Study Provides Overview of COVID-19 and Cardiovascular Health

This post originally appeared on HCPLive.

The impact of the novel coronavirus (COVID-19) on cardiovascular health is an urgent question for clinicians around the world during this global pandemic.

A new study published in Circulation offers an overview of available data on COVID-19 and cardiovascular health. The study team examined the impact on heart transplantation as well as potential treatments.

The study, authored by Nir Uriel, MD, MSc, and a team of colleagues, contains information from more than 60 articles to provide clinicians and cardiologists a much-needed outline of the disease and how its impact on those with cardiovascular disease (CVD) differs from those without.

Existing information suggests cardiovascular diseases are a common comorbidity among patients with COVID-19—as was seen with SARS and MERS—and 5 sets of data provided were referenced in support of this. Of note, an analysis of 8 studies including more than 45,000 infected patients found the most prevalent comorbidities were hypertension (17±7%, 95% CI, 14-22%), diabetes mellitus (8±6%, 95% CI 6-11%), and cardiovascular diseases (5±4%, 95% CI 4-7%). Another study, which analyzed 1099 infected patients, found hypertension was present in 36% of patients that died or required intubation.

An analysis of 138 hospitalized patients with COVID-19 indicated hypertension was present in 31% of patients and 58% that required placement in an intensive care unit (ICU) while CVD was presented in 15% overall and 25% that required ICU. This same study is referenced in the next section of the article, which examines COVID-19 and myocardial injury. In this analysis, elevated high sensitivity Troponin I (hs-cTnI) or new ECG or echocardiographic abnormalities were presented in 7.2% of the cohort and 22% of those requiring ICU.

Uriel and colleagues note available data suggest 2 apparent patterns of myocardial injury associated with COVID-19. The first, indicates a rise in hs-cTnI—as well as D-dimer, ferritin, IL-6, and lactate dehydrogenase—suggest this is more indicative of a cytokine storm or secondary hemophagocytic lymphohistiocytosis rather isolated myocardial injury. The second, which occurs in patients with predominantly cardiac symptoms, is more indicative of potential viral myocarditis or stress cardiomyopathy—they reference 3 reports to evidence this point.

The investigators briefly touch on the role of ACE inhibitors and ARBs in the disease and go on to point out most major cardiology organizations advise against adding or stopping these therapies given the lack of evidence currently available. They also touch on heart transplantation and COVID-19, explaining available data appears to indicate it remains safe even during the pandemic.

A survey in Wuhan found the risk of infection with SARS-CoV-2 did not increase if routine preventive measures were used. Additionally, Uriel and colleagues note recommendations from major societies include avoiding donors with known or suspected COVID-19 and if a donor had COVID-19, they should be COVID-19 free as assessed by RT-PCR for at least 14 days.

The portion of Uriel and colleagues’ work that outlines potential treatments includes more than half-a-dozen therapies, including chloroquine and hydroxychloroquine. In regard to these therapies, investigators note the therapy blocks SARS-CoV-2 cell entry in vitro at concentrations comparable to that achieved with treatment for rheumatoid arthritis and trials are still ongoing.

Other treatments that have been examined or could, at least in theory, provide some form of benefit referenced in this section include remdesevir, camostat mesylate, lopinavir/ritonavir, tocilizumab, sarilumab, and recombinant human ACE2 (APN01). At multiple points throughout the section highlighting treatments, Uriel and colleagues note none of these treatments have proven clinical efficacy to date.

Uriel and colleagues also point out that research into the mechanisms behind many of the aforementioned associations requires further investigation and many other questions surrounding COVID-19 and its impact on cardiovascular health remain unanswered.

“COVID-19, caused by SARS-CoV-2, is a global pandemic evolving in real time,” Uriel and colleagues wrote.