Abstract
BackgroundSignificance of totally occluded culprit coronary artery in patients presenting with non-ST segment elevation myocardial infarction (NSTEMI) is underestimated. The aim of the study was to evaluate the incidence and impact of totally occluded culprit artery on in-hospital and 6 months follow-up outcomes of NSTEMI acute coronary syndrome (ACS) patients.ResultsWe collected retrospectively data of 500 NSTEMI patients who presented to our hospital from June 2016 to June 2017. All patients underwent PCI within 72 h of presentation. We excluded patients with cardiogenic shock, prior CABG, and STEMI. Patients were divided into two groups according to pre-procedural culprit vessel thrombolysis in myocardial infarction (TIMI) flow. Group 1, TIMI flow 0 total coronary occlusion, included 112 patients (22.4%). Group 2, TIMI flow 1–3 non-total occlusion, included 388 patients (77.6%). Group 1 patients had significantly higher incidence of smoking (p=0.01), significantly higher level of cardiac enzymes (p<0.001), significantly more collaterals (p<0.001), and significantly more LCX and RCA as the culprit vessel (p<0.01), while group 2 patients had significantly higher incidence of diabetes (p=0.02) and significantly more LAD as the culprit vessel. There were no significant differences between the two groups regarding the major adverse cardiac and cerebrovascular events (MACCE) in-hospital (5.3% in totally occluded group vs. 1% in non-totally occluded group, p=0.07), but group 1 patients had significantly higher incidence of in-hospital arrhythmia (8.9% in group 1 vs. 1% in group 2, p=0.007). After 6 months follow-up, there were no significant differences regarding MACCE between the 2 groups after 6 months follow-up (5.4% in group 1 vs. 4.6% of group 2, P=0.24).Conclusion22.4% of NSTEMI patients have a totally occluded culprit artery. The presence of an occluded culprit artery did not significantly affect the clinical outcomes of NSTEMI patients either in-hospital or after 6 months follow-up but was associated with significantly higher incidence of in-hospital arrhythmia.
Highlights
Significance of totally occluded culprit coronary artery in patients presenting with non-ST segment elevation myocardial infarction (NSTEMI) is underestimated
Previous studies have shown that nearly 25% of NSTE Myocardial infarction (MI) patients present with a totally occluded coronary artery, and two-thirds of the occlusions are already collateralized at the time of angiographic examination [8, 9]; this was more common in patients presenting with either right coronary artery (RCA) or left circumflex artery (LCX) involvement [8,9,10,11,12,13,14], which could be explained by the lack of ECG sensitivity in detecting acute ischemia in the inferolateral and posterior walls
We aimed to evaluate the incidence and impact of totally occluded culprit artery on in-hospital and after 6 months follow-up outcomes of NSTEMI patients
Summary
Significance of totally occluded culprit coronary artery in patients presenting with non-ST segment elevation myocardial infarction (NSTEMI) is underestimated. The aim of the study was to evaluate the incidence and impact of totally occluded culprit artery on in-hospital and 6 months follow-up outcomes of NSTEMI acute coronary syndrome (ACS) patients. The spectrum of acute coronary syndrome (ACS) including ST-segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina have become the leading cause of death globally [1,2,3]. The lack of classic ST-segment elevation on ECG in these subset of NSTEMI patients, despite the presence of totally occluded culprit artery, lead to either delay in or no revascularization [15] Previous studies have shown that nearly 25% of NSTE MI patients present with a totally occluded coronary artery, and two-thirds of the occlusions are already collateralized at the time of angiographic examination [8, 9]; this was more common in patients presenting with either right coronary artery (RCA) or left circumflex artery (LCX) involvement [8,9,10,11,12,13,14], which could be explained by the lack of ECG sensitivity in detecting acute ischemia in the inferolateral and posterior walls.
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