Evaluation of regression of left ventricular hypertrophy in hypertensive patients treated with captopril as assessed by magnetic resonance imaging.

Magnetic resonance imaging (MRI) was used to assess left ventricular mass (LVM) in 20 mild to moderate essential hypertensive patients with left ventricular hypertrophy (LVH) (LVM > 120 g/m2), treated with captopril alone or combined with hydrochlorothiazide. MRI examination was performed at the beginning (T0) and after 3 months (T3) of active treatment, by using a Philips Gyroscan S15 superconducting system, operating at 1.5 Tesla. We used a multislice-multiphase spin-echo sequence on the short-axis and transverse plane (TE = 30 ms; TR = 80-90% RR). End-diastolic thickness of interventricular septum (IVST) and lateral wall (LWT) were measured. LVM was calculated according to Simpson's rule. The results were: IVST 12.2 mm +/- 0.7 vs 10.9 mm +/- 0.5 (p < 0.001); LWT 11.5 mm +/- 0.9 vs 10.5 mm +/- 0.9 (p < 0.001); LVM 160 (g/m2) +/- 5.5 vs 138.4 g/m2 +/- 6 (p < 0.001), at T0 and T3, respectively. Our study demonstrates a significant regression of LVH in hypertensive patients after 3 months of treatment with captopril and a high accuracy of MRI as a noninvasive technique of measuring the LVM reduction

Intima-media thickness after pravastatin stabilizes also in patients with moderate to no reduction in LDL-cholesterol levels: the carotid atherosclerosis Italian ultrasound study

The Carotid Atherosclerosis Italian Ultrasound study (CAIUS), a multicenter, double-blind clinical trial, performed in 305 asymptomatic, moderately hypercholesterolemic patients, clearly demonstrated beneficial effects of pravastatin on the carotid intima-media thickness (IMT) progression. The database of the CAIUS study was examined in order to investigate the presence of a relationship, if any, between the activity of pravastatin on IMT progression rate and its hypocholesterolemic effect. Quantitative B-mode ultrasound imaging was used to quantify the individual mean maximum IMT progression rate in 3 years. In the overall group of patients (placebo and pravastatin) covariance analysis showed that while the variable 'treatment' (0 = placebo, 1 = pravastatin) was significantly related to the reduction of IMT progression (F= 6.6, P = 0.01), the IMT progression did not correlate with the extent of LDL-C lowering (F= 0.00, P = 0.98). To further investigate this issue. the pravastatin treated group was stratified into quartiles of LDL-C reduction. In contrast to what was observed in the placebo group, in which a positive mean IMT progression rate was observed, independent of the extent of LDL-C reduction, no IMT progressionwas observed in any subgroup treated with pravastatin. No significant difference was found among quartiles and no trend could be identified. In conclusion, the effect of pravastatin treatment on carotid IMT progression rate is beneficial; however the CAIUS study demonstrated that lowering LDL-C by itself, does not explain the variability of beneficial changes in IMT