COVID-19 Infection Is Associated With High Rates of New-Onset Hypertension

CITATION:
Bloch MJ. COVID-19 infection is associated with high rates of new-onset hypertension. Consultant360. Published online October 19, 2023. 

Previous reports have suggested that mean blood pressure (BP) increased during the early years of the COVID-19 pandemic across the United States.¹ There have been many hypotheses regarding why–including weight gain, less healthy diet, reduced opportunities for exercise, psychosocial stress, and effects of social isolation. But there is also the intriguing possibility that COVID-19 infection itself may trigger increases in BP and even the development of new-onset hypertension.

To analyze the effect of acute COVID-19 infection on incident hypertension, Zhang and colleagues² performed a retrospective observational study examining records from a large academic health system, which includes 15 hospitals and many outpatient clinics, in a demographically diverse cross-section of New York City. The investigators identified positive cases of COVID-19 infection, both hospitalized and non-hospitalized, and then examined follow-up data for a new diagnosis of persistent hypertension 3 to 9 months after infection. Patients with a previous history of hypertension or who were taking anti-hypertensive medications at the time of their COVID-19 diagnosis were excluded as were patients who did not return for outpatient follow-up within the medical system.

The primary outcome, new onset persistent hypertension, was defined as any patient who met the following criteria at follow-up: systolic BP greater than 140 mmHg or greater than 90 mmHg diastolic, a new diagnosis code for hypertension, or prescribed antihypertensive medications. As a control group, the investigators did a similar analysis on a retrospective sample of patients diagnosed with acute influenza.

Overall, from March 1, 2020, to February 20, 2022, 45,398 people tested positive for COVID-19 infection; of those, 28,576 did not have a previous diagnosis of hypertension. In total, there were 5562 patients hospitalized, of which 1455 returned for a follow-up visit. Of the 23,014 patients who had COVID-19 infection but who were not hospitalized, 5565 returned for a follow-up visit. The incidence of new-onset hypertension was 20.6% among hospitalized and 10.9% among non-hospitalized patients with COVID-19. This incidence was significantly higher than the control group with influenza infection.

The incidence of new-onset hypertension remained relatively constant in patients who were hospitalized but decreased over time in those who were not, suggesting that perhaps disease severity may be a risk factor for the development of hypertension. Risk factors for the development of new-onset hypertension with COVID infection included age, Black race, baseline systolic BP, chronic kidney disease, chronic obstructive pulmonary disease, coronary artery disease, and corticosteroid administration, suggesting that COVID-19 infection likely accelerated the process of hypertension in patients who may have already been prone to increased BP. The incidence of new-onset hypertension appeared similar when the analysis was performed only on patients who had more than one visit during the ascertainment window, suggesting that the BP elevations were persistent.

This analysis is certainly subject to certain limitations. Most importantly, as a purely observational study, it can only identify association rather than causation. Important unidentified confounders may have impacted the results. Certainly, background prevalent hypertension may have been underdiagnosed in this patient population. And, since New York City was a major early epicenter of the COVID-19 pandemic, the results here may not be representative of the experience in other areas of the country. The comparison to those with influenza certainly mitigates (but does not completely resolve) many of these issues.

These limitations aside, the findings in Zhang and colleagues have important implications for our health care system. The prevalence of hypertension, and suboptimally controlled BP, have reached epidemic proportions in the United States. If the COVID-19 pandemic truly does accelerate the development of hypertension in at-risk individuals, we could be facing a new “wave” of hypertension diagnoses, burdening our delivery system which is already stretched too thin.

Of course, this study cannot elucidate the exact mechanism by which COVID-19 infection triggers incident hypertension, but the possibilities are intriguing. We know that the SARS-CoV-2 virus enters cells via the ACE2 receptor. As such, relatively severe COVID-19 infection may lead to long-term deleterious effects on the balance of the renin-angiotensin system.³ Relatively severe COVID-19 infection also leads to endothelial injury and inflammation and could have subtle effects on kidney structure and function. Finally, we are learning that many of the hemodynamic changes associated with long COVID syndrome may be mediated through dysregulation of the sympathetic nervous system, which could also have effects on BP.

In this analysis, most patients who developed incident hypertension already had risk factors for the condition. This report should highlight the importance of lifestyle modification and careful BP monitoring in patients with such risk factors, whether they have experienced known COVID-19 infection.  

References:

1. Laffin LJ, Kaufman HW, Chen Z, et al. Rise in blood pressure observed among US adults during the COVID-19 pandemic. Circulation. 2022;145:235-237
2. Zhang V, Fisher M, Hou W, Zhang, L, Duong T. Incidence of new-onset hypertension post-covid-19: comparison with influenza. Hypertension. 2023;80:2135-2148
3. Bloch MJ. Renin-angiotensin system blockade in COVID-19: Good, bad, or indifferent? J Am Coll Cardiol. 2020:76(3):277-279