COVID-19 and Cardiovascular Disease
Patients with cardiovascular risk factors and established cardiovascular
disease, including heart failure (HF), are particularly vulnerable when
suffering from COVID‐19[4][5] and patients with cardiac injury
in the context of COVID‐19 have an increased risk of morbidity and
mortality.[6]
Guzik et al.[7] report a mortality rate ∼0.9% for patients with no
comorbidities and much higher for patients with comorbidities (10.5%
for patients with CV disease, 7.3% for those with diabetes, 6% for
those with hypertension and 6.3% for those with chronic respiratory
disease.[8]
SARS-CoV-2 anchors on transmembrane ACE2 to enter the host cells
including type 2 pneumocytes, macrophages, endothelial cells, pericytes,
and cardiac myocytes,[9] leading to inflammation, severe
microvascular[10] and macrovascular dysfunction and multiorgan
failure.
Furthermore, COVID-19 infection leads to systemic inflammation and
immune cell overactivation, and a ‘cytokine storm’, with resultant
release of in an elevated level of cytokines such as IL-6, IL-7, IL-22,
and CXCL10. Subsequently, activated T cells and macrophages may
infiltrate infected myocardium, resulting in the development of
fulminant myocarditis and severe cardiac damage and impairment of left
ventricular function.[11]
Thus, the mechanisms by which COVID-19 affects the cardiovascular system
possibly include direct myocardial injury, indirect injury through
sepsis, hypoxia, cytokine release, a prothrombotic state causing
microvascular thrombosis, and exacerbation of underlying cardiovascular
disease, for example, plaque rupture in susceptible
patients.[12][13][14] Supply/demand mismatch (Type 2
myocardial infarction (MI)) or microvascular thrombosis can lead to left
ventricular dysfunction and ventricular arrhythmias. Fulminant
myocarditis can lead to rapidly progressive cardiogenic shock from
decompensation in patients with known or subclinical cardiomyopathy.
Among hospitalized patients, the presence of cardiac injury has been
independently associated with a 4-fold increased risk of mortality in
patients infected with COVID-19.[15]
In patients with COVID-19 infection, hypoxemic respiratory failure and
ARDS can exacerbate pulmonary vasoconstriction and interstitial oedema,
worsening pulmonary hypertension even in patients without pre-existing
lung disease.[16] In patients with pre-existing biventricular
failure, further elevation in pulmonary pressures secondary to ARDS can
worsen right ventricular function.
In a large cohort study of 138 patients, 8.7% of patients presented
with shock, 7.2% with acute cardiac injury and 16.7% with
arrhythmias.[17] Various other reports show new-onset heart
failure/cardiomyopathy in up to one-third of critically ill patients
admitted with COVID-19 infection.[18][19]
A special population at risk for COVID‐19 includes patients supported
with left ventricular assist devices (LVADs). These patients are
chronically affected by long‐standing cardiovascular diseases and are
subjected to variations of the normal cardiovascular physiology due to a
non‐pulsatile blood flow, exposure of the blood to artificial surfaces,
and risk of haemorrhagic and thrombotic events. Patients with advanced
HF, including those with durable LVAD support, have severely reduced
functional capacity[20][21], as measured by peak
VO2, and impaired ability to augment cardiac output in
response to physiological stressors. These factors collectively decrease
their cardiopulmonary reserve.
Patients with COVID-19 infection are at higher risk for thrombosis in
the arterial and venous circulations due to endothelial dysfunction,
inflammation, oxidative stress, and platelet activation[22]; both
may trigger decompensation of pre-existing HF or development of de novo
acute HF. Right ventricular failure can also develop secondary to
elevated pulmonary pressures in the setting of ARDS and/or pulmonary
embolism.[23]
HF incidence, prevalence, and undertreatment will likely grow as a
result of new COVID-19-related heart disease, delays in the recognition
and treatment of ischemic heart disease, rising unemployment, and loss
of income and health benefits for large segments of the population.
Special considerations are needed for patients with advanced HF,
including those supported by durable LVADs and heart transplantation
(HT) recipients.