Muhammad N Tariq, Ahmed T Abdel Halim, Jennifer A Evans
Enclomiphene citrate is increasingly prescribed off-label for secondary male hypogonadism, and its cardiovascular safety profile remains poorly characterised. We report a 46-year-old man with a mitral valve repair performed 20 years earlier and chronic immune thrombocytopenia (ITP) in whom atrial flutter was first documented shortly after he inadvertently increased his enclomiphene dose, taking 50 mg daily in place of 25 mg daily. Laboratory evaluation demonstrated chronic thrombocytopenia with a platelet count of 36 × 10⁹/L, while thyroid function, cardiac biomarkers, and electrolytes were normal. Transthoracic echocardiography showed preserved left ventricular systolic function with mild asymmetric left ventricular hypertrophy, mild left atrial enlargement, and mildly reduced right ventricular systolic function. Computed tomography pulmonary angiography (CTPA) excluded pulmonary embolism. Rate control was achieved with metoprolol and diltiazem. Anticoagulation was deferred because of severe thrombocytopenia, and high-dose prednisone was initiated to raise the platelet count before planned anticoagulation and elective cardioversion. Testosterone was elevated at presentation and the arrhythmia was detected soon after the dose increase, but causality cannot be established. The patient had a remote atriotomy and echocardiographic evidence of chronic atrial and ventricular remodelling, a substrate sufficient on its own to sustain macro-reentrant atrial flutter, and earlier asymptomatic or self-limiting episodes could not be excluded. Formal causality assessment using the Naranjo scale placed the association in the possible category only. The case is presented for two reasons: as an illustration of how a hormonal agent should be weighed against a pre-existing structural substrate rather than assumed to be causal, and as an example of the difficulty of balancing thromboembolic and bleeding risk when atrial flutter coexists with severe ITP.