Biomedical subjects

Shuichi Ichikawa

Publications and source records attributed to Shuichi Ichikawa.

10 recordsLinked to original sources

PubMed2003

Effect of spironolactone on cardiac sympathetic nerve activity and left ventricular remodeling in patients with dilated cardiomyopathy.

OBJECTIVES: We sought to evaluate the effects of spironolactone on cardiac sympathetic nerve activity and left ventricular (LV) remodeling in patients with dilated cardiomyopathy (DCM). BACKGROUND: Aldosterone prevents the uptake of norepinephrine and promotes structural remodeling of the heart. Spironolactone, an aldosterone receptor blocker, improves LV remodeling in patients with DCM, but its influence on cardiac sympathetic nerve activity has not been determined. METHODS: We selected 30 patients with DCM who were treated with an angiotensin-converting enzyme inhibitor and a loop diuretic. Fifteen patients were assigned to receive spironolactone additionally, whereas the remaining 15 patients continued their current regimen. The delayed heart/mediastinum (H/M) count ratio, delayed total defect score (TDS), and washout rate (WR) were determined from iodine-123 ((123)I)-meta-iodobenzylguanidine (MIBG) images before and six months after treatment. The left ventricular end-diastolic volume (LVEDV) and left ventricular ejection fraction (LVEF) were determined by echocardiography, and New York Heart Association (NYHA) functional class was estimated. RESULTS: In the spironolactone group, the TDS decreased from 36 +/- 9 to 24 +/- 13 (p < 0.0001), the H/M ratio increased from 1.64 +/- 0.20 to 1.86 +/- 0.27 (p < 0.0001), and WR decreased from 55 +/- 12% to 41 +/- 15% (p < 0.0005). In addition, the LVEDV decreased from 187 +/- 26 to 154 +/- 41 ml (p < 0.005), and LVEF increased from 33 +/- 6% to 39 +/- 6% (p < 0.005). However, there were no significant changes in these parameters in the control group. There was a significant correlation between changes in the (123)I-MIBG findings and changes in LVEDV with spironolactone treatment (TDS: r = 0.684, p = 0.0038; H/M ratio: r = -0.878, p < 0.0001; and WR: r = 0.737, p = 0.0011). The NYHA functional class improved in both groups but showed a greater improvement in the spironolactone group than in the control group (p < 0.01). CONCLUSIONS: Spironolactone improves cardiac sympathetic nerve activity and LV remodeling in patients with DCM.

Adult↗

PubMed2003

Hormone replacement therapy causes a decrease in hepatocyte growth factor in hypertensive women.

OBJECTIVE: Serum hepatocyte growth factor (HGF) is associated with blood pressure. We investigated whether the serum HGF level differs between hypertensive and normotensive postmenopausal women (PMW) and whether hormone replacement therapy (HRT) alters the serum HGF level and blood pressure in hypertensive and normotensive PMW. DESIGN: Prospective observational study. METHODS: A total of 33 PMW with mild to moderate essential hypertension controlled by antihypertensive treatment (mean age, 57 +/- 6 years) and 23 normotensive PMW (mean age, 57 +/- 7 years) received continuous HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) once a day orally for 12 months, and we measured serum HGF levels and blood pressure before and 12 months after the start of HRT. RESULTS: The baseline serum HGF level was significantly higher in hypertensive PMW than in normotensive PMW. HRT significantly decreased the serum HGF level in hypertensive subjects, from 2.85 +/- 0.64 pmol/l to 2.49 +/- 0.65 pmol/l (P < 0.001), but not in normotensive subjects. HRT did not change blood pressure in either group. CONCLUSIONS: Serum HGF level before the start of HRT was higher in the hypertensive PMW than in the normotensive PMW. Furthermore, HRT decreases serum HGF without decreasing blood pressure in hypertensive PMW. The HRT-induced decrease in serum HGF was greater in hypertensive PMW than in normotensive PMW, and the decrease was independent of blood pressure changes.

Aged↗

PubMed2003

Hormone replacement therapy decreases insulin resistance and lipid metabolism in Japanese postmenopausal women with impaired and normal glucose tolerance.

OBJECTS: To investigate the effect of combined estrogen and progesterone therapy on insulin resistance (IR) and carbohydrate and lipid metabolism in postmenopausal women (PMW) with impaired (IGT) and normal glucose tolerance (NGT). METHODS: Sixteen Japanese PMW with IGT and 33 with NGT received daily oral hormone replacement therapy (HRT; 0.625 mg of conjugated equine estrogen plus 2.5 mg of medroxyprogesterone acetate) for 12 months. As controls, 13 Japanese PMW with IGT and 31 with NGT were enrolled and not treated by HRT. Fasting plasma glucose (FPG), fasting immunoreactive insulin (IRI), and IR were measured in each subject at study initiation and 12 months later. We used homeostasis model assessment (HOMA) to determine IR. RESULTS: FPG and HOMA IR were decreased in both HRT groups, and fasting IRI was reduced in the HRT-NGT group. In controls, FPG, fasting IRI, and HOMA IR were unaltered. Total and low-density lipoprotein cholesterol were decreased and high-density lipoprotein cholesterol was increased in both HRT groups, but triglyceride was unchanged. In controls, lipid metabolism was unaltered. CONCLUSION: HRT decreased IR and improved carbohydrate and lipid metabolism in Japanese PMW with IGT and NGT. These beneficial effects argue for the use of HRT in PMW with IGT as well as NGT.

Asian People↗

PubMed2003

Azelnidipine and amlodipine: a comparison of their pharmacokinetics and effects on ambulatory blood pressure.

We objected: 1) To compare the effects of azelnidipine and amlodipine on 24-h blood pressure; 2) To monitor the plasma concentration vs. the time profile in order to assess the association between pharmacokinetics and hypotensive activity after administration of either drug for 6 weeks. Blood pressure and pulse rate were measured by 24-h monitoring with a portable automatic monitor in a randomized double-blind study of 46 patients with essential hypertension. Azelnidipine 16 mg (23 patients) or amlodipine 5 mg (23 patients) was administered once daily for 6 weeks. Pharmacokinetics were analyzed after the last dose was taken. Both drugs showed similar effects on the office blood pressure and pulse rate. During 24-h monitoring, both drugs caused a decrease in systolic blood pressure of 13 mmHg and had a similar hypotensive profile during the daytime period (07:00-21:30). The pulse rate decreased by 2 beats/min in the azelnidipine group, whereas it significantly increased by 4 beats/min in the amlodipine group. Similar trends in the blood pressure and pulse rate were observed during the nighttime (22:00-6:30) and over 24 h. Excessive blood pressure reduction during the nighttime was not seen in either group. The pharmacokinetic results indicated that the plasma half-life (t1/2) of amlodipine was 38.5 +/- 19.8 h and that of azelnidipine was 8.68 +/- 1.33 h. Despite this difference in pharmacokinetics, the hypotensive effects of amlodipine and azelnidipine were similar throughout the 24-h administration period.

Amlodipine↗

PubMed2003

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.

Antihypertensive Agents↗

PubMed2003

Effects of hormone replacement therapy on serum angiotensin-converting enzyme activity and plasma bradykinin in postmenopausal women according to angiotensin-converting enzyme-genotype.

An insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene determines serum ACE levels. The D allele is associated with increased ACE activity and is linked to cardiovascular disease. Hormone replacement therapy (HRT) in postmenopausal women (PMW) decreases serum ACE activity and concomitantly increases plasma bradykinin. We investigated the effect of HRT on these parameters in PMW according to ACE-genotype. We assessed 68 PMW during 12-month oral HRT (0.625 mg conjugated estrogen +2.5 mg medroxyprogesterone acetate). ACE genotype was determined at baseline, and serum ACE activity and plasma bradykinin were measured at baseline and after 3-, 6-, and 12-month HRT. We divided the PMW into three groups according to ACE genotype: groups I/I (n = 26), I/D (n = 33), and D/D (n = 9). HRT resulted in a significant reduction in the genotype-associated increase in ACE activity in the ACE I/D and D/D groups after 6-month (p < 0.001 and p < 0.05, respectively) and 12-month HRT (p < 0.001 and p < 0.01, respectively), but not in the I/I group. While the reduction of ACE activity was expected to increase bradykinin in the ACE I/D and D/D groups, HRT significantly increased the bradykinin levels not only in these two groups but also in the ACE I/I group at both 6 months (p < 0.01, p < 0.05, and p < 0.001, respectively) and 12 months after the start of HRT (p < 0.01, p < 0.01, and p < 0.01, respectively). These results suggest that the increased plasma bradykinin of PMW by HRT might not be induced solely by the reduction in serum ACE activity.

Aged↗

PubMed2003

Effects of hormone replacement therapy on circulating docosahexaenoic acid and eicosapentaenoic acid levels in postmenopausal women.

Hormone replacement therapy (HRT) has antiatherosclerotic effects of which the mechanism remains unclear. The ingestion of fish oil or other sources of n-3 polyunsaturated fatty acids has been included in comprehensive strategies to prevent atherosclerosis. Many epidemiologic studies have shown that the dietary intake of docosahexaenoic acid and eicosapentaenoic acid has antiatherosclerotic effects. We investigated the effect of HRT on plasma docosahexaenoic acid and eicosapentaenoic acid concentrations in postmenopausal women. Fifty-nine postmenopausal women, who received conjugated estrogens (0.625 mg/day) and medroxyprogesterone (2.5 mg/day) for 12 months, and 45 control postmenopausal women, who did not receive HRT, volunteered to participate in this study. Plasma docosahexaenoic acid and eicosapentaenoic acid concentrations were measured at baseline and at 6 and 12 months after the start of HRT. HRT significantly increased the plasma docosahexaenoic acid and eicosapentaenoic acid concentrations from 134 +/- 5 microg/ml and 69 +/- 4 microg/ml at baseline to 156 +/- 7 microg/ml and 85 +/- 7 microg/ml after 12 months (both p<0.01). However, the control group showed no significant change in their plasma docosahexaenoic acid and eicosapentaenoic acid levels during the study. HRT increased plasma docosahexaenoic acid and eicosapentaenoic acid levels in postmenopausal women. We propose that the increase in docosahexaenoic acid and eicosapentaenoic acid may be partially responsible for the beneficial mechanisms by which HRT induces an antiatherosclerotic effect in postmenopausal women.

Adult↗

PubMed2003

Addition of valsartan to an angiotensin-converting enzyme inhibitor improves cardiac sympathetic nerve activity and left ventricular function in patients with congestive heart failure.

UNLABELLED: We determined whether the addition of the angiotensin-receptor blocker valsartan to an angiotensin-converting enzyme (ACE) inhibitor improves cardiac sympathetic nerve activity and left ventricular function in patients with congestive heart failure (CHF). METHODS: Thirty-two patients with CHF (left ventricular ejection fraction [LVEF] < 40%; mean, 33% +/- 6%) were treated with an ACE inhibitor and a loop diuretic. Sixteen patients (group A) were randomized to additionally receive valsartan (40-80 mg/d), and the remaining 16 patients (group B) continued their current regimen. Patients were studied before and 6 mo after treatment. The delayed heart-to-mediastinum count ratio (H/M ratio), delayed total defect score (TDS), and washout rate (WR) were determined from (123)I-metaiodobenzylguanidine images. The left ventricular end-diastolic volume (LVEDV) and LVEF were determined by echocardiography, and New York Heart Association (NYHA) functional class was estimated. RESULTS: Before treatment, TDS, H/M ratio, WR, LVEDV, LVEF, and NYHA functional class were similar in both groups. After treatment in group A, TDS decreased from 37 +/- 8 to 31 +/- 9 (P < 0.001), H/M ratio increased from 1.66 +/- 0.23 to 1.81 +/- 0.23 (P < 0.001), and WR decreased from 47% +/- 9% to 39% +/- 10% (P < 0.01). In addition, the LVEDV decreased from 193 +/- 36 mL to 169 +/- 51 mL (P < 0.005), and LVEF increased from 32% +/- 7% to 41% +/- 13% (P = 0.0005). In group B, these parameters did not change significantly. NYHA functional class improved in both groups (in group A, from 3.3 +/- 0.5 to 1.7 +/- 0.6 [P < 0.0005]; in group B, from 3.3 +/- 0.5 to 2.4 +/- 0.6; [P < 0.005]). The improvement was significantly greater in group A than in group B (P < 0.05). CONCLUSION: The addition of valsartan to an ACE inhibitor improves cardiac sympathetic nerve activity, left ventricular function, and symptoms in patients with CHF.

3-Iodobenzylguanidine↗

PubMed2002

Effects of hormone replacement therapy on left ventricular hypertrophy and growth-promoting factors in hypertensive postmenopausal women.

We investigated the effects of hormone replacement therapy (HRT) on left ventricular hypertrophy (LVH) and growth-promoting factors in hypertensive postmenopausal women (PMW) with LVH. Twenty-one Japanese hypertensive PMW (age 55.3+/-0.8 years) with LVH who had never received HRT volunteered to participate in this study. Eleven subjects received a daily dose of HRT (0.625 mg conjugated equine estrogen, 2.5 mg medroxyprogesterone acetate) orally for 12 months. Ten PMW who refused HRT were enrolled as controls. Blood pressure and serum angiotensin-converting enzyme (ACE) activity, plasma aldosterone, and insulin resistance were measured. M-mode echocardiography and blood pressure measurements were performed in all patients. Data obtained before and after 12 months of HRT were compared. No significant differences in blood pressure were observed between the two groups after 12 months of HRT. In the HRT group, the LV mass index (p<0.01), serum ACE activity (p<0.01), and plasma aldosterone (p<0.01) levels were reduced after 12 months of treatment. The changes in serum ACE activity and plasma aldosterone were not correlated with the change in LV mass index in the HRT group. No significant changes in blood pressure, LV mass index, serum ACE activity, plasma aldosterone, or insulin resistance were observed in the control group. HRT contributed to the reduction of LV mass in hypertensive PMW. However, the effect of HRT on LVH did not appear to be associated with changes in growth-promoting factors, such as blood pressure, serum ACE activity, plasma aldosterone, and insulin resistance.

Aldosterone↗

PubMed2002

Spironolactone improves cardiac sympathetic nerve activity and symptoms in patients with congestive heart failure.

UNLABELLED: We evaluated whether spironolactone would improve cardiac sympathetic nerve activity and symptoms in patients with congestive heart failure (CHF). METHODS: Thirty patients with CHF (left ventricular ejection fraction [LVEF] < 40%; mean, 30% +/- 9%) were treated with an angiotensin-converting enzyme inhibitor, a loop diuretic, and, in most cases, digoxin. Fifteen patients (group A) were assigned to additionally receive spironolactone (12.5-50 mg/day), and the remaining 15 patients (group B) continued their current regimen. Patients were studied before and 6 mo after treatment. 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) images. LVEF was determined by echocardiography, and New York Heart Association (NYHA) functional class was estimated. RESULTS: Before treatment, LVEF, TDS, H/M ratio, WR, and NYHA functional class were similar in both groups. With treatment, LVEF did not significantly improve in either group. However, after treatment in group A, TDS decreased from 37 +/- 9 to 25 +/- 13 (P = 0.0001), H/M ratio increased from 1.62 +/- 0.20 to 1.83 +/- 0.27 (P < 0.0001), and WR decreased from 51 +/- 9 to 40 +/- 15 (P < 0.001). In group B, these parameters did not significantly change. NYHA functional class improved in both groups (in group A, from 3.3 +/- 0.5 to 1.7 +/- 0.5 [P < 0.0001]; in group B, from 3.3 +/- 0.5 to 2.4 +/- 0.6 [P = 0.01]); this was a significantly greater improvement in group A than in group B (P < 0.01). CONCLUSION: Spironolactone improves cardiac sympathetic nerve activity and symptoms in patients with CHF.

3-Iodobenzylguanidine↗