Cardiovascular complications of severe acute respiratory syndrome

Abstract

Background and Aims: Severe acute respiratory syndrome (SARS) is a virulent viral infection that affects a number of organs and systems. This study examined if SARS may result in cardiovascular complications. Methods and Results: 121 patients (37.5 (SD13.2) years, 36% male) diagnosed to have SARS were assessed continuously for blood pressure, pulse, and temperature during their stay in hopsital. Hypotension occurred in 61 (50.4%) patients in hospital, and was found in 28.1%, 21.5%, and 14.8% of patients during the first, second, and third week, respectively. Only one patient who had transient echocardiographic evidence of impaired left ventricular systolic function required temporary inotropic support. Tachycardia was present in 87 (71.9%) patients, and was found in 62.8%, 45.4%, and 35.5% of patients from the first to third week. It occurred independent of hypotension, and could not be explained by the presence of fever. Tachycardia was also present in 38.8% of patients at follow up. Bradycardia only occurred in 18 (14.9%) patients as a transient event. Reversible cardiomegaly was reported in 13 (10.7%) patients, but without clinical evidence of heart failure. Transient atrial fibrillation was present in one patient. Corticosteroid therapy was weakly associated with tachycardia during the second (x 2 = 3.99, p = 0.046) and third week (x 2 = 6.53, p = 0.01), although it could not explain tachycardia during follow up. Conclusions: In patients with SARS, cardiovascular complications including hypotension and tachycardia were common but usually self limiting. Bradycardia and cardiomegaly were less common, while cardiac arrhythmia was rare. However, only tachycardia persisted even when corticosteroid therapy was withdrawn.

Pathophysiological characteristics and therapeutic approaches for pulmonary injury and cardiovascular complications of coronavirus disease 2019

“…Previous studies have confirmed that the immune abnormality is related to the pathogenesis of SARS-CoV infection 45 .…”

“…ACE2-dependent manner 45 . The trimers of the SARS-CoV spike protein initially extends into a hydrophobic pocket of ACE2 catalytic domain 46 , which consequentially leads to the endocytosis of SARS-CoV particles and fusion of virus to cardiomyocytes with the help of type II transmembrane serine proteases (TMPRSS2) 47 , finally downregulating ACE2 expression in cardiomyocytes 48,49 .…”

Angiotensin receptor blockers as tentative SARS‐CoV‐2 therapeutics

“…Losartan, telmisartan, olmesartan (and additional AT1R antagonists) are widely applied in the clinic since the 1990s for control of hypertension and kidney disorders, and are known as safe drugs that are rarely implicated in adverse drugs events (Deppe, Böger, Weiss, & Benndorf, 2010;McIntyre, Caffe, Michalak, & Reid, 1997). However, it should be noted that around half of SARS-CoV patients developed hypotension during their hospitalization (Yu et al, 2006). At time of writing this commentary, no comprehensive information is available on hypotension rates among hospitalized SARS-CoV-2 patients; it is thus premature to estimate what percentage of SARS patients of the currently ongoing epidemic can be safely treated with AT1R blockers without risking exacerbated hypotension.…”

Severe Acute Respiratory Syndrome (SARS)

“…Transient atrial fibrillation was seen in 1 patient. 95 ARF ARF occurred in 17% of patients admitted with probable SARS. 96 Most of the patients were men (77%), older, and more often had underlying illnesses (diabetes: 38% vs 6%, P<.01; and, heart failure: 38% vs 2%, P<.001).…”