Cardiovascular Medicine

What a remarkable first three months it has been for Cardiovascular Medicine! [...]

Long QT associated with pheochromocytoma is rare but clinically significant. A 43-year-old woman presented with palpitations, chest pain, and recurrent syncope. ECG showed ST-segment elevation, while coronary angiography revealed normal arteries but Takotsubo-like left ventricular dysfunction. Hypertension and tachycardia raised suspicion for pheochromocytoma, later confirmed by imaging and biochemical tests. The patient exhibited QT prolongation (QTc 570 ms) in parallel with Takotsubo episodes. Following adrenalectomy, both QT duration and ventricular function normalized. The European Society of Cardiology now classifies pheochromocytoma-induced cardiomyopathy within the Takotsubo spectrum. Early recognition is crucial due to the risk of sudden cardiac death.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for managing inflammation, but they are associated with gastrointestinal and renal toxicity upon long-term use. Selective cyclooxygenase-2 (COX-2) inhibitors, or coxibs, were developed to avoid these adverse effects while maintaining anti-inflammatory efficacy. However, accumulating evidence indicates that coxibs may increase the risk of cardiovascular complications. This review explores the pathophysiological mechanisms underlying adverse cardiovascular effects in patients treated with COX-2 inhibitors. These mechanisms include an imbalance between prothrombotic and antithrombotic factors, an altered endocannabinoid metabolism, and downregulation of PPARδ, contributing to thrombosis. Additionally, COX-2 inhibition disrupts renal prostaglandin synthesis, particularly PGE2 and prostacyclins, reduces EP4 receptor expression in macrophages, promotes chemotaxis, and elevates arterial pressure via increased iNOS, ADMA, and L-NMMA activity. At the molecular level, genetic polymorphisms, matrix metalloproteinases, signaling cross-talk, and direct cardiomyocyte injury are implicated. Collectively, these alterations promote a prothrombotic state, fluid retention, enhanced vasoconstriction, impaired vasodilation, myocardial injury, cell death, and cardiac fibrosis. Despite these risks, coxibs are often prescribed without adequate cardiovascular assessment, particularly in patients with pre-existing cardiovascular risk factors. Greater awareness of these mechanisms is essential to optimize the benefit–risk ratio in clinical decision-making involving selective COX-2 inhibitors.