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Myocarditis is a disease caused by inflammation of the heart that can progress to dilated cardiomyopathy, heart failure, and eventually death in many patients. Several etiologies are implicated in the development of myocarditis including autoimmune, drug-induced, infectious, and others. All causes lead to inflammation which causes damage to the myocardium followed by remodeling and fibrosis. This review aims to summarize recent findings in biomarkers for myocarditis and highlight the most promising candidates.Current methods of diagnosing myocarditis, including imaging and endomyocardial biopsy, are invasive, expensive, and often not done early enough to affect progression. Research is being done to find biomarkers of myocarditis that are cost-effective, accurate, and prognostically informative. These biomarkers would allow for earlier screening for myocarditis, as well as earlier treatment, and a better understanding of the disease course for specific patients. Early diagnosis of myocarditis with biomarkers may allow for prompt treatment to improve outcomes in patients.

PURPOSE OF REVIEW: This review aims to summarize the renal effects of sodium-glucose transporter-2 (SGLT-2) inhibitors and their potential implications in heart failure pathophysiology. RECENT FINDINGS: In patients with diabetes and established atherosclerosis, the SGLT-2 inhibitor empagliflozin versus placebo significantly reduced the rate of heart failure admissions with 35%. Moreover, empagliflozin slowed kidney disease progression and reduced the need for renal replacement therapy. SGLT-2 inhibitors inhibit proximal tubular sodium and chloride reabsorption, leading to increased nephron flux throughout the distal renal tubules, most notably at the level of the macula densa. Afferent arteriolar vasoconstriction is promoted through tubulo-glomerular feedback and reduces glomerular capillary hydrostatic pressure, relieving podocyte stress and explaining renal preservation. Further, plasma volume is contracted and natriuresis promoted without inducing neurohumoral activation. Finally, SGLT-2 inhibitors may improve endothelial function and energy metabolism efficiency. Together, these promising features place them as a potential novel treatment for heart failure.

Congestion, defined by elevated cardiac filling pressures, is the major driver of hospitalization in acute decompensated heart failure. Careful clinical assessment should allow to determine whether volume overload or volume misdistribution is the predominating mechanism of congestion. Differentiation is imperative because therapy differs. If volume overloads prevails, loop diuretics are considered the mainstay therapy. However, early use of combinational therapy with diuretics acting more proximal or distal in the nephron could allow for a more profound natriuresis and diuresis. A stepped guided pharmacological treatment should focus on achieving complete decongestion, because persistent congestion is a major driver of readmission. If diuretic strategies remain unsuccessful, ultrafiltration should be considered. Ultrafiltration should be used with caution in the setting of worsening of renal function. When volume misdistribution and impaired venous capacitance predominate the picture of congestion, unloading-more than diuretics-with arteriolar and venous vasodilators might mitigate the clinical picture of congestion. This review offers a thorough overview and practical insight in the use of current and potential decongestive therapies.