Background
Cardiovascular and thromboembolic complications have been reported in patients with Coronavirus disease-2019 (COVID-19)-related severe respiratory distress syndrome. Although myocarditis associated with COVID-19 pneumonia has been described, evidence of left ventricular (LV) mural thrombi with other multisystem events has not been reported.
Case summary
We report two cases with severe COVID-19 pneumonia and myocardial injury with large LV thrombi and other multisystem thrombotic events. The first patient represents an unusual case of large LV apical thrombus without concordant regional wall motion abnormality and mildly reduced LV function. A subsequent inferior ST-elevation myocardial infarction (STEMI) was likely related to either an embolic event or in situ coronary thrombosis. We could not ascertain whether the acute right ventricular dysfunction was due to in situ pulmonary thrombosis or inferior STEMI. The catastrophic cerebrovascular accident was likely an embolic phenomenon. Similarly, the second patient demonstrated multiple large pedunculated thrombi occupying one-third of the LV cavity with moderately reduced LV function. A segmental pulmonary embolism was diagnosed on computed tomography chest, confirming multiple territories of in situ thrombosis.
Discussion
COVID-19-related inflammatory cytokine release has been linked to activation of coagulation pathways. Marked elevation of ferritin and C-reactive protein levels in both patients were consistent with evidence of a hyperinflammatory state with ‘cytokine storm’. Furthermore, the finding of elevated D-dimer levels lends support to the altered coagulation cascade that plausibly explains the multisystem thrombosis observed in our patients. The direct viral endothelial involvement and subsequent endothelial dysfunction may play an important role in the development of thrombosis in different vascular beds, as seen in our patients.
Clinical Case:
A 37-year-old transgender (TG) woman off gender-affirming hormonal therapy (GAHT) presented with substernal chest pain radiating to the left arm, worse with exertion and relieved with res. She was hypertensive and tachycardic on admission. Initial bloodwork revealed an elevated troponin I of 0.57 ng/mL, which peaked at 1.48 ng/mL. EKG on admission showed hyperacute T waves in the anterior leads without ST elevation (see Figure 1). She was diagnosed with non-ST elevation myocardial infarction (NSTEMI) and taken for left heart catheterization (LHC).
Decision-Making:
TTE showed preserved LVEF and basal inferior, basal inferolateral, basal anterolateral and mid-anterolateral hypokinesis. LHC showed proximal-to-mid right coronary artery (RCA) occlusion. After failed aspiration thrombectomy indicating calcified plaque, two overlapping drug-eluting stents (DES) were successfully deployed with restoration of flow. She was discharged home on aspirin, ticagrelor, atorvastatin, and carvedilol.
Discussion:
Despite a recent push to increase awareness, research and healthcare equality specific to lesbian, gay, bisexual, transgender, and queer (LGBTQ+) patients, a significant gap persists. Specifically, stress, inflammation, dyslipidemia, and thromboembolism predispose this understudied population to increased coronary artery disease (CAD) and myocardial infarction (MI). Accordingly, greater effort needs to be taken to mitigate preventable cardiac morbidity and mortality in this patient population.
Conclusion:
CAD in LGBTQ+ adults is well studied. However, there are few published studies on CAD specifically among TG men and women. National cross-sectional data highlights this disproportionate risk of CAD and MI among TG men and women relative to their cisgender female and male peers, a healthcare disparity recently emphasized by the AHA. Consequently, care must be taken to eliminate these aforementioned inequalities.
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