Objectives: To evaluate the prevalence and pattern of congenital coronary artery anomalies (CAAs) in the adult population undergoing catheter coronary angiography.Methods: The coronary angiograms done between October 2015 and September 2020 were reviewed for the presence of coronary anomalies based upon Angelini's classification. The medical record of patients with anomalies was reviewed for symptomatology and indication of angiography.Results: CAAs were found in 129 (87 males and 42 females) of 6,258 patients giving a prevalence of 2.06%. The mean age was 57.8 ± 11.8 (range 32-81) years. Among these, the anomalous origin and course of the coronaries were the most common anomaly seen in 81 (1.29%) patients, followed by intrinsic anomalies of the coronary arterial system in 44 (0.7%) patients and anomalies of coronary termination and anomalous anastomotic vessels in 2 (0.03%) patients each. Overall, the absence of the left main trunk with a separate origin of the left anterior descending (LAD) and the circumflex artery was the commonest anomaly seen in 46 (0.74%) patients, followed by dual LAD in 35 (0.56%) patients. The anomalous origin of the right coronary artery (RCA) from the left sinus was seen in 14 patients (0.22%) and that of the circumflex artery from the right sinus or right coronary artery was seen in 11 patients (0.17%). The origin of the left main and RCA from ascending aorta was found in eight (0.13%) patients. One (0.02%) patient had a single coronary artery, and another one (0.02%) had all the three coronary arteries arising from the right sinus; however, with separate ostia. The split RCA was seen in nine (0.14%) patients and there were two (0.03%) patients each of coronary artery fistulae, and of anomalous anastomotic vessels.Conclusions: The prevalence of congenital coronary anomalies in this study was 2.06%. The commonest anomaly was that of origin and courses of the vessels, however, the pattern of anomalies is different from previous studies.

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Introduction: Women perform worse after acute coronary syndrome (ACS) than men. The reason for these differences is unclear. The aim was to ascertain gender differences in the culprit plaque characteristics in ACS. Methods:Patients with ACS undergoing percutaneous coronary intervention for the culprit vessel underwent optical coherence tomography (OCT) imaging. Culprit plaque was identified as lipid rich,fibrous, and calcific plaque. Mechanisms underlying ACS are classified as plaque rupture, erosion,or calcified nodule. A lipid rich plaque along with thin-cap fibroatheroma (TCFA) was a vulnerable plaque. Plaque microstructures including cholesterol crystals, macrophages, and microvessels were noted. Results: A total of 52 patients were enrolled (men=29 and women=23). Baseline demographic features were similar in both the groups except men largely were current smokers (P<0.001). Plaque morphology,men vs. women: lipid rich 88.0% vs. 90.5%; fibrous 4% vs 0%; calcific 8.0% vs. 9.5% (P = 0.64). Of the ACS mechanisms in males versus females; plaque rupture (76.9 % vs. 50 %), plaque erosion (15.4 % vs.40 %) and calcified nodule (7.7 % vs. 10 %) was noted (P = 0.139). Fibrous cap thickness was (50.19 ±11.17 vs. 49.00 ± 10.71 mm, P = 0.71) and thin-cap fibroatheroma (96.2% vs. 95.0%, P = 1.0) in men and women respectively. Likewise no significant difference in presence of macrophages (42.3 % vs. 30%, P = 0.76), microvessels (73.1% vs. 60 %, P = 0.52) and cholesterol crystals (92.3% vs. 80%, P = 0.38). Conclusion: No significant gender-based in-vivo differences could be discerned in ACS patients’ culprit plaques morphology, characteristics, and underlying mechanisms.

Background Not every patient achieves normal coronary flow following fibrinolysis in STEMI (ST-segment elevation myocardial infarction). The culprit lesion plaque characteristics play a prominent role in the coronary flow before and during percutaneous coronary intervention. The main purpose was to determine the culprit lesion plaque features by virtual histology-intravascular ultrasound (VH-IVUS) in patients with STEMI following fibrinolysis in relation to baseline coronary angiogram TIMI (thrombolysis in myocardial infarction) flow. Pre-intervention IVUS was undertaken in 61 patients with STEMI after successful fibrinolysis. After the coronary angiogram, they were separated into the TIMI1–2 flow group (n = 31) and TIMI 3 flow group (n = 30). Culprit lesion plaque composition was evaluated by VH-IVUS. Results On gray-scale IVUS, the lesion external elastic membrane cross-sectional area (EEM CSA) was significantly higher in the TIMI 1–2 groups as compared to the TIMI 3 group (15.71 ± 3.73 mm2 vs 13.91 ± 2.94 mm2, p = 0.041) with no significant difference in plaque burden (82.42% vs. 81.65%, p = 0.306) and plaque volume (108.3 mm3 vs. 94.3 mm3, p = 0.194). On VH-IVUS, at the minimal luminal area site (MLS), the fibrous area (5.83 mm2 vs. 4.37 mm2, p = 0.024), necrotic core (NC) area (0.95 mm2 vs. 0.59 mm2, p < 0.001), and NC percentage (11% vs. 7.1%, p = 0.024) were higher in the TIMI 1–2 groups in contrast to the TIMI 3 group. The absolute necrotic core (NC) volume (8.3 mm3 vs. 3.65 mm3, p < 0.001) and NC percentage (9.3% vs. 6.0%, p = 0.007) were significantly higher in the TIMI 1–2 groups as compared to the TIMI 3 group. Absolute dense calcium (DC) volume was higher in TIMI 1–2 groups with a trend towards significance (1.0 mm3 vs.0.75 mm3, p = 0.051). In multivariate analysis, absolute NC volume was the only independent predictor of TIMI 1–2 flow (odds ratio = 1.561; 95% CI 1.202–2.026, p = 0.001). Receiver operating characteristic curves showed absolute NC volume has best diagnostic accuracy (AUC = 0.816, p < 0.001) to predict TIMI 1–2 flow with an optimal cutoff value of 4.5 mm3 with sensitivity and specificity of 79% and 61%, respectively. Conclusions This study exemplifies that the necrotic core component of the culprit lesion plaque in STEMI is associated with the coronary flow after fibrinolysis. The absolute necrotic core volume is a key determinant of flow restoration post-fibrinolysis and aids in prognostication of less than TIMI 3 flow.

Very late stent thrombosis (VLST) is a catastrophic and life-threatening complication after percutaneous coronary intervention which presents as an acute coronary syndrome with significantly high mortality and morbidity. VLST is a rare entity with drug-eluting stents and even rarer with bare metal stents. The exact pathophysiologic mechanism of VLST after BMS implantation is not known although various mechanisms have been proposed. Recently, in-stent neoatherosclerosis with intimal plaque rupture has been proposed as a potential mechanism of VLST after BMS. We report a rare case of VLST occurring 17 years after BMS implantation with angiographic and intravascular imaging evidence which provides insight into the mechanisms of VLST.