Collateral formation and clinical variables in obstructive coronary artery disease: the influence of hypercholesterolemia and diabetes mellitus.

BACKGROUND

Collateral circulation is severely compromised in patients who have a limited degree of spontaneous myocardial angiogenesis and arteriogenesis.

METHOD

To determine the clinical characteristics associated with angiographic apparent collaterals (AAC) and myocardial blush score (MBS), this study compared the clinical variables in various AAC and MBS grades (0 = no, 1 = minimal, 2 = moderate and 3 = maximal collaterals defined by the two variables) among a consecutive group of 112 patients (aged 62 +/- 12 years, 76% men) with a native artery chronic total coronary occlusion studied by selective coronary angiograms.

RESULTS

By univariate analysis, including variables such as age, sex, diabetes, hypertension, hypercholesterolemia, smoking and ejection fraction, the only variable that was found more frequently in patients with greater AAC grade was hypercholesterolemia (59%, 63%, 71% and 78% in patients with AAC grade 0, 1, 2 and 3, P = 0.003). Ejection fraction tended to be more preserved in patients with greater AAC score (46%, 48%, 51% and 54% in patients with AAC grade 0, 1, 2 and 3, respectively, P = 0.052). Diabetes mellitus was the only factor that was negatively associated with MBS (23%, 22%, 18% and 16% in patients with MBS grade 0, 1, 2 and 3, P = 0.01). Using a multivariate logistic regression analysis to predict maximal AAC grade, the only independent predictor found was hypercholesterolemia (odds ratio = 1.3, confidence limits = 1.05-1.9, P = 0.048). Diabetes mellitus was the only predictor found to be negatively associated with MBS (odds ratio = 0.72, confidence limits = 0.46-0.98, P = 0.04). It is concluded that collateral grade is associated with hypercholesterolemia and myocardial blush is negatively associated with diabetes mellitus. These findings may reflect a conflicting impact of hypercolesterolemia and diabetes mellitus upon collateral formation, leading to enhanced or depressed angiogenesis in response to obstructive coronary artery disease.