Effect of diabetes mellitus on formation of coronary collateral vessels

A Abacı, A Oguzhan, S Kahraman, NK Eryol, S Ünal… - Circulation, 1999 - Am Heart Assoc
A Abacı, A Oguzhan, S Kahraman, NK Eryol, S Ünal, H Arınç, A Ergin
Circulation, 1999Am Heart Assoc
Background—Although myocardial ischemia is known to be significantly related to the
development of coronary collateral vessels (CCVs), there is considerable variation between
patients with ischemic heart disease in the presence of collateral development. The nature
of this variability is not well known. Likewise, it remains unclear whether diabetes mellitus
(DM) has any effect on CCVs. The aim of this study was to evaluate the effect of DM on
CCVs. Methods and Results—Of the patients who underwent coronary angiography during …
Background—Although myocardial ischemia is known to be significantly related to the development of coronary collateral vessels (CCVs), there is considerable variation between patients with ischemic heart disease in the presence of collateral development. The nature of this variability is not well known. Likewise, it remains unclear whether diabetes mellitus (DM) has any effect on CCVs. The aim of this study was to evaluate the effect of DM on CCVs.
Methods and Results—Of the patients who underwent coronary angiography during the interval between March 1, 1993, and June 20, 1998, in our institution, 306 were diabetic. Those patients in whom coronary angiography is normal or severity of coronary artery stenosis is thought not to be sufficient for the development of CCVs (<75%) were excluded from the study. A total of 205 patients (mean age, 59±8 years) met the criteria for the DM group. For case-control matching, 205 consecutive nondiabetic patients (mean age, 58±9 years) who had ≥1 diseased vessel with >75% stenosis were included in the control group. The CCVs were graded according to the Rentrop scoring system, and the collateral score was calculated by summing the Rentrop numbers of every patient. There was no statistical difference between patients with and without DM in clinical baseline characteristics. The mean number of diseased vessels in the DM group (1.58±0.68) was higher than that in the nondiabetic group (1.42±0.65, P=0.005). The mean collateral score was 2.41±2.20 in the DM group and 2.60±2.39 in the control group. After confounding variables were controlled for, the collateral score in the diabetic group was significantly different from that in the nondiabetic group (P=0.034).
Conclusions—Our findings suggest that CCV development is poorer in patients with than in patients without DM. Thus, we can speculate that DM is an important factor affecting CCV development.
Am Heart Assoc