Welcome to the first installment of our 8-part series on cardiovascular complications in patients with COVID-19. The severe systemic inflammatory processes and hypercoagulability occurring with COVID-19 illness increase the risk of atherosclerotic plaque disruption and acute myocardial infarction (AMI). Patients with previous history of coronary disease and/or other significant comorbidities are particularly predisposed to cardiovascular complications with COVID-19 infection.1 In this installment, we will discuss a COVID-19 patient with suspected acute ST-elevation myocardial infarction (STEMI) or non-ST–elevation myocardial infarction (NSTEMI).
A 56-year-old woman presents to a rural emergency department with complaints of severe substernal chest pain. Associated symptoms include fatigue, nausea, and vomiting. The 12-lead electrocardiography (ECG) is suggestive of acute AMI with 2.5-mm ST elevation in leads V2 to V4, serum cardiac biomarkers are positive with normal serum beta natriuretic peptide (BNP). Rapid COVID-19 test is positive and appropriate infection control precautions are implemented.
The patient is given 325-mg nonenteric coated aspirin (ASA), 2 doses of sublingual nitroglycerin 0.4-mg tablet given 5 minutes apart, 1 subcutaneous injection of heparin enoxaparin 1 mg/kg, and 3 doses of intravenous metoprolol 5 mg given 5 minutes apart. The patient is then emergently transferred to a tertiary care center for further treatment.
Upon arrival at the tertiary center, the patient is taken to the cardiac catheterization lab where angiography and percutaneous intervention (PCI) are performed. Angiography reveals a 100% occlusion of the proximal left anterior descending (LAD) artery. Angioplasty and deployment of a drug-eluting stent to the proximal LAD are completed. Left ventriculogram demonstrates a reduced ejection fraction (EF) of 37%. Subsequent echocardiogram confirms the reduced EF but does not demonstrate any evidence of pulmonary hypertension or elevation of right heart pressures.
Significant Medical History
The patient’s past medical history includes a previous diagnosis of coronary artery disease and PCI of the right coronary artery. She also had a history of dyslipidemia, hypothyroidism, and obesity with a BMI of 33.
On initial presentation, the patient is an anxious appearing middle-aged woman with obesity and complaints of substernal chest pain. Her lungs are clear bilaterally anterior and posterior; heart tones are normal. Vital signs include oxygen saturation, 95% on room air; blood pressure, 156/89 mm Hg; heart rate, 98 beats per minute; respiratory rate, 22 breaths per minute; and pain rating, 8/10. Cardiac monitor reveals a sinus rhythm in lead II. The recommended diagnostic and laboratory tests are ordered (Table 1).2
Table 1. Recommended Diagnostic/Laboratory Tests2
|• CBC: leukocytosis, anemia, and thrombocytopenia|
|• CMP: electrolytes, renal function, and elevated liver function|
|• Fasting lipid panel|
|• Coagulation PT/INR, d-dimer|
|• Cardiac biomarkers: troponin, BNP|
|• ECG to access ischemia, pericarditis, QTc monitor with rate and rhythm|
|• Continuous cardiac monitor: monitor for QTc|
|• CT chest without contrast for pneumonia evaluation, with contrast to rule out pulmonary embolus|
The American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend troponin as the only cardiac biomarker that should be measured in patients with suspected MI.3 Troponin, which is not normally found in serum, is only released when myocardial necrosis occurs.3 Serial measurement taken 3 to 6 hours after the initial level is obtained is recommended.3,4 If the initial troponin levels are negative and MI is still suspected, measurement beyond the 6-hour mark should be obtained.3
Other laboratory studies should include a complete blood cell count, comprehensive metabolic profile, and fasting lipid profile.4 Because of the proinflammatory state, patients with MI may have a modestly elevated white blood cell count.4 Moreover, if the patient is going to receive a thrombolytic agent, it is important to evaluate presence of anemia as well as the platelet count.3 Potassium and magnesium must be monitored closely in patients with MI because abnormalities can result in fatal cardiac dysrhythmias.4 Creatinine levels are also important prior to specific interventions (ie, cardiac catheterization or angiotensin-converting enzyme [ACE] inhibitor administration).4
Initial 12-lead ECG is obtained on presentation to rule out any ST-segment elevation. An ST-segment elevation in 2 contiguous leads of greater than or equal to 1 mm in all leads except V2 and V3 is considered significant. Leads V2 and V3 require ST elevation of greater than or equal to 1.5 mm for women aged 40 years or older, greater than or equal to 2.5 mm for men less than 40 years of age, and greater than or equal to 2.0 mm for men older than 40 years. Continuous cardiac monitoring is also recommended for early recognition of arrhythmias.5