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Serum cardiac enzyme elevation after percutaneous coronary intervention (PCI), a relatively common complication, is a prognostic determinant of long-term outcome in patients who undergo these procedures. Statins are postulated to reduce such complications. This study investigated the short-term effects of pravastatin on serum creatine kinase myocardial isoform (CK-MB) and serum cardiac troponin I (cTpI) levels after elective PCI. Of 93 patients studied, 72 (77.4%) were men, and 21 (22.6%) were women (mean age, 58.9+/-11.0 y). Patients were randomly divided into 3 groups before they underwent elective PCI. Preoperatively, group 1 patients (n=30) received pravastatin 10 mg/d, and group 2 patients (n=29) received pravastatin 40 mg/d. Control group patients (n=34) received no lipid-lowering medication. Serum CK-MB and serum cTpI levels were measured preoperatively and then again at 6, 24, and 36 h postoperatively. Demographic features of patients and characteristics of the PCI procedure, including number of vessels/lesions and duration and number of inflations, did not differ among groups (P>.05). Mean serum CK-MB and serum cTpI levels were significantly increased after PCI in all patients (P<.001). When compared with control group patients, those given pravastatin did not experience significantly lowered postprocedural serum CK-MB or serum cTpI levels (P>.05). Preprocedural pravastatin therapy at dosages of 10 mg/d and 40 mg/d seems inadequate for preventing serum cardiac enzyme elevations during short-term follow-up after PCI. Additional research on this topic is recommended.

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Basal septal hypertrophy (BSH), a cause of left ventricular outflow tract (LVOT) obstruction, is thought to occur by increased ventricular dynamics. The aim of the study was to evaluate the effect of pharmacologic stress on LVOT gradients in a group of hypertensive patients with BSH. Dobutamine stress was used in 24 hypertensive patients (mean age 56 +/-8 years; 11 women) with BSH and 20 normal controls (mean age 54 +/-9 years; 7 women). Ejection fraction and myocardial mass, basal septal dimension, and LVOT diameter were measured with 2-dimensional echocardiography. LVOT velocities and transmitral velocities before and at peak dobutamine infusion were determined by continuous wave Doppler and pulsed Doppler, respectively. There were no differences in mean ejection fraction and myocardial mass between BSH patients (58 +/-3%, 204 +/-24 g) and normals (56 +/-4%, 201 +/-32 g). The basal septum was thicker in patients (1.55 +/-0.2 cm) than in normals (1.03 +/-0.1 cm, p<0.001). Maximum LVOT velocities were similar in BSH (1.2 +/-0.4 m/sec) and normals (1.1 +/-0.2 m/sec) at rest. At peak stress, maximum LVOT velocities were higher in BSH (3.3 +/-0.6 m/sec) than normals (1.7 +/-0.4 m/sec, p<0.001). LV rate-pressure product at peak stress was higher in BSH (23,326 +/-4,388) than normals (17,592 +/-2,409, p<0.001). LV isovolumetric relaxation time was prolonged, and the E/A ratio was decreased in the patients at rest (130 +/-14 msec and 0.72 +/-0.18, respectively, p<0.001). At peak stress, diastolic function did not significantly change in two groups. The correlations between LVOT velocity change by stress and mean LVOT diameter (r=-0.668, p<0.001) and mean BS thickness (r=0.610; p<0.001) were significant in the whole group. High velocities appeared on LVOT at peak pharmacologic stress in the hypertensive patients with BSH compared with control group. This suggests dynamic ventricular ejection by stress may contribute to hypertrophy of the basal segment, which is the closest part of septum to increased afterload.

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