Cardiac manifestations of COVID-19 include myocarditis, demand ischemia, myocardial infarction and arrhythmias with prothrombotic state being a major underlying pathogenetic mechanism. In this report we present a case of a 57-year-old, otherwise healthy, woman who presented with chest pain and nausea and was found to have an inferior wall ST-elevation myocardial infarction (STEMI) in the setting of an active COVID-19 infection. Angiography revealed tortuous coronary arteries with a 100% right coronary artery occlusion with high thrombus burden and normal left coronary system. In light of the available literature regarding the pro-thrombotic effects of this novel corona virus, we continued full dose anticoagulation with Enoxaparin after the cardiac catheterization and transitioned to rivaroxaban and we also continued the patient on dual antiplatelet therapy prior to discharge.
Methotrexate (MTX) toxicity can affect multiple organ systems, manifesting as nephrotoxicity, myelosuppression, hepatotoxicity, mucositis, and gastrointestinal upset. Serious adverse events are rare in patients prescribed low-dose methotrexate. We present a case of an 86-year-old female on a weekly dose of oral MTX 12.5 mg for rheumatoid arthritis presenting with painful gingiva and oral bleeding during outpatient antimicrobial therapy (OPAT) for osteomyelitis with vancomycin and piperacillin-tazobactam. She had acute kidney injury (AKI), elevated serum MTX levels, thrombocytopenia, neutropenia, and a vancomycin level three times therapeutic concentration. MTX toxicity was suspected to have been triggered by vancomycin and piperacillin-tazobactam causing AKI and impaired renal clearance of MTX which itself is nephrotoxic. The patient was managed with leucovorin, alkalinized intravenous fluids, and filgrastim injections over a 2-week period. Her renal function continued to be reduced at 5-week outpatient follow-up, far after other markers of toxicity normalized. This case demonstrates the importance of considering potential drug-drug interactions and the need for robust monitoring for OPAT in select groups.
Coronary embolism is a cause of acute myocardial infarction (AMI)in which obstructive foci enter the coronary circulation, block normal blood flow and precipitate ischemia. Precise studies focusing on patient population affected, pathophysiological mechanisms, and treatment strategies are scanty, in spite of a reported prevalence estimated at 2.9%. As the understanding of myocardial infarction without evidence of coronary artery disease continues to grow, an in-depth review of this previously seldomly reported subtype of coronary ischemia was in order. Patients suffering coronary embolism are 15 to 20 years younger than traditional AMI patients with a slight predominance towards male sex, which resembles the gender data of the populations affected by non-traditional myocardial infarction in published reports. While the expected prevalence rate of cardiovascular disease risk factors such as hypertension and hyperlipidemia are present, this population also has a relatively high prevalence of atrial fibrillation and valve pathology, especially endocarditis. Initial presentation is indistinguishable from other causes of myocardial infarction however fever is commonly present, when endocarditis with valvular involvement is the primary cause of the coronary embolism. Mechanical thrombectomy is the mainstay of treatment, followed by percutaneous coronary intervention. Mortality is the highest in patients who do not receive targeted treatment for the coronary embolism, particularly if only antimicrobial agents or anticoagulation without thrombolytic agents are employed. The unique features of coronary embolism highlighted in this historical study justify further examination in contemporary patient populations.
Patients with human immunodeficiency virus (HIV) are at higher risk for coronary artery disease, due to accelerated atherosclerosis resulting from chronic inflammation, the prevalence of cardiovascular risk factors and the side effects of highly active antiretroviral therapy (HAART). The Wellens’ pattern is an electrocardiographic (ECG) finding that represents critical proximal left anterior descending (LAD) coronary artery stenosis that, that when is not promptly treated, can lead to extensive anterior wall myocardial infarction and death. Very few cases of Wellens’ syndrome in HIV positive patients have been reported. We present a case of Wellens’ syndrome in a 38-year-old male with HIV on HAART and hyperlipidemia, as his only traditional cardiovascular risk factor. Recognition of the characteristic biphasic T-waves in V2 and V3 on ECG in the setting of typical angina and elevated troponin levels directed the clinicians to proceed with an emergent cardiac catheterization and percutaneous coronary intervention with drug eluting stent placement in the proximal left anterior descending artery (LAD). Physicians should recognize Wellens’ syndrome as it indicates critical LAD stenosis requiring intervention. HIV positive patients can present with Wellens’ sign at a younger age, indicating premature coronary artery disease (CAD) in this population.
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