Right ventricular dysfunction after pericardiectomy for tuberculous constrictive pericarditis: A case report.

This case report provides a peculiar case of tuberculous constrictive pericarditis (TCP) who presented with right ventricular dysfunction after pericardiectomy. Right ventricular dysfunction is one of the main postoperative complications after pericardiectomy. Rapid and accurate identification of right ventricular dysfunction confirmed by transthoracic echocardiography (TTE), associated with the rapid initiation of diuretics and inotropic therapy is necessary for the patient's complete recovery. Abstract: TCP is a condition characterized by chronic inflammation and fibrosis of the pericardium. Pericardiectomy is the standard treatment for patients with constrictive pericarditis and persistent symptoms. One possible surgical complication is right ventricle (RV) failure. We report a case of a 44­year­old man who developed RV failure after pericardiectomy for TCP. A 41­year­old man with no medical history was referred to our hospital due to progressive dyspnea associated with edema of the lower limbs and significant weight loss (30 kg) over the past 5 months. TTE revealed significant pericardial thickening and mild pericardial effusion with normal RV function. Chest X­ray showed moderate bilateral pleural effusion. The patient underwent pericardiectomy and bilateral pleural drainage. Histopathological examination showed tuberculosis granulomas with caseous necrosis, and antituberculosis medication was initiated. Postoperative TTEs showed normal RV function and mild pericardial thickening. The patient was discharged home after successful postoperative recovery. Three weeks later, the patient was admitted to the emergency department with dyspnea and hypoxemia. TTE revealed RV systolic dysfunction. Chest CT showed a recurrence of moderate pleural effusion, this time loculated, with restrictive atelectasis of the adjacent lung parenchyma. Diuretics and inotropic therapy were initiated, and the patient underwent lung decortication after confirmation of tuberculous empyema. The patient experienced significant clinical improvement. TTE before discharge showed a decreased RV chamber size with improved RV systolic function. The patient was discharged in a stable condition 30 days after admission with a low dose of oral furosemide. Four months after discharge, he remained asymptomatic with good functional status. Pericardiectomy for TCP may carry the risk of developing RV dysfunction. Furthermore, TCP itself may be associated with other complications, such as empyema. We emphasize the importance of conducting a thorough clinical evaluation for patients with TCP, particularly those undergoing pericardiectomy, to mitigate potential adverse outcomes.

Dyslipidemia: A Narrative Review on Pharmacotherapy.

Dyslipidemia plays a fundamental role in the development and progression of atherosclerosis. Current guidelines for treating dyslipidemia focus on low-density lipoprotein-cholesterol (LDL-C). Despite advances in the pharmacotherapy of atherosclerosis, the most successful agents used to treat this disease-statins-remain insufficient in the primary or secondary prevention of acute myocardial infarction. Advancing therapy for hypercholesterolemia with emerging new drugs, either as monotherapy or in combination, is expected to improve cardiovascular outcomes. An emerging field in dyslipidemia pharmacotherapy is research on genetic therapies and genetic modulation. Understanding the genetic mechanisms underlying lipid alterations may lead to the development of personalized treatments that directly target the genetic causes of dyslipidemia. RNA messenger (mRNA)-based therapies are also being explored, offering the ability to modulate gene expression to normalize lipid levels. Furthermore, nanotechnology raises new possibilities in drug delivery for treating dyslipidemia. Controlled-release systems, nanoparticles, and liposomes can enhance the effectiveness and safety of medications by providing more precise and sustained release. This narrative review summarizes current and emerging therapies for the management of patients with dyslipidemia.

Diagnostic Management and Surgical Treatment of Isolated Tricuspid Regurgitation.

Severe tricuspid regurgitation is especially caused by pulmonary hypertension. Primary tricuspid regurgitation in the absence of pulmonary hypertension and of unknown etiology is a very rare condition with scarce data about its diagnosis, treatment, and follow-up. The particularities of surgery indication and outcomes are still not clearly known. A 72-year-old woman with a medical history of coronary artery bypass grafting three years ago presented with shortness of breath and low limb edema. Physical examination revealed a prominent bilateral jugular turgescence, hepatomegaly, peripheral edema, and a left midsternal border holosystolic murmur, suggestive of tricuspid regurgitation. The echocardiogram confirmed the diagnosis and showed preserved right and left ventricular dimensions and function. Coronary angiography showed no new obstructive lesions and patent surgical grafts. Right cardiac catheterization revealed mild pulmonary hypertension and increased right atrium pressure. Cardiac magnetic resonance showed mild right ventricular dilation with normal systolic function and normal left chambers. No late gadolinium enhancement was detected. Because of persistent symptoms, even after optimization of medical therapy, the patient was submitted to tricuspid valve replacement surgery. Immediately after the surgery, the patient developed significant right ventricular dysfunction, with the need of continuous hemodynamic support. She had progressive clinical recovery that was confirmed by serial echocardiograms that showed improvement in right ventricular volume and function. The patient was discharged with no signs or symptoms of right heart failure. The histopathological examination showed significant and diffuse myxomatous degeneration of the leaflets. No signs of infection or vegetation nor disruption of strands were observed. This report illustrates a very rare case of symptomatic primary isolated severe tricuspid regurgitation caused by myxomatous degeneration of the leaflets. The thoroughly diagnostic workup is presented, and only the histopathological analysis of the leaflets revealed the etiologic process. Surgical treatment indicated before the onset of right ventricular failure was essential to patient's full recovery.