Evaluation of myocardial bridging of the left anterior descending coronary artery by 64-slice multidetector computed tomographic angiography.

The purpose of this study was to use the unique characteristics of multidetector computed tomographic coronary angiography to evaluate the prevalence and characteristics of myocardial bridging (MB) in a large series of patients and to assess the relation between atherosclerosis and MB. Three hundred consecutive coronary angiograms obtained by 64-slice multidetector computed tomography were evaluated retrospectively. For comparison of symptoms and concomitant atherosclerosis, 245 patients were included in the study and categorized into group 1 (n = 108) with MB and group 2 (n = 137) with no MB in the left anterior descending coronary artery (LAD). Axial and multiplanar reformatted images of all arteries were analyzed for the presence of measurable obstructive coronary disease (>25% stenosis) and minor luminal (<25% stenosis) calcified and noncalcified plaque and for MB in the LAD. Longitudinal and cross-sectional views were used for MB measurements. MB was found in 44% of patients (108 of 245) and was present equally in men and women (45% and 41%, p = NS). The mid LAD was the most common location (66%, p <0.001). There were no atherosclerotic lesions within the MB segments. The presence of MB did not influence the presence or severity of atherosclerotic lesions in the nonbridged segments of the LAD. In conclusion, MB as demonstrated by 64-slice multidetector computed tomographic coronary angiography is more common than previously reported by coronary angiography. The bridged segment appears to be free of atherosclerosis.

Coronary artery disease risk factors in patients with diastolic dysfunction.

Diastolic dysfunction (DD) is a common entity associated with advanced age and hypertension, often present in patients with ischemic heart disease. The correlation of DD and coronary artery disease (CAD) in asymptomatic young patients is not known. We sought to determine the prevalence of CAD risk factors in asymptomatic patients with DD. We present data from a retrospective chart review of CAD risk factors in asymptomatic patients diagnosed with DD during an echocardiograph examination. We screened all patients that had an echocardiographic examination at Lenox Hill Hospital from January 2004 until July 2007. DD was diagnosed if an impaired filling pattern with an E/A ratio less than one was noted on the mitral inflow pulse wave doppler. One-hundred and one patients met study criteria. Data regarding the presence of the following risk factors was collected: sex, hypertension, hyperlipidemia, smoking, diabetes, peripheral artery disease, and family history of CAD. The mean age of patients was 48 +/- 6; 50% were male. The most prevalent CAD risk factor in this group of patients with DD was hypertension (53%), followed by hyperlipidemia (31%) and diabetes (22%). These data can help identify those patients who are asymptomatic in terms of DD who may be at risk for the condition. These patients should undergo an echocardiograph examination in order to rule out presence of DD, even if symptoms are not present.

Platelet aggregation inhibition in patients receiving statins either fully or partially metabolized by CYP3A4.

Clopidogrel therapy is the standard for prevention of cardiovascular thrombotic events. Clopidogrel is converted to an active thiol by the cytochrome P450 CYP 3A4 and 2C19 enzymes. Recent studies suggest that statins metabolized by CYP3A4 attenuate the anti-aggregatory effect of clopidogrel. We evaluated the effect of CYP3A4-metabolized statins (atorvastatin, group 1) and partially-CYP3A4-metabolized statins (simvastatin, group 2) on platelet aggregation inhibition (PAI) when given concomitantly with clopidogrel as compared to patients who were statin naive (group 3). PAI was measured by PlateletWorks (Helena Laboratories ICHOR) using the platelet P2Y12 receptor agonist ADP (20 micromol). All patients were on clopidogrel therapy (75 mg/day). Non-responsiveness was defined as a PAI of < 35%. There was no statistical difference in mean PAI among groups; a higher prevalence of clopidogrel non-responders was noted in group 1 compared to group 3 (p=0.002). Multivariate analysis, adjusting for unequal presence of metabolic syndrome and hypertension, we found no statistical difference between groups. Our data suggests that statins, either fully or partially metabolized by CYP3A4, do not influence PAI when clopidogrel is used at 75 mg/day, even after adjusting for risk factors. We concluded that concomitant statins with clopidogrel therapy does not influence the effect of clopidogrel in PAI.