Increased BP common after nonsevere COVID-19

Blood pressure (BP) tends to rise following a mild or moderate SARS-CoV-2 infection, indicating a potential hypertensive consequence, reveals a study.

This finding “suggests a hypertensive sequela, which might contribute to adverse cardiovascular events after COVID-19 and constitute a potential therapeutic target,” the investigators said.

In this cross-sectional study, BP profiles of individuals who had nonsevere COVID-19 were compared with a matched population-based cohort without prior COVID-19. The investigators obtained data from the ongoing and prospective Hamburg City Health Study, which included participants at least 4 months after COVID-19 infection. Matching was based on age, sex, education, and pre-existing hypertension.

A total of 432 individuals who had SARS-CoV-2 infection (mean age 56.1 percent) were matched to 1,728 controls without prior COVID-19 (mean age 56.2 years). Of the COVID-19 cases, 92.8 percent were mild or moderate in severity, 7.2 percent were hospitalized, and none were treated in an intensive care unit. [J Hypertens 2023;41:1721-1729]

Diastolic (D)BP remained significantly higher in individuals after COVID-19 (4.7 mm Hg, 95 precent confidence interval [CI], 3.97‒5.7; p<0.001) even after adjustment for relevant competing risk factors. An increasing trend was also noted for systolic (S)BP (1.4 mm Hg, 95 percent CI, ‒0.4 to 3.2; p=0.120).

A significantly higher occurrence of hypertensive BP (at least 130/80 mm Hg according to the ACC/AHA guideline and at least 140/90 based on the ESC/ESH guideline) was observed among individuals who had COVID-19 (odds ratio [OR], 2.0, 9 5percent CI, 1.5‒2.7; p<0.001) than among matched controls (OR, 1.6, 95 percent CI, 1.3‒2.0; p<0.001), driven primarily by DBP changes.

“[T]his study found significantly higher BPs in individuals after nonsevere COVID-19 as compared to matched controls with predominant differences in DBP,” the investigators said.

Potential mechanisms of increased BP following a mild or moderate SARS-CoV-2 infection remain in doubt, but more and more evidence suggests that hypertension is not only mediated by a direct increase in hydrostatic pressure but that inflammation affects the pathophysiology and contributes to the harmful consequences of COVID-19, according to the investigators.

“Cells of the innate immune system, including monocyte, macrophages, and dendritic cells, can promote BP elevation via effects mostly on kidney and vascular function,” they said.

In addition, previous studies found that T and B cells from the adaptive immune system play a role in hypertension and hypertensive end-organ damage. Thus, inflammation due to COVID-19 could result in a hypertensive sequela. [Cell Mol Immunol 2022;19:561-576; Cell Tissue Res 2021;385:393-404]

“SARS-CoV-2 mediated inflammatory effects on the microcirculation and activation of endothelial cells could contribute to such linkage between SARS-CoV-2 and subsequent hypertension,” the investigators said. [Circulation 2020;142:1609-1611; Lancet 2020;395:1417-1418; Angiogenesis 202226:53-61]

“Future studies are needed to clarify the cause and the relevance of this SARS-CoV-2 BP axis for the observed cardiovascular outcomes after COVID-19 and identify possible treatment options including hypertensive surveillance and control,” they said.