COVID-19 and Cardiovascular Disease
COVID-19 and Cardiovascular Disease Image Source: Kateryna Kon/Shutterstock.com
Background
One significant long-term clinical effect of COVID-19 appears to be heart damage. This has been identified since the outbreak in Wuhan, China. At the time, several patients hospitalized with the disease had elevated cardiac troponin levels, a molecular biomarker of myocardial injury.
These patients' echocardiographic examinations revealed functional deficits in the heart. The obvious conclusion was that the severity of COVID-19 was associated with myocardial injury.
However, due to the high number of asymptomatic cases and a severe lack of focused research, the question of the prevalence of this complication remains unanswered. Furthermore, it is unknown whether the damage to the heart muscle is caused by the systemic inflammatory response to COVID-19 or by myocarditis.
Most importantly, the possibility of long-term injury is unclear at this time, though it is a very real possibility given the large number of infections that have occurred thus far.
Myocarditis
Inflammation of the heart appears to be prevalent in COVID-19, at least in some patients. This condition can affect both the myocardium and the pericardium, resulting in severe fatigue in the absence of other obvious symptoms.
COVID-19 myocarditis is frequently fulminant and self-resolving, though it can occasionally result in arrhythmias, heart failure, cardiac arrest, or sudden death. In this case, cardiogenic shock is the cause of death.
Myocarditis is a relatively imprecise diagnosis due to a dearth of tests and diagnostic protocols. Thus, the course of the illness is unknown at the moment, but early reports indicate that symptoms persisted for a median of 47 days before being diagnosed via cardiac magnetic resonance (CMR) imaging.
In one study, more than half of the patients had edema, indicating active inflammation, and a significant proportion had scarring and impaired right ventricular function.
However, another study from Germany found that up to 60% of patients who had cleared the virus as confirmed by a negative nasal swab after 2-3 months continued to have signs of myocardial inflammation. Numerous others had elevated troponin levels. In comparison to controls, this study detected heart enlargement and inefficient pumping.
In a few patients with severe changes on CMR, active inflammation was confirmed via heart muscle biopsy. The majority of patients in this study were not hospitalized, including several who were asymptomatic, with a mean age of 50 years. COVID-19 severity, underlying medical conditions, and time since onset were not associated with an increased risk of heart inflammation.
In one study, recovered athletes demonstrated the same signs of myocarditis, whether active or recovering, following mild or asymptomatic COVID-19 infection. 12/26 competitive athletes exhibited these characteristics up to 53 days after quarantine in this study.
Notably, many of the patients in the German study had symptoms consistent with myocarditis, which could have influenced the study's findings. When compared to controls with the same risk factors, many of the patients with abnormal imaging findings had borderline positive results.
Due to the absence of CMR or troponin monitoring for other viral respiratory illnesses, the data are insufficient to make a valid comparison between COVID-19 and this data or to conclusively state that the abnormalities are a specific sequelae of COVID-19.
Myocarditis is typically caused by viral infection of the heart muscle, but in COVID-19, it could also be caused by cytokines circulating as part of systemic inflammation. The latter could account for the arrhythmias and even cardiac ischemic events that occur as a result of plaque rupture and fragmentation of the heart vessels.
Downregulation of ACE2 and myocardial edema
On the other hand, the angiotensin-converting enzyme 2 (ACE2), which functions as the viral receptor, is widely distributed and has significant cardiovascular functions, including normal vascular permeability. As a result of the decreased ACE2 expression caused by COVID-19, the influx of fluid into the heart muscle is enhanced, resulting in mild edema.
This may be exacerbated by systemic inflammation, another characteristic of COVID-19. This cardiac edema can result in severe persistent fatigue and may play a significant role in the cardiac injury caused by COVID-19. Given the rapid control of such inflammatory swelling by glucocorticoids, this may be one mechanism by which these drugs decrease mortality in patients with severe COVID-19 who require respiratory support.
COVID-19 can also result in an oxygen supply-demand imbalance, blood clots, sepsis, stress-induced cardiomyopathy, and multisystem inflammatory syndrome. Cardiovascular disease that is already present may be accelerated by severe COVID-19, as measured by troponin levels.
Cardiovascular damage and a prolonged COVID
Severe fatigue, palpitations, chest pain, shortness of breath, postural orthostatic tachycardia syndrome (POTS) due to neurologic disturbances, post-exercise fatigue, and increased troponin levels with an abnormal electrocardiogram are all signs and symptoms of possible heart damage following COVID-19.
According to some cardiologists, these symptoms are caused by cardiac damage. Hospitalized COVID-19 patients with elevated troponin levels exhibited persistent myocardial scarring in the absence of edema, indicating that the virus's damage is permanent and predisposes them to a higher risk of heart failure.
The right side of the heart is strained by the requirement to pump blood through inflamed lungs, a task that is frequently complicated by the formation of clots within the heart and lungs' blood vessels, which, in conjunction with the inflammation, reduces the level of oxygenation in these vital organs. This may be exacerbated by the use of a higher positive end-expiratory pressure during mechanical ventilation, which places additional stress on the right ventricle.
In patients with pre-existing heart failure, COVID-19
The prognosis is poor in patients who already have heart failure, as the co-occurrence of COVID-19 can result in myocardial injury, causing the patient's heart to fail suddenly. Heart failure is most likely caused by the cytokine storm associated with severe COVID-19 infection, which includes elevated levels of interleukins (IL) such as IL3, IL6, and IL7, as well as other pro-inflammatory mediators.
As a result of elevated cytokine levels, this may result in stress cardiomyopathy and myocardial dysfunction. This results in acute decompensation of pre-existing heart failure, even in previously stable patients.
While ACE inhibitors have been associated with beneficial effects during COVD-19, their role should be evaluated in patients with lung involvement, such as pneumonia or acute respiratory distress syndrome (ARDS), to avoid adverse effects. Similarly, drugs that have the potential to cause arrhythmias in the presence of electrolyte imbalance and other risk factors, such as hydroxychloroquine and azithromycin, should be closely monitored, even more so if the patient has structural heart disease and/or coronary artery disease.
Clinical repercussions
However, additional research will be required to correlate imaging findings with clinically significant events. The implications must be considered, as myocarditis places a strain on the heart, accounting for more than a tenth of sudden cardiac deaths in young adults and being recognized as a potentially fatal condition in competitive athletes.
Athletes with asymptomatic or mild COVID-19 may return to high-level training too soon, putting them at risk of death from myocarditis. The American College of Cardiology (ACC) recommends that athletes with moderate-to-severe infections undergo cardiac imaging and other tests prior to resuming training, a measure that has revealed some previously undetected cases.
However, the clinical implications may not be trivial. According to some scientists, some of the heart scarring observed in previous studies could have been caused by intense athletic training rather than the viral infection.
Myocarditis can result in the death of myocardial cells, scarring, heart attacks, and endothelial damage. If irreversible fibrosis occurs, patients may present five to twenty years later with heart failure and arrhythmias.
References:
Abbasi, J. et al. (2021). Researchers Investigate What COVID-19 Does to The Heart. JAMA Network. doi:10.1001/jama.2021.0107. Retrieved from: https://jamanetwork.com/journals/jama/fullarticle/2776538. Accessed on 6 September 2021.
Post-COVID Conditions (2021). Retrieved from: https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html. Accessed on 6 September 2021.
Sisti, N. et al. (2021). COVID-19 in Patients with Heart Failure: The New and The Old Epidemic. Postgraduate Medical Journal. Retrieved from: https://pmj.bmj.com/content/97/1145/175. Accessed on 6 September 2021.
Post a Comment for " COVID-19 and Cardiovascular Disease"