COVID-19 isn’t just a respiratory illness; it’s a long-term heart risk. This study reveals that the virus’s impact on your heart lingers, putting survivors at an elevated risk of life-threatening cardiac events for years.

Study: COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction with ABO Blood Type. Image Credit: crystal light / Shutterstock.com

A recent study published in Arteriosclerosis, Thrombosis, and Vascular Biology explores the risk of coronary artery disease (CAD) due to the coronavirus disease 2019 (COVID-19).

COVID-19 and MACE

COVID-19 is associated with numerous acute and chronic complications, including major adverse cardiac events (MACEs), some of which include myocardial infarction (MI), stroke, and death from any cause. The incidence of MACE is particularly high during the first 30 days following infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for COVID-19, with the risk of MACE remaining high for up to two years.

“CAD risk equivalence has historically been used as a benchmark for escalation of global CVD prevention efforts.”

Multiple genetic loci have been linked to increased susceptibility to COVID-19 and disease severity. The ABO locus that determines the blood type, for example, has been shown to modify the risk of atherosclerotic plaque rupture and MI.

About the study

Data for the current study were obtained from the United Kingdom Biobank on COVID-19 patients between January 1, 2020, and December 31, 2020. A total of 8,062 COVID-19 diagnoses were confirmed by polymerase chain reaction (PCR) tests, whereas 1,943 individuals received hospital-based diagnoses. Data for the control cohort of 217,730 from the same period were also obtained from the U.K. Biobank.

The researchers from the current study examined the risk of MACE with COVID-19 in association with the ABO locus.

COVID-19 increases MACE

COVID-19 patients were more likely to be males and have a comorbid cardiometabolic disease as compared to controls. The most common cause of death in both COVID-19 and control patients was cardiovascular disease (CVD) and other disorders of the circulatory system.

The risk of MACE was doubled in COVID-19 patients, irrespective of the severity of the infection-related illness. However, the risk of MACE was highest, nearly fourfold, among those hospitalized for COVID-19. This pattern persisted when the MACE risk in hospitalized COVID-19 cases was compared with that in control patients hospitalized for other causes.

MACE risk remained higher for three years after COVID-19, irrespective of severity; however, this risk was highest among hospitalized patients. The increased risk of MACE was independent of other CVD risk factors.

Males, younger people, as well as obese or diabetic patients, had differences in the risk of MACE. Hospitalization for COVID-19 was also associated with an increased risk of CVD mortality. 

COVID-19 as a CAD risk equivalent

Patients without a history of CVD who were hospitalized for COVID-19 had a seven-fold increased risk of MAE as compared to non-hospitalized controls without CVD risk factors. If CVD history was present, the risk of MACE increased by 12-fold.

Among controls, the MACE risk increased by two- and five-fold among those with diabetes and peripheral artery disease or CVD, respectively. Hospitalization for COVID-19 without a history of CVD increased MACE risk by 20% as compared to COVID-free patients with CVD.

Among patients who were not prescribed antiplatelet drugs when enrolled in the U.K. Biobank, the risk of thrombosis was higher for those hospitalized for COVID-19 despite the absence of prior CVD. Conversely, neither MI nor stroke risk rose among COVID-19 patients without CVD who were prescribed antiplatelet drugs.

ABO and COVID-19 risk

The ABO locus mediated differences in the risk of hospitalization for COVID-19. Blood types other than O were more likely to test positive for COVID-19 but not to be hospitalized for this infection.

Aside from the O blood type, all other blood types were associated with a 65% increased risk of thrombotic events, including MI and stroke, if hospitalized for COVID-19 as compared to controls.

Conclusions

The current study identified an increased long-term risk of MACE following COVID-19, irrespective of disease severity. This risk remained elevated three years from the onset of the illness, thus indicating a significant and persistent increased risk associated with COVID-19.

Severe COVID-19, which is defined as COVID-19 requiring hospitalization, is a CAD risk equivalent associated with an increased thrombosis risk. Therefore, additional studies are needed to determine whether this population of COVID-19 survivors should be targeted for aggressive primary prevention using cholesterol-lowering interventions and antiplatelet agents. This observation also suggests a potential mechanism involved in CVD-associated complications in severe COVID-19.