Thrombi straddling patent foramen ovale: A case series with various management strategies.

This case series explores four cases of thrombi straddling patent foramen ovale (TSFO), an exceedingly rare event. The cases are compared regarding their presentations, evaluations, and management strategies including the first documented uses of percutaneous thromboembolectomy for the removal of a TSFO.

Peripheral Administration of Nitroglycerin in Pulseless Ventricular Tachycardia due to Cocaine-Induced Coronary Vasospasm.

Cocaine use accounts for 40% of the annual drug use related emergency department visits in the United States. Cocaine use is hence recognized as a major health problem. Cocaine blocks the presynaptic reuptake of norepinephrine and dopamine. The resulting increased adrenergic activity leads to vasoconstriction. Additionally, via various mechanisms, cocaine leads to a prothrombotic state and increases myocardial demand. Cocaine can cause coronary vasospasm and is therefore, associated with acute myocardial injury even in the absence of pre-existing atherosclerotic coronary artery disease. Nitroglycerin has a class 1C indication by the ACCF/AHA guidelines for patients with ST-segment elevation or depression that accompanies ischemic chest discomfort in the setting of cocaine use. It has been shown to reverse cocaine-induced coronary vasospasm and chest pain. In this case report, for the first time, we discuss how intravenous administration of high dose nitroglycerin to a patient in pulseless ventricular tachycardia with angiographically confirmed vasospasm induced by cocaine resulted in return of spontaneous circulation.

Atrial fibrillation: the role of hypoxia-inducible factor-1-regulated cytokines.

Atrial fibrillation (AF) is a common arrhythmia that has major morbidity and mortality. Hypoxia plays an important role in AF initiation and maintenance. Hypoxia-inducible factor (HIF), the master regulator of oxygen homeostasis in cells, plays a fundamental role in the regulation of multiple chemokines and cytokines that are involved in different physiological and pathophysiological pathways. HIF is also involved in the pathophysiology of AF induction and propagation mostly through structural remodeling such as fibrosis; however, some of the cytokines discussed have even been implicated in electrical remodeling of the atria. In this article, we highlight the association between HIF and some of its related cytokines with AF. Additionally, we provide an overview of the potential diagnostic benefits of using the mentioned cytokines as AF biomarkers. Research discussed in this review suggests that the expression of these cytokines may correlate with patients who are at an increased risk of developing AF. Furthermore, cytokines that are elevated in patients with AF can assist clinicians in the diagnosis of suspect paroxysmal AF patients. Interestingly, some of the cytokines have been elevated specifically when AF is associated with a hypercoagulable state, suggesting that they could be helpful in the clinician's and patient's decision to begin anticoagulation. Finally, more recent research has demonstrated the promise of targeting these cytokines for the treatment of AF. While still in its early stages, tools such as neutralizing antibodies have proved to be efficacious in targeting the HIF pathway and treating or preventing AF.

Algorithm for cavo-tricuspid isthmus flutter on surface ECGs: the ACTIONS study.

OBJECTIVE: Cavo-tricuspid isthmus atrial flutter (CTI-AFL) is an important arrhythmia to recognise because there is a highly effective and relatively low-risk ablation strategy. However, clinical experience has demonstrated that providers often have difficulty distinguishing AFL from atrial fibrillation. METHODS: We developed a novel ECG-based three-step algorithm to identify CTI-AFL based on established CTI flutter characteristics and verified on consecutive ablation cases of typical flutter, atypical flutter and atrial fibrillation. The algorithm assesses V1/inferior lead F-wave concordance, consistency of P-wave morphology and the presence of isoelectric intervals in the inferior leads. In this observation study, the algorithm was validated on a cohort of 50 second-year medical students. Students were paired in a control and experimental group, and each pair received 10 randomly selected ECGs (from a pool of 50 intracardiac electrogram-proven CTI-AFL and 50 AF or atypical AFL cases). The experimental group received a cover sheet with the CTI algorithm, and the control group received no additional guidance. RESULTS: There was a statistically significant difference in the mean number of correctly identified ECGs among the students in the experimental and control groups (8.12 vs 5.68, p<0.001). Students who used the algorithm correctly identified 2.44 more ECGs as being CTI-AFL or not CTI-AFL. Using the electrophysiology study as the gold standard, the algorithm had an accuracy of 81%, sensitivity of 81%, specificity of 82%, positive predictive value of 78% and negative predictive value of 84% in identifying CTI-AFL. CONCLUSION: We developed a three-step ECG algorithm that provides a simple, sensitive, specific and accurate tool to identify CTI-AFL.

How transforming growth factor contributes to atrial fibrillation?

Atrial fibrillation (AF) is the most common clinically significant arrhythmia. There are four fundamental pathophysiological mechanisms of AF including: electrical remodeling, structural remodeling, autonomic nervous system changes, and Ca2+ handling abnormalities. The transforming growth factor-ß (TGF-ß) superfamily are cytokines that have the ability to regulate numerous cell functions including proliferation, differentiation, apoptosis, epithelial-mesenchymal transition, and production of extracellular matrix. During the last decade numerous studies have demonstrated that TGF-ß affects the architecture of the heart. TGF-ß1 has been shown to be involved in the development and propagation of atrial fibrillation (AF). Investigators have studied TGF-ß signaling in AF with the aim of discovering potential therapeutic agents. In this review we discuss the role of TGF-ß in atrial fibrillation and specifically its role in atrial structural and electrical remodeling.

Arrhythmia in COVID-19.

The current outbreak of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) also known as coronavirus disease 2019 (COVID-19) has quickly progressed to a global pandemic. There are well-documented cardiac complications of COVID-19 in patients with and without prior cardiovascular disease. The cardiac complications include myocarditis, heart failure, and acute coronary syndrome resulting from coronary artery thrombosis or SARS-CoV-2-related plaque ruptures. There is growing evidence showing that arrhythmias are also one of the major complications. Myocardial inflammation caused by viral infection leads to electrophysiological and structural remodeling as a possible mechanism for arrhythmia. This could also be the mechanism through which SARS-CoV-2 leads to different arrhythmias. In this review article, we discuss arrhythmia manifestations in COVID-19.

Myocardial injury and COVID-19: Possible mechanisms.

Coronavirus Disease 2019 (COVID-19) has quickly progressed to a global health emergency. Respiratory illness is the major cause of morbidity and mortality in these patients with the disease spectrum ranging from asymptomatic subclinical infection, to severe pneumonia progressing to acute respiratory distress syndrome. There is growing evidence describing pathophysiological resemblance of SARS-CoV-2 infection with other coronavirus infections such as Severe Acute Respiratory Syndrome coronavirus and Middle East Respiratory Syndrome coronavirus (MERS-CoV). Angiotensin Converting Enzyme-2 receptors play a pivotal role in the pathogenesis of the virus. Disruption of this receptor leads to cardiomyopathy, cardiac dysfunction, and heart failure. Patients with cardiovascular disease are more likely to be infected with SARS-CoV-2 and they are more likely to develop severe symptoms. Hypertension, arrhythmia, cardiomyopathy and coronary heart disease are amongst major cardiovascular disease comorbidities seen in severe cases of COVID-19. There is growing literature exploring cardiac involvement in SARS-CoV-2. Myocardial injury is one of the important pathogenic features of COVID-19. As a surrogate for myocardial injury, multiple studies have shown increased cardiac biomarkers mainly cardiac troponins I and T in the infected patients especially those with severe disease. Myocarditis is depicted as another cause of morbidity amongst COVID-19 patients. The exact mechanisms of how SARS-CoV-2 can cause myocardial injury are not clearly understood. The proposed mechanisms of myocardial injury are direct damage to the cardiomyocytes, systemic inflammation, myocardial interstitial fibrosis, interferon mediated immune response, exaggerated cytokine response by Type 1 and 2 helper T cells, in addition to coronary plaque destabilization, and hypoxia.

The role of long noncoding RNAs in atrial fibrillation.

Atrial fibrillation (AF) is a common arrhythmia with serious clinical sequelae, yet little is known about its genetic origins. Recently, the untranscribed 98% of the human genome has been increasingly implicated in important processes such as cardiac organogenesis, physiology, and pathophysiology. Specifically, long noncoding RNAs (lncRNAs) have been shown to interact with the transcriptome in various ways that alter gene expression. Previously, multiple lncRNAs have been identified in disease processes such as heart failure, coronary artery disease, and diabetes. Multiple studies now show lncRNAs are involved in each fundamental mechanism leading to the development of AF, including structural remodeling, electrical remodeling, renin angiotensin system effects, and calcium handling abnormalities. The altered expression of lncRNAs offers genetic targets for the diagnosis and treatment of AF. This article discusses the role of lncRNAs in AF and its pathogenesis.