Coronary Artery Calcification and Complications in COVID-19 Patients
- The presence and extent of CAC on chest CT is associated with a worse prognosis in hospitalized COVID-19 patients.
- CAC is associated with increase in requirement of ventilators, ECMO, and death independent of age and major atherosclerotic CVD risk factors.
Is coronary artery calcification (CAC) a marker for worse prognosis in coronavirus disease 2019 (COVID-19) patients?
A cross-sectional study was conducted from March 15-May 3, 2020 in consecutive patients 40-80 years of age without cardiovascular disease (CVD) who were hospitalized with COVID-19 and had a noncontrast chest computed tomography (CT) on the day of admission. The presence or absence of CAC (CAC+ and CAC-, respectively) was defined as any area ≥1 mm2 with a density >130 Hounsfield units along the known coronary tract. There was no ECG gating. Primary outcome segmented by median age was the first occurrence of mechanical noninvasive or invasive ventilation, extracorporeal membrane oxygenation (ECMO), or death within 30 days of admission.
After 147 exclusions, 209 consecutive patients were included, with median age 62 years [(interquartile range) 51-70], 72% men, and all were hospitalized without or with nasal oxygen. CAC was detected in 106 (50.7%) patients. The primary outcome occurred in 50% of CAC+ compared to 17.5% CAC- (p < 0.0001). In those <62 years, 32% were CAC+ with the primary outcome in 55% compared to 20% in those CAC- (hazard ratio [HR], 5.4; p = 0.0001). In those ≥62 years, 69% were CAC+ with the primary outcome in 48% compared to 13% in those CAC- (HR, 3.2; p = 0.02). In a Cox proportional hazard model including age, sex, hypertension, smoking, and diabetes, CAC was independently associated with the primary outcome (HR, 4.4; p < 0.0001). There was one acute myocardial infarction (MI) and no strokes during follow-up.
The presence and extent of CAC is associated with a worse prognosis in hospitalized COVID-19 patients. The severity of immune response, endothelial dysfunction, and myocardial stress due to COVID-19 could be exacerbated in patients with subclinical coronary atherosclerosis.
Despite the crude methods that would underestimate the calcium scores, the frequency of detecting calcium is similar to that published in the MESA (Multi-Ethnic Study of Atherosclerosis) cohort of about the same age. That the CAC association with hard pulmonary endpoints was independent of age and major coronary risk factors is surprising. There was only one MI and 9% had detectable high-sensitivity cardiac troponin I (hs-cTnI) in those CAC+ and 3.4% in CAC- (p = not significant). It is possible that this cohort was not as ill as patients in some other studies. I would have expected a much higher percent of hs-cTnI reflecting global myocardial demand ischemia, vasculitis, and myocarditis. The majority of COVID-19 patients have detectable hs-cTnI and it is present in 50% who die.
Keywords: Atherosclerosis, Coronary Artery Disease, Coronavirus, COVID-19, Diagnostic Imaging, Endothelium, Extracorporeal Membrane Oxygenation, Myocardial Infarction, Myocardial Ischemia, Oxygen, Plaque, Atherosclerotic, Secondary Prevention, Risk Factors, severe acute respiratory syndrome coronavirus 2, Tomography, X-Ray Computed, Troponin I, Ventilators, Mechanical
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