Fact checked byErik Swain

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October 09, 2024
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COVID-19 a CV risk equivalent to prior heart disease; type O blood may be protective

Fact checked byErik Swain
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Key takeaways:

  • COVID-19 hospitalization may be a risk equivalent to coronary artery disease for MI and stroke.
  • Having type O blood may be partly protective against risk for MI and stroke after SARS-CoV-2 infection.

Prior SARS-CoV-2 infection was associated with a twofold increased risk for heart attack and stroke for SARS-CoV-2 up to 3 years, even among people with no history of heart disease, researchers reported.

For more serious SARS-CoV-2 infection, such as those requiring hospitalization, the long-term risk was even higher.

Graphical depiction of data presented in article
Data were derived from Hilser JR, et al. Arterioscler Thromb Vasc Biol. 2024;doi:10.1161/ATVBAHA.124.321001.

In addition, the researchers noted that individuals with non-O blood types were at greater risk for major adverse cardiac events following COVID-19 hospitalization compared with those with the type O blood type, according to data published in Arteriosclerosis, Thrombosis, and Vascular Biology.

“It's known that there's CV risk associated with having COVID-19, but what isn't known is how long that lasts, how big an impact that has and, from a clinical perspective, should that be impacting the way we approach our patients for CV risk assessment,” Stanley L. Hazen, MD, PhD, co-section head of preventive cardiology and chair of cardiovascular and metabolic sciences at the Cleveland Clinic Lerner Research Institute, told Healio.

Stanley L. Hazen

Using data from the UK Biobank, Hazen and colleagues examined data from nearly a quarter million people and identified 10,005 individuals with either a positive PCR test for SARS-CoV-2 or a hospital-based ICD-10 code for COVID-19 between Feb. 1, 2020, and Dec. 31, 2020. The studies explore the impact of COVID-19 effect on long-term heart disease risks pre-vaccination.

COVID-19 and risk for MI and stroke

Risk for MI and stroke following SARS-CoV-2 infection and hospitalization in this cohort was compared to risk among two control groups: a population control cohort already in the UK Biobank who never tested positive for SARS-CoV-2 or assigned a COVID-19 ICD-10 code during the study period (n = 217,730); and a propensity-matched control cohort who never tested positive (n = 38,860) to reduce confounding due to preexisting risk factors.

COVID-19 as a CAD-equivalent risk factor was also evaluated over 1,000 days of follow-up.

Major adverse CV events — defined as MI, stroke or all-cause death — were significantly elevated among those with a positive SARS-CoV-2 PCR test at all levels of infection severity (HR = 2.09; 95% CI, 1.94-2.25; P < .0005) compared with individuals without SARS-CoV-2, and was especially higher among patients hospitalized for COVID-19 (HR = 3.85; 95% CI, 3.51-4.24; P < .0005). The association between major adverse CV events and COVID-19 hospitalization was consistent when compared with propensity-matched controls (HR = 3.65; 95% CI, 3.3-4.05; P < .0005).

Risk for MI, stroke and all-cause death remained elevated out to 1,000 days follow-up among those hospitalized with COVID-19, even among those without CVD at the time of hospitalization (HR = 7.04; 95% CI, 6.25–7.92; P < .0005), according to the study.

“That's the most surprising, and important, finding. The increased risk was persistent for as long as follow-up is available with no sign of attenuation at all,” Hazen told Healio. “The heightened risk that we saw in the first year after infection was the same magnitude as the heightening of risk in between years 2 and 3 after the sentinel infection. Somehow, having COVID-19 rewires us to make us, long-term, more susceptible to CV event risk, at least for 3 years. For all we know, it could be indefinite.”

Compared with patients with CVD and no history of SARS-CoV-2 infection, individuals without CVD who were hospitalized with COVID-19 had an approximately 20% increased risk for major adverse cardiac events during follow-up (HR = 1.21; 95% CI, 1.08-1.37; P < .005).

“If someone was hospitalized for COVID-19, based on this data, their long term risk for a heart attack, stroke or dying is equivalent to a prior diagnosis of heart disease like a bypass surgery, heart attack or stroke,” Hazen said. “As a preventive cardiology physician, it makes me wonder whether or not we should be taking COVID-19 positivity into our risk assessment for CV risk reduction efforts. If you have a CAD risk equivalent, we lower the LDL goals and we are more aggressive with antiplatelet agents. All of the antiplatelet studies in primary prevention are pre-COVID-19 era endpoint trials … Should we look at a history of COVID-19, especially severe COVID-19, as a thing that changes the way that we do preventive CV risk assessment? These studies suggest we should.”

Blood type may have downstream benefit

To assess whether thrombosis risk after SARS-CoV-2 infection was affected via interaction with genetic susceptibility factors, Hazen and colleagues analyzed the ABO locus — patients’ blood type.

The researchers reported that COVID-19 hospitalization was associated with greater risk for MI and stroke in patients with non-O blood types (HR = 1.65; 95% CI, 1.29-2.09; P = .000048) compared with O blood type (HR = 0.96; 95% CI, 0.66-1.39; P = .82; P for interaction = .01).

“[We] saw the remarkable finding that your blood type is related to your downstream risk for developing heart disease post COVID-19 infection. We saw COVID-19 infection amongst the entire cohort was  linked to heightened long-term risk, but the risk was especially larger among the non-O genotypes,” Hazen told Healio. “That's all we know at this point. ABO blood type is a carbohydrate group on the surface of the red blood cell, but it's also a carbohydrate group on the surface of many other cells too. If I had to guess, the blood type is having its effect on something other than a red blood cell.”

The researchers wrote that thrombosis risk among patients hospitalized with COVID-19 differs as a function of ABO blood type, but identified no interactions with genetic determinants of COVID-19 severity, SARS-CoV-2 infection susceptibility or atherosclerotic CAD.

For more information:

Stanley Hazen, MD, PhD, can be reached at 9500 Euclid Ave., Mail Code NC-I O, Cleveland, OH 44195.

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