Thread: A summary of "COVID-19 can affect the heart" by @EricTopol in @ScienceMagazine. See https://bit.ly/3nkxPM8 . #COVID19 #CardiacTwitter #LongCovid

1/ The four “common cold” coronaviruses have not been associated with heart problems, and only isolated reports of cardiac issues in MERS patients. SARS-CoV-2 is distinctive in its more extensive cardiac involvement.

2/ SARS-CoV-2 enters cells via the ACE2 protein (note: ACE2 'receptor' is a misnomer), which is highly expressed in the heart. SARS-CoV-2 can directly infect cardiomyocytes, or indirectly damage them through systemic inflammation and reduced blood supply.

3/ Direct or indirect damage to cardiomyocytes leads to necrosis, myocarditis (heart muscle inflammation), and cardiogenic shock (fatal inability to pump). Cardiac injury occurs in at least 20% of hospitalised patients, rising to >50% for those with pre-existing heart conditions.

4/ Cardiac injury is reflected by troponin concentrations > troponin concentration correlates with mortality > patients with higher troponin concentrations have markers of increased inflammation (CRP, IL-6, etc) and heart dysfunction (NT-proBNP).

5/ SARS-CoV-2 infection exhibits lymphocyte infiltration and can result in injury to all layers of the heart & pericardium (which surrounds the heart). Effects on layers of myocytes (involved in electrical conduction) can result in conduction block, arrhythmias, cardiac arrest.

6/ In a cohort of 100 patients who recovered from COVID-19, 78 had cardiac abnormalities and 60 had ongoing myocardial inflammation consistent with myocarditis. The majority of >1200 patients in another cohort had echocardiographic abnormalities. #LongCovid

7/ This raises possibility that, as 30-40% of SARS-CoV-2 infections occur w/o symptoms, many recovered individuals may have underlying cardiac pathologies. Half of asymptomatic people showed symptomatic lung features on CT, but few studies have done the same for cardiac imaging.

8/ Though an immunologic basis for #longcovid is likely, it has yet to be determined. Many of the symptoms (fatigue, chest pain, difficulty breathing) point to cardiovascular problems as well as, if not in place of, immunology.

9/ COVID-19 heart dysfunction can also manifest from other pathways: Takotsubo syndrome, ischaemia (from endothelitis), thrombosis/atherosclerotic plaque rupture. Not just the direct effects!

10 (last)/ First recognised a few months into the pandemic, now known to be more common – the driver behind this cardiac pathogenesis needs to be determined. Is it individual inflammatory responses, autoimmunity, or something(s) else entirely? Work to be done!