Publications by authors named "Christia Panagiota"

Background: Imaging with late gadolinium enhancement (LGE) magnetic resonance (MR) and F-fluorodeoxyglucose (F-FDG) PET allows complementary assessment of myocardial injury and disease activity and has shown promise for improved characterization of active cardiac sarcoidosis (CS) based on the combined positive imaging outcome, MR(+)PET(+).

Objectives: This study aims to evaluate qualitative and quantitative assessments of hybrid MR/PET imaging in CS and to evaluate its association with cardiac-related outcomes.

Methods: A total of 148 patients with suspected CS underwent hybrid MR/PET imaging.

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Article Synopsis
  • A study was conducted with 1,047 COVID-19 patients from 18 sites to understand myocardial injury linked to the virus, using cardiac magnetic resonance imaging.
  • Results showed that 20.9% of patients had nonischemic injury patterns like acute myocarditis, while 6.7% had ischemic injury patterns.
  • Key factors associated with acute myocarditis included elevated troponin and chest discomfort, while acute ischemic patterns were linked to known coronary disease and abnormal ECG findings.
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Background Amiodarone causes less drug-induced torsade de pointes (TdP) compared to other class III antiarrhythmics. Two theories proposed for this finding include that amiodarone has less repolarization heterogeneity, and/or decreases early after depolarization (EADs). Corrected QT (QTc) dispersion as measured on a surface electrocardiogram (ECG) represents spatial heterogeneity of ventricular repolarization.

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Background: HIV and HCV have been linked to an increased risk of cardiovascular disease (CVD). Their impact on long-term outcomes following ST-segment myocardial infarction (STEMI) has not been previously studied.

Methods: We leveraged data from a STEMI registry (n = 1208) at an inner-city health system to assess the influence of HIV and HCV on post-STEMI outcomes.

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Left ventricular outflow tract obstruction is a serious complication of mitral valve surgery (repair and replacement) and transcatheter mitral valve replacement. An appreciation of the various mechanisms which cause outflow obstruction in these settings is critical to avoiding this complication and to initiating appropriate treatment. This article discusses the mechanisms, pathophysiology, and imaging of left ventricular outflow tract obstruction which can arise following insertion of a variety of mitral valve prosthetics.

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Left ventricular outflow tract obstruction resulting from strut impingement upon the interventricular septum is a rare complication of bioprosthetic mitral valve insertion. Obstruction is more likely to develop when a small, high profile prosthetic valve is inserted into a patient with a small outflow tract. The likelihood of this complication may be reduced by appropriate modification of surgical technique.

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Unstable angina is a clinical diagnosis that may present with or without electrocardiographic changes. The "giant R wave" on electrocardiogram has been reported as a manifestation of acute ischemia; however, it is a rare finding in current clinical practice. We describe a case of a patient with unstable angina and a transient "giant R wave" pattern with a culprit lesion in the right coronary artery.

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Takotsubo cardiomyopathy (TCM) is a variant of stress-induced cardiomyopathy, characterized by transient left ventricular dysfunction that may be associated with emotional or physical triggers. We present the case of a 51-year-old Caucasian female with severe chronic obstructive pulmonary disease (COPD) who presented with syncope and was found to have her second lifetime episode of stress-induced cardiomyopathy. Eight months prior, she had been admitted with a COPD exacerbation and was found to have left ventricular (LV) dysfunction with ejection fraction (EF) of 22% attributed to TCM with subsequent normalization of her left ventricular function.

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Background: The benefit of ≤6-month compared with 12-month dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) with drug-eluting stent (DES) placement remains controversial. We performed a meta-analysis and meta-regression of ≤6-month versus 12-month DAPT in patients undergoing PCI with DES placement.

Methods: We conducted electronic database searches of randomized controlled trials (RCTs) comparing DAPT durations after DES placement.

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Background: Stroke is the major cause of disability and the fifth leading cause of death in the United States. In 30-40% of strokes the etiology remains uncertain or unknown. Identifying the cause of a cerebrovascular event offers the opportunity for an intervention that may decrease the risk of future stroke and thus prevent the resultant impairment.

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Article Synopsis
  • Cocaine use is a significant factor in STEMI cases, especially in socioeconomically disadvantaged urban areas, where the patient demographic is primarily younger, male, and often engaging in high-risk behaviors.
  • Compared to non-users, cocaine users with STEMI received fewer advanced treatments like drug-eluting stents and β blockers and had similar rates of adverse health outcomes during a follow-up period of 2.7 years.
  • The findings highlight the need for targeted programs addressing cocaine use and associated behaviors to improve health outcomes and prevent disease in low-income communities.
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Background: Studies suggest that thrombocytopaenia is associated with a higher mortality in several diseases. Little is known about the effect of low platelet count on mortality in patients with heart failure with reduced ejection fraction (HFrEF). The aim of this study was to determine the prognostic value of thrombocytopaenia in these patients by assessing all-cause mortality.

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Aims: Guidelines recommend mild therapeutic hypothermia (MTH) for survivors of out-of-hospital cardiac arrest (OHCA). However, there is little literature demonstrating a survival benefit. We performed a meta-analysis of randomized controlled trials (RCTs) assessing the efficacy of MTH in patients successfully resuscitated from OHCA.

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The foramen ovale is a remnant of the fetal circulation that remains patent in 20-25% of the adult population. Although long overlooked as a potential pathway that could produce pathologic conditions, the presence of a patent foramen ovale (PFO) has been associated with a higher than expected frequency in a variety of clinical syndromes including cryptogenic stroke, migraines, sleep apnea, platypnea-orthodeoxia, deep sea diving associated decompression illness, and high altitude pulmonary edema. A unifying hypothesis is that a chemical or particulate matter from the venous circulation crosses the PFO conduit between the right and left atria to produce a variety of clinical syndromes.

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Understanding the role of fibroblasts in pathologic conditions is hampered by the absence of specific markers. Fibroblast-specific protein (FSP)1 has been suggested as a fibroblast-specific marker in normal and fibrotic tissues; FSP1 reporter mice and FSP1-Cre-driven gene deletion are considered reliable strategies to investigate fibroblast biology. Because fibroblasts are abundant in normal and injured mammalian hearts, we studied the identity of FSP1(+) cells in the infarcted and remodeling myocardium using mice with green fluorescent protein (GFP) expression driven by the FSP1 promoter.

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Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns (DAMPs), activating complement and Toll-Like Receptor (TLR)/Interleukin (IL)-1 signalling and triggering an intense inflammatory reaction. Infiltrating leucocytes clear the infarct from dead cells, while activating reparative pathways that lead to formation of a scar. As the infarct heals the ventricle remodels, the geometric, functional and molecular alterations associated with postinfarction remodelling are driven by the inflammatory cascade and are involved in the development of heart failure.

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Mouse models of myocardial infarction are essential tools for the study of cardiac injury, repair, and remodeling. Our current investigation establishes a systematic approach for quantitative evaluation of the inflammatory and reparative response, cardiac function, and geometry in a mouse model of reperfused myocardial infarction. Reperfused mouse infarcts exhibited marked induction of inflammatory cytokines that peaked after 6 hr of reperfusion.

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Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators.

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