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Covid Cardiac Sequelae

On 8th December 2019, in Hubei province in China Dr Zhang Jixian confirmed a virus, which would prove to be the greatest medical challenge of the 21st century!!!

As the virus travelled around the world, a large number of countries were affected! Slowly, it had the whole world in its grasp! Without a cure, it resulted in a large number of deaths! Soon the medical fraternity were looking for a cure! Research for a vaccine was also underway! A few drugs did prove to be of benefit, and were used with care!

What is this virus and how does it cause disease?

So SARS CO-V 2 is a single stranded positive sense RNA virus. It has a crown of 4 structural proteins viz, M , E, N ,and S! Among these, the S protein has pivotal role in virus attachment and disease pathogenesis. After proteolytic cleavage by serine proteases the S protein binds to the transmembrane ACE2 rec and enters the Type 2 Pneumocyte, macrophages, perivascular pericytes and cardiomyocytes! This then leads to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability and myocardial infarction. The initial immune and inflammatory responses induce a severe cytokine storm which mediates the multi-organ dysfunction that sets in.
It is mostly transmitted from person to person by inhalation of respiratory droplets or aerosols , from an infected person

How do the patients usually present?

The usual symptoms are fever, dry cough, fatigue, loss of smell and taste, and headache. They may also have nasal congestion, rhinorrhea, sore throat, myalgia, poor appetite and diarrhea. About 50 percent of those infected may have asymptomatic disease. And 80 percent of those infected will have mild disease, unless they have comorbid conditions [ advanced age, male sex, HT, DM, COPD,Cancer, Cardiovascular issues.] two thirds of the patients with comorbidities may need ICU care and so this subset should present to a hospital early on!
The incubation period is 14 days and usually exposure to the appearance of first symptom takes 5-6 days.

What are the most common cardiovascular complications seen?

The most common complications observed were cardiac arrhythmias [ atrial fibrillation, ventricular tachycardia or fibrillation], fulminant myocarditis, myocardial ischaemia, pulmonary embolism, strokes, heart failure and DIC.

Effect of covid on cardiac variables/ events

1. Hypertension

Considering the importance of ACE2 in the development of hypertension and diabetes mellitus, patients with COVID-19 exhibit severe comorbidities including hypertension and diabetes with poor prognosis.

2. Myocardial injury and Heart failure

Apart from hypertension and age, acute cardiac injury, chronic heart damage and heart failure have all been observed in patients treated for COVID-19 infection. Due to acute inflammation, procoagulant stimulus and endothelial cell dysfunction, various influenza RNA viruses are involved in the development of human atherosclerotic plaques and progression of atherosclerosis. De-stabilization of vulnerable atherosclerotic plaques triggers acute myocardial infarction (MI) or cardiovascular death.

Acute heart failure can be the primary presenting manifestation of COVID-19 infection. It is currently unknown if heart failure is due to new cardiomyopathy versus an exacerbation of previously undiagnosed heart failure . It is important to be conscious of this potential cardiac dysfunction when administering intravenous fluids and avoid overaggressive fluid replacement. Importantly, right heart failure may also occur, particularly among those with ARDS and acute lung injury

3. Myocardialischaemia

Severe systemic inflammation increases the risk of atherosclerotic plaque disruption and AMI. Due to extensive inflammation and hypercoagulability, the risk of AMI is likely present in patients with COVID-19. These patients may need fibrinolysis or PTCA along with medical management.

4. Myocarditis

Myocarditis is a disease marked by the inflammation of the heart muscle, most often due to viral infection. This inflammation interferes with the electrical system and compromises the pumping capacity of the heart and results in arrhythmia and cardiac arrest. Acute myocarditis presents across a variable range of clinical severity and is a significant diagnostic challenge in the COVID-19 era. Patients with COVID-19 can present with chest pain, dyspnea, dysrhythmia, and acute left ventricular dysfunction . In patients with myocarditis and myocardial injury, serum troponin values will be abnormal. The electrocardiogram (ECG) can demonstrate a range of findings, in some cases mimicking acute coronary syndrome (ACS). The ECG abnormalities result from myocardial inflammation and include non-specific ST segment-T wave abnormalities, T wave inversion, and PR segment and ST segment deviations (depression and elevation). Echocardiography and consultation with cardiology, if either are available, is encouraged, as differentiating myocarditis and ACS is difficult. Echocardiographic evaluation is more likely to demonstrate a focal wall motion abnormality with active, significant ACS while severe forms of COVID-19-related myocarditis will show either no wall motion defects or global wall motion dysfunction. ECG and echocardiographic abnormalities in the setting of COVID-19 are markers of illness severity and are correlated with worse outcomes . Moreover, troponin elevations in patients with COVID-19 infection have been directly associated with an increased risk of adverse outcome in those patients with severe infection, including mortality

5. Myocardial arrhythmias

In patients with COVID-19, it is plausible that myocardial involvement can be the initiator of a pathway of inflammation and subsequent fibrosis. If the extent and distribution of fibrosis produces electrophysiological abnormalities that predispose to atrial fibrillation and ventricular arrhythmias, early detection and intervention could improve long-term outcomes.

Palpitations may be a presenting symptom in over 7% of patients with COVID-19 . A range of dysrhythmias have been encountered in patients with COVID-19 infection. Most frequently, sinus tachycardia is seen in such patients, resulting from multiple, simultaneous causes (hypoperfusion, fever, hypoxia, anxiety, etc). Dysrhythmias may occur in the setting of viral illness due to hypoxia, inflammatory stress, and abnormal metabolism . If dysrhythmias are associated with an elevation in serum troponin, the clinician should consider myocardial injury, acute myocarditis, and ACS in the differential diagnosis .

6. Coagulation abnormalities and Thromboembolic events

COVID-19 infection has been associated with venous and arterial thromboembolism. Studies have shown abnormalities of the coagulation cascade, with elevated D-dimer, thrombocytopenia, slightly elevated prothrombin time, and higher levels of fibrinogen and von Willebrand factor. The hypercoagulable state in COVID-19 infection is thought to be related to severe inflammatory response, cytokine storm, and endothelial damage, along with underlying patient comorbidities

Patients with COVID-19 are also at an increased risk of Venous thromboembolism. Systemic inflammation, abnormal coagulation status, multi-organ dysfunction, and critical illness are all potential contributing factors to the increased risk of VTE. Anticoagulation, mainly with low molecular weight heparin, may be associated with reduced mortality in severe COVID-19 infections or those with D-dimer greater than six times the upper limit of normal.

COVID-19 infection has been associated with cerebrovascular accidents. The incidence of acute ischemic stroke in patients with COVID-19 is approximately 1%–3%. these patients have higher mortality. In addition to arterial strokes, cerebral venous thrombosis has also been seen frequently in Covid patients.

Peripheral arterial thrombo-embolism causing acute limb ischemia also has been described in COVID-19. It has ,also, been seen in patients without any comorbidities. Results of revascularization has been less than satisfactory in this subset.

In a nutshell

The SARS-CoV-2 infection has been often reported to be complicated with cardiac dysfunction. Preexisting cardiac diseases predispose to the severity of the disease and worsening of the cardiac condition. Early detection of cardiovascular disease by clinical and laboratory parameters and treatment is of paramount importance. Clinical trials are underway, and more research will follow to evaluate the disease and its therapies, which will guide the clinicians in treatment and policymakers to set the guidelines for better management of cardiovascular aspects of COVID-19.

So how do we protect ourselves?

During this pandemic time, patients should avoid close contact with another patient with suspected or confirmed COVID-19 or having signs and symptoms of respiratory infection. Get vaccinated, wearing masks, hand washing, and social distancing are principles to reduce the risk of infection. Patients with underlying cardiac disease, hypertension, cardiac transplant patients, or patients taking immunosuppressive medications should take extra caution to avoid getting infected, considering the complications, already explained above.