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Background: Eosinophilic myocarditis (EM) secondary to eosinophilic granulomatosis with polyangiitis (EGPA) is a rare disease, for which cardiac magnetic resonance imaging (CMRI) is a useful non-invasive modality for diagnosis. We present a case of EM in a patient who recently recovered from COVID-19 and discuss the role of CMRI and endomyocardial biopsy (EMB) to differentiate between COVID-19-associated myocarditis and EM. Case summary: A 20-year-old Hispanic male with a history of sinusitis and asthma, and who recently recovered from COVID-19, presented to the emergency room with pleuritic chest pain, dyspnoea on exertion, and cough. His presentation labs were pertinent for leucocytosis, eosinophilia, elevated troponin, and elevated erythrocyte sedimentation rate and C-reactive protein. The electrocardiogram showed sinus tachycardia. Echocardiogram showed an ejection fraction of 40%. The patient was admitted, and on day 2 of admission, he underwent CMRI which showed findings of EM and mural thrombi. On hospital day 3, the patient underwent right heart catheterization and EMB which confirmed EM. The patient was treated with steroids and mepolizumab. He was discharged on hospital day 7 and continued outpatient heart failure treatment. Discussion: This is a unique case of EM and heart failure with reduced ejection fraction as a presentation of EGPA, in a patient who recently recovered from COVID-19. In this case, CMRI and EMB were critical to identify the cause of myocarditis and helped in the optimal management of this patient.

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Recognizing early cardiac sarcoidosis (CS) imaging phenotypes can help identify opportunities for effective treatment before irreversible myocardial pathology occurs. We aimed to characterize regional CS myocardial remodeling features correlating with future adverse cardiac events by coupling automated image processing and data analysis on cardiac magnetic resonance (CMR) imaging datasets. A deep convolutional neural network (DCNN) was used to process a CMR database of a 10-year cohort of 117 consecutive biopsy-proven sarcoidosis patients. The maximum relevance - minimum redundancy method was used to select the best subset of all the features-24 (from manual processing) and 232 (from automated processing) left ventricular (LV) structural/functional features. Three machine learning (ML) algorithms, logistic regression (LogR), support vector machine (SVM) and multi-layer neural networks (MLP), were used to build classifiers to categorize endpoints. Over a median follow-up of 41.8 (inter-quartile range 20.4-60.5) months, 35 sarcoidosis patients experienced a total of 43 cardiac events. After manual processing, LV ejection fraction (LVEF), late gadolinium enhancement, abnormal segmental wall motion, LV mass (LVM), LVMI index (LVMI), septal wall thickness, lateral wall thickness, relative wall thickness, and wall thickness of 9 (out of 17) individual LV segments were significantly different between patients with and without endpoints. After automated processing, LVEF, end-diastolic volume, end-systolic volume, LV mass and wall thickness of 92 (out of 216) individual LV segments were significantly different between patients with and without endpoints. To achieve the best predictive performance, ML algorithms selected lateral wall thickness, abnormal segmental wall motion, septal wall thickness, and increased wall thickness of 3 individual segments after manual image processing, and selected end-diastolic volume and 7 individual segments after automated image processing. LogR, SVM and MLP based on automated image processing consistently showed better predictive accuracies than those based on manual image processing. Automated image processing with a DCNN improves data resolution and regional CS myocardial remodeling pattern recognition, suggesting that a framework coupling automated image processing with data analysis can help clinical risk stratification.

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BACKGROUND Various physical and emotional factors have been previously described as triggers for stress induced cardiomyopathy. However, acute myocardial infarction as a trigger has never been reported. CASE REPORT We describe four patients who presented with an acute myocardial infarction, in whom the initial echocardiography revealed wall motion abnormalities extending beyond the coronary distribution of the infarct artery. Of the four patients identified, the mean age was 59 years; three patients were women and two patients had underlying psychiatric history. Electrocardiogram revealed ST elevation in the anterior leads in three patients; QTc was prolonged in all cases. All patients had ≤ moderately elevated troponin. Single culprit lesion was found uniformly in the proximal or mid left anterior descending artery. Initial echocardiography revealed severely reduced ejection fraction with relative sparing of the basal segments, whereas early repeat echocardiography revealed significant improvement in the left ventricular function in all patients. CONCLUSIONS This is the first case series demonstrating that acute myocardial infarction can trigger stress induced cardiomyopathy. Extensive reversible wall motion abnormalities, beyond the ones expected from angiography, accompanied by modest elevation in troponin and marked QTc prolongation, suggest superimposed stress induced cardiomyopathy.

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BACKGROUND: Chronic kidney disease (CKD) is associated with increased rates of adverse events after percutaneous coronary intervention. We sought to determine the impact of CKD on platelet reactivity in clopidogrel-treated patients and whether high platelet reactivity (HPR) confers a similar or differential risk for adverse events among patients with CKD and non-CKD. METHODS AND RESULTS: We performed a post hoc analysis of the Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents (ADAPT-DES) registry, which included 8582 patients undergoing percutaneous coronary intervention with drug-eluting stents and platelet function testing using the VerifyNow assay. We compared HPR and its impact on ischemic and bleeding events >2 years among patients with CKD and non-CKD. Patients with CKD (n=1367) were older, more often female, diabetic, and had lower ejection fraction compared with their non-CKD counterparts (n=7043). Although HPR prevalence increased with worsening renal function in unadjusted analyses, these associations were no longer present after adjustment. Major adverse cardiac event rates at 2 years among those without CKD or HPR, HPR alone, CKD alone, and both CKD and HPR were 9.0%, 11.2%, 13.3%, and 17.5%, respectively (P<0.001). Associations between HPR and adverse events were uniform across CKD strata without evidence of interaction. CONCLUSIONS: HPR is more common among those with versus without CKD, an association that is attributable to confounding risk factors that are more prevalent in CKD. The impact of HPR on ischemic and bleeding events is similar irrespective of CKD status. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00638794.

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BACKGROUND: Increasing numbers of balloon aortic valvuloplasty (BAV) are performed in the management of symptomatic aortic stenosis as bridge and therapeutic challenge in the work-up for transcatheter aortic valve replacement. However, the significance of gender in outcomes following BAV remains controversial. METHODS: We retrospectively reviewed 664 consecutive patients who underwent BAV from January 2005 to December 2012. Patients were stratified according to gender. Clinical and procedural characteristics as well as in-hospital outcomes and 1-year mortality were collected. Cumulative survival curves for women and men were constructed using the Kaplan-Meier method and were compared by the log-rank test. Cox regression analysis was performed to identify the independent effect of sex on 1-year mortality. RESULTS: Of the 664 patients, 333 (52%) were women. Women had lower body surface area, tended to be frailer and were less likely to have history of coronary artery disease. Women were more likely to present with heart failure whereas men presented more commonly with chest pain. In hospital death was significantly higher in women compared to men, mainly driven by the difference in cardiac death (8.1% vs 3.9%, P = .02 and 6.3% vs 2.6%, P = .02 respectively). One-year mortality rates were similar in women and men (25.4% vs 29.4%, P = .42) and after multivariate analysis gender had no association with 1-year mortality (HR = 0.9, P = .65). CONCLUSIONS: Significant differences exist in baseline characteristics and presentation between genders. Although in hospital mortality after BAV was significantly higher in women, 1-year mortality was similar between women and men.

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PURPOSE OF REVIEW: To provide updates regarding the optimal duration of dual antiplatelet therapy (DAPT) in patients with acute coronary syndromes (ACS). RECENT FINDINGS: Within the past years, five moderate-sized randomized controlled trials evaluated different DAPT durations after percutaneous coronary intervention. These studies included a significant percentage of ACS patients that varied from 30 to 75% depending on the study. Results suggest that in selected populations prolonging DAPT does not offer additional protection from ischemic events and increases bleeding complications. However, results from a large-scale registry illustrate that DAPT durations beyond 6 months are associated with lower cardiovascular risk. Moreover, a multicenter registry demonstrated that the context underlying DAPT cessation is an additional correlate of outcomes after stent implantation. SUMMARY: Current guidelines suggest 12 months of DAPT after an initial presentation with ACS. Emerging evidence suggest that in selected populations shorter duration might be acceptable.

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The role of high-density lipoprotein (HDL) in cardiovascular atheroprotection is well established. Epidemiological data have clearly demonstrated an inverse relationship between HDL levels and the risk for coronary artery disease, which is independent of the low-density lipoprotein levels. However, more recent data provide evidence that high HDL levels are not always protective and that under certain conditions may even confer an increased risk. Thus, a new concept has arisen, which stresses the importance of HDL functionality, rather than HDL concentration per se, in the assessment of cardiovascular risk. HDL functionality is genetically defined but can also be modified by several environmental and lifestyle factors, such as diet, smoking or certain pharmacologic interventions. Furthermore, HDL is consisted of a heterogeneous group of particles with major differences in their structural, biological and functional properties. Recently, the cholesterol efflux capacity from macrophages was proven to be an excellent metric of HDL functionality, because it was shown to have a strong inverse relationship with the risk of angiographically documented coronary artery disease, independent of the HDL and apolipoprotein A-1 levels, although it may not actually predict the prospective risk for cardiovascular events. Thus, improving the quality of HDL may represent a better therapeutic target than simply raising the HDL level, and assessment of HDL function may prove informative in refining our understanding of HDL-mediated atheroprotection.

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Coronary artery disease (CAD) is the leading cause of death in the United States. Although CAD was formerly considered a lipid accumulation-mediated disease, it has now been clearly shown to involve an ongoing inflammatory response. Advances in basic science research have established the crucial role of inflammation in mediating all stages of CAD. Today, there is convincing evidence that multiple interrelated immune mechanisms interact with metabolic risk factors to initiate, promote, and ultimately activate lesions in the coronary arteries. This review aims to provide current evidence pertaining to the role of inflammation in the pathogenesis of CAD and discusses the impact of inflammatory markers and their modification on clinical outcomes.

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Coronary heart disease (CHD) is one of the leading causes of death in the United States. Traditional risk factors such as family history, hypertension, hypercholesterolemia, diabetes mellitus and smoking cannot account for the entire risk for incident coronary events. Several other potential risk factors have been identified in an effort to improve risk assessment for CHD. This article reviews the current evidence on new and emerging risk factors for CHD and their current utility in screening, specifically focusing on coronary artery calcium score, C-reactive protein, lipoprotein (a), carotid intima-media thickness, homocysteine, lipoprotein-associated phospholipase A2, as well as high-density lipoprotein functionality.

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