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Recent data suggest that epicardial left atrial appendage closure (LAAC) is associated with several short-term neurohormonal effects. However, the long-term effects are currently unknown. To investigate the effects of percutaneous epicardial left atial appendage (LAA) exclusion using LARIAT on neurohormonal profiles at long-term follow-up. In a prospective single centre study, 60 patients with long-standing, persistent atrial fibrillation (AF) LARIAT were treated. The major hormones of the adrenergic system, renin-angiotensin-aldosterone system (RAAS), and natriuretic peptides were assessed before the intervention and at regular intervals during the following two years. In patients with epicardial LAAC, atrial natriuretic peptide (ANP) levels were significantly increased from baseline at 24 h and decreased at 7 days, 1 month, and 3 months, while remaining unchanged at 12 and 24 months. Noradrenaline levels were significantly lower at 24 h, 7 days, 1 month, 6 months, 12 months, and 24 months, while epinephrine levels decreased significantly at 1 month, 6 months, 12 months, and 24 months. Plasma renin activity significantly decreased at 7 days, 1 month, 6 months, 12 months, and 24 months, while aldosterone levels significantly decreased at 6 months, 12 months, and 24 months. Endothelin-1 and vasopressin showed a significant increase and decrease, respectively, at 24 h, 7 days, 1 month, 6 months, 12 months, and 24 months. There was also a significant decrease in systolic and diastolic blood pressure at 3 months, 6 months, 1 year, and 2 years after the intervention. Epicardial LAAC in AF patients is associated with persistent neurohormonal changes favouring blood pressure reduction.

Myocarditis refers to inflammation of the myocardium caused by infectious and non-infectious process. It should be considered in any patient presenting with unexplained congestive heart failure, ventricular arrhythmias, atrial fibrillation or dilated cardiomyopathy . Prompt diagnosis and treatment is required, otherwise unrecognized myocarditis can rapidly progress to cardiogenic shock with increase in mortality and morbidity. Although various etiologies such as viruses and autoimmune phenomenon have been proposed, there are many unanswered questions regarding the underlying pathophysiology that initiate and trigger myocardial inflammation. These gaps in knowledge need to addressed by developing appropriate myocarditis disease models for understanding the interaction of initial insult, autoimmunity, and host genetics so as to develop novel therapeutic modalities that can halt the disease progression for better clinical outcomes. This review focuses on etiology, pathophysiology, symptomatology, diagnosis, treatment and directions of myocarditis. [ABSTRACT FROM AUTHOR]