Clinical review of COVID-19 and CVD: What the cardiovascular practitioner needs to know

You will want to talk to your doctor if you are using ACE inhibitors or angiotensin receptor blockers.

Hypertension is on the risk list but doesn't say whether controlled or not. I have no idea if the definition of CVD here is old and thus includes stroke or is new and just heart stuff.

Found the most common comorbidities were hypertension (19%), diabetes (8.2%) and CVD (2.7%; Zhao X, et al. MedRxIV. 2020;doi:10.1101/2020.03.17.20037572).

 

ace inhibitor medications

angiotensin receptor blockers list 

This is on the second page; Currently, the American College of Cardiology and American Heart Association have recommended against preemptively stopping or starting an ACE inhibitor or angiotensin receptor blocker in the setting of COVID-19.

The latest here:

Clinical review of COVID-19 and CVD: What the cardiovascular practitioner needs to know

by Eamon Duffy, MD, MBA; Andrew Ayers; Miguel Caínzos-Achirica, MD, MPH, PhD; and Roger S. Blumenthal, MD

Eamon Duffy

The novel coronavirus disease, or COVID-19, is now a global pandemic. Clinicians, scientists and public health officials around the world are racing to define the molecular pathway and clinical presentation of the virus, identify risk factors for infection and poor clinical outcomes, and develop effective treatments and preventive interventions.
Although the data on each of these ventures continue to develop on a daily basis across the globe, several trends have emerged showing that CV comorbidities are common in patients with COVID-19 and are independently associated with a greater risk for morbidity and mortality.
This summary reviews the evolving molecular and clinical data on COVID-19, with a focus on the intersection of this virus with CVD and its potential impact on patients with CV and professionals.
The molecular pathway

Andrew Ayers

COVID-19 is caused by the pathogen SARS-CoV-2, a novel enveloped RNA betacoronavirus that is thought to originate in bats (Zhou P, et al. Nature. 2020;doi:10.1038/s41586-020-2012-7). Infection with SARS-CoV-2 is caused by binding of a spike protein on the viral surface to the ACE2 receptor. The virus is then internalized and propagated with viral replication (Walls AC, et al. Cell. 2020;doi:10.1016/j.cell.2020.02.058). This ACE2 receptor is found on type 2 pneumocytes in the lungs, the primary route of infection, but it is also found in high levels in the heart, arteries, kidneys and intestines (Hamming TW, et al. J Pathol. 2014;doi:10.1002/path.1570). ACE2, when activated, converts angiotensin 2 to angiotensin 1-7, leading ultimately to vasodilation, diuresis and reduced oxidative stress. When SARS-CoV-2 binds to ACE2, it leads to ACE2 downregulation, increased angiotensin II, and increased pulmonary vascular permeability as well as the clinical state of acute respiratory distress syndrome (ARDS) seen in so many severely ill patients with COVID-19 (Zhang H, et al. Intensive Care Med. 2020;doi:10.1007/s00134-020-05985-9).
The potential impact of ACE inhibitors and angiotensin receptor blockers, ubiquitously used in patients with CVD, on this pathway has so far been studied primarily in rodent models. These models have shown that ACE inhibitors lead to an increase in ACE2 (Ferrario CM, et al. Circulation. 2005;doi:10.1161/CIRCULATIONAHA.104.510461). This raises that concern that these medications could, by increasing the viral target, increase a patient’s susceptibility to the virus. 
4 more pages at link.