Effect of bezafibrate therapy on atherosclerotic aortic plaques detected by MRI in dyslipidemic patients with hypertriglyceridemia

Fibrates reduce triglycerides (TG) and increase HDL-cholesterol levels, but there was no report showing plaque regression by fibrates. Using MRI, we investigated the effects of bezafibrate on aortic plaques in 22 dyslipidemic patients. All patients were asked to receive 400mg bezafibrate, but 8 who declined to have bezafibrate became the control group. Changes in vessel wall area (VWA) and lumen area (LA) from baseline to 1-year were evaluated. Bezafibrate reduced TG (-55%) and increased HDL-cholesterol levels (+29%). Bezafibrate reduced HDL size and increased LDL size. In thoracic plaques, bezafibrate reduced VWA (-6%, P<0.001) with no LA change, but VWA slightly progressed without bezafibrate (+5%). In abdominal plaques, bezafibrate reduced VWA (-8%, P<0.001) with LA increase (+3%, P<0.02), but VWA progressed without bezafibrate (+6%). VWA changes in thoracic and abdominal plaques correlated with TG reduction and HDL-cholesterol increase. Notably, VWA change in only abdominal plaques correlated with HDL size reduction and LDL size increase. Thus, bezafibrate induced plaque regression in thoracic and abdominal aortas with marked TG reduction and HDL-cholesterol increase, but the processes of plaque regression and vascular remodeling may differ between thoracic and abdominal aortas. However, because our study was not a controlled, randomized trial, further study is needed.     

Comparison between objective measures of smoking and self-reported smoking status in patients with asthma or COPD: are our patients telling us the truth?

OBJECTIVE:

Smoking prevalence is frequently estimated on the basis of self-reported smoking status. That can lead to an underestimation of smoking rates. The aim of this study was to evaluate the difference between self-reported smoking status and that determined through the use of objective measures of smoking at a pulmonary outpatient clinic.

METHODS:

This was a cross-sectional study involving 144 individuals: 51 asthma patients, 53 COPD patients, 20 current smokers, and 20 never-smokers. Smoking status was determined on the basis of self-reports obtained in interviews, as well as through tests of exhaled carbon monoxide (eCO) and urinary cotinine.

RESULTS:

All of the asthma patients and COPD patients declared they were not current smokers. In the COPD and asthma patients, the median urinary cotinine concentration was 167 ng/mL (range, 2-5,348 ng/mL) and 47 ng/mL (range, 5-2,735 ng/mL), respectively (p < 0.0001), whereas the median eCO level was 8 ppm (range, 0-31 ppm) and 5 ppm (range, 2-45 ppm), respectively (p < 0.05). In 40 (38%) of the patients with asthma or COPD (n = 104), there was disagreement between the self-reported smoking status and that determined on the basis of the urinary cotinine concentration, a concentration > 200 ng/mL being considered indicative of current smoking. In 48 (46%) of those 104 patients, the self-reported non-smoking status was refuted by an eCO level > 6 ppm, which is also considered indicative of current smoking. In 30 (29%) of the patients with asthma or COPD, the urinary cotinine concentration and the eCO level both belied the patient claims of not being current smokers.

CONCLUSIONS:

Our findings suggest that high proportions of smoking pulmonary patients with lung disease falsely declare themselves to be nonsmokers. The accurate classification of smoking status is pivotal to the treatment of lung diseases. Objective measures of smoking could be helpful in improving clinical management and counseling.     

Heart and sports: modifications of electrocardiogram,late potentials and echocardiography. Study of 75 sportsmen and 46 witnesses

The authors report the results of prospective study, which compared 75 sports subjects and 45 witnesses. All subjects were male, the differentiating parameter being the type of sport practiced. This work analysed surface Electrocardiogramme, thransthoracic echocardiography and high amplification ECG. The statistical study used the student test t compare means and the Chi2 test for the percentages, the signification limit was fixed to 5%. Clinically, our two series didn't show a significant statistical difference, concerning: age, weight, height or arterial pressure. On the electrocardiographical level, the sport's men have a lower cardiac frequency (p = 0.005), a larger PR space (p = 0.05), an important Sokolow parameter (p < 0.005), and repolarisation disorders represented, essentially by negative T waves (p = 0.02) and an upper movement of ST segment in V2-V3 (p < 0.005). Echocardiography showed a dilatation of the right cavities: right auricular (p = 0.0125) and right ventricular (p = 0.025). Move over, it has been showed that the sport's men left ventricular walls were tabor (septal wall, p = 0.0125), (posterior wall, p = 0.025), despite a difference in the values of the left ventricular telediastolic diameter (4 mm average in the two series). The signification limit was not reached and it was also showed that the left auricular was also dilated (p = 0.025). The study of the delayed Potentials, tried to bring an explication to certain sudden deaths of sport's men which are to date unexplained and which could have a rhythmical origin? It is also to be noted that sport's men present more delayed ventricular Potentials. However, the statistical signification was not reached (p = 0.07).     

Statin therapy alone and in combination with an acyl-CoA:cholesterol O-acyltransferase inhibitor on experimental atherosclerosis

The ability to modify the enzymatic processes involved in promoting atherosclerotic plaque disruption and to serially monitor atherosclerotic evolution could provide novel information in the management of patients with atherosclerosis. We studied the effects of a statin (atorvastatin) and its combination with an acyl-CoA:cholesterol O-acyltransferase (ACAT) inhibitor (avasimibe) on atherosclerotic regression and plaque stability as measured by matrix metalloproteinase 1 and 3 (MMP-1 and MMP-3) levels. Watanabe Heritable Hyperlipidemic (WHHL) rabbits treated with atorvastatin alone experienced an attenuated increase in atherosclerotic burden versus controls as determined by MR imaging. The mean vessel wall area (VWA) prior to drug therapy was 5.57 +/- 0.01 mm2. The VWA increased to 6.71 +/- 0.03 and 7.16 +/- 0.03 mm2, respectively, in atorvastatin-treated and control groups (p < 0.0001 for both). The combination of atorvastatin and avasimibe induced a significant regression of the previously established atherosclerotic lesions, with the VWA decreasing to 4.54 +/- 0.04 mm2 (p = 0.009). Atorvastatin alone induced a nonsignificant reduction in the percent staining of MMP-1 in atherosclerotic lesions, but the combination treatment with avasimibe led to a significant reduction versus controls (p = 0.005). However, a reduction in MMP-3 staining was significant for rabbits treated with both atorvastatin alone (p = 0.007) and in combination with avasimibe (p = 0.04) versus controls. In this animal model, the addition of avasimibe to atorvastatin has beneficial effects on both atherosclerotic plaque regression and stabilization.