[Effect of trimetazidine on cardiac function and exercise tolerance in hypertension patients with diabetic].

OBJECTIVE: To determine the effect of trimetazidine on cardiac function and exercise tolerance in primary hypertension patients with type 2 diabetic. METHODS: In this randomized, double-blind, placebo-controlled prospective study, 60 primary hypertensive patients with diabetic were equally assigned into two groups, patients received trimetazidine (20 mg, 3 times a day) or placebo for 1 year. Echocardiography, cardiopulmonary exercise testing were performed; and the plasma N terminal pro B type natriuretic peptide (NT-ProBNP), hr-CRP, TNF-α, angiotensin Ⅱ and endothelin concentration were determined before and after treatment. RESULTS: In trimetazidine group, the left ventricular mass index, the mitral flow velocity E wave to A wave ratio (E/A), the peak early diastolic velocity (VE) to late diastolic velocity (VA) ratio (VE/VA) and the peak systolic velocity (Vs) were significantly improved, the plasma NT-ProBNP level was significantly decreased, and the exercise time, metabolic equivalent, maximal oxygen uptake and anaerobic threshold were significantly increased (all P<0.05); plasma concentration of hr-CRP, TNF-α, angiotensin Ⅱ and endothelin were significantly reduced after trimetazidine treatment, compared with baseline (all P<0.05) and with placebo (all P<0.05). There were no significant differences in any of above parameters after treatment in placebo group (all P>0.05). No severe adverse reaction was observed in both groups. CONCLUSIONS: For patients with both hypertension and diabetes, trimetazidine can improve cardiac function and increase exercise tolerance.

[Effect of atorvastatin on exercise tolerance in patients with diastolic dysfunction and exercise-induced hypertension].

OBJECTIVE: To investigate the effect of atorvastatin on exercise tolerance in patients with diastolic dysfunction and exercise-induced hypertension. METHODS: A randomized, double-blind, placebo-controlled prospective study was performed. Sixty patients with diastolic dysfunction (mitral flow velocity E/A <1) and exercise-induced hypertension (SBP>200 mm Hg) treated with atorvastatin (20 mg q.d) or placebo for 1 year. Cardiopulmonary exercise test and exercise blood pressure measurement were performed. Plasma B-natriuretic peptide (BNP) concentration at rest and at peak exercise, plasma high sensitive-C reaction protein (hs-CRP) and endothelin (ET) concentration were determined at baseline and after treatment. RESULTS: After treatment by atorvastatin, the resting SBP, pulse pressure, the peak exercise SBP and BNP were significantly decreased; and the exercise time, metabolic equivalent, maximal oxygen uptake and anaerobic threshold were increased. All of these parameters had significant differences with baseline levels (P<0.05) and the rest pulse pressure, the peak exercise SBP and BNP, and the exercise time had significant differences compared with placebo treatment (P<0.05). Plasma concentrations of hs-CRP and ET were markedly reduced by atorvastatin treatment compared with baseline and placebo (P<0.05). No difference in above parameters was found before and after placebo treatment (P>0.05). CONCLUSION: In patients with diastolic dysfunction at rest and exercise-induced hypertension, atorvastatin can effectively reduce plasma hs-CRP and ET level, lower blood pressure and peak exercise SBP, decrease peak exercise plasma BNP concentration, and ultimately improve exercise tolerance.

[Reduced cardiopulmonary exercise capacity in patients with essential hypertension: impact of left ventricular hypertrophy].

OBJECTIVE: To evaluate the cardiopulmonary exercise capacity in patients with essential hypertension (EH) complicating with or without left ventricular hypertrophy (LVH). METHODS: Graded maximal exercise test on the bicycle ergometer with respiratory gas analysis were performed in 30 gender and age matched normotensive controls, 40 EH patients without LVH and 30 EH patients with LVH (LVMI>125 g/m2 in males and > 120 g/m2 in females). Metabolic equivalents (METs), oxygen uptake (VO2), oxygen uptake to body mass ratio (VO2/kg) and oxygen uptake to heart beat ratio (VO2/HR) at time of reaching anaerobic threshold (AT) and at maximal oxygen uptake (VO2max) were measured and compared. RESULTS: METs and VO2/kg were significantly reduced in EH patients with or without LVH compared with controls [at AT, METs: 3.57 +/- 0.8 and 4.34 +/- 1.47 vs. 5.21 +/- 1.45; VO2/kg: 12.38 +/- 2.85 and 14.42 +/- 4.33 vs. 18.48 +/- 4.52, all P < 0.01; at VO2max, METs: 4.94 +/- 1.24 and 5.90 +/- 1.51 vs. 6.96 +/- 1.85; VO(2)/kg: (17.20 +/- 4.34) mlxmin(-1)xkg(-1) and (20.41 +/- 4.59) mlxmin(-1)xkg(-1) vs. (24.04 +/- 5.21) mlxmin(-1)xkg(-1), all P < 0.01]. METs and VO2/kg at both time points were also significantly reduced in EH patients with LVH compared EH patients without LVH (all P < 0.05). The lower VO2/kg in hypertensive patients was significantly correlated to higher LVMI (P < 0.05). CONCLUSIONS: Cardiopulmonary exercise capacity was reduced in hypertensive patients, especially in hypertensive patients with LVH.

[Effects of liposomal prostaglandin E(1) on myocardial reperfusion injury in rabbits]

OBJECTIVE: To probe into the role of liposomal prostaglandin E(1) (Lipo-PGE(1)) on reperfusion injury in a rabbit ischemia-reperfusion model. METHODS: Twenty-four open-chest rebbits were randomized to receive a 10 min intravenous infusion of either liposome diluent, free PGE(1), or Lipo-PGE(1) after 60 min of left anterior desending (LAD) ligation just before reperfusion. Serum creatine phosphokinase (CPK), malodialdehyde (MDA), superoxide dismutase (SOD) were detected; infarct size and region at risk were measured. RESULTS: Infarct size as a ratio of weight of infarcted tissue to weight at risk (MI/RISK) was significantly reduced with Lipo-PGE(1) (32.20+/-4.70)% compared with PGE(1) (42.09+/-6.93)% or placebo (44.57+/-5.46)% infusion (P<0.01). The values of serum CPK, MDA during reperfusion in treatment of Lipo-PGE(1) group were significantly reduced than in treatment of PGE(1) group or control group (P<0.05), and the values of serum SOD were significantly increased (P<0.05). CONCLUSION: Lipo-PGE(1) can effectively decrease the serum CPK and MDA contents, elevate the SOD activity, and attenuate myocardial reperfusion injury.