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BACKGROUND Constrictive pericarditis occurs due to chronic pericardial inflammation and adherence of the cardiac pericardial layer. Etiologies include toxins, infection, cardiac surgery, and idiopathic causes. Outside the United States, the most common cause of constrictive pericarditis is tuberculosis (TB). Constrictive pericarditis is the most severe complication of tuberculous pericardial disease. CASE REPORT A 31-year-old man who recently immigrated to the United States presented with a 2-week history of constitutional symptoms, dyspnea, and pleuritic chest pain. Physical examination was pertinent for bilateral lower extremity pitting edema, decreased bilateral breath sounds, and jugular venous distension. Transthoracic echocardiogram revealed a left ventricular ejection fraction of 45%, pericardial thickening, and an exaggerated septal bounce. Right heart catheterization showed discordant and concordant right ventricular pressure tracings. Cardiac magnetic resonance imaging revealed bilateral pleural effusions and circumferential pericardial thickening. Thoracocentesis was significant for an exudative effusion, with elevated adenosine deaminase levels. Subsequent QuantiFERON-TB Gold testing was positive, and he underwent elective pericardiectomy. Pericardial histopathology revealed necrotizing caseating granulomas. He was discharged on a 6-month course of rifampicin, isoniazid, pyrazinamide, and ethambutol therapy, with close multidisciplinary care team outpatient follow-up. CONCLUSIONS This case highlights the importance of a high index of clinical suspicion for tuberculous pericarditis in patients presenting with constitutional and heart failure symptoms and a relevant travel history, to ensure prompt diagnosis and treatment. This case also reflects the importance of coordination of care between cardiology, infectious disease, pathology, and cardiothoracic surgery teams in the management of tuberculous constrictive pericarditis.

Symptomatic women with angina are more likely to have ischemia with no obstructive coronary arteries (INOCA) compared to men. In both men and women, the finding of INOCA is not benign and is associated with adverse cardiovascular events, including myocardial infarction, heart failure and angina hospitalizations. Women with INOCA have more angina and a lower quality of life compared to men, but they are often falsely reassured because of a lack of obstructive coronary artery disease (CAD) and a perception of low risk. Coronary microvascular dysfunction (CMD) is a key pathophysiologic contributor to INOCA, and non-invasive imaging methods are used to detect impaired microvascular flow. Coronary vasospasm is another mechanism of INOCA, and can co-exist with CMD, but usually requires invasive coronary function testing (CFT) with provocation testing for a definitive diagnosis. In addition to traditional heart disease risk factors, inflammatory, hormonal and psychological risk factors that impact microvascular tone are implicated in INOCA. Treatment of risk factors and use of anti-atherosclerotic and anti-anginal medications offer benefit. Increasing awareness and early referral to specialized centers that focus on INOCA management can improve patient-oriented outcomes. However, large, randomized treatment trials to investigate the impact on major adverse cardiovascular events (MACE) are needed. In this focused review, we discuss the prevalence, pathophysiology, presentation, diagnosis and treatment of INOCA.