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Biomedical subjects

Hisao Ogawa

Publications and source records attributed to Hisao Ogawa.

At least 19 recordsLinked to original sources
PubMed2007

The effects of long-term smoking on endothelial nitric oxide synthase mRNA expression in human platelets as detected with real-time quantitative RT-PCR.

Endothelium-derived nitric oxide (NO) plays an important role in the prevention of platelet aggregation and adhesion to the vascular wall. Endothelial nitric oxide synthase (eNOS) and L-arginine/NO pathway are both present in human platelets. Platelet-derived NO inhibits excessive activation and aggregation of platelets. However, the expression level of the eNOS gene in human platelets has yet to be elucidated. The current study investigates the individual expression level of platelet eNOS mRNA using the real-time reverse transcriptase-polymerase chain reaction (RT-PCR) detection method. eNOS mRNA expression was examined in platelets isolated from 50 subjects: 11 male smokers, 15 male nonsmokers, and 24 female non-smokers. After extraction of platelet total RNA, eNOS (target) and GAPDH (internal control) mRNA expression levels were quantitated using real-time RT-PCR. The expression levels of eNOS mRNA (relative copy numbers) were significantly lower in male smokers (59+/-17) than in male nonsmokers (195+/-71, P < .03), and higher in female nonsmokers (285+/-60) than in the male nonsmokers (195+/-71, P < .03). By multiple linear regression analysis, cigarette smoking (P = .008) and diabetes mellitus (P = .047) were found to be significantly negative predictors, and antioxidant (vitamin E) treatment (P = .01) was a significantly positive predictor of platelet eNOS mRNA expression. Age, other medications, and other risk factors for coronary artery disease were not significant. Using this method, eNOS mRNA abundance in human platelets was detected and quantitated in real-time. The intraplatelet eNOS mRNA expression levels were significantly decreased in cigarette smokers. Low platelet NO synthesis in smokers may result in the augmentation of platelet aggregation and thrombus formation, developing into acute coronary syndromes.

Adult↗
PubMed2006

Pravastatin enhances beneficial effects of olmesartan on vascular injury of salt-sensitive hypertensive rats, via pleiotropic effects.

OBJECTIVE: This work was undertaken to investigate comparative effect of AT1 receptor blocker (ARB), 3-hydroxy-3-methylglutaryl (HMG) coenzymeA (CoA) reductase inhibitor (statin), and their combination on vascular injury of salt-sensitive hypertension. METHODS AND RESULTS: Salt-loaded Dahl salt-sensitive hypertensive rats (DS rats) were treated with (1) vehicle, (2) hydralazine (5 mg/kg/d), (3) olmesartan (0.5 mg/kg/d), (4) pravastatin (100 mg/kg/d), and (5) combined olmesartan and pravastatin for 4 weeks. Olmesartan or pravastatin significantly and comparably improved vascular endothelium-dependent relaxation to acetylcholine, coronary arterial remodeling, and eNOS activity of DS rats. Olmesartan prevented vascular eNOS dimer disruption or the downregulation of dihydrofolate reductase (DHFR) more than pravastatin, whereas Akt phosphorylation was enhanced by pravastatin but not olmesartan, indicating differential pleiotropic effects between olmesartan and pravastatin. Add-on pravastatin significantly enhanced the improvement of vascular endothelial dysfunction and remodeling by olmesartan in DS rats. Moreover, pravastatin enhanced the increase in eNOS activity by olmesartan, being associated with additive effects of pravastatin on phosphorylation of Akt and eNOS. CONCLUSIONS: Olmesartan and pravastatin exerted beneficial vascular effects in salt-sensitive hypertension, via differential pleiotropic effects. Pravastatin enhanced vascular protective effects of olmesartan. Thus, the combination of ARB with statin may be the potential therapeutic strategy for vascular diseases of salt-sensitive hypertension.

Animals↗
PubMed2006

The relationship between endothelial function in the brachial artery and intima plus media thickening of the coronary arteries in patients with chest pain syndrome.

Endothelial dysfunction precedes the development of clinical atherosclerosis. A decrease in endothelium-derived nitric oxide activity shows impaired vasodilator function and causes arterial intimal hyperplasia or thickening. Others and we have reported the close relation of endothelial function in brachial artery and coronary artery. To compare the flow-mediated endothelium-dependent vasodilation (FMD) in brachial artery and the intima+media area in coronary artery, we measured brachial artery vasodilator response following transient occlusion with high resolution ultrasound transducer and intima+media area in coronary arteries with intravascular ultrasound in 25 patients with normal coronary angiograms (age 61.6+/-8.7 years old, men 14 and women 11). FMD was measured at least 7 days after the cessation of all vasodilators. The mean FMD of 25 patients was 3.83+/-2.38%, the mean intima+media area in coronary arteries of 25 patients was 39.9+/-15.5% of total vessel wall. FMD has a close negative relation with the largest percent intima+media area (r=-0.77, p<0.01). Especially, the patients whose FMD was less than 3.83% had larger percent intima+media area than those whose FMD was 3.83% or more (48.7+/-10.7% versus 30.3+/-14.2%, p<0.01). There is an intima+media thickening even in the patients who had normal coronary angiograms, and that the percent intima+media area correlated with FMD. The measurement of FMD is useful for screening the coronary artery intima+media thickening noninvasively. The pathogenesis of acute coronary syndrome has been reported to be the plaque rupture even in the patients with normal coronary angiograms. Thus, we must pay much attention in the patients with impaired FMD even in the normal coronary angiograms.

Aged↗
PubMed2006

Pravastatin improved glucose metabolism associated with increasing plasma adiponectin in patients with impaired glucose tolerance and coronary artery disease.

Reduced incidence of type-2 diabetes has been shown in patients treated with pravastatin. Adiponectin can exhibit beneficial effects on glucose metabolism. We investigated whether pravastatin could improve glucose tolerance associated with increasing adiponectin levels in patients with impaired glucose tolerance (IGT). This study consisted of 40 coronary artery disease (CAD) patients with IGT assessed by oral glucose tolerance test (OGTT). Patients were randomized to receive pravastatin (n=20) or no lipid-lowering medications (control group, n=20) for 6 months, after which OGTT was repeated and adiponectin levels were measured. Pravastatin treatment significantly decreased levels of total cholesterol (16%), low-density lipoprotein cholesterol (23%) and high-sensitivity C-reactive protein (37%) (p<0.01, respectively). At 2h in OGTT, pravastatin significantly improved hyperglycemia (-14%) and hyperinsulinemia (-23%). Pravastatin treatment significantly elevated plasma adiponectin levels (35%; p<0.001) but not in the control group. The glucose reduction at 2h post-OGTT was significantly associated with increased levels of adiponectin (r=-0.462; p=0.003). Pravastatin treatment is an independent predictor for improvement of post-loaded hyperglycemia (odds ratio; 5.7; 95% confidence interval 1.7-19.3; p=0.003) and achieved beneficial conversion from IGT to normal glucose tolerance (40%; p=0.03). Pravastatin exhibits beneficial effects on glucose metabolism especially in the postprandial state associated with increasing plasma adiponectin levels in CAD patients with IGT.

Adiponectin↗
PubMed2006

Future adverse cardiac events can be predicted by persistently low plasma adiponectin concentrations in men and marked reductions of adiponectin in women after acute myocardial infarction.

There is conflicting information about whether mortality after AMI is higher in women than men. We investigated the significance of plasma adiponectin concentrations on major adverse cardiac events (MACE) after acute myocardial infarction (AMI) to delineate any differences between men and women. The study patients consisted of 114 men and 42 women with AMI. The incidence of MACE was significantly higher in women than men during the entire follow-up period (p<0.05). Compared with men for post-AMI MACE, the hazard ratio for women was 5.6 after adjustment for prognostic factors. Killip class (p<0.001) and sex differences (p<0.05) were independent predictors of MACE at 1 year post-AMI. Plasma adiponectin levels in women were significantly higher than men on admission (8.66 microg/mL [range: 6.6-14.08] versus 4.71 microg/mL [range: 3.47-7.27], p<0.0001) and during the post-AMI course (all p<0.0001). Multivariate analysis identified plasma adiponectin level on admission as an independent predictor of MACE in men (p<0.001) and the difference between plasma adiponectin levels at discharge and on admission in women (p<0.05). Patterns of serial changes in plasma adiponectin concentrations are different between men and women and plasma adiponectin concentrations can be used to predict future adverse cardiac events in AMI patients.

Acute Disease↗
PubMed2006

Plasma adiponectin levels are associated with coronary lesion complexity in men with coronary artery disease.

OBJECTIVES: We sought to assess whether plasma adiponectin levels correlate with angiographic coronary lesion complexity in patients with coronary artery disease (CAD). BACKGROUND: Metabolic disorders, including diabetes mellitus and metabolic syndrome, are important risk factors for acute cardiovascular events, and adiponectin is a key molecule of metabolic disorders, with anti-atherogenic properties. Low plasma adiponectin levels are associated with CAD and future incidence of myocardial infarction. The involvement of adiponectin in coronary plaque vulnerability, which may be reflected by angiographic complex lesions, remains to be elucidated. METHODS: We measured plasma adiponectin levels in 207 men (152 with stable CAD and 55 with acute coronary syndromes [ACS]). Coronary lesions were classified as of simple or complex appearance. RESULTS: Plasma adiponectin levels were significantly lower in stable CAD patients with complex coronary lesions (n = 60) than in those with simple lesions (n = 92) (4.14 [range 2.95 to 6.02] vs. 5.27 [range 3.67 to 8.12] microg/ml, p = 0.006). Multiple logistic regression analysis demonstrated that adiponectin level was independently associated with complex lesions (odds ratio 0.514, 95% confidence interval 0.278 to 0.951; p = 0.034). Polytomous logistic regression revealed that adiponectin correlated independently with both single and multiple complex lesions. Among patients with ACS, who had lower adiponectin levels than stable CAD patients, those with multiple complex lesions had significantly lower adiponectin than those with a single complex lesion (3.26 [range 2.26 to 4.46] vs. 4.21 [range 3.36 to 5.41] microg/ml, p = 0.032). CONCLUSIONS: Plasma adiponectin levels are significantly associated with coronary lesion complexity in men with CAD. Low adiponectin levels may contribute to coronary plaque vulnerability.

Acute Disease↗
PubMed2006

Subacute thrombosis after coronary stenting occurring with resistance to ticlopidine.

A 79-year-old man underwent stent implantation from the proximal site to the left main trunk with one bare metal stent after rotation atherectomy. He received 200 mg/day ticlopidine and 200 mg/day aspirin from 2 days pre-stenting. Subacute thrombosis occurred 5 days after coronary stenting. We performed a test of platelet aggregation one month after the commencement of dual antiplatelet therapy and the test showed no response to ticlopidine in this case. An increased dose of ticlopidine was not effective for suppressing platelet aggregation. We report a case of subacute stent thrombosis which is related to ticlopidine resistance.

Aged↗
PubMed2006

Prognostic value of flow-mediated dilation of the brachial artery in patients with cardiovascular disease.

OBJECTIVE: Endothelial dysfunction is thought to represent the initial stage in the development of atherosclerosis. Recently, noninvasive examination of endothelial function has become possible using flow-mediated endothelium-dependent dilation of the brachial artery (FMD) during reactive hyperemia. We examined whether FMD has prognostic value for the prediction of subsequent cardiovascular events. METHODS: Patients were followed prospectively every month until the occurrence of the cardiovascular events. PATIENTS: The study subjects comprised 221 consecutive patients (men 108, mean age 61.4+/-10.6, ischemic heart disease 152, cardiomyopathy 28, arrhythmia 12, valvular disease 5, congenital heart disease 3, and cardioneurosis 21). The mean FMD was 4.77+/-2.85% and this value was used to divide the patients into the 2 groups (Group 1: FMD > or =4.7%; Group 2: FMD <4.7%). RESULTS: There were 110 patients in Group 1 (men 36, mean age 60.5+/-10.9), and 111 patients in Group 2 (men 72, mean age 62.2+/-10.3). Patients were followed until the occurrence of at least 1 of the major clinical cardiovascular events. Seven cardiovascular events occurred in Group 1 (6.4%, 1.14 events per 100 patient-years), while 16 occurred in Group 2 (2.88 events per 100 patient-years). Kaplan-Meier analysis demonstrated a significantly higher probability of developing cardiovascular events in Group 2 than in Group 1. CONCLUSION: The present results demonstrated that the magnitude of FMD in the brachial artery was a good predictor of subsequent cardiovascular events.

Aged↗
PubMed2006

Usefulness of combined white blood cell count and plasma glucose for predicting in-hospital outcomes after acute myocardial infarction.

Admission white blood cell (WBC) count and plasma glucose (PG) have been associated with adverse outcomes after acute myocardial infarction (AMI). This study investigated the joint effect of WBC count and PG on predicting in-hospital outcomes in patients with AMI. WBC count and PG were measured at the time of hospital admission in 3,665 patients with AMI. Patients were stratified into tertiles (low, medium, and high) based on WBC count and PG. Patients with a high WBC count had a 2.0-fold increase in in-hospital mortality compared with those with a low WBC count. Patients with a high PG level had a 2.7-fold increase in mortality compared with those with a low PG level. When a combination of different strata for each variable was analyzed, a stepwise increase in mortality was seen. There was a considerable number of patients with a high WBC count and low PG level or with a low WBC count and high PG level. These patients had an intermediate risk, whereas those with a high WBC count and high PG level had the highest risk, i.e., 4.8-fold increase in mortality, compared with those with a low WBC count and low PG level. Multivariate analysis was performed to assess the predictor for in-hospital mortality using WBC count and PG level as continuous variables and showed that WBC count and PG level were independently associated with in-hospital mortality. These findings suggested that a simple combination of WBC count and PG level might provide further information for predicting outcomes in patients with AMI.

Aged↗
PubMed2006

Effects of early statin treatment on symptomatic heart failure and ischemic events after acute myocardial infarction in Japanese.

Statins have been shown to prevent coronary artery disease and to preserve left ventricular function in dilated cardiomyopathy. We hypothesized that early use of statins would decrease cardiovascular events, including heart failure in patients with acute myocardial infarction (AMI). To examine the effect of statins in Japanese patients with AMI, a prospective, randomized, open-label trial was conducted in 486 patients with normal total cholesterol levels. Patients were randomly assigned to receive any available statin (n = 241) within 96 hours of AMI onset or no statin (n = 245) and were followed for up to 24 months. The primary end point was a composite of cardiovascular death, nonfatal AMI, recurrent symptomatic myocardial ischemia, congestive heart failure, and stroke. Event rate for the primary end point was lower in the statin group than in the nonstatin group (6.1% vs 11.4%, p = 0.0433). The statin group had a lower risk of congestive heart failure and symptomatic myocardial ischemia (p = 0.0154 and 0.0264, respectively). In conclusion, early lipid-lowering therapy with statins decreases recurrent cardiovascular events, in particular, congestive heart failure.

Aged↗
PubMed2006

Elevated levels of remnant lipoproteins are associated with plasma platelet microparticles in patients with type-2 diabetes mellitus without obstructive coronary artery disease.

AIMS: Platelets participate in the pathogenesis of arterial thrombosis and it has been demonstrated that enhanced platelet activation occurs in patients with diabetes mellitus (DM). Dyslipidaemia is a common feature of diabetes. We investigated the association between certain lipid fractions and plasma platelet-derived microparticle (PMP) levels in patients with type-2 DM. METHODS AND RESULTS: We measured fasting serum levels of remnant-like lipoprotein particles-cholesterol (RLP-cholesterol) and assessed in vivo platelet activation by quantifying the number of PMP in the plasma detected as CD42b-positive microparticles by flow cytometry in Japanese type-2 DM patients without obstructive coronary artery disease who were more slender when compared with Western diabetic patients. The levels of total cholesterol, triglycerides, RLP-cholesterol, and plasma glucose were significantly higher in patients with type-2 DM (n = 105) than in non-diabetic patients (n = 92). The plasma levels of PMP were elevated significantly in type-2 DM patients when compared with non-diabetic control subjects [7.41(5.39-10.50) x 10(6) vs. 3.44(2.43-4.41)x10(6), P < 0.001]. We found that RLP-cholesterol levels were the best predictor of PMP in multivariable linear regression analyses (beta = 0.375, P < 0.001). Lipid-lowering medication with bezafibrate successfully reduced levels of both RLP-cholesterol and PMP in patients with type-2 DM (P < 0.05). CONCLUSIONS: RLP-cholesterol and platelet microparticles are both elevated in type-2 DM patients when compared with controls. RLP-cholesterol is the primary and only predictor of platelet microparticles in the multivariable analysis, which include several standard atherosclerosis risk factors. This suggested that reducing elevated RLP-cholesterol with lipid-lowering therapy may be an effective strategy to prevent thrombogenic vascular complications in type-2 DM.

Angina Pectoris↗
PubMed2006

The effect of 6 months of treatment with pravastatin on serum adiponection concentrations in Japanese patients with coronary artery disease and hypercholesterolemia: a pilot study.

BACKGROUND: Pravastatin has been reported to reduce cardiovascular events and mortality in patients with coronary artery disease (CAD). Hypoadiponectinemia is a known risk factor for CAD. OBJECTIVE: This study analyzed the effects of shortterm pravastatin treatment on serum lipid and adiponectin concentrations in patients with CAD and hypercholesterolemia. METHODS: This was a multicenter, observational pilot study of the effect of 6 months of treatment with pravastatin 10 to 20 mg/d on serum adiponection concentrations in patients with documented CAD and total cholesterol (TC) levels> or =180 mg/dL. Patients from 13 medical centers in Japan were monitored at visits every 4 weeks for assessment of compliance and adverse effects. For the assessment of pravastatin's effects, patients were categorized according to baseline serum adiponectin concentrations: quartile 1 (Q1) = < 4.83 microg/mL; quartile 2 (Q2) = 4.83 to 7.20 microg/mL; (Q4) = > 10.38 microg/mL. The primary end point of the study was the percent change from baseline in adiponectin nectin concentrations at 6 months. Secondary end points were changes in lipids, high-sensitivity C-reactive protein (hsCRP), and glycosylated hemoglobin (HbA1c). RESULTS: One hundred thirty consecutive patients were enrolled; 11 were excluded and 4 discontinued due to adverse events. Thus, 115 patients were included in the study analyses (83 men, 32 women; mean age, 68 years). No patient had a cardiac event during the 6-month follow-up period. After 6 months of pravastatin treatment, 74 (64.3%) patients had increases in serum adiponectin concentrations. Median (interquartile range) adiponectin concentrations increased significantly from 7.2 (4.8-10.4) mug/mL at baseline to 7.8 (5.4-11.2) microg/mL after 6 months of pravastatin treatment (P<0.001); the mean percent increase from baseline was 16.3%. The percent increase from baseline in serum adiponection concentrations was significantly higher among patients in Q1 (39.3%) compared with those in Q3 (4.5%) and Q4 (6.3%) (P<0.003 and P<0.005, respectively). The relative increase in adiponectin concentrations was significantly correlated with the relative increase in high-density lipoprotein cholesterol (HDL-C) (f=0.47; P<0.001). After 6 months of pravastatin treatment, TC and low-density lipoprotein cholesterol levels had decreased, by 14.6% and 23.3%, respectively, and HDL-C levels had increased by 14.0% (all, P<0.001). The change in triglycerides (-13.3%) was not statistically significant. Serum hsCRP levels were significantly decreased from baseline after 6 months of pravastatin treatment (P<0.001). HbA1c did not change significantly. CONCLUSION: In this pilot study in Japanese patients with CAD and hypercholesterolemia, 6 months of treatment with pravastatin 10 to 20mg/d was associated with significant increases in serum adiponectin concentrations.

Adiponectin↗
PubMed2006

Relation between platelet microaggregates and ankle brachial index in patients with peripheral arterial disease.

INTRODUCTION: Peripheral arterial disease is one of the systemic atherosclerotic diseases, and patients with the disorder are classified in the high risk group of coronary artery disease. A lower ankle brachial index is a frequent finding in peripheral arterial disease. While platelet microaggregates are a significant predictor of adverse clinical outcome in coronary artery disease, the significance of platelet aggregability in peripheral arterial disease has not been elucidated. MATERIALS AND METHODS: Small platelet aggregates measured using laser-light scattering and ankle brachial index were determined in 42 patients with both coronary artery disease and peripheral arterial disease (peripheral group), 56 patients with only coronary artery disease (coronary group) and 32 patients without both (control group). RESULTS: The level of small platelet aggregates was increased significantly in the peripheral group (4.3 x 10(4) [range 2.2 x 10(4) to 7.4 x 10(4)]) compared with both the coronary (1.1 x 10(4) [range 0.3 x 10(4) to 5.0 x 10(4)]) and control groups (0.5 x 10(4) [range 0.1 x 10(4) to 0.9 x 10(4)]). There was a significant inverse correlation between log small platelet aggregates and ankle brachial index (n=130, r=-0.422, p<0.001). Multivariate logistic regression analysis revealed that a lower ankle brachial index (<0.90) was an independent determinant of increased levels of small platelet aggregates. CONCLUSIONS: Platelet aggregability was increased in patients with peripheral arterial disease with the degree of platelet aggregation being closely associated with ankle brachial index. It is possible that this change in platelet activity may be one mechanism to explain why a lower ankle brachial index is a predictor of poor prognosis in patients with peripheral arterial disease.

Aged↗
PubMed2006

A -786T>C polymorphism in the endothelial nitric oxide synthase gene reduces serum nitrite/nitrate levels from the heart due to an intracoronary injection of acetylcholine.

We identified a -786T>C polymorphism in the eNOS gene, and this polymorphism was strongly associated with coronary spasm. The present study aimed to elucidate whether the -786T>C polymorphism or acetylcholine (ACh)-induced coronary spasm affects serum nitrite/nitrate (NOx) levels. The study population comprised three groups: (i) 26 patients without coronary spasm in the left anterior descending coronary artery (LAD) with the T/T genotype (group A); (ii) 20 patients with coronary spasm in the LAD with the T/T genotype (group B); and (iii) 16 patients with coronary spasm in the LAD with the C/T genotype (group C). Paired blood samples were obtained from the coronary sinus (CS) and the aortic tract (Ao) before and after an intracoronary injection of ACh. Serum NOx and plasma lactate levels were measured. The delta NOx level was calculated as the serum concentration of NOx in the CS minus that in the Ao. We compared lactate extraction ratios (LERs) and delta NOx levels between the three groups. The LERs after the provocation test in groups A, B and C were 18.9+/-2.4%, -0.5+/-3.9% and -13.5+/-4.2%, respectively. The LER in group C was significantly lower than in group B. The delta NOx levels after the provocation test in groups A, B and C were 11.5+/-1.7 micromol/l, 10.4+/-3.5 micromol/l and -2.1+/-4.8 micromol/l, respectively. The delta NOx levels in group C were significantly lower (P<0.05). Although the NOx level was significantly increased after the provocation test in group A (P<0.05), the NOx level was significantly decreased after the provocation test in group C (P=0.001). In group B, the provocation test did not significantly change the delta NOx level. In conclusion, the -786T>C polymorphism reduces the NOx level from the heart due to an intracoronary injection of ACh, and thereby predisposes the patients to severe coronary spasm.

Acetylcholine↗
PubMed2006

Enhancement of cardiac oxidative stress by tachycardia and its critical role in cardiac hypertrophy and fibrosis.

OBJECTIVE: To examine the mechanism and significance of tachycardia-induced cardiac damage, using azelnidipine, a relatively new dihydropyridine calcium channel blocker which does not increase heart rate. METHODS: Comparing azelnidipine and amlodipine, we examined the cardiac effects and the direct effects on a sinus node/atrial preparation in stroke-prone spontaneously hypertensive rats (spSHRs). By pacing the right atrium, we examined the effect of tachycardia per se on cardiac oxidative stress. Using apocynin, a reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, we investigated the role of oxidative stress in cardiac remodelling. RESULTS: Azelnidipine suppressed cardiac hypertrophy, fibrosis, NADPH oxidase and superoxide in spSHRs more potently than amlodipine, and was associated with lower heart rates than amlodipine. Azelnidipine caused a greater reduction than amlodipine in the beat rate of the sinus node/atrial preparation of spSHRs. A 10 or 20% increase in heart rate, independent of blood pressure or sympathetic nerve activity, significantly enhanced cardiac NADPH oxidase activity, superoxide and activated mitogen-activated protein kinases. Reduction of cardiac oxidative stress by apocynin led to the suppression of cardiac hypertrophy, inflammation and fibrosis in spSHRs, beyond its hypotensive effect. CONCLUSIONS: Our work provided evidence that the increase in heart rate per se, independent of sympathetic nerve activity, enhances cardiac oxidative stress and activates mitogen-activated protein kinases, which seem to be responsible for cardiac remodelling. Azelnidipine, without causing an increase in heart rate, has the potential to be useful for the treatment of cardiac remodelling.

Amlodipine↗
PubMed2006

Spontaneous polymorphic ventricular tachycardia after administration of pilsicainide in a patient resuscitated from ventricular fibrillation.

We performed a pilsicainide challenge test in a 38-year-old man who was resuscitated from ventricular fibrillation without apparent baseline electrocardiogram (ECG) abnormality. His father had a history of ventricular fibrillation and his brother had multiple episodes of syncope. Pilsicainide (1 mg/kg) induced short coupled ventricular premature beats followed by repetitive polymorphic ventricular tachycardia without apparent J wave and ST elevation, and excessive changes in QRS duration and QT interval. An implantable cardioverter defibrillator was implanted.

Adult↗
PubMed2006

Sex differences in early mortality of patients undergoing primary stenting for acute myocardial infarction.

BACKGROUND: Limited information exists regarding the impact of gender on in-hospital outcome after primary stenting for acute myocardial infarction (AMI). METHODS AND RESULTS: A total of 2,981 patients (790 women and 2,191 men) participated in the study who were admitted within 24 h after symptom onset and underwent emergency primary stenting for AMI. Compared with men, women were significantly older; had higher incidences of hypertension, diabetes mellitus, hyperlipidemia, Killip class > or =2, and cardiogenic shock; had a higher blood glucose level and a lower serum creatinine level on admission. Other baseline characteristics, including the incidences of ST-segment elevation AMI, anterior infarction, 3-vessel disease, initial or final Thrombolysis in Myocardial Infarction (TIMI) flow grade did not significantly differ between the sexes. The in-hospital mortality rate was significantly higher in women than in men (9.4% vs 5.2%, p<0.001). On multivariate analysis, age, Killip class, blood glucose level, serum creatinine level, and final TIMI grade were independent predictors of in-hospital death, but female gender was not (odds ratio 1.01, p=0.69). CONCLUSIONS: Our findings suggest that in patients undergoing primary stenting for AMI, women have higher in-hospital mortality than men, but female gender itself is not independently associated with increased in-hospital mortality after adjustment for baseline differences.

Acute Disease↗