Abstract
Numerous factors have been implicated in the pathogenesis of cocaine associated myocardial infarction (CAMI). However, the relative contributions each of these mechanisms provide to the pathogenesis of CAMI have not been well defined. We hypothesized that significant angiographic differences exist between CAMI patients vs thrombotic AMI patients (TAMI) and normal controls. The TIMI Flow Grade, corrected TIMI Frame Count (CTFC), TIMI Myocardial Perfusion Grade (TMPG), presence of triple-vessel disease, stenosis severity, and presence of angiographically apparent thrombus were compared in patients who sustained CAMI to TAMI patients and normal controls. 2495 angiograms were analyzed (CAMI = 57, TAMI = 2403, Controls = 35). Impairment in both epicardial and microvascular flow in patients with CAMI was intermediate between TAMI and controls. Compared to TAMI patients, CAMI patients were less likely to have 3 vessel disease (8.9% vs. 19.1%; p < 0.05), epicardial stenosis was less severe (14.9+/-30.2 vs. 72.6+/-18.6; p < 0.0001), less thrombus was present (6.5% vs. 33.1%; p < 0.001) and TIMI grade 3 flow was observed more frequently (76% vs. 59%). Normal TMPG 3 perfusion was significantly impaired in both CAMI and TAMI patients when compared to controls without AMI (TMPG 3 was 40% and 26.6% vs. 100% respectively; p < 0.001 for both). The majority of patients in both AMI groups had diminished or absent tissue level perfusion (TMPG 0 flow, CAMI 53.9 vs. TAMI 56.8%). Both epicardial and microvascular flow is impaired in CAMI. While epicardial flow among CAMI patients is slightly better than TAMI patients, the incidence of little or severely impaired tissue level perfusion is nearly identical.
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