**7. Cardiovascular findings in COVID-19**

*Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions*

consolidative opacity. 56% of subjects had normal CT images in the early phase (0 to 2 days) of the disease but more frequent in longer infections with consolidation, bilateral and peripheral and greater total lung involvement. Bilateral involvement occurred in 28%, 76% and 88% of early (0–2 days), intermediate (3–5 days) and late (6–12 days) infection times respectively. Further notable CT findings include linear

*Representative characteristic findings of COVID-19 infection on thoracic CT imaging: (a) axial CT image obtained without intravenous contrast. 36y male showing bilateral ground-glass opacities in upper lobes with rounded morphologies (arrows); (b) axial CT image. 65 y female, showing bilateral ground-glass and consolidative opacities with striking peripheral distribution (arrows); (c) axial CT image obtained without intravenous contrast material in a 43 y female, demonstrating crazy-paving pattern manifested by right lower lobe ground-glass opacification with interlobular septal thickening (arrows) with intralobular lines. (d) Axial CT image obtained in a 22y female, showing an area of faint ground-glass opacification in left upper lobe with a ring of denser consolidation or reverse halo sign (arrow). [source: Images modified from Bernheim* 

Following isolation and treatment, most COVID-19 patients stabilise and become well. Further CT imaging demonstrates regression of infection with

Gastrointestinal (GI) symptoms are emerging in patients with COVID-19. This is

= 74%). The pooled prevalence of digestive symptoms was 15%

= 96%) with nausea or vomiting, diarrhoea, and loss

due to the presence of the ACE2 receptor expressed in the GI tract [33, 34]. COVID-19 patients present with GI symptoms such as diarrhoea (10% of patients) with nausea and vomiting less common [35]. In a meta-analysis of 35 studies, 29 studies reported gastrointestinal symptoms in 6,064 COVID-19 patients with a pooled prevalence of gastrointestinal comorbidities of 4%. (95% CI 2 to 5%;

opacity, crazy-paving patterns and reverse halo sign (**Figure 8**).

absorbed lesions, and some cord-like shadows.

**6. Gastrointestinal symptoms in COVID-19**

2

of appetite being the three most common [36].

**134**

**Figure 8.**

*et al. [32]].*

range 0 to 15%; *I*

2

(10 to 21%; range: 2 to 57%; *I*

In addition to respiratory and gastrointestinal symptoms, cardiovascular involvement is also common amongst patients with COVID-19. The symptoms are wide-ranging in manifestation and severity and are more common in the elderly and those hospitalised with the infection. Previous influenza epidemics have been associated with an increased prevalence of myocardial infarction, myocarditis and chronic/congestive heart failure [37]. Both SARS and MERS were associated with either bradycardia, tachycardia, cardiomegaly, diastolic impairments, cardiac arrest, cardiomegaly and acute cardiac failure [38–40].

Patients with cardiovascular risk factors or established cardiovascular disease disproportionately suffer with severe forms of the infection with worse clinical prognosis and outcome. In one of the earliest reports of clinical characteristics of COVID-19 from Wuhan China; 14% of 138 patients demonstrated baseline cardiovascular disease and 31% had hypertension [41]. Similar data has been reported in other population studies from Wuhan, China [42–44]; Italy [45, 46]; Iran [47], United Kingdom [48] and the USA [49] to varying cardiac involvement.

The pathophysiological mechanism of cardiac injury in COVID-19 infection are similar to those associated with other influenza pandemics and human coronavirus diseases (SARS and MERS). Although the pathophysiological mechanisms injury is not fully established in COVID-19 patients, it is likely that the elevation is related to (1) Systemic inflammatory involvement, cytokine storm mediated through T-cell and monocytes resulting in myocarditis. Often patients have concomitant elevations in C-reactive protein (CRP), eosinophil sedimentation rate (ESR) (2) Hypercoagulability.

**Figure 9.** *Pathophysiological mechanisms of acute myocardial injury in COVID-19 infection.*

Haematological differentials along with abnormal clotting factors and elevated D-dimer result in haemostasis and thrombosis as evident of coronary microvascular disease. (3) Endothelial injury causing diffuse disruption to the vasculature in several organs including the heart. (4) Down regulation of ACE2 expression in cardiomyocytes and loss of the protective signalling pathway (5) Inflammatory and stress response causing plaque rupture in those subjects with active coronary artery disease (**Figure 9**).
