
What Pharmacists Should Know About COVID-19's Cardiovascular Toll
Key Takeaways
- Acute COVID-19 substantially increases risk of MI, stroke, arrhythmias, myocarditis, heart failure, and thromboembolism, with severe cases approximating the cardiovascular risk magnitude of established coronary disease.
- Underlying hypertension, diabetes, obesity, and preexisting CVD heighten post-infectious vascular susceptibility, while age-related endothelial dysfunction and reduced arterial elasticity further compound adverse cardiovascular outcomes.
Learn how COVID-19 drives heart and vascular risks, why vaccines and antivirals help, and how pharmacists manage dangerous drug interactions.
COVID-19, the virus caused by SARS-CoV-2, is now recognized as a disease with profound cardiovascular consequences, both in the acute phase and in the persistent condition known as long COVID, rather than just a respiratory illness. Researchers outlined what is known about COVID-19's vascular effects and how best to prevent them in a new review published in the BMJ.1
"In many respects, COVID-19 is a vascular disease masquerading as a respiratory one," Andy Benest, PhD, a vascular biologist at the University of Nottingham, said in the review.1
Understanding Acute Cardiovascular Complications
The cardiovascular burden of acute COVID-19 infection has been well documented, as previous studies have found that acute cardiac injury has occurred in 6% to 25% of hospitalized patients. One large study using UK Biobank data found that early variants of SARS-CoV-2 doubled the risk of cardiovascular events overall. For patients with severe infections requiring hospitalization, the risk of myocardial infarction and stroke was 4 times that of uninfected controls, which is a magnitude equivalent to having preexisting coronary artery disease.1
A 2022 analysis of nearly 154,000 United States veterans similarly found that COVID-19 survivors faced elevated risks of dysrhythmias, ischemic heart disease, heart failure, myocarditis, pericarditis, and thromboembolic disease compared with more than 5 million controls. The analysis also found that even mild infections conferred measurable additional risk.1
Notably, patients with hypertension, diabetes, obesity, and preexisting cardiovascular disease (CVD) face the greatest risk. As Benest explained in the review, these underlying cardiometabolic conditions magnify post-COVID vascular vulnerability, while age compounds that risk through accumulated endothelial dysfunction and reduced vascular elasticity.1
Long COVID and the Heart
Cardiovascular symptoms rank as the third most frequent category of long COVID complaints, after neurological-neuropsychiatric and pulmonary manifestations. Postural orthostatic tachycardia syndrome (POTS) and other forms of dysautonomia have emerged as particularly notable features of the condition, alongside chest pain, palpitations, dyspnea, and syncope.1
A 2025 systematic review and meta-analysis published in Nature Communications found that individuals who received COVID-19 vaccination had a significantly lower risk of developing long COVID compared with unvaccinated individuals during the phase of the Omicron variant, with booster doses conferring additional protection. The same analysis noted that influenza vaccination and cardiovascular preventive treatments were associated with reduced risk of hospitalization due to long COVID, underscoring the additive benefit of comprehensive preventive care in this population.2
Navigating Cardiovascular Drug Interactions With Antiviral Therapy
Among the pharmacological tools available to reduce the cardiovascular sequelae of COVID-19, antiviral therapy, particularly nirmatrelvir/ritonavir (Paxlovid; Pfizer), has shown real-world benefit. A target trial emulation study published in Nature Communications found that nirmatrelvir/ritonavir was associated with significantly lower 1-year risks of cardiovascular mortality, major adverse cardiac events, and cerebrovascular complications among hospitalized patients with COVID-19. The same study found that molnupiravir (Lagevrio; Merck and Co., Ridgeback Biotherapeutics) did not confer the same degree of cardiovascular protection, reinforcing nirmatrelvir/ritonavir as the preferred antiviral for high-risk patients.3
However, prescribing nirmatrelvir/ritonavir in patients with CVD presents a significant pharmacist challenge. Because ritonavir is a potent CYP3A4 inhibitor and P-glycoprotein inhibitor, it carries substantial drug-drug interaction (DDI) potential with many common cardiovascular medications, including statins, direct oral anticoagulants, antiarrhythmics, and antiplatelet agents. A review in European Cardiology Review emphasizes that careful medication reconciliation, including all prescription medications, OTC drugs, and herbal supplements, is essential before dispensing.4
The FDA has authorized pharmacists to prescribe nirmatrelvir/ritonavir directly under certain conditions, provided patients bring recent health records, including kidney and liver function results and a comprehensive medication list, to enable pharmacist screening for DDIs and eligibility assessment. This expanded scope places pharmacists at the center of COVID-19 antiviral stewardship for the very patients, such as those with existing CVD, who have the most to gain from early treatment and the most to lose from drug interactions.5
Vaccination is Still the Most Powerful Preventive Tool
Both the BMJ review and supporting research make clear that vaccination remains the single most effective strategy for reducing COVID-19's cardiovascular burden. Pharmacists, who administer the majority of COVID-19 vaccinations in community settings, are uniquely positioned to counsel high-risk patients, particularly those with hypertension, diabetes, and established CVD, on the importance of staying current with both COVID-19 and influenza vaccinations as part of an integrated cardiovascular risk reduction strategy.


































































































































