Coronary Embolism and Myocardial Infarction in a Transgender Male Undergoing Hormone Therapy: A Case Report and Review of the Literature.

Introduction. Due to the complex interaction between the underlying disease, psychosocial factors, and the high-dose hormonal therapy, transgender patients pose a therapeutic and diagnostic challenge, especially during emergencies. This case presents one such clinical dilemma using the example of a case of myocardial infarction. CASE: A 35-year-old transgender male presented to our clinic with an acute inferior wall myocardial infarction. For the past 6 years, he was receiving high-dose testosterone therapy for the maintenance of hormone levels after female-to-male gender conversion. The emergency coronary angiography revealed a distal right coronary artery occlusion. Recanalization of the vessel was achieved by catheter-driven direct thrombectomy and subsequent intracardiac lysis. The appearance of the remaining coronary arteries bore no angiographic evidence of advanced coronary artery disease. We suspected a thromboembolic origin as the primary cause of the myocardial infarction. The presentation also fulfilled the proposed National Cerebral and Cardiovascular Center criteria for the clinical diagnosis of coronary embolism. In the diagnostic work-up, the most common causes of coronary embolism like atrial fibrillation, cardiomyopathies, endocarditis, and intracardiac tumors could be ruled out. The screening for hereditary thrombophilia was also negative. Likewise, the presence of a haemodynamically relevant right to left shunt could be excluded. In the end, the high-dose testosterone therapy seemed to be the most likely cause. CONCLUSION: Following major thromboembolic cardiovascular events, we believe that transgender males treated with high-dose testosterone therapy should receive oral anticoagulation, preferably with a DOAC, especially keeping in mind that the discontinuation of the hormone therapy is not always possible due to the various underlying psychosocial factors.

Matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, B⁺ tenascin-C and ED-A⁺ fibronectin in dilated cardiomyopathy: potential impact on disease progression and patients' prognosis.

BACKGROUND: Dilated cardiomyopathy (DCM) is associated with heart failure and increased mortality and there is no reliable biomarker to estimate patients' prognosis. During cardiac remodeling, an extensive reorganization of the extracellular matrix occurs. The study was aimed to investigate matrix metalloproteinase 9 (MMP-9), tissue inhibitor of metalloproteinase 1 (TIMP-1) and fetal tenascin-C (B(+) Tn-C) and fibronectin (ED-A(+) Fn) variants known to be involved in that process. METHODS AND RESULTS: In 187 patients with DCM, levels of MMP-9, TIMP-1 and B(+) Tn-C in serum as well as B(+) Tn-C and ED-A(+) Fn in tissue were quantified and subjected to univariate analysis. For all serum markers, concentrations above a calculated threshold were associated with decreased survival (MMP-9: p = 0.008, TIMP-1: p = 0.001, B(+) Tn-C: p < 0.001) and a significantly higher risk to die or undergo transplantation. In tissue, a reexpression of B(+) Tn-C and ED-A(+) Fn could be shown. Protein deposition levels of ≥4.5% for B(+) Tn-C and ≥2.1% for ED-A(+) Fn were associated with a significantly decreased survival (p = 0.001 for B(+) Tn-C, p = 0.031 for ED-A(+) Fn) and an increased risk to die or undergo transplantation. In a multivariate analysis, TIMP-1 is the superior parameter to predict transplantation free survival (p = 0.027). CONCLUSIONS: Serum levels of MMP-9, TIMP-1 and B(+) Tn-C and tissue levels of B(+) Tn-C and ED-A(+) Fn are promising markers for risk assessment. The reoccurrence of ED-A(+) Fn and the availability of a human antibody usable as a vehicle for targeted drug delivery might be the basis for novel therapeutic strategies.

Delayed recovery of left ventricular function after recanalization of a chronic coronary occlusion.

An unusually prolonged course of recovery of severely impaired left ventricular (LV) function (EF 32%) was observed in a patient after recanalization of a chronically occluded LAD. Despite persistent vessel patency, LV function remained depressed for almost 2 years after the percutaneous transluminal coronary angioplasty until complete recovery (EF 82%) could be observed. The possibility of a delayed recovery should be considered when assessing new therapeutic strategies to improve LV function of chronically ischemic myocardium.