New research indicates that among patients with hypertension, COVID-19 contributes to an increased risk of poorer cardiovascular (CV) outcomes.
In a large retrospective cohort of adults with hypertension and no prior CV events, those with hospitalized COVID-19 had between 1.4- and 2.5-fold higher risks of first-time myocardial infarction (MI) (adjusted hazard ratio [aHR], 1.40, 95 percent confidence interval [CI], 1.21–1.63), heart failure (HF) (aHR, 1.59, 95 percent CI, 1.45–1.75), stroke (aHR, 1.35, 95 percent CI, 1.17–1.57), major adverse CV events (MACE) (aHR, 1.65, 95 percent CI, 1.54–1.77), and all-cause mortality (aHR, 2.51, 95 percent CI, 2.17–2.90) compared with those who were COVID-negative. [J Hum Hypertens 2026;doi:10.1038/s41371-026-01147-4]
Patients with nonhospitalized COVID-19 also had elevated risks of HF (aHR, 1.17, 95 percent CI, 1.06–1.30) and MACE (aHR, 1.14, 95 percent CI, 1.05–1.23) compared with COVID-negative patients, suggesting that “even mild or asymptomatic SARS-CoV-2 infections may carry lasting adverse CV consequences,” the investigators noted.
In an analysis stratified by hypertension stage based on average systolic and diastolic measurements in the year prior to index, the association between hospitalized COVID-19 and first-time MACE was more pronounced among patients with elevated BP (aHR, 2.26, 95 percent CI, 1.80–2.84) and stage 1 hypertension (aHR, 2.48, 95 percent CI, 2.04–3.02) than among those with normal BP (aHR, 1.71, 95 percent CI, 1.39–2.21).
Abnormal levels of C-reactive protein (≥1.1 mg/dL), creatinine (≥1.1 mg/dL), lactate dehydrogenase (≥400 U/L), D-dimer (≥1.5 µg/mL), and haemoglobin (≤9.2 g/dL), as well as a high neutrophil-to-lymphocyte ratio (≥10) during acute COVID-19 infection were predictive of the future risk of MACE among hospitalized COVID-19 patients.
Why patients with hypertension are vulnerable to post-COVID cardiovascular complications may be explained by the patients’ elevated baseline risk profiles and unique pathophysiological features that may be worsened by COVID-19 illness, according to the investigators.
“SARS-CoV-2 virions bind to angiotensin-converting enzyme 2 receptors and this leads to buildup of angiotensin II, resulting in vasoconstriction and potential exacerbation of high BP [in] hypertensive patients, [who already] have a dysregulated renin-angiotensin-aldosterone system,” the investigators explained.
“COVID-19 may also induce systemic inflammation, endothelial dysfunction, hypoxia, and coagulopathy, which in the context of hypertension can exacerbate already elevated thrombotic and cardiovascular risk,” they added.
The findings from this study have important public health implications, given the high global burden of hypertension and the widespread impact of COVID-19, according to the investigators.
They highlighted the need for long-term cardiovascular monitoring not only in hypertensive patients with high-risk or hospitalized COVID-19 but also in those with milder COVID-19 presentations.
The study included 75,153 hypertensive patients, among whom 22,147 were COVID-positive and 53,006 were COVID-negative. Mean age at index date was 55.36 and 54.68 years in the respective groups, around 63 percent were female, and 35 percent were Black. Mean BP level was 133/79 and 134/80 mm Hg, and 60.33 percent and 55.72 percent of the patients were using BP-lowering medications, respectively. The most common pre-existing comorbidities were obesity, diabetes, and asthma.
Outcome events were recorded in the electronic health record (EHR) >30 days to up to 4.5 years after index date. Mean follow-up was 24.53 and 27.33 months.
The analyses were adjusted for demographics, comorbidities, socioeconomic status, and COVID-19 vaccination.
The investigators acknowledged several limitations to the study, including its reliance on the accuracy of the EHR in the Montefiore Health System and the inability to examine the associations of various acute COVID-19 treatments with outcomes, among others.