follow-up on day 1 and at 1, 3 and 6 months and 1 year after successful percutaneous transluminal coronary angioplasty. Quantitative measurement of coronary stenosis was achieved by cinevideodensitometric analysis. Actuarial restenosis rate was 12.7% at 1 month, 43.0% at 3 months, 49.4% at 6 months and 52.5% at 1 year. In 219 patients followed up for greater than or equal to 3 months, mean stenosis diameter was 1.91 +/- 0.53 mm immediately after coronary angioplasty, 1.72 +/- 0.52 mm on day 1, 1.86 +/- 0.58 mm at 1 month and 1.43 +/- 0.67 mm at 3 months. In 149 patients followed up for greater than or equal to 6 months, mean stenosis diameter was 1.66 +/- 0.58 mm at 3 months and 1.66 +/- 0.62 mm at 6 months. In 73 patients followed up for 1 year, mean stenosis diameter was 1.65 +/- 0.56 mm at 6 months and 1.66 +/- 0.57 mm at 1 year. Thus, stenosis diameter decreased markedly between 1 month and 3 months after coronary angioplasty and reached a plateau thereafter. In conclusion, restenosis is most prevalent between 1 and 3 months and rarely occurs beyond 3 months after coronary angioplasty.