Cardiovascular Diseases as a Risk for COVID-19 Infection
Since the beginning of the COVID-19 pandemic in Wuhan, China, many studies and case reports have shown adverse outcomes related to COVID-19 in patients with preexisting cardiovascular diseases such as hypertension, coronary artery disease (CAD), and heart failure (HF). Furthermore, the occurrence of severe disease requiring critical care management and mortality is also reported to be higher in individuals with such comorbidities. In a meta-analysis of 6 studies with 1527 patients, the prevalence of hypertension, cardio-cerebrovascular diseases, and diabetes in patients with COVID-19 were 17.1%, 16.4%, and 9.7%, respectively, with high critical care unit admissions (Table 1-1).
TABLE 1-1Pathogenesis of Cardiovascular Disease in COVID-19 Infection ||Download (.pdf) TABLE 1-1 Pathogenesis of Cardiovascular Disease in COVID-19 Infection
|S.N. ||Cardiovascular Effects ||Incidence ||Pathogenesis |
|1. ||Arrhythmia ||17% in ICU patients || |
Hypoxia due to ARDS
Angiotensin II–mediated electrolyte disturbances
Systemic hyperinflammation affecting cardiac ion channels
Drug effect (hydroxychloroquine, chloroquine, antivirals)
|2. ||Myocardial injury: myocarditis, heart failure, cardiogenic shock ||7%-20% || |
Cytokine–mediated release of ROS, NO, and superoxide ion–mediated injury
Systemic hyperinflammation–mediated apoptosis of cardiac cells
Direct myocardial cytotoxicity by SARS-CoV-2
Hypoxia–mediated myocardial damage
Hyperinflammation and catecholamine surge due to stress causing stress cardiomyopathy
ARDS causing pulmonary HTN and right heart failure
|3. ||Acute coronary syndrome ||2%-4% || |
Systemic inflammation, microthrombi formation resulting in endothelial damage and plaque rupture
Microvascular dysfunction caused by direct cytotoxicity of SARS-CoV-2 in pericytes of coronary arteries
|4. ||Hypertension ||17% || |
Angiotensin II–mediated vasoconstriction, sodium and water retention, inflammation, fibrosis
Reduced activity of angiotensin, which is anti-inflammatory, antifibrotic, and vasodilatory
|5. ||Thromboembolism || |
6% (in wards)
Cytokine–mediated damage of endothelial cell-activating coagulation cascade
Angiotensin II–mediated vascular inflammation
Prolonged immobility in critical cases
Reduced thrombolysis due to hyperinflammation
|6. ||Valvular damage ||Rare || |
|7. ||Pericardial disease ||Unknown || |
Prevention of COVID-19 Infection in Cardiovascular Disease
Preexisting cardiovascular disease has been associated with severe COVID-19 illness and poor outcomes. Hence, it is important to make all efforts to prevent transmission of the virus. Exposure to infected people should be minimized as much as possible. Since hospital-associated transmission is a possibility, hospital visits should be kept to a minimum and when necessary, inpatient stay duration should be as short as possible.
Chronic cardiovascular conditions that require outpatient monitoring or follow-up should be managed by telemedicine. Additionally, the use of remote monitoring devices such as pulmonary artery pressure sensors and CardioMEMS should be considered. All the standard precautions should be taken for patients with acute cardiac disease or those requiring a hospital visit or admission. Furthermore, they should be managed in a COVID-free zone of the hospital if possible, proper hygiene precautions should be adopted, and all the healthcare workers should be donned in appropriate personal protective equipment (PPE). Elective procedures should be kept to a minimum during the COVID surge to decrease transmission and avoid overloading the health system. Nevertheless, patients should be educated to seek medical attention whenever required and instructed to practice safety precautions to avoid transmission.
Hemodynamic Monitoring in COVID-19
Cardiovascular sequelae in patients with COVID-19 such as myocarditis, shock, and coagulopathy, along with high positive end-expiratory pressure (PEEP) mechanical ventilation for ARDS, demand meticulous hemodynamic monitoring as patients are highly susceptible to end-organ hypoperfusion. Various noninvasive and invasive technologies can be used for monitoring of intravascular volume status.
Noninvasive techniques include echocardiography (transthoracic or transesophageal), and noninvasive cardiac monitoring (NICOM). Echocardiogram gives us valuable information regarding ventricular function, size, and pressures as well as volume responsiveness by assessing inferior vena cava (IVC) diameter. However, it can only provide cross-sectional information, which makes it unsuitable for continuous monitoring. It also requires expert individuals and increases exposure of healthcare workers.
Minimally invasive techniques like pulse index contour cardiac output (PiCCO), lithium dilution cardiac output (LiDCO), and FloTrac devices can be used. Invasive techniques like pulmonary artery catheterization (PAC) can be used for continuous monitoring of intravascular volume status and cardiac function, but PAC can overestimate left ventricular volume in ARDS patients requiring high PEEP ventilation and carries risk for pulmonary artery perforation.
Cardiac Arrest Management in COVID-19
SARS-CoV-2, through its direct effect on the heart, causes myocardial dysfunction, which itself and/or in conjunction with ARDS contributes to cardiac arrhythmias and cardiac arrest. Management of cardiac arrest in COVID-19 follows the advanced cardiac life support (ACLS) protocol with some modifications that emphasize preventing or limiting risk of aerosolization to healthcare workers. The number of individuals involved should be kept to a required minimum. All the health personnel involved in the cardiac arrest management should be donned in full PPE. For airway management, use of nonrebreather or face mask with high-flow oxygen and insertion of oral airway is recommended for oxygenation until additional help arrives for cardiopulmonary resuscitation (CPR). Also, a bag valve mask attached to a high-efficiency particulate absorbing (HEPA) filter can be used while ensuring a tight seal with the face mask. Video laryngoscopy should be preferred over direct laryngoscopy for intubation and chest compressions should be held during intubation, which help in minimizing the risk of aerosol transmission to the person performing intubation. The patient should be attached to a ventilator with a HEPA filter attached and the ventilator closed circuit should be ensured to prevent leakage of aerosol to the environment. Intraosseous (IO) access should be considered whenever a peripheral or central intravenous (IV) line is difficult because it is faster, minimizing the exposure time. Mechanical CPR devices should be used whenever available. Defibrillation, being a non–aerosol-generating procedure, is recommended early in the case of shockable rhythm, which will shorten the duration of resuscitation and minimize exposure time.
Management of COVID-19 in Patients with LVAD or Heart Transplant
Patients with left ventricular assist device (LVAD) or HF are considered a vulnerable population for severe COVID-19 given their high cardiovascular risk, risk for infection, and thrombosis; thus extra precautions are required to prevent transmission of SARS-CoV-2. Whenever possible, remote monitoring of LVAD should be preferred. Thromboembolic predisposition in COVID-19 increases the risk of pump thrombosis in LVAD recipients, so therapeutic anticoagulation should be ensured in those patients. As discussed previously, hyperinflammation and cytokine storm plays a major role in the pathogenesis of COVID-19-related cardiovascular diseases and use of an LVAD is believed to be associated with an overall improved inflammatory profile in the setting of COVID-19.
Patients with a heart transplant have been reported to be infected with COVID-19. An early study in China involving 87 heart transplant patients reported that the patients who used extra precautionary measures to avoid exposure did not have a high rate of infection. Similarly, a multicenter survey from Germany involving 21 heart transplant patients with COVID-19 reported clinical presentation similar to nontransplant patients with 8 of 21 patients developing severe disease. However, mortality was found to be elevated in patients with severe disease (87.5%). Right ventricular dysfunction, arrhythmias, and thromboembolic events were seen in a group with severe disease compared with the nonsevere disease group. Heart transplant patients are on high-dose immunosuppression, but the effect of immunosuppression on the disease course is unclear. It is believed to be obscuring the typical manifestations of COVID and may even confuse lab findings due to preexisting lymphopenia. Management initially is supportive, and several protocols have been used by transplant centers in terms of immunosuppressants, such as pausing mycophenolate mofetil, switching sirolimus to tacrolimus, and using high-dose corticosteroids. Due to the high mortality of heart transplant patients with COVID-19, utmost importance should be given to preventive measures. (1-5)