Unmasking the Hidden Threat: COVID-19 and Its Impact on Blood Pressure


As the COVID-19 pandemic continues to disrupt lives worldwide, the focus has primarily been on the immediate health implications of the virus.

To date, over 770 million confirmed cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections and approximately 6.9 million deaths related to coronavirus disease 2019 (COVID-19) have been globally recorded [source].

The concern for global health security has been driven by both short-term and long-term severe complications of infection, including cardiovascular manifestations, respiratory failure, and post-intensive care syndrome.

However, recent research has unveiled a concerning and specific effect of SARS-CoV-2 on blood pressure (BP) during and after the acute phase of infection. This article delves into the implications and mechanisms behind this phenomenon, which carries significant clinical and public health importance.

Evidence of Elevated Blood Pressure in COVID-19 Patients

One of the earliest prospective studies reporting the impact of COVID-19 on blood pressure was conducted by a group of researchers. They evaluated BP changes among hospitalized patients with confirmed diagnosis of COVID-19 pneumonia and compared them to patients with bacterial pneumonia.

The study’s main clinical outcome was the development of persistent high blood pressure (defined as BP values ≥140 mmHg systolic or 90 mmHg diastolic for at least two consecutive days) requiring new or intensified anti-hypertensive treatment during hospitalization.

The results were striking: systolic and diastolic BP values recorded during the acute phase were significantly higher in COVID-19 patients compared to the bacterial pneumonia group. Moreover, a persistent increase in BP was detected in a substantial number of COVID-19 patients, far exceeding the bacterial pneumonia group.

Multivariable regression models confirmed that COVID-19 pneumonia was associated with a remarkable 7-fold higher risk of uncontrolled hypertension, even after adjusting for significant confounders [1].

These findings were substantiated by subsequent reports. A retrospective analysis of 153 confirmed COVID-19 patients showed that both systolic and diastolic BP were significantly higher in the post COVID-19 period than on admission, causing new-onset hypertension in 12% of patients.

Moreover, a large registry analysis revealed that 21.0% of hospitalized COVID-19 patients without a history of hypertension developed in-hospital hypertension [3].

Long-term consequences are also a concern. Data from health plans, administrative claims, and healthcare organizations have indicated an increased risk of new-onset hypertension in COVID-19 survivors for up to 12 months. A meta-analysis confirmed that new-onset hypertension represents a significant post-acute COVID-19 sequela, with recovered patients at a 1.70-fold higher risk of developing hypertension compared to controls [4].

Epidemiological Burden of New-Onset Hypertension

To further understand the epidemiological burden, a pooled analysis of four studies reporting incidence rates of new-onset hypertension among COVID-19 patients and controls was performed.

The results revealed that COVID-19 was associated with a 65% increased risk of new-onset hypertension compared to controls, with an incidence of 9% among COVID-19 patients and 5% among controls [3, 5, 6, 7].

Clinical Implications

The implications of COVID-19-induced hypertension are three-fold. First, acute elevations in blood pressure and uncontrolled in-hospital BP are significant predictors of organ damage and worse outcomes in COVID-19 patients. Hypertension is associated with more frequent admissions to intensive care units, worsening heart failure, and increased mortality in COVID-19 patients.

Second, new-onset hypertension is suspected to be a potential risk factor for long COVID and the occurrence of cardiovascular events after recovery from SARS-CoV-2 infection. Finally, new variants of SARS-CoV-2 share a common feature – mutations in the spike protein that promotes entry into viral cells via ACE2. This enhanced spike affinity for ACE2 of new variants may increase the risk of new-onset hypertension compared to the original Wuhan strain.

Mechanisms Underlying COVID-19-Induced Hypertension

The pathophysiological mechanisms linking COVID-19 with new-onset hypertension are not yet fully understood. However, the interaction between the spike proteins of SARS-CoV-2 and ACE2 receptors appears to be the most plausible explanation for the increase in blood pressure.

During infection, the contact between spike proteins and ACE2 receptors leads to ACE2 malfunction, predominantly due to spike occupancy and ACE2 down-regulation. This dysregulates the protective axis of the renin–angiotensin–aldosterone system (RAAS), leading to an increased generation and activity of Angiotensin II (Ang II) and reduced formation of Angiotensin1,7 (Ang1,7). This accumulation of Ang II promotes an increase in blood pressure [18, 19, 20, 21, 22].

A similar mechanism may be at play after recovery from COVID-19. Even after the acute phase of infection, viral RNA or viral fragments, in the form of spike proteins, can persist in various organs. This suggests the possibility of persistent circulating spike proteins interacting with ACE2 receptors, promoting ACE2 internalization and degradation, and leading to the accumulation of Ang II [24].


The data accumulated thus far underscore new-onset hypertension as one of the most prevalent cardiovascular sequelae of COVID-19. While the duration and appropriate treatment options for this condition remain to be explored, it is crucial to implement screening measures for individuals after their recovery from COVID-19.

Early identification of patients at increased risk of developing abnormal blood pressure levels and hypertension-related cardiovascular events is imperative. The research presented here opens a new chapter in our understanding of COVID-19 and its multifaceted impact on global health.

reference link: https://www.sciencedirect.com/science/article/pii/S0953620523003710


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