Effect of COVID-19 pandemic on six-month mortality and clinical outcomes of patients with ST-elevation myocardial infarction.

Introduction: The coronavirus disease 2019 (COVID-19) infection has changed everyday clinical practice, with a shortage of solid data about its implications for ST-elevation myocardial infarction (STEMI) patients. Aim: To evaluate the impact of COVID-19 on 6-month clinical outcomes of patients with STEMI and determine the mortality predictors after STEMI during the COVID-19 pandemic. Material and methods: This prospective observational study was conducted on consecutive STEMI patients who presented to our hospital between April and October 2021. A total of 74 COVID-19-positive patients were included in group I and compared to 148 COVID-19-negative patients (group II). We compared the two cohorts' rates of major adverse cardiovascular events (MACEs; composite of death from any cause, recurrent MI, target-vessel revascularization, and stroke) at 6 months. Results: COVID-19 STEMI patients were more likely to present with angina equivalent symptoms, had higher Killip class at admission, and higher levels of high-sensitive cardiac troponin T and serum C-reactive protein. The 6-month rates of MACEs were significantly higher in STEMI patients with COVID-19 compared to non-COVID-19 patients (41.9% vs. 16.9%, respectively; p < 0.001) and were mainly due to higher in-hospital mortality (20.3% vs. 6.1%, respectively; p = 0.001). The independent predictors of 6-month mortality in STEMI patients during the COVID-19 pandemic were the absence of ST resolution, low systolic blood and higher Killip class on admission, presence of severe MR and atrial fibrillation, and anterior wall STEMI. Conclusions: STEMI patients with superimposed COVID-19 infection had worse clinical outcomes, with almost three times higher in-hospital mortality and 6-month MACEs.

Predictors and 3-year outcomes of compromised left circumflex coronary artery after left main crossover stenting.

BACKGROUND: There are few predictors of decreased fractional flow reserve (FFR) in the left circumflex coronary artery (LCx) after left main (LM) crossover stenting. OBJECTIVES: We aimed to determine the predictors for low FFR at LCx and possible treatment strategies for compromised LCx, together with their long-term outcomes. METHODS: Altogether, 563 patients who met the inclusion criteria were admitted to our hospital from February 2015 to November 2020 with significant distal LM bifurcation lesions. They underwent single-stent crossover percutaneous coronary intervention (PCI) under intravascular ultrasound (IVUS) guidance with further LCx intervention based on the measured FFR. RESULTS: The patients showed significant angiographic LCx ostial affection post-LM stenting, but only 116 (20.6%) patients had FFR < 0.8. The three-year composite major adverse cardiac events (MACE) rates were comparable between the high and low FFR groups (16.8% vs. 15.5; p = 0.744). In a multivariate analysis, low FFR at the LCx was associated with post-stenting minimal luminal area (MLA) of LCx (odds ratio [OR]: 0.032, p < .001), post-stenting LCx plaque burden (OR: 1.166, p < .001), poststenting LM MLA (OR: 0.821, p = .038), and prestenting LCx MLA (OR: 0.371, p = .044). In the low FFR group, those with compromised LCx managed with drug-eluting balloon had the lowest three-year MACE rate (8.1%), as compared to either those undergoing kissing balloon inflation (KBI) (17.5%) or stenting (20.5%) (p = 0.299). CONCLUSION: Unnecessary LCx interventions can be avoided with FFR-guided LCx intervention. Poststenting MLA and plaque burden of the LCx, and main vessel stent length are poststenting predictors of low FFR.

Predictors of suboptimal coronary blood flow after primary angioplasty and its implications on short-term outcomes in patients with acute anterior STEMI.

BACKGROUND: Suboptimal coronary blood flow after primary percutaneous coronary intervention (PCI) is a complex multifactorial phenomenon. Although extensively studied, defined modifiable risk factors and efficient management strategy are lacking. This study aims to determine the potential causes of suboptimal flow and associated impact on 30-day outcomes in patients presenting with anterior ST-elevation myocardial infarction (STEMI). METHODS: We evaluated a total of 1104 consecutive patients admitted to our hospital from January 2016 to December 2018 with the diagnosis of anterior wall STEMI who had primary PCI. RESULTS: Overall, 245 patients (22.2%) had final post-PCI TIMI flow ≤2 in the LAD (suboptimal flow group) and 859 (77.8%) had final TIMI-3 flow (optimal flow group). The independent predictors of suboptimal flow were thrombus burden grade (Odds ratio (OR) 1.848; p < 0.001), age (OR 1.039 per 1-year increase; p < 0.001), low systolic blood pressure (OR 1.017 per 1 mmHg decrease; p < 0.001), total stent length (OR 1.021 per 1 mm increase; p < 0.001), and baseline TIMI flow ≤1 (OR 1.674; p = 0.018). The 30-day rates of major adverse cardiovascular events (MACE) and cardiac mortality were significantly higher in patients with TIMI flow ≤2 compared to those with TIMI-3 flow (MACE: adjusted risk ratio [RR] 2.021; P = 0.025, cardiac mortality: adjusted RR 2.931; P = 0.031). CONCLUSION: Failure to achieve normal TIMI-3 flow was associated with patient-related (age) and other potentially modifiable risk factors (thrombus burden, admission systolic blood pressure, total stent length, and baseline TIMI flow). The absence of final TIMI-3 flow carried worse short-term clinical outcomes.

Kawasaki Disease: Global Burden and Genetic Background.

Kawasaki disease (KD) is a childhood vasculitides associated with serious coronary artery lesions. It is the most common cause of pediatric acquired heart disease in developed countries, and is increasingly reported from many rapidly industrializing developing countries. The incidence varies widely among different nations and is highest in North-East Asian countries, where almost 1 in 100 children in Japan having the disease by age of 5, where the lowest incidence reported in sub-Saharan Africa. The etiology of KD is still uncertain; interaction between a genetic predisposition and several environmental and immunological factors has been hypothesized. Several susceptibility genes were identified to be associated with the development of KD and increased risk of coronary artery lesions. Gene-gene associations and alteration of deoxyribonucleic acid (DNA) methylation are also found to play key roles in the pathogenesis and prognosis of KD. This article will focus on the global epidemiological patterns of KD, and the currently known genetic predisposition.