Why the study?
Coronary artery anatomy frequently affects plaque and culprit lesion location, but whether the presence or absence of a Ramus Intermedius coronary artery affects culprit lesion location in acute LCX occlusion was unclear.
Does the presence of a Ramus Intermedius artery affect the location of culprit lesions in patients with acute left circumflex coronary artery occlusion?
Does the presence of a Ramus Intermedius artery affect the location of culprit lesions in patients with acute left circumflex coronary artery occlusion?
The presence of a Ramus Intermedius artery does not significantly alter the proximal location of culprit lesions or infarct size in acute left circumflex coronary artery occlusion.
RI presence should not guide LCX lesion expectations in acute occlusion; leaves open anatomic effects on plaque location.
BACKGROUND AND AIM: Coronary artery anatomy frequently affects location of atherosclerotic plaques and subsequent culprit lesions. We sought to clarify whether presence or absence of Ramus Intermedius coronary artery (RI) would affect location of culprit lesions in acute left circumflex (LCX) coronary artery occlusion. METHODS: The study included 180 patients, 100 with a diagnosis of non-ST elevation myocardial infarction (NSTEMI) and 80 with ST elevation myocardial infarction (STEMI). All culprit lesions were located in the LCX coronary artery. RI group included 45 patients and the No RI group included 135 patients. RESULTS: Culprit LCX lesions were similarly located at a comparable distance from LCX ostium in both groups and the presence of RI was not associated with significantly more proximally located culprit LCX lesions (34.7 ± 15.2 mm compared to 30.8 ± 17.9 mm respectively, p > 0.05). The frequency distribution of culprit lesions' distance from LCX ostium showed no significant difference between both groups in any of the segments studied (10 mm each). There was no significant difference between both groups regarding markers of myocardial necrosis size as cardiac biomarkers (peak cardiac troponin-T 1077.4 ± 361.2 pg/dl vs 926 ± 462.2 pg/dl respectively, p = 0.13), (peak creatine kinase-MB 232.2 ± 81 ng/dl vs 194.7 ± 99.2 ng/dl respectively, p = 0.07) or left ventricular ejection fraction (EF 46.3 ± 6.3% vs 48.3 ± 8.3% respectively, p = 0.76). CONCLUSION: Presence of RI coronary artery, as an additional flow divider, may not be associated with more proximal culprit lesions, compared to its absence, in cases of acute LCX coronary artery occlusion. Possible underlying pathophysiologic mechanisms remain to be clarified.
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Zayat et al. (2021) studied this question.
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