The Impact of COVID-19 on Arterial Stiffness and Cardiovascular Complications


The COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has had profound global consequences since its emergence. By June 2023, there were over 765 million confirmed cases and nearly 7 million reported deaths [1,2].

Initially considered primarily a respiratory illness, research has revealed that COVID-19 is a complex multisystemic disease associated with long-term complications and a close link to cardiovascular (CV) issues [3,4].

This article delves into the significant relationship between COVID-19 and cardiovascular complications, including the impact on arterial stiffness and the emergence of long COVID-19.

The Link Between COVID-19 and Cardiovascular Complications

Patients with pre-existing cardiovascular conditions are at a higher risk of experiencing unfavorable outcomes when infected with COVID-19 [5]. Moreover, the virus itself can directly or indirectly contribute to significant CV complications [5]. Even after recovering from the acute phase of the infection, these complications may persist [6,7].

The duration of COVID-19 symptoms has been suggested to influence vascular function, and the emergence of long COVID-19, affecting at least 76 million people worldwide, presents ongoing CV concerns [8].

COVID-19’s CV manifestations encompass arrhythmias, asymptomatic myocardial damage, congestive heart failure, and thromboembolic events [5,11,12]. These conditions result from the virus’s cytotoxic effects and the subsequent systemic inflammatory cytokine storm. Notably, endothelial dysfunction is a critical mediator of COVID-19’s pathophysiologic pathways [13].

Endothelial cells, which play a pivotal role in vascular health, have angiotensin-converting enzyme 2 cellular receptors (ACE2-R) and the transmembrane serine protease 2 (TMPRSS2), enabling SARS-CoV-2 entry into host cells. Infected endothelial cells elevate cytokine production, leading to inflammation and thrombosis [14]. The resulting vasculitis affects various body parts, contributing to multiorgan failure in some COVID-19 patients [15].

There is evidence suggesting that COVID-19 accelerates macrovascular vascular aging. Mechanisms contributing to cellular senescence and vascular stiffness include mitochondrial dysfunction, local reactive oxygen species (ROS) formation, and oxidative telomere shortening [17]. The breakdown of elastin fibers in arterial walls and their replacement with fibrous tissue may result in arterial stiffness, which might persist as a long-term CV consequence, irrespective of the initial infection’s severity [15,18]. Notably, vascular changes, particularly endothelial dysfunction and arterial stiffness, can endure long after the COVID-19 infection has resolved [19].

Arterial Stiffness as an Indicator of Cardiovascular Health

Arterial stiffness serves as a reliable indicator of vascular system age and overall CV health. It is a composite biomarker that assesses the cumulative impact of genetic and environmental factors on arteries, as well as the influence of established CV risk factors [20]. Numerous studies have established strong correlations between arterial stiffness, as measured by pulse wave velocity (PWV), and the increased risk of CV disease, independently of traditional risk variables [21,22,23]. Several tests, including the augmentation index (Aix), the cardio-ankle vascular index (CAVI), the arterial stiffness index (ASI), Young’s modulus of elasticity, and pulse pressure (PP), help confirm arterial stiffness in COVID-19 patients [24,25,26,27].

Pulse wave velocity (PWV), particularly carotid-femoral pulse wave velocity (cfPWV), is vital in assessing vascular age and may correlate more strongly with the onset of CV disease than chronological age [28]. CfPWV, being noninvasive and reproducible, is now regarded as the gold standard for assessing arterial stiffness. The progressive stiffening of arteries negatively affects arterial-ventricular interactions, limiting the vessel’s ability to adapt to blood pressure changes, potentially leading to heart failure. CfPWV holds high prognostic value, helping to identify individuals at a higher risk not only for future CV events but also for all-cause mortality [19,29].

Research Objectives

This research aims to investigate the impact of COVID-19 on carotid-femoral pulse wave velocity (cfPWV) as a measure of arterial stiffness and its potential contribution to subsequent cardiovascular complications. Understanding the long-term consequences of COVID-19 on arterial health and cardiovascular outcomes is essential for effective patient management and healthcare strategies in the post-pandemic era.


The meta-analysis conducted in this study has shed light on the significant correlation between COVID-19 infection and an increase in carotid-femoral pulse wave velocity (cfPWV) in a majority of the analyzed studies. The observed rise in arterial stiffness, a well-recognized marker of cardiovascular (CV) risk, suggests that COVID-19 may have a profound impact on vascular health. Nevertheless, it’s important to note the contrasting findings of Van der Sluijs et al., who did not observe such a correlation, and Skow et al., who found a positive but statistically insignificant correlation [38,39]. These variations may be attributed to differences in study populations, the timing of assessments, or other factors.

Arterial stiffness, as measured by cfPWV, reflects alterations in blood pressure, blood flow, and vascular diameter, serving as an indicator of both mechanical and functional properties of arterial walls. The degradation of elastic fibers is a primary factor influencing arterial stiffness, but other factors, including fibrosis, collagen, elastin cross-linking, and medial calcifications, also contribute to this phenomenon.

Several studies have highlighted the multifactorial nature of arterial stiffness, encompassing factors such as endothelial dysfunction, inflammation, oxidative stress, extracellular matrix turnover, and the regulation of smooth muscle tone in muscular arteries [40,44]. SARS-CoV-2 targets endothelial cells by binding to ACE2 receptors, leading to endothelial dysfunction.

This dysfunction is further exacerbated by systemic inflammatory responses and cytokine storms, which activate platelets and release leukocytes into circulation. Uncontrolled inflammation may directly stimulate arterial remodeling and impair vascular responsiveness.

Nitric oxide (NO) deficiency in COVID-19 patients can worsen endothelial dysfunction, further contributing to increased arterial stiffness and oxidative stress. These changes in NO bioavailability, combined with direct actions of SARS-CoV-2 on endothelial cells, can result in structural alterations in the vascular wall’s extracellular matrix, promoting arterial stiffness.

The increase in arterial stiffness observed in COVID-19 patients raises the risk of CV complications, including high blood pressure, heart attacks, and strokes, particularly in individuals with pre-existing CV conditions. Faria et al. demonstrated that COVID-19 patients experienced over-activation of the sympathetic nervous system, vascular dysfunction, and elevated cfPWV values.

Importantly, pulse wave velocity (PWV) has been established as a strong predictor of future CV events and all-cause mortality, with its predictive power being higher in subjects with a higher baseline CV risk. This indicates that the increased arterial stiffness contributes to the elevated CV risk observed in COVID-19 survivors. Elevated risks of stroke are attributed to both COVID-19 and increased arterial stiffness.

Long COVID-19, characterized by persistent symptoms, presents an additional concern. Nandadev et al. noted heightened arterial pressure and cfPWV values in long COVID-19 patients, suggesting they may be at an increased risk of CV problems. The correlation between COVID-19 infection and CV complications appears complex, with cardioembolic and cryptogenic etiologies being identified in CV diseases among COVID-19 patients. Risk factors such as atrial fibrillation, coronary artery disease, diabetes, and hypertension are prevalent in COVID-19-positive individuals, further increasing the risk of CV complications.

Importantly, Ratchford et al. demonstrated a strong association between increased cfPWV and mortality among COVID-19 patients, particularly those with pre-existing chronic conditions. Additionally, Schnaubelt et al. found that cfPWV among COVID-19 survivors was significantly lower than in healthy patients, potentially indicating a link to long-term complications. Kumar et al. also showed increased cfPWV in severe COVID-19 cases, suggesting a correlation between COVID-19 severity and arterial stiffness.

Research also highlights the role of pre-existing conditions in accelerating arterial aging in the context of COVID-19. Tudoran et al. demonstrated a correlation between aortic and arterial stiffness and diastolic dysfunction in seemingly healthy individuals with post-acute COVID-19 syndrome. Oikonomou et al. found that while some improvement was observed, values remained worse than in the control group, indicating a persistent increase in arterial stiffness post-COVID-19. Iconomidis and their team similarly found higher cfPWV values in COVID-19 survivors at the 12-month follow-up evaluation.

Addressing post-COVID complications, including chronic arterial stiffness, is essential. While arterial stiffness is not easily reversible with medication or surgical interventions, comprehensive rehabilitation strategies, including exercise, physiotherapy, lifestyle changes, and cardiovascular rehabilitation, could mitigate the long-term consequences of arterial stiffness and improve patient outcomes.

It’s important to consider that the impact of COVID-19 may vary depending on the virus’s mutation. Skow et al.’s research during the Omicron wave did not find significant differences in arterial stiffness between individuals with the Omicron variant and controls. However, this research pertained specifically to the Omicron variant, and the correlation between other COVID-19 types and arterial stiffness remains inconclusive.

In conclusion, the research indicates a strong association between COVID-19 infection and increased arterial stiffness, suggesting a potential link between the virus and elevated CV risk. Early identification of individuals with augmented arterial stiffness can facilitate targeted interventions to reduce the CV risks associated with COVID-19. Timely medical and rehabilitation interventions can help improve patient outcomes. Future research should provide further insights into the connection between COVID-19 infection, arterial stiffness, and subsequent CV events, making cfPWV measurements a valuable diagnostic and prognostic tool.

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