Resistance exercise and lipoproteins in postmenopausal women.

The specific aims of this study were to quantify the effects of 12 weeks of resistance training, as well as a single session of resistance exercise on lipids and lipoproteins in obese, postmenopausal women. 21 obese, postmenopausal women, not on hormone replacement therapy (age=65.9 ± 0.5 yr; BMI=32.7 ± 0.8 kg/m(2)), were randomly assigned to control (n=12) and exercise (n=9) groups matched for age and BMI. For 12 weeks, 3 days/week, the exercise group performed 10 whole body resistance exercises (3 sets at 8-RM). Fasting (10 h) blood samples were collected immediately prior to and 24 h after the first and last exercise and control session. Serum was assayed for concentrations of total cholesterol, triglycerides, LDL-C, HDL-C, HDL 2-C, HDL 3-C, non-HDL-C and TC:HDL and LDL:HDL ratios. The exercise group exhibited a significant (P<0.01) improvement in muscular strength, but no change in BMI, body mass or body composition post-training. Total cholesterol, LDL-C and non-HDL-C were significantly (P<0.05) lower in the exercise compared to the control group following the 12 weeks of resistance training. Whole body resistance training provides obese, postmenopausal women a non-pharmacological approach for the reduction of lipid and lipoprotein-cholesterol concentrations.

Major improvement of percutaneous cardiovascular procedure outcomes with radial artery catheterisation: results from the PREVAIL study.

OBJECTIVE: To obtain a "snapshot" view of access-specific percutaneous cardiovascular procedures outcomes in the real world. DESIGN: Multicentre, prospective study performed over a 30-day period. SETTING: Nine hospitals with invasive cardiology facilities, reflecting the contemporary state of healthcare. PATIENTS: Unselected consecutive sample of patients undergoing any percutaneous cardiovascular procedure requiring an arterial access. INTERVENTIONS: Percutaneous cardiovascular procedures by radial or femoral access MAIN OUTCOME MEASURES: The primary outcome was the combined incidence of in-hospital (a) major and minor haemorrhages; (b) peri-procedural stroke; and (c) entry-site vascular complications. The secondary outcome was the combined incidence of in-hospital death and myocardial infarction/reinfarction. For analysis purposes, outcomes were allocated to arterial access-determined study arms on an intention-to treat basis. Multivariable analysis adjusted using propensity score was performed to correct for selection bias related to arterial site. RESULTS: A total of 1052 patients were enrolled: 509 underwent radial access and 543 femoral access. In both groups, 40% underwent a coronary angioplasty. Relative to femoral access, radial access was associated with a lower incidence both of primary (4.2% vs 1.96%, p = 0.03, respectively) and secondary endpoints (3.1% vs 0.6%, p = 0.005, respectively). Multivariate analysis, adjusted for procedural and clinical confounders, confirmed that intention-to-access via the radial route was significantly and independently associated with a decreased risk both of primary (OR 0.37, 95% CI 0.16 to 0.84) and secondary endpoints (OR 0.14, 95% CI 0.03 to 0.62). CONCLUSIONS: Our study indicates strikingly better outcomes of percutaneous cardiovascular procedures with radial access versus femoral access in contemporary, real-world clinical settings.

Coronary artero-venous gradient of endogenous urokinase.

Experimental data indicate that urokinase-type plasminogen activator (u-PA) contributes significantly to endogenous fibrinolysis and vascular remodeling in proportion to its local concentrations. In humans, however, it is not known whether u-PA levels vary at different sites and across specific vascular beds. We investigated possible regional and artero-venous differences in plasma u-PA concentrations in 15 patients undergoing cardiac catheterization. Three pairs of simultaneous samples were taken from: (1) the ascending aorta and coronary sinus; (2) left ventricle and right atrium; (3) femoral artery and femoral vein. Single-chain urokinase-type plasminogen activator (scu-PA) was measured by bioimmunoassay, and total u-PA antigen (including scu-Pa and two-chain urokinase-type plasminogen activator complexed with inhibitors (tcu-PA)) by enzyme-linked immunosorbent assay. Scu-PA represented, on average, 51+/-15% of total u-PA concentrations. Scu-PA and total u-PA levels were correlated (r=.72, P<.0001) and did not differ significantly among the arterial or venous locations. There was a small but consistent increase in mean (+/-standard deviation (S.D.)) scu-PA concentrations from all arterial to all venous samples (1.5+/-0.6 vs. 1.6+/-0.5 ng/ml, P=.038) and from ascending aorta to coronary sinus (1.6+/-0.5 vs. 1.7+/-0.6 ng/ml, P=.046). Similarly, total u-PA levels increased from femoral artery to femoral vein (2.9+/-0.7 vs. 3.0+/-0.8 ng/ml, P<.001). In contrast, across the lungs, no significant concentration-gradient was seen in either scu-PA or total u-PA. The changes in total u-PA roughly followed those of scu-PA. These data identify an artero-venous gradient in human plasma u-PA across the coronary and peripheral beds, but not across the lungs, suggesting differences in u-PA kinetics according to vascular location.

Effect of sildenafil citrate upon myocardial ischemia in patients with chronic stable angina in therapy with beta-blockers.

BACKGROUND: It has been suggested that phosphodiesterase 5 (PDE5) inhibition is potentially hazardous and that it increases the risk of cardiac events in patients with coronary artery disease. This study sought to evaluate whether PDE5 inhibition with sildenafil exerts any effect on exercise-induced myocardial ischemia in patients on beta-blockers. METHODS: Fourteen patients underwent a baseline exercise test off-therapy and were then started on atenolol (100 mg once daily). After a run-in phase of 1 week, patients underwent a second exercise test and were randomized to receive either sildenafil (50 mg) or placebo given in a random order on two different occasions, 2 days apart. Exercise test was repeated 2 hours after the administration of sildenafil or placebo. RESULTS: All patients had a > 1 mm ST-segment depression while off-therapy. Eight patients had a negative exercise test response after atenolol, which was unaltered by the adjunct of either sildenafil or placebo. In the remaining subjects, atenolol significantly prolonged the time to 1 mm ST-segment depression and the exercise time. Sildenafil and placebo did not reverse the beneficial effect of atenolol upon exercise-induced myocardial ischemia. CONCLUSIONS: PDE5 inhibition does not worsen exercise capacity and exercise-induced myocardial ischemia in patients with chronic stable angina whose symptoms and exercise test response are well controlled by beta-blocker therapy.

Effect of estrogen replacement therapy on heart rate variability and heart rate in healthy postmenopausal women.

Increased sympathetic drive in symptomatic menopausal women was reduced after estrogen replacement therapy for 4 months, which has a potentially beneficial effect on cardiovascular functions.

Significance of transient ST-T segment changes during dobutamine testing in Q wave myocardial infarction.

OBJECTIVES: We evaluated dobutamine stress electrocardiography for detecting potentially reversible contractile dysfunction or residual ischemia in the infarct-related area. BACKGROUND: ST-T segment changes in pathologic Q wave leads during stress testing may reflect contractile reserve, inducible ischemia or passive mechanical stretching. Dobutamine echocardiography allows detection of contractile reserve at low doses and inducible ischemia at high doses. METHODS: We used low (5 to 10 microg/kg body weight per min) and high doses (20 to 40 microg/kg per min) of dobutamine in 49 patients with a previous Q wave myocardial infarction and analyzed the relation between ST-T segment changes in pathologic Q wave leads and regional contraction. RESULTS: At low dose dobutamine, regional contraction improved in the infarct-related area in 23 patients. New or further ST segment elevation and pseudonormalization of negative T waves developed at low doses more frequently in patients with than without contractile reserve (both p < 0.001), giving a sensitivity of 43.5% and 60.9% and a specificity of 100% and 96.2%, respectively. At high dose dobutamine (43 patients), new or further ST segment elevation and pseudonormalization of negative T waves, occurring beyond those observed at low doses, had a low predictive accuracy for contractile reserve (sensitivity of 9.5% and 14.3% and specificity of 68.2% and 81.8%, respectively). Pseudonormalization of negative T waves at high dose dobutamine was 100% specific (but only 25% sensitive) for homozonal ischemia. CONCLUSIONS: ST segment elevation or pseudonormalization of negative T waves, or both, is indicative of contractile reserve in the infarct-related area when either develops at low dose dobutamine, but may be associated with worsening or no change in contractile function at high doses.