Long-term survival and fate of the leg in de novo intermittent claudication.

Aims: The long-term life expectancy and fate of the leg, including progression rate to critical limb ischaemia (CLI), were analysed in de novo patients with intermittent claudication (IC). Methods and results: A prospective cohort study was performed in 1107 patients with de novo IC. The endpoints were overall survival (OS), freedom from major adverse cardiovascular events (MACE), freedom from major adverse cardiovascular and limb events (MACLE), and fate of the leg. The 5-, 10-, 15-, and 20-year rates were 73.3, 47.8, 28.1, and 14.9% for OS, and 63.0, 35.6, 18.5, and 5.7% for freedom from MACE, respectively. In Cox multivariable analysis, body mass index, diabetes, haemodialysis, and C-reactive protein (CRP) level were correlated with OS (P < 0.05). Ankle brachial pressure index, diabetes, coronary artery disease, haemodialysis, and CRP level were independently correlated with freedom from MACE and MACLE. Statins improved mortality, MACE, and MACLE (P < 0.05). Revascularization did not improve mortality and MACE, and femoropopliteal revascularization increased MACLE (P < 0.05). There was no deterioration of claudication in 881 patients (79.6%). Worsening claudication was noted in 211 patients (14.8% per 5 years), and 15 patients (1.1% per 5 years) worsened to CLI. Diabetes and haemodialysis were independent predictors of CLI. A history of cerebral infarction and femoropopliteal revascularization tended to increase CLI. Conclusions: Life expectancy in patients with IC was poor, but the rate of IC progression to CLI was low. Statins improved mortality and morbidity, revascularization did not improve mortality and MACE, and femoropopliteal revascularization reduced freedom from MACLE with a risk of CLI.

15-Year Patency and Life Expectancy After Primary Stenting Guided by Intravascular Ultrasound for Iliac Artery Lesions in Peripheral Arterial Disease.

OBJECTIVES: The purpose of this study was to evaluate 15-year patency and life expectancy after endovascular treatment (EVT) with primary stenting guided by intravascular ultrasound (IVUS) for iliac artery lesions. BACKGROUND: Fifteen-year patency, factors causing restenosis, and survival after IVUS-guided EVT are unclear based on the TransAtlantic Inter-Society Consensus II (TASC-II) classification in peripheral arterial disease (PAD). METHODS: EVT was performed for 507 lesions in 455 patients with PAD. The 15-year endpoints were primary, primary-assisted, and secondary patency; overall survival; freedom from major adverse cardiovascular events (MACE); and freedom from major adverse cardiovascular and limb events (MACLE). RESULTS: The 5-, 10-, and 15-year primary and secondary patencies were 89%, 83%, and 75%, respectively, and 92%, 91%, and 91%, respectively. There were no significant differences among TASC-II categories. CONCLUSIONS: IVUS-guided stenting for the iliac artery had favorable 15-year patency in all TASC categories. Life expectancy after EVT was poor, but stenting is feasible for patients with PAD.

A surgical experience of symptomatic sigmoid septum: drastic exacerbation of mitral regurgitation after sufficient ventricular septal myectomy.

A 74-year-old woman presented with progressive dyspnea on exertion. Transthoracic echocardiography (TTE) demonstrated significant left ventricular outflow tract (LVOT) obstruction with a pressure gradient of 100 mmHg caused by a sigmoid septum (SS). Mitral regurgitation (MR) of a mild to moderate degree occurred due to systolic anterior motion (SAM) of the anterior mitral leaflet (AML), with no intrinsic mitral valve (MV) abnormality. Myectomy of the hypertrophied septal bulge ameliorated the pressure gradient to 8 mmHg with similar MR. However, just before the sternal closure, hemodynamic status deteriorated drastically to ventricular fibrillation. MR exacerbated to a severe degree with an uncertain etiology; thus, a mechanical prosthetic valve was implanted. The postoperative course was complicated by prolonged mechanical ventilation due to massive pulmonary edema and complete atrioventricular block (CAVB) requiring permanent pacemaker implantation. One year postoperatively, the patient is asymptomatic and TTE revealed no residual pressure gradient with an iatrogenic ventricular septal defect (VSD). This case, the first published surgical experience of SS, may indicate that secondary MR, which is usually relieved by sufficient myectomy in hypertrophic cardiomyopathy (HCM), can exacerbate markedly, and that myectomy might not be advisable in SS. The therapeutic strategy must be considered carefully before embarking on surgical intervention.

A recurrent vagal schwannoma in the middle mediastinum after surgical enucleation.

A 50-year-old man underwent repeat surgery for a benign vagal schwannoma in the middle mediastinum. He had undergone tumor enucleation at another hospital 4 months before presentation. The tumor (99 × 88 × 76 mm) was located in the aortopulmonary window and arose from the left vagus nerve. It had been enucleated, leaving its sheath behind to preserve the nerve. Imaging studies showed tumor regrowth without distant metastasis, and the tumor was extirpated along with the involved nerve during cardiopulmonary bypass. There was no nerve dysfunction, recurrence, or metastasis 6 months after the operation. A benign vagal schwannoma can be excised with nerve transection or enucleated without nerve transection. The present case suggests that a vagal mediastinal schwannoma should be extirpated along with the nerve because insufficient enucleation might lead to tumor regrowth.

Effects of oral nicorandil therapy on sympathetic nerve activity and cardiac events in patients with chronic heart failure: subanalysis of our previous report using propensity score matching.

PURPOSE: Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, improves cardiac sympathetic nerve activity (CSNA) in patients with ischaemic heart disease. However, the long-term effects on both CSNA, as evaluated by (123)I-metaiodobenzylguanidine (MIBG) scintigraphy, and prognosis have not been determined in patients with chronic heart failure (CHF). METHODS: This study was a subanalysis of our previous results that serial (123)I-MIBG scintigraphic studies are the most useful prognostic indicator in CHF patients. The study group comprised 208 patients with CHF (left ventricular ejection fraction <45 %) but no cardiac events for at least 5 months identified on the basis of a history of decompensated acute heart failure requiring hospitalization. These patients underwent (123)I-MIBG scintigraphy and echocardiography just before leaving the hospital and again 6 months later. We selected 170 patients and used propensity propensity score matching to compare patients who received oral nicorandil (85 patients) and those who did not (85 patients). The patients were followed up for a median of 5.03 years, with the primary and secondary study end-points defined as the occurrence of a fatal cardiac event and a major adverse cardiac event (MACE), respectively. RESULTS: After treatment, the extent of changes in (123)I-MIBG scintigraphic and echocardiographic parameters in the nicorandil group were more favourable than in those not receiving nicorandil. Of the 170 patients, a fatal cardiac event occurred in 42, and a MACE in 68 during the study. Multivariate Cox regression analyses revealed that no nicorandil treatment was a significant predictor of both cardiac death and MACE in our patients with CHF. On Kaplan-Meier analysis, the rates of freedom from cardiac death or from MACE in the nicorandil group were significantly higher than in those not receiving nicorandil (all p<0.05). CONCLUSION: Long-term nicorandil treatment improves CSNA and left ventricular parameters in patients with CHF. Furthermore, this agent is potentially effective for reducing the incidence of cardiac events in patients with CHF.

Differences in brain natriuretic peptide and other factors between Japanese peripheral arterial disease patients with critical limb ischemia and intermittent claudication.

AIM: The goal of this study was to analyze differences in risk factors, including the level of brain natriuretic peptide (BNP) and the distribution of lesions, between cases of critical limb ischemia (CLI) and intermittent claudication (IC) among patients with peripheral arterial disease. METHODS: Risk factors and clinical characteristics were prospectively investigated in 817 consecutive patients, including 185 patients with CLI and 632 patients with IC. RESULTS: The patients in the CLI group were older than those in the IC group (p＜0.001). The prevalence of diabetes and cerebral infarction and the proportion of women were higher in the CLI group (p＜0.05). The plasma BNP levels in the CLI group were higher than those observed in the IC group (333±538 vs. 136±354 pg/mL, p＜0.001). In contrast, the levels of homocysteine and fibrinogen were higher and the levels of albumin and the estimated glomerular filtration rate were lower in the CLI group (p＜0.05). According to a multiple logistic analysis, the BNP level, diabetes, female gender, the albumin level, body mass index (BMI) and ankle-brachial pressure index (ABI) were associated with CLI (p＜0.05). Aortoiliac artery lesions were less common, whereas femoropopliteal and below-the-knee (BK) lesions were more common, in the CLI group (p＜0.05). The number of affected BK arteries was also higher in the CLI group (p＜0.001). Correlations were found between the presence of aortoiliac lesions and smoking and a low HDL cholesterol level, while femoropopliteal lesions were found to correlate with age, BMI and hypertension and BK lesions were found to correlate with diabetes, age, female gender and BMI (p＜0.05). The plasma BNP level correlated with the number of affected BK arteries (p＜0.05). CONCLUSIONS: A high BNP level, diabetes, female gender, a low albumin level, ABI and BMI are risk factors for CLI. In this study, differences in the levels of anatomical lesions and correlated risk factors were found between the CLI and IC groups.

A successful surgical repair of pulmonary stenosis caused by isolated pulmonary Takayasu's arteritis.

A 48-year-old man underwent surgery to treat pulmonary stenoses of unknown origin. The right main pulmonary artery was severely stenotic, and the orifice of the left pulmonary artery was focally constricted. The patient was nearly asymptomatic, despite marked pulmonary hypertension and right heart strain. The pressure gradients beyond the stenotic regions were 88 mmHg bilaterally. The cause of the stenoses could not be established before operation. The right main pulmonary artery and ascending aorta were successfully replaced. It was suspected that the ascending aorta was involved because it was markedly thickened and adhered tightly to the right pulmonary artery. It was therefore also replaced. However, only the transected right pulmonary artery showed histological evidence consistent with a diagnosis of Takayasu's arteritis. The postoperative course was uneventful. The patient was completely free of symptoms six months after the operation. To our knowledge, this is the thirteenth surgically treated case of isolated pulmonary Takayasu's arteritis to be reported.

Relationship between late ventricular potentials and myocardial 123I-metaiodobenzylguanidine scintigraphy in patients with dilated cardiomyopathy with mild to moderate heart failure: results of a prospective study of sudden death events.

PURPOSE: Late ventricular potentials (LPs) are considered to be useful for identifying patients with heart failure at risk of developing ventricular arrhythmias. (123)I-metaiodobenzylguanidine (MIBG) scintigraphy, which is used to evaluate cardiac sympathetic activity, has demonstrated cardiac sympathetic denervation in patients with malignant ventricular tachyarrhythmias. This study was undertaken to clarify the relationship between LPs and (123)I-MIBG scintigraphy findings in patients with dilated cardiomyopathy (DCM). METHODS: A total of 56 patients with DCM were divided into an LP-positive group (n = 24) and an LP-negative group (n = 32). During the compensated period, the delayed heart/mediastinum count (H/M) ratio, delayed total defect score (TDS), and washout rate (WR) were determined from (123)I-MIBG images and plasma brain natriuretic peptide (BNP) concentrations were measured. Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), and left ventricular ejection fraction (LVEF) were simultaneously determined by echocardiography. RESULTS: LVEDV, LVESV, LVEF and plasma BNP concentrations were similar in the two groups. However, TDS was significantly higher (35 ± 8 vs. 28 ± 6, p < 0.005), the H/M ratio was significantly lower (1.57 ± 0.23 vs. 1.78 ± 0.20, p < 0.005), and the WR was significantly higher (60 ± 14% vs. 46 ± 12%, p < 0.001) in the LP-positive than in the LP-negative group. The average follow-up time was 4.5 years, and there were nine sudden deaths among the 56 patients (16.1%). In logistic regression analysis, the incidences of sudden death events were similar in those LP-negative with WR <50%, LP-negative with WR ≥ 50% and LP-positive with WR <50% (0%, 10.0% and 14.3%, respectively), but was significantly higher (41.2%) in those LP-positive with WR ≥ 50% (p < 0.01, p < 0.05, and p < 0.05, respectively). CONCLUSION: The present study demonstrated that the values of cardiac (123)I-MIBG scintigraphic parameters were worse in LP-positive DCM patients than in LP-negative DCM patients. Furthermore, in LP-positive DCM patients with a high WR, the incidence of sudden death events was higher than that in other subgroups of DCM patients.

Sex-related differences in Japanese patients with peripheral arterial disease.

OBJECTIVE: The goal of the study was to examine possible sex-related differences in the clinical characteristics and risk factors in Japanese patients with peripheral arterial disease (PAD). METHODS: Sex-related differences in clinical profiles, risk factors and treatments were examined in 730 consecutive patients with PAD (148 women (20.3%) and 582 men (79.7%)). RESULTS: The mean age of the women was higher than that of the men (73.6 ± 11.2 vs. 70.9 ± 9.1 years old, p = 0.002) and the proportion of subjects aged ≥ 75 years old was also higher in women (P=0.005). Women more frequently had critical limb ischemia (P < 0.001) and diabetes mellitus (P = 0.026), but less frequent smoking and alcohol intake, compared to men (P< 0.001). Total cholesterol (P < 0.001) and LDL cholesterol (P = 0.014) were higher in women. Fontaine stages were correlated with age, diabetes, cerebral infarction and women (p < 0.001). The prevalence of iliac artery lesions was higher in men (p< 0.001), whereas that for below the knee lesions was higher in women (p < 0.001). The number of affected below the knee arteries was also higher in women than in men (p < 0.001). The prevalence of medical treatment was higher in women (P = 0.009) and major amputation tended to be higher in women (p = 0.056). CONCLUSIONS: Women had more severe symptomatic states and uncontrolled risk factors. The prevalence of iliac artery lesions was lower, but below the knee lesions were more severe in women.

The influence of the obesity paradox and chronic kidney disease on long-term survival in a Japanese cohort with peripheral arterial disease.

BACKGROUND: This study analyzed risk factors for mortality in peripheral arterial disease (PAD), including body mass index (BMI) and estimated glomerular filtration rate (eGFR). Risk factors for long-term survival are unclear in patients with PAD. The origin of the obesity paradox, a paradoxical decrease in mortality with increasing BMI, is also uncertain in these patients. METHODS: A prospective cohort study was performed in 652 patients (aged 71.3 +/- 9.4 years old) with PAD. RESULTS: The 1-, 5-, 10- and 15-year survival rates were 94.5%, 70.4%, 45.2%, and 21.1%, respectively, in patients with intermittent claudication, and 72.7%, 27.2%, 11.6%, and 5.8%, respectively, in those with critical limb ischemia (CLI). In Cox multivariate analysis, a significant association with all-cause mortality was found for CLI (hazard ratio [HR], 1.931; 95% confidence interval [CI], 1.089-3.422; P = .024), diabetes (HR, 2.111; 95% CI, 1.247-3.572; P = .005), BMI (HR, 0.879; 95% CI, 0.804-0.962; P = .005), and eGFR (HR, 0.985; 95% CI, 0.971-0.998l; P = .028). These parameters were also significant risk factors for cardiovascular mortality. Fibrinogen (HR, 1.003; 95% CI, 1.001-1.005; P = .014) and cerebrovascular disease (HR, 1.730; 95% CI, 1.021-2.930; P = .045) were identified as risk factors for all-cause mortality. The adjusted HR for mortality of BMI <21.5 vs >or=21.5 kg/m(2) was 1.772 (95% CI, 1.378-2.279; P < .001). BMI had positive correlations with triglyceride and albumin concentrations and negative correlations with the fibrinogen level and chronic obstructive pulmonary disease (P = .005). CONCLUSIONS: Low BMI, eGFR, CLI, and diabetes are significant risk factors for mortality in PAD. The obesity paradox was verified and may be partly explained by low BMI mediated by malnutrition and systemic inflammation due to PAD or chronic obstructive pulmonary disease.

Effects of raloxifene on brachial arterial endothelial function, carotid wall thickness, and arterial stiffness in osteoporotic postmenopausal women.

The beneficial effects of raloxifene, a selective estrogen receptor modulator, on cardiovascular risks and events have been investigated. Brachial arterial flow-mediated vasodilatation (FMD), carotid intima-media thickness (IMT), and pulse wave velocity (PWV) have been widely used in clinical settings as surrogate markers of atherosclerosis. This study investigated the simultaneous effects of raloxifene on brachial arterial FMD, carotid IMT, and PWV in osteoporotic postmenopausal women. A total of 31 postmenopausal women with osteoporosis or osteopenia were divided into 2 groups: a raloxifene group (n = 15; mean age +/- SD, 66.1 +/- 8.2 years) was treated with raloxifene hydrochloride (60 mg/day) orally for 12 months, and an untreated control group (n = 16; 64.1 +/- 7.8 years). Brachial arterial FMD, carotid IMT, and brachial-ankle PWV (baPWV) were measured at baseline and at 12 months after the start of the study. The brachial arterial FMD increased significantly, from 4.5 +/- 1.8% to 9.2 +/- 3.0%, in the raloxifene group (P < 0.01) but did not change in the control group. Nitroglycerin-induced vasodilatation did not change in either group. The carotid IMT decreased significantly, from 0.82 +/- 0.15 mm to 0.72 +/- 0.11 mm, in the raloxifene group (P < 0.01) but did not change in the control group. The baPWV did not change in either group. In conclusion, raloxifene may have beneficial effects on brachial arterial endothelial function and carotid wall thickness in osteoporotic postmenopausal women.

Effects of raloxifene on the renin-angiotensin-aldosterone system and blood pressure in hypertensive and normotensive osteoporotic postmenopausal women.

AIM: An increase in blood pressure after menopause has been documented. The renin-angiotensin-aldosterone system (RAAS) plays a central role in the regulation of blood pressure and in the pathophysiology of hypertension. This study investigated the effects of raloxifene, a selective estrogen receptor modulator, on components of the RAAS and blood pressure in hypertensive and normotensive osteoporotic postmenopausal women. METHODS: A total of 41 hypertensive or normotensive postmenopausal women with osteoporosis or osteopenia were divided into four groups. Eleven hypertensive and eight normotensive women received raloxifene hydrochloride (60 mg/day) p.o. for 6 months, and 12 hypertensive and 10 normotensive women did not receive raloxifene hydrochloride for 6 months. In all of the hypertensive women, blood pressure had been controlled prior to the start of the study using a variety of antihypertensive drugs other than angiotensin-converting enzyme (ACE) inhibitors, angiotensin (Ang)II type 1 receptor antagonists or diuretics. Plasma renin activity (PRA), serum ACE activity, plasma AngI, AngII and aldosterone concentrations, and blood pressure were measured before and 6 months after the start of the study. RESULTS: No significant changes in PRA, ACE activity, or the AngI, AngII or aldosterone levels were observed in any of the groups. In all the groups, blood pressure remained unchanged. CONCLUSION: Raloxifene may have no significant effect on the RAAS or blood pressure in hypertensive and normotensive osteoporotic postmenopausal women.

Long-term nicorandil therapy improves cardiac sympathetic nerve activity after reperfusion therapy in patients with first acute myocardial infarction.

UNLABELLED: Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, reduces plasma norepinephrine concentration in patients with ischemic heart disease. However, long-term effects on cardiac sympathetic nerve activity (CSNA) as evaluated by (123)I-metaiodobenzylguanidine (MIBG) scintigraphy have not been determined for patients with acute myocardial infarction (AMI). METHODS: We studied 40 patients with their first AMI who were treated with intravenous nicorandil before and after primary coronary angioplasty. After suspension of the initial intravenous nicorandil treatment, 20 patients were randomized to receive oral nicorandil (15 mg/d) (group A) and the other 20 patients received a placebo (group B). All patients were also treated with an angiotensin-converting enzyme (ACE) inhibitor or beta-blockers. The delayed heart-to-mediastinum count ratio (H/M ratio), delayed total defect score (TDS), and washout rate (WR) were determined from (123)I-MIBG scintigraphy 3 wk and 6 mo after angioplasty. The left ventricular (LV) end-diastolic volume (EDV), LV end-systolic volume (ESV), and LV ejection fraction (EF) were determined by contrast left ventriculography, whereas plasma procollagen type III amino-terminal peptide (PIIINP) concentrations were also measured at the same time points. RESULTS: Three weeks after angioplasty, TDS, H/M ratios, WR, LVEDV, LVESV, and LVEF were similar in both groups. After 6 mo, all of these parameters had improved in both groups. However, the extent of change in TDS was -9 +/- 6 in group A and -5 +/- 6 in group B (P < 0.05), whereas that in the H/M ratio was 0.15 +/- 0.13 and 0.07 +/- 0.11 (P < 0.05) and that in the WR was -12% +/- 8% and -5% +/- 11% (P < 0.05). The extent of change in LVEDV, LVESV, and LVEF in group A tended to exceed that in group B, but these changes were not statistically significant. We found significant correlations between the percent change in PIIINP and that of TDS from baseline to 6 mo in group A (r = 0.456, P < 0.05). CONCLUSION: Long-term nicorandil therapy can be more beneficial for CSNA and LV remodeling than short-term therapy in patients with AMI.

Different effects of oral conjugated estrogen and transdermal estradiol on arterial stiffness and vascular inflammatory markers in postmenopausal women.

AIMS: We compared the effects of oral conjugated equine estrogen (CEE) therapy and transdermal estradiol therapy on pulse wave velocity (PWV) and circulating levels of vascular inflammatory markers in postmenopausal women and we also explored the interrelationship between the change in PWV and the changes in vascular inflammatory markers. METHODS AND RESULTS: In a randomized 12-month trial, 28 postmenopausal women received a continuous oral CEE plus cyclic medroxyprogesterone acetate (MPA), 28 received a continuous transdermal estradiol patch plus cyclic MPA, and 27 did not receive either therapy. In each subject, we measured the brachial-ankle PWV (baPWV) using an automated device, the blood pressure, and the circulating levels of vascular inflammatory markers (C-reactive protein [CRP], cell adhesion molecules [CAMs], monocyte chemoattractant protein-1 [MCP-1], and matrix metalloproteinase [MMP-9]) before and 12 months after the start of the study. Oral CEE therapy did not change the baPWV but significantly increased the CRP and MMP-9 levels (P<0.05, each) and significantly decreased the CAMs and MCP-1 levels (P<0.05, each). Transdermal estradiol therapy significantly decreased the baPWV, and the CAMs and MCP-1 levels (P<0.05, each) but had no effect on the CRP or MMP-9 levels. No significant changes were seen in the control group. The blood pressures of the subjects remained unchanged. In the transdermal estradiol group, the change in baPWV was not significantly correlated with the changes in vascular inflammatory markers. CONCLUSION: Transdermal estradiol, but not oral CEE therapy, may have antiatherosclerotic effects by improving arterial stiffness. The reduction in baPWV may contribute to the direct effect of estrogen, but not to the decrease in estrogen-induced vascular inflammatory markers.

Effect of transdermal hormone replacement therapy on carotid artery wall thickness and levels of vascular inflammatory markers in postmenopausal women.

Carotid intima-media thickness (IMT) and vascular inflammatory markers have been shown to be involved in atherosclerosis. This study was designed to investigate the effect of transdermal hormone replacement therapy (HRT) on carotid IMT and vascular inflammatory markers in postmenopausal women and to explore the interrelationship between the change in carotid IMT and the changes in vascular inflammatory markers. Thirty-five postmenopausal women (mean age 57.0+/-7.7 years) received transdermal HRT (continuous 17beta-estradiol patch [36 microg/day] plus cyclic oral medroxyprogesterone acetate [2.5 mg/day, for 12 days/ month]) for 12 months, and 32 controls (mean age 58.0+/-7.5 years) did not. Carotid IMT, assessed by ultrasound, and circulating vascular inflammatory markers, i.e., C-reactive protein (CRP), intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, E-selectin, monocyte chemoattractant protein (MCP)-1, and matrix metalloproteinase (MMP)-9 were measured before and after 12 months of treatment. In the HRT group, carotid IMT decreased significantly (p<0.01), from 0.71+/-0.13 mm to 0.65+/-0.12 mm, and the ICAM-1, VCAM-1, E-selectin, and MCP-1 levels decreased significantly (p<0.01 for all), but the CRP and MMP-9 levels remained unchanged. Carotid IMT and vascular inflammatory markers were unchanged in the control group. In the HRT group, the change in carotid IMT was significantly correlated with the change in serum E-selectin (r=0.38, p<0.05), but not with the changes in other vascular inflammatory markers. These results suggest that transdermal HRT reduced carotid artery wall thickness, and that the reduction may have been induced by an antiatherosclerotic effect combined with the direct effect of estrogen and decreased levels of estrogen-induced E-selectin.

Comparative effects of nicorandil with isosorbide mononitrate on cardiac sympathetic nerve activity and left ventricular function in patients with ischemic cardiomyopathy.

BACKGROUND: Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, improves left ventricular (LV) remodeling after myocardial infarction in rat models. However, the effects of chronic nicorandil therapy on cardiac sympathetic nerve activity in patients with ischemic cardiomyopathy have not been determined. METHODS: Thirty-six patients with ischemic cardiomyopathy (LV ejection fraction [LVEF] < 40%) who underwent successful revascularization procedure before 6 months were treated by standard conventional therapy. Eighteen patients were randomized to additionally receive nicorandil (15 mg/d), whereas the other 18 patients received isosorbide mononitrate (40 mg/d). The delayed heart-to-mediastinum count ratio (H/M ratio), delayed total defect score (TDS), and washout rate (WR) were determined from (123)I-meta-iodobenzylguanidine (MIBG) scintigraphy before and 6 months after treatment. Left ventricular end-diastolic volume (LVEDV) and LVEF were determined by echocardiography. RESULTS: Total defect score, H/M ratio, WR, LVEDV, and LVEF at baseline were similar for both groups. After treatment, in patients receiving nicorandil, TDS decreased from 50 +/- 6 to 40 +/- 11 (P < .005), H/M ratio increased from 1.68 +/- 0.23 to 1.79 +/- 0.26 (P = .005), and WR decreased from 46% +/- 9% to 40% +/- 12% (P < .005). In addition, LVEDV decreased from 178 +/- 31 to 157 +/- 30 mL (P < .0005), and LVEF increased from 33% +/- 6% to 39% +/- 7% (P < .05). In patients receiving isosorbide mononitrate, no significant changes were observed in these parameters. Moreover, there was a significant correlation between the percent change of LVEF and that of TDS from baseline to 6 months in the patients receiving nicorandil (r = -0.569, P < .05). CONCLUSIONS: The present study demonstrates improvements in cardiac (123)I-MIBG scintigraphic and echocardiographic parameters with nicorandil treatment. These findings indicate that nicorandil can improve cardiac sympathetic nerve activity and LV function in patients with ischemic cardiomyopathy.

Effects of hormone replacement therapy on office and ambulatory blood pressure in Japanese hypertensive postmenopausal women.

No study has demonstrated that hormone replacement therapy (HRT) affects blood pressure (BP) measured by 24-h ambulatory blood pressure monitoring (ABPM) in Japanese postmenopausal women (PMW) with normotension or mild-to-moderate essential hypertension. In the present study, we examined the effects of HRT on office BP and 24-h ambulatory blood pressure (ABP) in Japanese hypertensive or normotensive PMW. Thirty-one hypertensive (HT-HRT group) and 17 normotensive PMW (NT-HRT group) received HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) orally for 12 months, and 30 hypertensive (HT-Control group) and 19 normotensive PMW (NT-Control group) did not receive HRT. In all of the hypertensive PMW, BP was controlled by a variety of antihypertensive drugs before starting HRT. The hypertensive PMW were divided into two groups according to the results of ABP before HRT: nondippers (those without a diurnal change in BP) and dippers (those with a diurnal change in BP). In all patients, office BP measurements and 24-h ABPM were performed before and 12 months after the start of HRT. HRT did not change either the office or the 24-h ambulatory systolic, diastolic, or mean BP in any of the groups. Therefore, HRT did not significantly alter the proportion of nondippers. We conclude that with respect to BP, HRT might not be harmful in hypertensive PMW whose BP has been well-controlled prior to the initiation of HRT, as well as in normotensive PMW.