Localization of culprit lesions in coronary arteries of patients with ST-segment elevation myocardial infarctions: relation to bifurcations and curvatures.

BACKGROUND: Although culprit lesions in ST-segment elevation myocardial infarction (STEMI) cluster in the proximal coronary arteries, their relationship to bifurcations and curvatures, where blood flow is disturbed, is unknown. We hypothesized that (a) culprit lesions localize to disturbed flow distal to bifurcations and curvatures and (b) the distribution of culprit lesions in the left (LCA) and right coronary arteries (RCA) and resulting infarct size are related to the location of bifurcations and curvatures. METHODS: Emory University's contribution to the National Cardiovascular Data Registry was queried for STEMIs. Using quantitative coronary angiography, the distances from the vessel ostium, major bifurcations, and major curvatures to the culprit lesion were measured in 385 patients. RESULTS: Culprit lesions were located within 20 mm of a bifurcation in 79% of patients and closer to the bifurcation in the LCA compared with the RCA (7.4 ± 7.3 vs 17.7 ± 14.8 mm, P < .0001). Of RCA culprit lesions, 45% were located within 20 mm of a major curvature. Compared with those in the RCA, culprit lesions in the LCA were located more proximally (24.4 ± 16.5 vs 44.7 ± 28.8 mm, P = .0003) and were associated with larger myocardial infarctions as assessed by peak creatine kinase-MB (208 ± 222 vs 140 ± 153 ng/dL, P = .001) and troponin I (59 ± 62 vs 40 ± 35 ng/dL, P = .0006) and with higher in-hospital mortality (5.2% vs 1.1%, P = .04). CONCLUSIONS: In patients with STEMI, culprit lesions are frequently located immediately distal to bifurcations and in proximity to major curvatures where disturbed flow is known to occur. This supports the role of wall shear stress in the pathogenesis of STEMI.

Comparison of location of "culprit lesions" in left anterior descending coronary artery among patients with anterior wall ST-segment elevation myocardial infarction having ramus intermedius coronary arteries versus patients not having such arteries.

Disturbed, nonlaminar flow distal to arterial bifurcations contributes to atherosclerosis development and progression. We hypothesized that the presence of a ramus intermedius (RI) amplifies the flow disturbances in the proximal left anterior descending (LAD) artery causing more proximal LAD lesions and larger ST-segment elevation myocardial infarction (STEMI). Emory University's contribution to the National Cardiovascular Data Registry was queried for STEMIs from January 2006 to July 2008. The distance from the LAD ostium to the lesion was measured in patients with angiographically visible culprit lesions. The peak troponin-I, creatinine kinase-MB, and left ventricular ejection fraction were used as markers for infarct size. Of the 386 patients with STEMI, 150 had LAD culprit lesions. The mean lesion distance from the LAD ostium was 15.2 +/- 11.0 mm in the patients with RI (n = 44) and 29 +/- 19 mm in those without RI (n = 106; p <0.01). LAD lesions were more proximal in the patients with RI, with 43% and 63% of lesions occurring in the first 10 and 20 mm of the LAD, respectively, versus 10% and 32% in those without RI (p <0.01). Patients with RI had greater peak troponin-I (69 +/- 40 ng/ml vs 50 +/- 39 ng/ml, p = 0.01) and peak creatinine kinase-MB (277 +/- 271 ng/ml vs 174 +/- 190 ng/ml, p = 0.01). A trend was seen toward a lower left ventricular ejection fraction in patients with RI (36 +/- 10% versus 40 +/- 11%, p = 0.06). In conclusion, the presence of RI was associated with more proximal LAD lesions and larger anterior infarctions, suggesting anatomy-induced flow disturbances have important clinical implications.