BEYOND the effects of acute Covid-19 infection, the resolution of the acute infection results in lingering effects for which terms such as "long Covid" or "post-acute Covid-19 syndrome" have been used. In this article, we will take a learning journey into the short and long-term cardiovascular effects of Covid-19 based on the latest evidence.

Covid-19 - attacking our cells

Key to the Covid-19 story is a protein enzyme found on the surface of many cells including the nasopharynx, intestines, kidney, testis and heart, known as Angiotensin-converting enzyme 2 (ACE2).

ACE2 is the "doorway" for the Covid-19 virus. This ACE2 protein has other important functions such as helping to dilate the vessels and anti-clot formation effect. The Covid-19 virus has a protein, the spike (S) protein, which allows it to bind to the ACE2, akin to inserting a key into a lock, thereby facilitating the entry of the virus into cells.

The entry of the Covid-19 virus into the cells triggers a cascade of reactions where the body mounts an attack on the virus in bid to fend off the virus. In the initial stage, the body will try to "size" up the invading virus and understand its molecular structures via special proteins called pattern recognition receptors (PRR) which will bind to the virus.

The binding of PRR to the viral proteins will allow the body to start sending instructions to the white blood cells and endothelial cells (lining of blood vessels) to activate the genes responsible for the production of several proteins required to mount an inflammatory response against the virus, including cytokines.

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When released, cytokines will cause an influx of white blood cells to the site of the infected tissue. Excessive production of cytokines (cytokine storm) in severe Covid-19 patients can trigger damage to the lining of blood vessels, damage the cells of organs, cause the blood to become hypercoagulable (more likely to form clots), and result in the clotting of microvascular blood vessels in the lung and heart microcirculation, damage of heart muscle cells and dysfunction of multiple organs.

The resulting damage leads to leakage of fluid into the lungs and decreased heart pump function - the two key factors that drive Sars-CoV-2related mortality.

Covid-19 and risk factors for death

Studies have shown that age, cardiovascular disease, diabetes, obesity, respiratory diseases, history of malignancy, kidney diseases, liver diseases, neurological diseases and autoimmune diseases were all associated with increased risk of death.

A UK population-based study using the QCovid research database have reported about 5 to 6 times higher risk of death in type 2 diabetics - this is consistent with the higher prevalence of diabetes in patients with severe Covid-19 disease and a higher death rate of Covid-19 among diabetic patients compared with non-diabetic patients.

Epidemiological data show that compared to patients with a BMI less than 30 kg/m2, those with a BMI ranging from 30 to 34 kg/m2 and BMI equal or more than 35 kg/m2 had a 2-fold and 3.6-fold increase in the probability of ICU admission respectively. In addition, a BMI more than 35 kg/m2 increased the risk of invasive mechanical ventilation 7-fold and was associated with lower survival rates. Among these factors, age appears to be the strongest predictor for severe disease and mortality in Covid-19.

Mechanism of Covid-19  heart injury

Current evidence suggests that damage to the heart is not via direct infection of heart muscle cells by the virus, but rather by damage to the microcirculation and the formation of clots.

Hence, viral myocarditis (inflammation of the heart muscle) related to Covid-19 infection is rare. Sars-CoV-2 viral infection injures endothelial cells and reduces ACE2 function, which leads to activation of the blood clotting system.

This increased hypercoagulability (prothrombotic state) is also accompanied by a decreased ability to break down clots and dissolve clots. It can lead to significantly reduced heart muscle function by obstruction of the heart microcirculation by clots and the progression of atherosclerosis by plaque rupture precipitated by vessel inflammation.

Covid-19 heart damage facts

More heart damage means more deaths. Heart muscle damage results in troponin (heart biomarker) release, and if the level exceeds the upper reference limit, death is about 22 per cent. If the levels exceed the upper reference limit by more than 10 times, the death rate increases to 61.5 per cent.

Most with heart injury have impaired heart function. About two thirds of those with elevated troponin had abnormal findings on echocardiogram (heart ultrasound), including impairment of the left and right heart pumping chambers and fluid accumulation around the heart (pericardial effusion).

Heart damage is aggravated by lung complications. Acute heart muscle injury is also caused by pulmonary embolism (presence of clots in lung arteries) which can be present in up to 80 per cent of Covid-19 ICU patients.

Severe heart damage results in heart failure. The damage to the heart can lead to acute heart failure in 23 per cent to 33 per cent of hospitalised Covid-19 patients and even in those without pre-existing cardiovascular disease.

Covid-19 arrhythmia facts

Abnormal heart rhythms (arrhythmias) is a contributing cause to death. Incidence of arrhythmias are as high as 18 per cent in a recent international survey of more than 4,500 patients.

The commonest arrhythmia is atrial fibrillation/flutter (AF). AF is associated with poor prognosis. Arrhythmias can kill. Life-threatening arrhythmias (ventricular tachycardia/ ventricular fibrillation) can occur in 4 to 6 per cent of hospitalised Covid-19 patients

The heart can stop beating. Cardiac arrest, either in or out of hospital, is common in critically ill patients with Covid-19 and is associated with poor survival, particularly among women and men aged 80 or older. In-hospital ECG monitoring to detect life threatening shockable rhythm can result in saved lives through prompt defibrillations.

"Long Covid" facts

Covid-19 effects can linger after the acute infection. Unlike the usual virus, the consequences of Covid-19 infection may not end when the acute infection resolves.

Incidence of residual heart injury can be high. Cardiac MRI data at a median time interval of 71 days since Covid-19 diagnosis suggest about 80 per cent of patients had heart injury and 60 per cent had ongoing heart inflammation, even in asymptomatic patients.

Another study in the United Kingdom published by Fontana et la in the European Heart Journal in January 2021 reported that 49 per cent of the convalescent acute Covid-19 patients who underwent MRI scan of the heart showed evidence of heart muscle scarring.

Post-acute Covid-19 patients with heart damage have "weaker" hearts. Post-acute Covid-19 patients, when compared to health controls, have lower heart pump capacity, larger left ventricular size, evidence of heart muscle scarring on MRI and inflammation of the lining of the heart (pericardium).

Residual lung damage is common. Residual lung damage including scarring was reported in one third of patients at 6-month follow-up chest CT scan, resulting in impaired lung function.

Worsening diabetes post-Covid-19 increases heart risk. The impact of Covid-19 on the incidence of newly diagnosed or worsening diabetic control has long term implications as diabetes is a major risk factor for heart disease.

Covid-19 infection has a significant impact on the cardiovascular system and many convalescent patients continue to have residual cardiovascular changes. The impact of these changes on the long-term health of the individual remains to be understood and will require further research.

As we walk this Covid-19 journey together, we will gradually understand the long term implications of these findings but one thing's for sure - for many post-acute Covid-19 patients, the scars on the cardiovascular system will remain.

• This article is produced in collaboration with Royal Healthcare Heart, Stroke & Cancer Centre