Coronavirus disease 2019 and cardiovascular complications: focused clinical review

Abstract

The coronavirus disease 2019 (COVID-19) may cause not only an acute respiratory distress syndrome (ARDS) but also multiple organ damage and failure requiring intensive care and leading to death. Male sex, advanced age, chronic lung disease, chronic kidney disease and cardiovascular disease, such as hypertension, diabetes and obesity have been identified as risk factors for the COVID-19 severity. Presumably, as these three cardiovascular risk factors are associated with a high prevalence of multiorgan damage. In the present focused clinical review, we will discuss the cardiovascular complications of COVID-19 including acute cardiovascular syndrome (acute cardiac injury/COVID cardiomyopathy, thromboembolic complications and arrhythmias) and post-COVID-19 sequelae. Preliminary data shows that the cause of acute cardiovascular syndrome may be multifactorial and involve direct viral invasion of the heart and vascular system, as well as through the immune and inflammation-mediated systemic cytokine storm. COVID-19 survivors may also show persistently elevated blood pressure and sinus tachycardia at rest. Furthermore, poor diabetic control, persistent renal damage and cerebral sequelae, such as persistent cognitive and neuropsychiatric alterations are also frequently reported. A particular attention should be paid towards cardiovascular protection in COVID-19 patients who develop acute cardiovascular syndromes during hospitalization, and/or permanent/semipermanent sequelae after recovery from COVID-19. These conditions may require careful clinical assessment, treatment and close follow-up to avoid short-term and long-term complications.

Characteristics of 24-hour Ambulatory Blood Pressure Monitoring in a COVID-19 Survivor

“…However, after the COVID-19 infection and discharge from hospital, he showed worsening of hypertension with a sustained elevated BP. This observation is in line with current attention to the possibility that COVID-19 may lead to permanent or semipermanent post-COVID sequelae [2]. A 24-hour ambulatory BP monitoring should be performed to evaluate patient's true hypertensive state in previously apparently normotensive patients and BP control in patients with known hypertension.…”

“…After recovery, COVID-19 leads to worsening of hypertension, poor diabetic control and renal damage [2]. Hypertension and obesity are together with male sex common comorbidities and risk factors for unfavorable outcome in patients with COVID-19.…”

“…Shortly after its outbreak, reports suggested that male sex and advanced age increased the risk of severe infection and mortality [1]. Furthermore, hypertension (although not adjusted for age and other unmeasured confounders), diabetes, obesity and cardiovascular disease were reported as the most common comorbid conditions among patients with COVID-19 infection with significant increased mortality [1][2][3]. COVID-19 infection primarily affects the lungs and cause severe pneumonia complicated by acute respiratory distress syndrome (ARDS), respiratory failure and shock requiring intensive care with ventilator support, as well as vasopressors and renal replacement therapy [4].…”

Arterial stiffness and COVID‐19: A bidirectional cause‐effect relationship

“…Resistance to the virus may be further reduced by the pathogenetic nature of some of these organ alterations, that is, by the fact the most common cause of risk factor-dependent complications, atherosclerosis, is likely to be codetermined by an inflammatory process that may adversely interact with that of the coronavirus. 1 As far as obesity, a major component of the metabolic syndrome, is concerned, its relationship with the COVID-19 severity may be due to its association with chronic low grade inflammation, higher leptin and lower adiponectin levels, immune response dysregulation, and abnormal pro-inflammatory cytokine production. 2 The association between increased arterial stiffness and the severity and duration of chronic inflammation in a number of systemic inflammatory diseases are well established.…”

Antithrombotic therapy in COVID-19

“…In details, endothelial dysfunction, subintimal inflammation, hemorrhage, edema, dysregulation of vascular tone, as well as disseminated intravascular coagulopathy (DIC), sepsis induced coagulopathy (SIC), increased D-dimer/FDP (fibrin degradation factors) are all possible contributing factors to vascular thrombosis both on arterial and venous side. [1][2][3][4] However, optimal antithrombotic treatment has so far not been established, and the results from Commentary Antithrombotic therapy in COVID-19 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.…”