These pooled results provide strong evidence that pravastatin reduces the risk of cardiovascular events in patients with atherosclerotic disease and mildly to moderately elevated lipid levels. The benefit for reducing myocardial infarction is evident in older and younger patients, men and women, and patients with and without histories of hypertension and prior infarction.

We investigated whether left ventricular hypertrophy in elite cyclists is associated with functional changes or abnormal energy metabolism. Left ventricular hypertrophy is a powerful risk factor for sudden cardiac death with different prognostic significance among the various geometric forms. Cyclists may have a combination of mixed eccentric and concentric hypertrophy. Magnetic resonance imaging was used to define left ventricular mass, geometry and function. Thirteen highly trained male cyclists and 12 healthy controls were investigated. Proton-decoupled phosphorus-31 cardiac spectroscopy was performed to assess parameters of myocardial high-energy phosphate metabolism. Left ventricular mass and end-diastolic volumes normalized for body surface area were significantly higher in cyclists (124.1 +/- 9.4 g.m-2 and 106.2 +/- 11.4 ml.m-2, respectively) than in controls (85.9 +/- 9.3 g.m-2 and 79.1 +/- 11.6 ml.m-2, respectively), (both P < 0.0001). The left ventricular mass to end-diastolic volume ratio, as a parameter of left ventricular geometry, was not significantly increased in cyclists compared to controls. Resting left ventricular ejection fraction, cardiac index, and systolic wall stress in cyclists did not differ significantly from those of controls. The phosphocreatine to adenosine triphosphate ratio was not significantly different between cyclists and controls (2.2 +/- 0.34 vs 2.2 +/- 0.17, ns). Cyclists show prominent left ventricular hypertrophy with normal geometry. The finding that the hypertrophic hearts of the cyclists had normal left ventricular function and a normal phosphocreatine to adenosine triphosphate ratio suggests that sport-induced left ventricular hypertrophy is a physiological adaptation rather than a pathophysiological response.

Objective-To determine whether the angiotensin converting enzyme (ACE) and the angiotensin II type 1 receptor (AT 1 R A1166C) gene polymorphism interact to increase the risk of ischaemic events, and whether this can be explained by the progression of angiographically defined coronary atherosclerosis. Design-Prospective defined substudy of the lipid lowering regression trial (REGRESS). Setting-University hospital. Patients-885 male patients with stable coronary artery disease. Main outcome measures-Incidence of ischaemic events during a two year follow up; serial quantitative coronary arteriography (mean segment diameter and minimum obstruction diameter) at baseline and after two years. Results-Patients who carried both the ACE-DD and AT 1 R-CC genotype had significantly more ischaemic events during the two year follow up than those carrying other genotype combinations (p = 0.035, Mantel-Haenszel test for linear association). There was no association between the two genotypes and mean segment diameter or minimum obstruction diameter at baseline or after two years. Conclusions-The suggestion that ACE-DD and AT 1 R-CC genotypes interact to increase the risk of ischaemic events is confirmed. However, this increased risk was not accompanied by increased progression of angiographically defined coronary atherosclerosis. (Heart 2001;85:458-462)

Background Lipid-lowering therapy during 2 years in the Regression Growth Evaluation Statin Study (REGRESS) was associated with less progression of coronary atherosclerosis in the pravastatin group compared with the placebo group. The effect of lipid-lowering therapy on the functional state of the coronary circulation is less well known. The purpose of this study was to evaluate this effect. Methods and Results In a substudy of REGRESS, 69 patients were randomized to pravastatin or placebo. Thirty-seven of these patients were allocated to the medical management stratum. Quantitative coronary angiography, regional myocardial perfusion, exercise testing, and classification of angina pectoris were assessed at baseline and after 2 years of therapy. Regional myocardial perfusion was assessed by digital subtraction angiography after intracoronary papaverine with videodensitometric calculation of the hyperemic mean transit time (HMTT) of contrast. In the medical management stratum, regional myocardial perfusion was assessed in 31 regions in the pravastatin group and 25 regions in the placebo group. The change in HMTT in the pravastatin group was −0.18 seconds (−5%) and in the placebo group +0.52 seconds (+18%), a difference of 0.70 seconds ( P =.004). The mean difference in change in classification of angina pectoris (scale, 1 to 4) between pravastatin and placebo was 0.7 ( P =.03) in favor of the pravastatin-treated patients. The change in HMTT was correlated with the change in exercise time ( r =−.65, P =.002). Conclusions In patients with symptomatic coronary artery disease, treatment with the HMG-coenzyme A reductase inhibitor pravastatin during 2 years resulted in a preserved regional myocardial perfusion, whereas patients on placebo deteriorated. The classification of angina pectoris improved only in patients receiving pravastatin. In lipid-lowering therapy, the evaluation of myocardial perfusion by assessment of the HMTT reveals a combined measure of functional and structural changes in the coronary circulation.

After myocardial infarction, left ventricular volume and ejection fraction can be assessed by echocardiography, magnetic resonance imaging and radionuclide angiography to guide therapy and determine prognosis. Whether a measured parameter gives the same results irrespective of the method used and the observer who performs the analysis is only partly known. Intra-observer and inter-observer variability were determined for echo and magnetic resonance imaging. Left ventricular ejection fraction measured by these techniques was related to radionuclide angiograms performed in the same period. Intra-observer variability for both echo and MRI was low and in most instances below 5%. Inter-observer variability for the echo and MRI measurements were substantially higher than intra-observer variability. Comparison of the three imaging modalities revealed systematic differences. Therefore, in clinical studies, left ventricular volume and function parameters have to be measured with the same technique and by the same observer in qualified core laboratories.

In quantitative coronary arteriography (QCA), the outer diameter of the contrast catheter is used almost exclusively as the calibration device. Since the true outer diameter of these catheters are smaller than the French sizes listed by the manufacturer, it has been advocated to measure the actual sizes with a precision micrometer. However, this represents a significant effort in the organizations of the QCA Angiographic Core Laboratories and of the participating cardiac catheterization laboratories. In the Dutch REGRESS trial on regression/progression of coronary artery disease, we have measured a total of 2,104 catheters from four different manufacturers. In 2,048 of the 2,104 catheters the variabilities in the measurements were 0.02-0.03 mm, which represents an error of only 1% of the average catheter sizes. In the remaining 56 catheter measurements, the variability was 0.04 mm. From these data we may conclude that from now on the stated mean values can be used for calibration purposes. This has important practical consequences for running clinical trials and QCA Core Laboratory operations.

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