Short-term simvastatin therapy increased maximal myocardial blood flow in stenotic segments by ≈45% (from 1.29 to 1.89 mL/min/g during high-dose adenosine, P<0.01).
Does simvastatin 40 mg daily improve coronary vasodilator response and maximal perfusion in patients with ischemic heart disease?
Short-term simvastatin therapy significantly improves maximal myocardial blood flow in stenotic segments in patients with ischemic heart disease.
Absolute Event Rate: 1.89% vs 1.29%
p-value: p=<0.01
Background —We tested the hypothesis that correction of hyperlipidemia improves coronary vasodilator response and maximal perfusion in myocardial regions having substantial impairment of pretreatment vasodilator capacity. Methods and Results —Measurements of myocardial blood flow were made with PET 13 Nammonia in 12 patients with ischemic heart disease (11 men; age, 65±8 years mean±SD) at rest and during adenosine at 70 and then 140 μg · kg −1 · min −1 for 5 minutes each before and ≈4 months after simvastatin treatment (40 mg daily). Simvastatin reduced LDL (171±13 before versus 99±18 mg/dL after simvastatin, P <0.001) and increased HDL (39±8 versus 45±9 mg/dL, P <0.05). Myocardial segments were classified on the basis of pretreatment blood flow response to 140 μg · kg −1 · min −1 adenosine as normal (flow ≥2 mL · min −1 · g −1 ) or abnormal (flow <2 mL · min −1 · g −1 ). In normal segments, baseline myocardial blood flow (0.95±0.32) increased ( P <0.001) at both low- (1.62±0.81) and high- (2.63±0.41) dose adenosine and was unchanged both at rest and with adenosine after simvastatin. In abnormal segments, myocardial blood flow at rest (0.73±0.19) increased at low- (1.06±0.59, P <0.02) and high- (1.29±0.33, P <0.01) dose adenosine. After simvastatin, myocardial blood flow increased more compared with pretreatment at both low- (1.37±0.66, P <0.05 versus pretreatment) and high- (1.89±0.79, P <0.01 versus pretreatment) dose adenosine. Conclusions —Short-term lipid-lowering therapy increases stenotic segment maximal myocardial blood flow by ≈45%. The mechanism involves enhanced, flow-mediated dilation of stenotic epicardial conduit vessels and may account at least in part for the efficacy of lipid lowering in secondary prevention trials and in reducing ischemic episodes in ambulatory patients.
Huggins et al. (Tue,) conducted a other in ischemic heart disease and hyperlipidemia (n=12). simvastatin vs. pretreatment baseline was evaluated on myocardial blood flow during high-dose adenosine in abnormal segments (p=<0.01). Short-term simvastatin therapy increased maximal myocardial blood flow in stenotic segments by ≈45% (from 1.29 to 1.89 mL/min/g during high-dose adenosine, P<0.01).