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Aims: To evaluate the acute and chronic patterns of myocardial injury among patients with coronavirus disease-2019 (COVID-19), and their mid-term outcomes., Methods and Results: Patients with laboratory-confirmed COVID-19 who had a hospital encounter within the Mount Sinai Health System (New York City) between 27 February 2020 and 15 October 2020 were evaluated for inclusion. Troponin levels assessed between 72 h before and 48 h after the COVID-19 diagnosis were used to stratify the study population by the presence of acute and chronic myocardial injury, as defined by the Fourth Universal Definition of Myocardial Infarction. Among 4695 patients, those with chronic myocardial injury (n = 319, 6.8%) had more comorbidities, including chronic kidney disease and heart failure, while acute myocardial injury (n = 1168, 24.9%) was more associated with increased levels of inflammatory markers. Both types of myocardial injury were strongly associated with impaired survival at 6 months [chronic: hazard ratio (HR) 4.17, 95% confidence interval (CI) 3.44-5.06; acute: HR 4.72, 95% CI 4.14-5.36], even after excluding events occurring in the first 30 days (chronic: HR 3.97, 95% CI 2.15-7.33; acute: HR 4.13, 95% CI 2.75-6.21). The mortality risk was not significantly different in patients with acute as compared with chronic myocardial injury (HR 1.13, 95% CI 0.94-1.36), except for a worse prognostic impact of acute myocardial injury in patients <65 years of age (P-interaction = 0.043) and in those without coronary artery disease (P-interaction = 0.041)., Conclusion: Chronic and acute myocardial injury represent two distinctive patterns of cardiac involvement among COVID-19 patients. While both types of myocardial injury are associated with impaired survival at 6 months, mortality rates peak in the early phase of the infection but remain elevated even beyond 30 days during the convalescent phase., (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: Myocardial injury is frequent among patients hospitalized with coronavirus disease-2019 (COVID-19) and is associated with a poor prognosis. However, the mechanisms of myocardial injury remain unclear and prior studies have not reported cardiovascular imaging data., Objectives: This study sought to characterize the echocardiographic abnormalities associated with myocardial injury and their prognostic impact in patients with COVID-19., Methods: We conducted an international, multicenter cohort study including 7 hospitals in New York City and Milan of hospitalized patients with laboratory-confirmed COVID-19 who had undergone transthoracic echocardiographic (TTE) and electrocardiographic evaluation during their index hospitalization. Myocardial injury was defined as any elevation in cardiac troponin at the time of clinical presentation or during the hospitalization., Results: A total of 305 patients were included. Mean age was 63 years and 205 patients (67.2%) were male. Overall, myocardial injury was observed in 190 patients (62.3%). Compared with patients without myocardial injury, those with myocardial injury had more electrocardiographic abnormalities, higher inflammatory biomarkers and an increased prevalence of major echocardiographic abnormalities that included left ventricular wall motion abnormalities, global left ventricular dysfunction, left ventricular diastolic dysfunction grade II or III, right ventricular dysfunction and pericardial effusions. Rates of in-hospital mortality were 5.2%, 18.6%, and 31.7% in patients without myocardial injury, with myocardial injury without TTE abnormalities, and with myocardial injury and TTE abnormalities. Following multivariable adjustment, myocardial injury with TTE abnormalities was associated with higher risk of death but not myocardial injury without TTE abnormalities., Conclusions: Among patients with COVID-19 who underwent TTE, cardiac structural abnormalities were present in nearly two-thirds of patients with myocardial injury. Myocardial injury was associated with increased in-hospital mortality particularly if echocardiographic abnormalities were present., (Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Purpose: Our study investigated the impact of coronary artery calcification (CAC) and systemic inflammation on risks for major adverse cardiovascular events (MACE) following percutaneous coronary intervention (PCI)., Background: CAC and systemic inflammation are known to be associated with an increased risk of cardiovascular events., Methods: A total of 17,711 consecutive patients who underwent PCI in our hospital between January 1, 2009 and December 31, 2015 were categorized according to the degree of CAC (moderate/severe vs. none/mild) and high-sensitivity C-reactive protein (hsCRP) level (≥2 vs. <2 mg/L). MACE was defined as death, myocardial infarction (MI), or target vessel revascularization (TVR) occurring over 1 year., Results: Within the four groups, patients with both moderate/severe CAC and elevated hsCRP (n = 1,814 [10.2%]) were older with more comorbid risk factors compared to those with moderate/severe CAC alone (n = 1,687 [9.5%]), elevated hsCRP alone (n = 7,597 [42.9%]) or neither abnormality (n = 6,613 [37.3%]). The analogous 1-year MACE rates were 21.2, 14.9, 11.5, and 7.8%, respectively (p-trend < .001). Results were unchanged after multivariable adjustment, suggesting synergistic adverse effects in patients with both CAC and elevated hsCRP., Conclusions: The presence of both moderate/severe CAC and systemic inflammation confers a synergistic effect on risk for MACE following PCI, indicating the need for novel or more intense therapeutic interventions to mitigate risk in such patients., (© 2020 Wiley Periodicals, Inc.)

Objectives: We sought to determine the prevalence, predictors, and clinical impact of target lesion calcification in patients undergoing percutaneous coronary intervention (PCI) with newer generation drug-eluting stents (DES) and devices., Background: Coronary calcification is independently associated with adverse outcomes following PCI. While newer DES and contemporary devices are considered safer and more efficacious, their influence on outcomes following PCI of heavily calcified lesions is unknown., Methods: We performed a retrospective analysis of a large, multiethnic cohort of patients undergoing PCI with new generation DES at an academic center between 2009 and 2013. Coronary calcification was qualitatively assessed as none/mild, moderate, or severe. Independent demographic, clinical, and anatomic predictors of moderate/severe calcification were identified using logistic regression. Associations between coronary calcification and 1-year MACE (death, myocardial infarction, or target vessel revascularization) were examined using Cox modeling., Results: Compared to patients with none/mild (n = 10,180; 82.0%), those with moderate (n = 1,271; 10.0%) or severe (n = 994; 8.0%) calcification were older, more often Caucasian, had more complex target lesions, and worse renal function. The strongest demographic, clinical, and anatomic correlates of moderate/severe calcification were age, Caucasian race, renal dysfunction, lesion length, and left main location. Unadjusted MACE rates among those with none/mild, moderate, and severe calcification were 8.3, 14.6, and 17.8%, respectively (P < 0.001). After multivariable adjustment, the hazard ratio (95% CI) for MACE associated with moderate or severe coronary calcification was 1.63., Conclusions: Target lesion calcification remains independently associated with adverse outcomes in patients treated with newer generation DES and modern devices., (© 2017 Wiley Periodicals, Inc.)

Objectives: To compare the discriminatory value of differing risk scores for predicting clinical outcomes following PCI in routine practice., Background: Various risk scores predict outcomes after PCI. However, these scores consider markedly different factors, from purely anatomical (SYNTAX risk score [SRS]) to purely clinical (ACEF, modified ACEF [ACEFmod], NCDR), while other scores combine both elements (Clinical SYNTAX score [CSS], NY State Risk Score [NYSRS])., Methods: Patients with triple vessel and/or LM disease with 12 month follow-up were studied from a single center PCI registry. Exclusion criteria included STEMI presentation, prior revascularization and shock. Clinical events at 12 months were compared to baseline risk scores, according to score tertiles and area under receiver-operating-characteristic curves (AUC)., Results: We identified 584 eligible patients (69.8±12.3yrs, 405 males). All scores were predictive of mortality, with the SRS being least predictive (AUC=0.66). The most accurate scores for mortality were the CSS and ACEF (AUC=0.76 for both: P = 0.019 and 0.08 vs. SRS, respectively). For TLR, while the SRS trended toward being positively predictive (P = 0.075), several scores trended towards a negative association, which reached significance for the NCDR (P = 0.045). The SRS and CSS were the only scores predictive of MI (both P < 0.05). No score was particularly accurate for predicting MACE (death+MI+TLR), with AUCs ranging from 0.53 (NCDR) to 0.63 (SRS)., Conclusions: Competing factors influence mortality, MI and TLR after PCI. An increasing burden of comorbidities is associated with mortality, whereas anatomical complexity predicts MI. By combining these outcomes to predict MACE, all scores show reduced utility., (Copyright © 2013 Wiley Periodicals, Inc.)

Objectives: Patients with congenital bicuspid aortic valves have aortic valve stenosis at a relatively young age compared with patients with tricuspid aortic valves. We hypothesize that aortic valve stenosis evolves from a more aggressive inflammatory process, with increased macrophage/T-cell and neovessel content in congenital bicuspid aortic valveswhen compared with that seen in tricuspid valves., Methods: Fifty-one severely stenotic aortic valves were obtained at the time of aortic valve replacement. A total of 17 bicuspid and 34 tricuspid aortic valves were evaluated. Macrophage/T-cell infiltration (CD68 plus CD3) and neovessel density (CD34) were evaluated with immunohistochemical staining. Leaflet calcification and ossification were also quantified. Real-time polymerase chain reaction was used to assess expression of chondromodulin 1 and vascular endothelial growth factor., Results: The density of macrophages/T cells was greater in congenital bicuspid aortic valves than in tricuspid valves (51 ± 31 vs 23 ± 13 cells/mm(2), P = .002). Neovascularization was more frequently noted in congenital bicuspid aortic valves when compared with tricuspid valves (31 ± 10 vs 21 ± 9 vessels/mm(2), P = .0005), and calcification was more severe (P = .03). Expression of chondromodulin 1 demonstrated a 6-fold downregulation (P = .0003) and expression of vascular endothelial growth factor demonstrated a 2-fold increase (P = .02) in congenital bicuspid aortic valves compared with that seen in tricuspid valves. Multivariable analyses demonstrated significant associations between bicuspid aortic valve anatomy and increased inflammatory cell infiltration (β = 25.8, P = .0007) and neovascularization (β = 9.4, P = .001), despite adjusting for measured covariates., Conclusions: The pathogenesis of aortic valve stenosis in bicuspid aortic valves is associated with a more aggressive inflammatory process with increased macrophage infiltration and neovascularization when compared with that seen in tricuspid valves., (Copyright © 2011 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.)

Objectives: We seek to identify predictors of 30-day mortality after balloon aortic valvuloplasty (BAV)., Background: To date, there is no validated method of predicting patient outcomes after percutaneous aortic valve interventions., Methods: Data for consecutive patients with severe aortic stenosis who underwent BAV at the Mount Sinai Medical Center from January 2001 to July 2007 were retrospectively reviewed. Cox-proportional hazards regression was used to identify significant predictors of 30-day mortality, and the resultant model was compared to the EuroSCORE using Akaike's Information Criterion and area under the receiver-operating curve (AUC)., Results: The analysis included 281 patients (age 83 ± 9 years, 61% women, aortic valve area: 0.64 ± 0.2 cm(2)) and 36 (12.8%) of whom died within 30 days of BAV. With identified risk factors for 30-day mortality, critical status, renal dysfunction, right atrial pressure, and cardiac output, we constructed the CRRAC the AV risk score. Thirty-day survival was 72% in the highest tertile versus 94% in the lower two tertiles of the score. Compared to the additive and logistic EuroSCORE, the risk score demonstrated superior discrimination (AUC = 0.75 vs. 0.60 and 0.63, respectively)., Conclusions: We derived a risk score, the CRRAC the AV score that identifies patients at high-risk of 30-day mortality after BAV. Validation of the developed risk prediction score, the CRRAC the AV score, is needed in other cohorts of post-BAV patients and potentially in patients undergoing other catheter-based valve interventions., (Copyright © 2010 Wiley-Liss, Inc.)

Objectives: This study evaluated the outcomes of patients discharged the day of percutaneous coronary intervention (PCI) by analyzing the data from a single-center, large, multioperator registry of interventions., Background: Although same-day discharge is likely safe after interventions on low-risk stable patients, there is limited data to guide selection of a broader population of patients. Due to numerous patient variables and physician preferences, standardization of the length of stay after PCI has been a challenge. Most of the reported studies on same-day discharge have strict inclusion criteria and hence do not truly reflect a real-world population., Methods: We analyzed the outcomes of consecutive same-day discharge in 2,400 of 16,585 patients who underwent elective PCI without any procedural or hospital complication. Composite end point included 30-day major adverse cardiac cerebral events and bleeding/vascular complications., Results: The mean age of the study population was 57.0 +/- 23.7 years with 12% aged over 65 years. Twenty-eight percent received glycoprotein IIb/IIIa inhibitor with closure devices in 90.5%. Clinical and angiographic success was noted in 97% of all PCIs. The average length-of-stay following PCI was 8.2 +/- 2.5 h. The composite end point was reached in 23 patients (0.96%). Major adverse cardiac cerebral events occurred in 8 patients (0.33%) and vascular/bleeding complications in the form of Thrombolysis In Myocardial Infarction minor bleeding in 14 patients (0.58%) and pseudoaneurysm in 1 patient (0.04%)., Conclusions: When appropriately selected, with strict adherence to the set protocol, same-day discharge after uncomplicated elective PCI is safe despite using femoral access in a wide spectrum of patients., (Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Creatine kinase-MB (CK-MB) and troponin I elevations after successful percutaneous coronary intervention (PCI) are common, and different gradations have been correlated with mortality. To establish which of these 2 markers of myonecrosis, CK-MB and troponin I, accurately predicts mortality after successful PCI, we analyzed 2,873 patients without acute myocardial infarction who underwent PCI for in-hospital events and mid-term mortality. Patients were stratified into 4 groups based on peak post-PCI cardiac markers values: group I: normal CK-MB (<16 U/L) or troponin I (<2 ng/ml); group II: CK-MB or troponin I levels 1 to 3 times normal; group III: >3 to 5 times normal; and group IV: >5 times normal. CK-MB elevation occurred in 16.1% of patients, with 12.2%, 2.3%, and 1.6% in groups II to IV, respectively. Troponin I elevation was detected in 38.9% of patients, with 16.4%, 8.4%, and 14.1% in groups II to IV, respectively. There was poor correlation between postprocedural CK-MB and troponin I values (r = 0.10) and in their individual subgroups. Kaplan-Meier estimates of death for postprocedure CK-MB were 2.1%, 2.7%, 1.7%, and 10.3% (p = 0.002) for groups I to IV, respectively; for troponin I, these estimates were 2.2%, 2.3%, 2.9%, and 2.1% for groups I to IV, respectively (p = 0.58). A Cox proportional hazards model showed that CK-MB >5 times normal was the strongest predictor of mortality (hazard ratio 6.7, 95% confidence interval 1.9 to 22.9; p = 0.002), although heart failure, peripheral vascular disease, pre-PCI digoxin therapy, and post-PCI renal failure also predicted mortality. However, neither troponin I peak elevation nor any subgroup predicted mortality. Troponin I is frequently elevated after PCI, but does not predict mortality. Periprocedural CK-MB elevation >5 times normal remains an independent predictor of mid-term mortality and a valuable marker for PCI prognosis in low-to-medium risk patients.