"When," "Where," and "How" of SARS-CoV-2 Infection Affects the Human Cardiovascular System: A Narrative Review.

Coronavirus disease 2019 (COVID-19) is caused by the novel severe acute respiratory coronavirus-2 (SARS-CoV-2). Several explanations for the development of cardiovascular complications during and after acute COVID-19 infection have been hypothesized. The COVID-19 pandemic, caused by SARS-CoV-2, has emerged as one of the deadliest pandemics in modern history. The myocardial injury in COVID-19 patients has been associated with coronary spasm, microthrombi formation, plaque rupture, hypoxic injury, or cytokine storm, which have the same pathophysiology as the three clinical variants of Kounis syndrome. The angiotensin-converting enzyme 2 (ACE2), reninaldosterone system (RAAS), and kinin-kallikrein system are the main proposed mechanisms contributing to cardiovascular complications with the COVID-19 infection. ACE receptors can be found in the heart, blood vessels, endothelium, lungs, intestines, testes, neurons, and other human body parts. SARS-CoV-2 directly invades the endothelial cells with ACE2 receptors and constitutes the main pathway through which the virus enters the endothelial cells. This causes angiotensin II accumulation downregulation of the ACE2 receptors, resulting in prothrombotic effects, such as hemostatic imbalance via activation of the coagulation cascade, impaired fibrinolysis, thrombin generation, vasoconstriction, endothelial and platelet activation, and pro-inflammatory cytokine release. The KKS system typically causes vasodilation and regulates tissue repair, inflammation, cell proliferation, and platelet aggregation, but SARS-CoV-2 infection impairs such counterbalancing effects. This cascade results in cardiac arrhythmias, cardiac arrest, cardiomyopathy, cytokine storm, heart failure, ischemic myocardial injuries, microvascular disease, Kounis syndrome, prolonged COVID, myocardial fibrosis, myocarditis, new-onset hypertension, pericarditis, postural orthostatic tachycardia syndrome, pulmonary hypertension, stroke, Takotsubo syndrome, venous thromboembolism, and thrombocytopenia. In this narrative review, we describe and elucidate when, where, and how COVID-19 affects the human cardiovascular system in various parts of the human body that are vulnerable in every patient category, including children and athletes.

Nighttime Home Blood Pressure in Children: Association with Ambulatory Blood Pressure and Preclinical Organ Damage.

[Figure: see text].

Twenty-four-hour ambulatory central blood pressure in adolescents and young adults: association with peripheral blood pressure and preclinical organ damage.

OBJECTIVES: To investigate the relationship of 24-h ambulatory central blood pressure (ABP) with preclinical organ damage in youth. METHODS: Individuals aged 10-25 years referred for suspected hypertension and healthy volunteers had simultaneous 24-h peripheral and central ABP monitoring (Mobil-O-Graph 24 h PWA). Central BP was calculated using two different calibration methods (c1 using oscillometric systolic/diastolic ABP; c2 using mean arterial/diastolic ABP). Their association with preclinical organ damage [left ventricular mass index (LVMI), carotid intima-media thickness (IMT), 24-h pulse wave velocity (PWV)] was investigated. RESULTS: A total of 136 participants were analyzed (age 17.9 ±â€Š4.7 years, 54% adolescents, 77% males, 34% with elevated ABP). Twenty-four-hour peripheral systolic ABP (pSBP) was higher than c1 systolic ABP (c1SBP) by 14.1 ±â€Š3.7 mmHg, but lower than c2SBP by 6.5 ±â€Š7.6 mmHg (all P < 0.01). c2SBP quartiles provided better stratification of preclinical organ damage than pSBP. Both c1SBP/c2SBP were significantly associated with LVMI (r = 0.35/0.33) and IMT (r = 0.23/0.42; all P < 0.01; primary endpoint). These associations were stronger for c2SBP compared with those of pSBP in adolescents but not in adults. PWV was more closely associated with pSBP than c2SBP (r = 0.94/0.83, P < 0.01). LVMI variation was best determined by c2SBP in adolescents and pSBP in adults; IMT by c2SBP and PWV by pSBP in both subgroups. CONCLUSION: These findings suggest that in young individuals, the calibration method for 24-h central ABP plays a major role in determining its association with preclinical organ damage. In adolescents, 24-h central ABP appears to be more strongly associated with early cardiac and carotid damage than peripheral BP.

Home and ambulatory blood pressure monitoring in children, adolescents and young adults: comparison, diagnostic agreement and association with preclinical organ damage.

OBJECTIVES: To compare the association of home (HBP), ambulatory (ABP) and office blood pressure (OBP) measurements with preclinical organ damage in young individuals. METHODS: Individuals referred for elevated blood pressure and healthy volunteers aged 6-25 years were evaluated with OBP (2-3 visits), 7-day HBP and 24-h ABP monitoring. Organ damage was assessed by echocardiographic left ventricular mass index (LVMI), carotid ultrasonography [intima--media thickness (IMT)] and pulse wave velocity (PWV) using piezo-electronic or oscillometric technique. RESULTS: Analysis included 251 individuals (mean age 14 ±â€Š3.9 years, 70.9% men: 31.1% children, 54.6% adolescents, 14.3% young adults) of whom 189 had LVMI, 123 IMT and 198 PWV measurements. Office, ambulatory and home hypertension was diagnosed in 29.5, 27.1 and 26.3% of participants. The agreement of OBP with ABP was 74.5% (kappa 0.37) and HBP 76.1% (kappa 0.41), with closer agreement between HBP and ABP (84.9%, kappa 0.61). LVMI gave comparable correlations with systolic OBP, 24-h ABP and HBP (r = 0.31/0.31/0.30, all P < 0.01). The same was the case for IMT (0.33/0.32/0.37, all P < 0.01) and piezo-electronic PWV (0.55/0.53/0.52, all P < 0.01), whereas oscillometric PWV gave stronger correlations with OBP than ABP or HBP. In linear regression analysis, the variation of LVMI was determined by night-time ABP, of IMT by HBP and of PWV by OBP and 24-h ABP. CONCLUSION: These data suggest that in young individuals, target organ damage is mainly determined by out-of-office rather than office BP. Home and ambulatory BP give comparable associations with preclinical organ damage.

Cardiovascular involvement in pediatric systemic autoimmune diseases: the emerging role of noninvasive cardiovascular imaging.

Cardiac involvement in pediatric systemic autoimmune diseases has a wide spectrum of presentation ranging from asymptomatic to severe clinically overt involvement. Coronary artery disease, pericardial, myocardial, valvular and rythm disturbances are the most common causes of heart lesion in pediatric systemic autoimmune diseases and cannot be explained only by the traditional cardiovascular risk factors. Therefore, chronic inflammation has been considered as an additive causative factor of cardiac disease in these patients. Rheumatic fever, juvenile idiopathic arthritis, systemic lupus erythematosus, ankylosing spondylitis/spondyloarthritides, juvenile scleroderma, juvenile dermatomyositis/polymyositis, Kawasaki disease and other autoimmune vasculitides are the commonest pediatric systemic autoimmune diseases with heart involvement. Noninvasive cardiovascular imaging is an absolutely necessary adjunct to the clinical evaluation of these patients. Echocardiography is the cornerstone of this assessment, due to excellent acoustic window in children, lack of radiation, low cost and high availability. However, it can not detect disease acuity and pathophysiologic background of cardiac lesions. Recently, the development of cardiovascular magnetic resonance imaging holds the promise for early detection of subclinical heart disease and detailed serial evaluation of myocardium (function, inflammation, stress perfusion-fibrosis) and coronary arteries (assessment of ectasia and aneurysms).