Abstract
Cardiovascular disease causes almost one third of deaths worldwide, and more than half are related to primary arterial hypertension (PAH). The occurrence of several deleterious events, such as hyperactivation of the renin–angiotensin system (RAS), and oxidative and inflammatory stress, contributes to the development of small vessel disease in PAH. Small resistance arteries are found at various points through the arterial tree, act as the major site of vascular resistance, and actively regulate local tissue perfusion. Experimental and clinical studies demonstrate that alterations in small resistance artery properties are important features of PAH pathophysiology. Diseased small vessels in PAH show decreased lumens, thicker walls, endothelial dysfunction, and oxidative stress and inflammation. These events may lead to altered blood flow supply to tissues and organs, and can increase the risk of thrombosis. Notably, PAH is prevalent among patients diagnosed with COVID-19, in whom evidence of small vessel disease leading to cardiovascular pathology is reported. The SARS-Cov2 virus, responsible for COVID-19, achieves cell entry through an S (spike) high-affinity protein binding to the catalytic domain of the angiotensin-converting enzyme 2 (ACE2), a negative regulator of the RAS pathway. Therefore, it is crucial to examine the relationship between small resistance artery disease, ACE2, and PAH, to understand COVID-19 morbidity and mortality. The scope of the present review is to briefly summarize available knowledge on the role of small resistance artery disease and ACE2 in PAH, and critically discuss their clinical relevance in the context of cardiovascular pathology associated to COVID-19.
Highlights
Hypertension remains the leading cause of death globally, accounting for 10.4 million deaths worldwide every year [1]
The objective of this review is to briefly summarize available knowledge on the role of small resistance artery disease in primary arterial hypertension (PAH) and the contribution of the angiotensin-converting enzyme 2 (ACE2) pathway, and critically discuss their clinical relevance in the context of cardiovascular pathology associated to COVID-19
Few works have been focused on describing the anomalies and potential underlying mechanisms of small resistance artery disease in COVID-19 (Figure 1)
Summary
Hypertension remains the leading cause of death globally, accounting for 10.4 million deaths worldwide every year [1]. Diseased small vessels in PAH show decreased lumens, thicker walls, endothelial dysfunction, and increased oxidative stress and inflammation, events that may lead to altered blood flow supply to tissues and organs, and increase the risk of thrombosis. PAH is prevalent among patients diagnosed with coronavirus disease 2019 (COVID-19), in whom rapid disease progression has been reported. It is still not clear if raised blood pressure is a risk factor for increase COVID-19 lethality [3, 4]. Given the importance of small resistance artery disease and ACE2 in PAH, it is crucial to examine their relationship with SARS-CoV-2-induced endothelial cell injury [5] to understand COVID-19 morbidity and mortality
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