The current COVID-19 pandemic (caused by the SARS-CoV-2 virus) represents the biggest medical challenge in decades. Whilst COVID-19 mainly affects the lungs it also affects multiple organ systems, including the cardiovascular system. There are documented associations between severity of disease and risk of death and To provide all the information required by review bodies and research information systems, we ask a number of specific questions. This section invites you to give an overview using language comprehensible to lay reviewers and members of the public. Please read the guidance notes for advice on this section. 5 DRAFT Full Set of Project Data IRAS Version 5.13 advancing age, male sex and associated comorbid disease (hypertension, ischaemic heart disease, diabetes, obesity, COPD and cancer). The most common complications include cardiac dysrhythmia, cardiac injury, myocarditis, heart failure, pulmonary embolism and disseminated intravascular coagulation. It is thought that the mechanism of action of the virus involves binding to a host transmembrane enzyme (angiotensin- converting enzyme 2 (ACE2)) to enter some lung, heart and immune cells and cause further damage. While ACE2 is essential for viral invasion, it is unclear if the use of the common antihypertensive drugs ACE inhibitors or angiotensin receptor blockers (ARBs) alter prognosis. This study aims to look closely at the health of the vascular system of patients after being treated in hospital for COVID-19 (confirmed by PCR test) and compare them to patients who had a hospital admission for suspected COVID-19 (negative PCR test) . Information from this study is essential so that clinicians treating patients with high blood pressure understand the impact of the condition and these hypertension medicines in the context of the current COVID-19 pandemic. This will allow doctors to effectively treat and offer advice to patients currently prescribed these medications or who are newly diagnosed with hypertension.
COVID-19 is pandemic and, though it primarily affects the lungs, there is evidence of
cardiovascular system involvement. Mechanistically, SARS-CoV-2, following proteolytic
cleavage of its S protein by a serine protease, binds to the transmembrane
angiotensin-converting enzyme 2 (ACE2) -a homologue of ACE-to enter type 2 pneumocytes,
macrophages, perivascular pericytes, and cardiomyocytes. This may lead to myocardial
dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque
instability, and myocardial infarction. While ACE2 is essential for viral invasion, it is
unclear if the use of the common antihypertensive drugs ACE inhibitors or angiotensin
receptor blockers alter prognosis.
Diagnostic Test: ABPM
24 hour ambulatory blood pressure monitoring
Diagnostic Test: ECG
Electrocardiogram
Diagnostic Test: FMD
Flow mediated dilatation
Diagnostic Test: PWV
Pulse wave velocity
Diagnostic Test: Rarefaction
nailbed capillaroscopy
Inclusion Criteria:
- Admission between 01/04/2020 and 31/12/2020 Clinically suspected or PCR confirmed
COVID-19 Age 30-60 years No history of hypertension or current drug treatment for
hypertension
Exclusion Criteria:
- Inability to give informed consent/lack of capacity Non-English speakers BMI >40 eGFR
<60 ml/min Pregnancy History of Cancer within 5 years Persistent atrial fibrillation
Severe illness, at investigator discretion Prescription of BP lowering drugs
Corticosteroid (chronic use) Immunosupressive agents NSAIDs (chronic use)
NHS Greater Glasgow and Clyde
Glasgow, United Kingdom
Katriona Brooksbank
01413302418
katriona.brooksbank@glasgow.ac.uk
Rhian M Touyz
01413307775
rhian.touyz@glasgow.ac.uk