"Coronavirus and Heart Disease – A Latest Update"
Coronavirus
and Heart Disease – A Latest Update
Introduction
Today, the world is facing a pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), etiological agent of COVID-19 disease. The first signs of the new virus began to show up in December 2019 in Wuhan, China. In this century, two coronavirus epidemics occurred, the severe acute respiratory syndrome coronavirus (SARS-CoV) in 2002 and the Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012. SARS-CoV-2 presents a transmissibility ten times faster than 2002 SARS-CoV. Due to its fast dissemination, COVID-19 was declared a pandemic by the World Health Organization (WHO). By the 10 September 2021, the world had already registered 22,30,22,538 individuals contaminated, with 46,02,882 deaths.
The
coronaviruses are single-stranded RNA viruses, with great capacity for fast
mutations and recombination, causing respiratory or intestinal infections in
humans and animals. Coronavirus infection occurs through the coupling of
S-protein located on the surface of the virus with angiotensin-converting
enzyme 2 (ACE2), which acts as a receptor for the virus. ACE2 is mostly present
in the lungs and seems to be the main gateway for the virus. It is also present
in great amounts in the heart, which can lead to cardiovascular (CV)
complications.
The
main clinical manifestations of COVID-19 are respiratory, varying from a mild
presentation to acute respiratory distress syndrome (ARDS), being potentially
fatal. Moreover, as in other respiratory infections, preexisting CV diseases
and risk factors can increase the severity of COVID-19, leading to the
aggravation and decompensation of chronic underlying cardiac pathologies as
well as acute-onset of new cardiac complications, highlighting that myocardial
injury can be present in approximately 12% of hospitalized patients with
SARSCoV-2 infection.
With incessant advances in science and
technology, cardiology has seen the most rapid advances in the last three
decades. In the midst of this, the world is now facing the worst pandemic of
the century. Although the most common presenting symptoms are fever, cough and
malaise, several reports have seen varied manifestations including myocardial ischemia
and heart failure. Also, the prognosis of COVID-19 patients is worse when there
is accompanying myocardial injury.
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Impact
of preexisting cardiovascular disease —
Symptoms
and signs of heart disease in a patient with COVID-19 may result from an acute
disease process, from hemodynamic demands in the setting of chronic heart
disease, or may be caused by an acute exacerbation of chronic disease. As
discussed separately, there is substantial evidence of association between
preexisting cardiovascular disease (such as hypertension and coronary artery
disease) and the risk and severity of COVID-19 infection. The causes of this
association have not been determined. Proposed mechanisms include impaired
physiologic reserve (cardiovascular and pulmonary), impaired immune response,
augmented inflammatory response, vulnerability to SARS-CoV-2-induced
endothelial dysfunction and effects mediated by the angiotensin-converting
enzyme 2 receptor.
Pathophysiology
SARS-CoV-2 uses its S-spike to bind to ACE2 receptors as the point
of entry into the cell. These ACE2 receptors are expressed in type 1 and type 2
pneumocytes and other cell types, including endothelial cells. ACE2 is an
inverse regulator of the renin-angiotensin-aldosterone system. Like other coronaviruses,
SARS-CoV-2 uses these ACE2 receptors to target the respiratory system
primarily.
SARS-CoV-2 and the Immune Response
There are two immune-response phases of COVID-19 disease. Phase 1
occurs during the incubation stage of the disease, during which the adaptive
immune system works to eliminate the virus; if any defects occur at this stage,
SARS-CoV-2 will disseminate and induce systemic organ damage, with more
significant destruction of organs with higher expression of ACE2 receptors,
including lung, endothelial cells, the heart, and the kidneys. This massive
damage leads to phase 2 severe inflammation in the affected organs.
Diabetes, atherosclerosis, and obesity, which are risk factors for
cardiovascular disease, downregulate the immune system. These have been
associated with a poor prognosis in COVID-19.
Mechanisms of Cardiac Damage in COVID-19
Multiple mechanisms have been suggested for cardiac damage, based
on studies conducted during the previous SARS and MERS epidemics and the
ongoing COVID-19 epidemic. Part of the systemic inflammatory response in severe
COVID-19 is the release of high levels of cytokines that can injure multiple
tissues, including vascular endothelium and cardiac myocytes.
Cytokine Release Syndrome
Cytokine release syndrome occurs in patients with severe COVID-19
infection. Many proinflammatory cytokines are significantly elevated in severe
cases, including interleukin (IL)-2, IL-10, IL-6, IL-8 and tumor necrosis
factor (TNF)-α. Cytokines play an important role during infection with the
virus (phase 1) and during ongoing severe inflammation (phase 2), resulting in
acute respiratory distress syndrome (ARDS) and other end-organ damage.
Direct Myocardial Cell Injury
The interaction of SARS-CoV-2 with ACE2 can cause changes to the
ACE2 pathways, leading to acute injury of the lung, heart and endothelial
cells. A small number of case reports have indicated that SARS-CoV2 might
directly infect the myocardium, causing viral myocarditis. However, in most
cases, myocardial damage appeared to be caused by increased cardiometabolic
demand associated with the systemic infection and ongoing hypoxia caused by
severe pneumonia or ARDS.
Acute Coronary Syndrome
Plaque rupture leading to acute coronary syndrome can result from
the systemic inflammation and catecholamine surge inherent in this
disease. Coronary thrombosis also has been identified as a possible cause
of acute coronary syndrome in COVID-19 patients.
Other Possible Mechanisms
Certain medications such as corticosteroids, antiviral medications
sand immunological agents may have cardiotoxic side effects. Electrolyte
disturbances can occur in any critical systemic illness and trigger
arrhythmias, for which patients with underlying cardiac disease are at higher
risk. There is particular concern about hypokalemia in patients with COVID-19,
given the interaction of SARS-CoV-2 with the renin-angiotensin-aldosterone
system. Hypokalemia is well known to increase vulnerability to various kinds of
arrhythmia.
Spectrum
of Clinical Presentations
Patients
with COVID-19 present with a broad spectrum of clinical cardiac presentations:
some patients manifest no clinical evidence of heart disease, some have no
symptoms of heart disease but have cardiac test abnormalities and some have
symptomatic heart disease. Cardiac complications include myocardial injury,
heart failure, cardiogenic shock, and cardiac arrhythmias including sudden
cardiac arrest. The following sections review the spectrum of cardiac
manifestations in patients with COVID-19.
Most
patients with COVID-19 with abnormalities on cardiac testing have typical
symptoms of COVID-19, including cough, fever, myalgia, headache, and dyspnea,
as described separately. A minority of patients with COVID-19 present with
symptoms that may suggest heart disease (such as palpitations or chest pain).
These symptoms may or may not be accompanied by prior or concurrent symptoms
typical of COVID-19 infection. Symptoms such as dyspnea and chest pain may be
caused by noncardiac and cardiac causes.
Asymptomatic
heart disease — Most patients with COVID-19 with
cardiac test abnormalities (such as cardiac troponin elevation, electrocardiographic
[ECG] abnormalities or cardiac imaging findings) lack symptoms of heart
disease.
As
noted above, some symptoms, such as dyspnea, are nonspecific and are evaluated
in the context of concurrent symptoms, signs, and test findings to determine if
they are more likely caused by a noncardiac condition (eg, pneumonia) or
cardiac disease.
Myocardial
injury — Myocardial injury as detected by troponin elevation
is commonly identified in patients hospitalized with COVID-19, but the causes
of myocardial injury have not been fully elucidated. Cardiac troponin elevation
does not distinguish among the causes of injury. As discussed above, there are
many putative causes of myocardial injury in patients with COVID-19, but the
cause in individual patients is frequently not identified. Clinical conditions
associated with myocardial injury include myocarditis, stress cardiomyopathy,
and myocardial infarction (MI).
The term "myocardial injury" encompasses all conditions causing cardiomyocyte death. Cardiac troponin elevation is the generally accepted marker for identifying myocardial injury. Myocardial injury is commonly clinically identified by the presence of at least one cardiac troponin value above the 99th percentile upper reference limit, in accordance with the definition of myocardial injury in the Fourth Universal Definition of Myocardial Infarction. While high-sensitivity cardiac troponin levels are sensitive markers of myocardial injury, some patients with disease processes causing cardiomyocyte death may have troponin levels below the 99th percentile URL.
Myocarditis —
Chen and colleagues also had a similar observation, with elevation of interleukin (IL)-2R, IL-6, IL-10, and tumour necrosis factor α among the cohort of severe COVID-19 patients in a single-centre retrospective study. Cytokine storm is not unique to severe COVID-19, because MERS-CoV and SARS-CoV have shown cytokine surge syndrome among the spectrum of coronavirus disease. Whether this phenomenon is the main cause of fulminant myocarditis still uncertain.
Another
potential cause of myocarditis is direct viral involvement. SARS-CoV-2 uses the
angiotensin-converting enzyme 2 via its S-spike to bind and anchor to the
receptors, hence an entry point to the cell. Hence, it is
reasonable to consider viral inclusion or associated myocardial inflammation as
the pathogenesis of myocarditis. This direct myocardial involvement was seen in
MERS, with one report showing evidence of subepicardial late gadolinium
enhancement, consistent with myocarditis. In this case, the distribution of late gadolinium enhancement in the
subepicardial region is consistent with myocarditis.
Stress
cardiomyopathy — Stress cardiomyopathy has been
reported in patients with COVID-19. In addition, some case reports of
clinically suspected myocarditis complicating COVID-19 have described marked
recovery of left ventricular systolic function within days, suggestive of
stress cardiomyopathy or fulminant myocarditis.
In a review of 12 cases of stress cardiomyopathy associated with COVID-19, the mean age was 70.8 and the majority of patients were female. An elevated troponin level was identified in 11 of the cases. There was no significant coronary artery disease on invasive coronary angiography in two patients, coronary artery disease in arteries supplying a different territory in one case, negative computed tomography coronary angiography in five cases, and no coronary artery disease on autopsy in one case; the coronary arteries were not examined in three cases. Complications included HF, cardiogenic shock, cardiac tamponade, and hypertensive crisis.
Myocardial
infarction — Studies suggest that COVID-19 increases the risk of
acute MI. In one study, there was an increased risk of acute MI in patients
with a new diagnosis of COVID-19 compared to noninfected controls. With
COVID-19 infection, the majority of MIs are type 2 and related to the primary
infection, hemodynamic, and respiratory derangement. As such, the primary
disorders should be treated, and in most cases the patient can be treated
conservatively with regard to coronary disease. If a type 1 infarction is
thought to be the primary etiology of the MI, standard therapies can be
considered.
Heart
failure
General
prevalence — HF in patients with COVID-19 may be
precipitated by acute illness in patients with preexisting known or undiagnosed
heart disease (eg, coronary artery disease or hypertensive heart disease),
acute hemodynamic stress or acute myocardial injury. Cardiovascular risk
factors and cardiovascular disease are highly prevalent in hospitalized
patients with COVID-19. Patients with a known history of HF may suffer an acute
decompensation due to the development of COVID-19 disease.
Although
acute HF incidence was not documented in some series of hospitalized patients
with COVID-19, elevated natriuretic peptides and N-terminal pro-BNP are common,
particularly in patients with evidence of cardiac injury, as described below.
Right
heart failure — Acute cor pulmonale (right HF
due to acute pulmonary hypertension) precipitated by acute pulmonary embolism
or adult respiratory distress syndrome (ARDS) has been described in patients
with COVID-19. Patients with COVID-19 are at risk for development of ARDS.
Venous thromboembolism (including extensive deep vein thrombosis and pulmonary
embolism) is common in acutely ill patients with COVID-19.
Cardiogenic
shock — The first confirmed instance of Cardiogenic
Shock due to COVID-19 infection through myocardial infiltration by viral particles was in a 69-year-old
patient from Italy. This was confirmed via biopsy. Since then, the two most probable mechanisms of cardiogenic shock related to COVID-19 are direct invasion and cytokine storm. According to a recent study out of an ICU in
Washington state, one-third of critically ill patients with COVID-19 had
clinical signs of cardiogenic shock and cardiomyopathy.
According to another observational study in China, COVID-19 associated cardiogenic shock has a poor prognosis.
The two most likely mechanisms that
contribute to COVID-19 cardiogenic
shock are:
·Direct invasion of the virus into the cardiomyocytes
· Cytokine storm activated
by T
helper cells that triggers a systemic
hyperinflammatory response
The causes of cardiogenic shock related
to COVID-19 may
include:
· Newly emerging COVID-19 associated myocarditis, cardiac
arrhythmias, cardiomyopathy, or an acute
coronary syndrome deteriorated into cardiogenic shock
· Worsening of previous left
ventricular failure due to COVID-19
· COVID-19-associated multisystem
inflammatory syndrome in children (MIS-C)
Cardiogenic Shock: A Critical Care Crisis in the Age of COVID-19
Multisystem
inflammatory syndrome in adults (MIS-A) — Multisystem
inflammatory syndrome (MIS) was initially described in children (MIS-C) with
recent COVID-19 infection as a Kawasaki-like illness associated with fever,
gastrointestinal symptoms, shock, LV systolic dysfunction and elevated
inflammatory markers.
Similar cases of MIS have been described in young to middle-aged adults (MIS-A) also presenting with fever, gastrointestinal symptoms, and shock with vasoplegia, LV systolic dysfunction and elevated inflammatory markers. Many of these patients had history of recent COVID-19 and had positive SARS-CoV-2 antibody tests, with fewer having positive SARS-CoV-2 reverse transcription polymerase chain reaction tests. This diagnosis should be considered in young adults presenting in inflammatory shock. This syndrome appears to be highly responsive to parenteral steroids.
Cardiac arrhythmias — The prevalence of arrhythmias and conduction system disease (and cardiovascular disease in general) in patients with COVID-19 varies from population to population. The vast majority of patients presenting with a systemic illness consistent with COVID-19 will not have symptoms or signs of arrhythmias or conduction system disease. Patients may be tachycardic (with or without palpitations) in the setting of other illness-related symptoms (eg, fever, shortness of breath, pain, etc). In most available reports, the specific cause of palpitations or type of arrhythmia have not been specified. Hypoxia and electrolyte abnormalities, both known to contribute to the development of acute arrhythmias, have been frequently reported in the acute phase of severe COVID-19 illness; therefore, the exact contribution of COVID-19 infection to the development of arrhythmias in asymptomatic, mildly ill, critically ill, and recovered patients is not known.
- The most common arrhythmia overall in patients with COVID-19 is sinus tachycardia, but the most likely pathologic arrhythmias include atrial fibrillation, atrial flutter, and monomorphic or polymorphic VT.
- The differentiation between various tachycardias based on regularity (ie, regular or irregular) and QRS width (ie, narrow or wide QRS complex) requires only a surface ECG.
- Bradyarrhythmias, including sinus pauses or high-grade heart block with slow escape rhythms, have not typically been seen but can be identified using a surface ECG if present.
CARDIAC
TEST FINDINGS
A
variety of cardiac test abnormalities have been described in patients with
COVID-19, as described in the following sections.
Biomarkers — Cardiac
troponin and natriuretic peptide (B-type natriuretic peptide [BNP] and
N-terminal pro-BNP [NT-proBNP]) biomarkers are commonly elevated among
hospitalized patients with COVID-19 and are associated with increased risk of
mortality.
Troponin — Cardiac
troponin elevation is a marker of myocardial injury and is commonly identified
in patients hospitalized with COVID-19, but the causes of troponin elevation
have not been fully elucidated. The frequency of myocardial injury (as
reflected by elevation in cardiac troponin levels) is variable among
hospitalized patients with COVID-19, with reported frequencies of 7 to 36
percent. The frequency of troponin elevation appears to be lower among patients
with mildly symptomatic COVID-19.
Natriuretic
peptides — Natriuretic peptides (BNP and NT-proBNP) are
commonly elevated in hospitalized patients with COVID-19 and natriuretic
peptide elevation is associated with mortality risk, as described above.
Electrocardiogram — The
various ECG findings observed in patients with COVID-19 likely reflect the
combined effects of acute illness and chronic heart disease. The range of ECG
findings was illustrated in a study of 756 patients (mean age 63 years)
hospitalized with COVID-19 in New York. The mortality rate was 11.9 percent
during the follow-up period of two to seven weeks. Cardiovascular risk factors
and conditions were common, including obesity (37 percent), diabetes mellitus
(29 percent), hypertension (57 percent), coronary artery disease (CAD, 14
percent) and HF (7 percent). This study did not include data on troponin levels
or comparison with prior ECGs.
●Atrial fibrillation or flutter was observed
in 5.6 percent. Atrial premature beats were observed in 7.7 percent and
premature ventricular contractions in 3.4 percent.
●Right bundle branch block was identified in
7.8 percent, left bundle branch block in 1.5 percent and nonspecific intraventricular
conduction delay in 2.5 percent.
●Repolarization abnormalities included
localized ST elevation in 0.7 percent, localized T-wave inversion in 10.5
percent and nonspecific repolarization abnormalities in 29 percent.
●In a multivariable model including age,
clinical characteristics, and ECG findings, the variables associated with risk
of death were presence of CAD, an immunosuppressed state, hypoxemia, and the
following ECG findings: APBs (OR 2.57, 95% CI 1.23-5.36), RBBB or IVCD (OR
2.61, 95% CI 1.32-5.18), localized T-wave inversion (OR 3.49, 95% CI
1.56-7.80), and nonspecific repolarization abnormality (OR 2.31, 95% CI
1.27-4.21).
Cardiac
imaging
Echocardiogram — A
variety of echocardiographic findings have been identified in patients with
COVID-19, as illustrated by a study of an unselected population of 100 patients
hospitalized with COVID-19.
●Transthoracic echocardiography findings
included right ventricular dilation and dysfunction (39 percent), LV diastolic
dysfunction (16 percent) and LV systolic dysfunction (10 percent). Patients
with an elevated troponin level or worse clinical condition had worse RV
function.
●Among the 20 percent of patients with subsequent
clinical deterioration, the most common echocardiographic findings were
worsened RV function (12 patients) and worsened LV systolic and diastolic
function (5 patients). Femoral deep vein thrombosis was identified in 5 of 12
patients with RV failure.
Cardiovascular magnetic resonance — Cardiovascular magnetic resonance abnormalities have been identified in patients with COVID-19 as well as in patients who have recently recovered from COVID-19, though most reported abnormalities have been nonspecific. CMR findings identified in some of these patients include elevations in native T1 (a nonspecific finding seen with acute myocardial injury, fibrosis, or infiltration), T2 (a marker of edema), and, less commonly, late gadolinium enhancement (a marker of acute myocardial injury, fibrosis, or infarction). Since limited endomyocardial biopsy data and no follow-up data have been reported, the clinical significance of these findings is uncertain. Moreover, since no patients had a CMR examination before COVID-19, it remains undetermined whether the abnormal findings might have already been present and therefore be unrelated to COVID-19.
Myocardial
histology and viral genome analysis — Myocarditis is
commonly suspected in patients with COVID-19 and elevated cardiac troponin
levels. However, there have been few reported cases of histologically confirmed
myocarditis and viral myocarditis caused by SARS-CoV-2 has not been
definitively confirmed by histologic and viral genome analysis.
Proof
that SARS-CoV-2 is a cause of viral myocarditis requires identification of
histologic findings of active myocarditis plus myocyte necrosis not typical of
ischemic injury, identification of the SARS-CoV-2 genome or viral particles in
cardiomyocytes and exclusion of known cardiotropic viruses. Cardiotropic
viruses that are known to be associated with myocarditis (eg, enterovirus,
which is associated with diarrhea and parvovirus B19, which is associated with
a pseudoinfarct presentation) were not searched for in most of the reported
cases and might be involved.
Comprehensive Cardiovascular Care for
COVID-19 Patients
Cardiac care needs to be optimized for
COVID-19 patients with an aim for early detection and management of cardiac
ailments with the simultaneous aim at triaging cases and proper protection to
prevent or minimize COVID-19 exposure. As Bonow et al. have rightly put,
the message to the patients should be clear that prompt emergency care to be
sought in case of warning cardiac symptoms. Mask-wearing, physical distancing
remains as essential as ever. Simultaneously, doctors and researchers are
finding the best practices for COVID-19 related cardiovascular disease.
ACE inhibitors (ACEI)/ Angiotensin Receptor
Blockers (ARB)
Early in 2020, a controversy grew regarding
the safe usage of these drugs in COVID-19 patients. The current consensus
agrees to the continued use of these medications. BRACE CORONA trial was
presented in ESC Congress 2020, which found no significant difference in the
number of days alive and out of hospital through 30 days among subjects
receiving continuous ACEI/ARB and hospitalized for COVID-19 compared to those
in whom these medicines were temporarily suspended. Five common classes of
antihypertensive medications are safe in patients of COVID-19 and do not
increase the likelihood of infection.
Remdesivir
Remdesivir is an antiviral (RNA polymerase
inhibitor) drug used to treat COVID-19. A multicenter, double-blind RCT from
China studied Remdesivir for adult patients hospitalized for severe COVID-19.
The study showed a reduction in clinical improvement in the treatment group
compared with controls, but the difference was not significant. A
subsequent trial, sponsored by the US National Institute of Allergy and
Infectious Disease, assessed 1063 hospitalized COVID-19 patients in a
remdesivir treatment trial. Results published in the New England Journal of
Medicine indicated a faster time to recovery for patients who received
remdesivir vs. placebo.
The US Food and Drug Administration (FDA) has
issued an emergency use authorization for remdesivir in all patients
hospitalized with COVID-19. Thus far, no prominent cardiovascular side effects
have been reported with Remdesivir, although these may become apparent with
future use during the COVID-19 pandemic.
Hydroxychloroquine and Chloroquine
Hydroxychloroquine was introduced
as a potential treatment for COVID-19 patients based on an open-label,
single-group study from France. However, an observational study of
hospitalized COVID-19 patients conducted at a large medical center in New York
City found no apparent benefit from hydroxychloroquine. The use of
hydroxychloroquine alone or hydroxychloroquine plus azithromycin did not
improve a composite endpoint of intubation or death.
Chloroquine has been noted to cause
atrioventricular blocks and prolonged QTc, especially when combined with
azithromycin. The lack of benefit seen in clinical trials and the
potential for cardiovascular side effects has led the FDA to revoke its
emergency use authorization of hydroxychloroquine and chloroquine for patients
in COVID-19.
Azithromycin
Azithromycin was commonly used in combination
with hydroxychloroquine as a treatment early in the pandemic. However, several
studies of this combination have not shown any clinical benefit. Azithromycin
is a macrolide and is known to prolong the QTc interval. Combining azithromycin
with chloroquine or hydroxychloroquine increases QTc prolongation and
potentially the risk for torsade de points. The lack of clinical benefit
and the potential for cardiac arrhythmias has discouraged physicians from using
azithromycin in COVID-19.
Lopinavir-ritonavir
Lopinavir and ritonavir are protease
inhibitors approved by the FDA for HIV-1 infection. In a recent study published
in the New England Journal of
Medicine, researchers observed
no survival benefit after treatment with lopinavir-ritonavir in hospitalized
adults with severe COVID-19. Lopinavir-ritonavir can interact with
cardiovascular drugs such as antiarrhythmic agents, antiplatelet drugs and
anticoagulants that are metabolized by cytochrome P-450 3A4; therefore, it
should be used with caution, especially in patients with underlying
cardiovascular disease.
Steroids
The World Health Organization has recommended
using systemic steroids to treat COVID-19 infection. Corticosteroids are
known to possess potent anti-inflammatory effects and they have been studied
extensively in the treatment of sepsis and ARDS. However, they are also known
to cause fluid retention, electrolyte derangement, hyperglycemia, and
hypertension. At the onset of the COVID-19 pandemic, concerns about potential
harm from steroids in COVID-19 were based on data collected and extrapolated
during the previous SARS-CoV outbreak. Nonetheless, the recent RECOVERY trial
compared dexamethasone 6 mg once daily for up to 10 days versus usual care
alone in hospitalized patients with COVID-19 receiving invasive mechanical
ventilation or oxygen. Dexamethasone reduced 28-day mortality by one-third in
patients on a mechanical ventilator and by one-fifth in patients requiring
oxygen therapy.
Aspirin
In a retrospective study, the use of low-dose
Aspirin in patients hospitalized with COVID-19 was associated with better
outcomes.
Tocilizumab
Tocilizumab, an anti–IL-6
receptor antibody, has been investigated to treat hospitalized COVID-19
patients. IL-6 levels are elevated in COVID-19 patients and significantly
elevated in patients with severe disease. Tocilizumab’s potential efficacy lies
in its ability to reduce the inflammatory response, including the cytokine
storm that contributes to ARDS and death. As for cardiac side effects,
tocilizumab is known to increase cholesterol levels, but there are conflicting
reports on its effect on long-term cardiac morbidity and mortality.
Convalescent Plasma
Convalescent plasma for the treatment of
COVID-19 patients is obtained from individuals who have recovered from COVID-19
and have generated an immune response. Small randomized trials and case studies
have shown some benefit from convalescent plasma in hospitalized patients with
severe COVID-19, especially if given early in the disease course. The FDA
has granted emergency use authorization for convalescent plasma in hospitalized
patients with COVID-19.
Ivermectin
Ivermectin was introduced as a potential
treatment for COVID-19 patients. Ivermectin is an antiparasitic drug used to
treat Strongyloides and onchocerciasis infection. A Meta-analysis by Dr. Andrew
Hill investigated Ivermectin in 18 randomized clinical trials. There was a 75%
reduction in mortality found in moderate or severe infection in six randomized
trials. In another randomized trial of 476 patients, Ivermectin did not shorten
the duration of the infection. Multiorgan failure was reported in four
patients. The FDA has issued a warning against using Ivermectin to prevent or
treat COVID-19 infection.
Vaccination
The SARS-CoV-2 genetic sequence was published
in January 2020 and since then, researcher teams worldwide have been working
actively to develop a vaccine against SARS-CoV-2. More than 90 vaccines are
being developed at this time. Vaccination has already started in various
countries. The mRNA- based vaccines developed by Pfizer and Moderna have been
granted emergency use authorization (EUA) by the US Food and Drug
Administration (FDA). Many healthcare workers have already received these
vaccines. Two
vaccines were granted emergency use authorization by the Central Drugs Standard
Control Organization (CDSCO) in India, Covishield® (AstraZeneca's vaccine
manufactured by Serum Institute of India) and Covaxin® (manufactured by Bharat
Biotech Limited). Sputnik - V has been granted EUA in the month of April 2021
in India.
Johnson
& Johnson The Johnson & Johnson vaccine is a viral vector vaccine like
the one developed by Oxford-AstraZeneca. The vaccine uses a modified adenovirus
to deploy the SARS-CoV-2 virus's "spike protein" to human cells,
which triggers an immune response. The
three-dose ZyCoV-D vaccine prevented symptomatic disease in 66% of those
vaccinated, according to an interim study quoted by the vaccine maker Cadila
Healthcare. The ZyCoV-D vaccine is also the world's first DNA vaccine
against Covid-19. Like other vaccines, a DNA vaccine, once administered,
teaches the body's immune system to fight the real virus.
No
significant cardiac complication has been reported with any of the vaccines
thus far.
Prognosis
Most of the patients (80%) will get a mild
form of the disease. The severe form of the disease occurs in about 15% of
patients requiring hospitalization and the critical form occurs in about 5% of
patients requiring intensive care. The current mortality rate ranges between 2%
to 5% of all patients with COVID-19 but is much higher in patients
requiring invasive mechanical ventilation. The major cause of death in COVID-19
is acute respiratory distress (ARDS); however, there is also significant other
vital organ involvement, including the cardiovascular system and
shock. The presence of chronic cardiac diseases or cardiac involvement
leads to a higher mortality rate in comparison to patients without
cardiovascular disease.
In this COVID-19 pandemic, fewer cardiac
patients have attended clinics or hospitals due to the fear of contracting the
infection. On the contrary, cardiac patients irrespective of SARS-CoV-2
infection need prompt evaluation and management, more so during this pandemic
as the resources and workforce are often compromised.
The prognostic significance of cardiovascular
disease was amply illustrated in a cohort of 191 patients in which 30% had
hypertension and constituted 48% of nonsurvivors, whereas 8% had cardiovascular
disease and constituted 13% of nonsurvivors. In a report of 44672
confirmed cases of COVID-19 from the Chinese Center for Disease Control and
Prevention, the overall case-fatality rate was 2.3% for the entire cohort but
significantly higher for patients with hypertension (6%), diabetes (7%), or
cardiovascular disease (11%).
Conclusion
COVID-19 is mainly a lung disease.
However, a hyperergic immune reaction, or “cytokine storm”, with a dramatic
systemic impact can be also observed in a later stage of the disease. In
addition, COVID-19 prognosis can be deteriorated by pre-existing cardiovascular
diseases, or acute cardiovascular events can be induced by COVID-19 even in the
absence of a related history. They include the possibility of thrombotic
manifestations in the form of local (i.e. pulmonary) or systemic (DIC) events,
as well as QT interval prolongation. Finally, in the lack of evidence regarding
the postulated harmful effect of ACE inhibitors and sartans in terms of
SARS-CoV-2 virulence, these drugs should not be discontinued. Indeed, whether
infection by coronaviruses might affect ACE2 function adversely, thus
potentially contributing to infectious disease burden in selected patients, is
a possibility that deserves investigation.
There is an interaction between COVID-19
and CVD. SARS-CoV-2 can cause CVD, including acute myocardial injury,
arrhythmia, and heart failure, through a variety of pathways. COVID-19 patients
with underlying CVD have a higher mortality rate. Therefore, close attention
should be paid to cardiovascular complications during the diagnosis and
treatment of COVID-19 to reduce the mortality of patients. At present, there is
insufficient evidence that the use of ACEIs/ARBs aggravates the condition of
COVID-19 patients. Therefore, it is not necessary to stop treatment with
ACEIs/ARBs in CVD patients after SARS-CoV-2 infection.
Dr. Mayank Chandrakar is a writer also. My first book "Ayurveda Self Healing: How to Achieve Health and Happiness" is available on Kobo and Instamojo. You can buy and read.
For Kobo-
https://www.kobo.com/search?query=Ayurveda+Self+Healing
The second Book "Think Positive Live Positive: How Optimism and Gratitude can change your life" is available on Kobo and Instamojo.
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