Background/Objectives: Venlafaxine (VEN) is a serotonin and norepinephrine reuptake inhibitor (SNRI) antidepressant. Arterial hypertension (HTN), heart failure (HF), and arrhythmias are side effects of VEN. Cardiotoxicity (CTOX) as a feature of VEN-associated side-effects has only rarely been described. Methods: We conducted a search of our database for cases of VEN-associated CTOX, analyzing symptoms, echocardiographic findings, and laboratory results. Results: We identified five patients (three females, two males) with VEN-associated CTOX, aged 51 to 87 years at presentation. VEN dose was 150 and 375 mg daily and treatment duration was 1.5 to 15 years. Presenting features were HTN in three, “hypertrophic cardiomyopathy” in two, heart failure in three, and atrial fibrillation in three patients. Symptoms and signs of CTOX were reversible in all patients after discontinuation or dose reduction of VEN, suggesting a causal relationship between VEN and CTOX. Conclusions: VEN-associated CTOX can occur and progress to severe cardiomyopathy or heart failure. Potential risk factors include cardiac sympathetic stimulation, high VEN dosage, and prolonged treatment duration; however, CTOX may also occur at standard doses. Therefore, patients taking VEN should be routinely monitored for signs of cardiotoxicity, including monitoring of serum concentrations of VEN.

Coronary artery fistulas (CAFs) are a rare, typically congenital coronary anomaly. They may cause myocardial ischemia through a coronary steal phenomenon. Acquired CAFs are exceptionally uncommon and are usually due to an intervention or trauma. We re-port the case of a 79-year-old man with history of clear cell renal cell carcinoma previ-ously treated with right nephrectomy in 2015. Seven years later, he underwent percu-taneous coronary intervention of severe LAD stenosis following out-of-hospital cardi-ac arrest. During follow-up, progressive exertional dyspnea and inducible lateral is-chemia led to repeated coronary angiography 15 months later revealing fistulous communications from the circumflex and right coronary arteries draining into a left pulmonary mass. Right-heart catheterization showed a small left-to-right shunt at rest (Qp/Qs 1.3). Thoracic computed tomography and biopsy confirmed a large pulmonary metastasis from clear cell renal cell carcinoma, suggesting that the fistulas developed as part of tumor angiogenesis. Transcatheter coil embolization would have been a strategy to reduce tumor perfusion and the coronary steal; however, we just limited our treatment to the tyrosine kinase inhibitor Axitinib due to the metastatic disease. This case describes a rare mechanism of acquired CAF formation in metastatic renal cell carcinoma.