COVID-19 in Cyanotic Congenital Heart Disease

Ammar, Lama A; Nassar, Joseph E; Bitar, Fadi; Arabi, Mariam

doi:https://doi.org/10.1155/2023/5561159

Canadian Journal of Infectious Diseases and Medical Microbiology

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Abstract Materials and Methods Discussion Conclusion Conflicts of Interest Authors’ Contributions Acknowledgments References Copyright Related Articles

Review Article | Open Access

Volume 2023 | Article ID 5561159 | https://doi.org/10.1155/2023/5561159

COVID-19 in Cyanotic Congenital Heart Disease

Lama A Ammar,¹Joseph E Nassar,¹Fadi Bitar,¹and Mariam Arabi¹

Academic Editor: Arif Siddiqui

Received24 Jan 2023

Revised30 Mar 2023

Accepted06 Apr 2023

Published18 Apr 2023

Abstract

Congenital heart disease (CHD) is the most prevalent congenital defect in newborn infants. Due to the various types of heart abnormalities, CHD can have a wide range of symptoms. Cardiac lesions comprise a range of different types and accordingly varying severities. It is highly helpful to classify CHD into cyanotic and acyanotic heart diseases. In this review, we are investigating the course of Coronavirus disease 2019 (COVID-19) in cyanotic CHD patients. The infection may directly or indirectly affect the heart by affecting the respiratory system and other organs. The effect on the heart that is pressure- or volume-overloaded in the context of CHD is theoretically more severe. Patients with CHD are at a higher risk of mortality from COVID-19 infection or suffering worse complications. While the anatomic complexity of CHD does not seem to predict the severity of infection, patients with worse physiological stages are more susceptible such as cyanosis and pulmonary hypertension. Patients with CHD exhibit continuous hypoxemia and have lower oxygen saturations because of a right-to-left shunt. Such individuals run the danger of rapidly deteriorating in the event of respiratory tract infections with inadequate oxygenation. Additionally, these patients have a higher risk of paradoxical embolism. Hence, critical care should be given to cyanotic heart disease patients with COVID-19 in comparison to acyanotic patients and this is through proper management, close observation, and adequate medical therapy.

1. Congenital Heart Disease

1.1. General Overview

CHD is the most prevalent congenital defect in newborn infants [1]. CHD accounts for about 30% of all congenital abnormalities. Its prevalence varies significantly amongst populations, averaging 8 per 1,000 live births per year. Due to advancements in screening and detecting techniques, the incidence of CHD has increased in recent decades [2].

The survival rate of CHD patients greatly increased with the quick advancements in surgery and detection approaches. It mainly depends on the kind and severity of CHD, with a survival rate of over 98 percent for milder illnesses [3]. However, these patients continue to have a very high risk of developing lower respiratory infections that cause increased morbidity and mortality [4].

Due to situations of various types of heart abnormalities, CHDs can have a variety of symptoms. A blue tint to the skin (cyanosis), clubbed fingernails, heavy perspiration, intense exhaustion, fatigue, poor feeding, rapid heartbeat, shortness of breath, and chest pain are some of the general symptoms of this illness [5]. Congenital cardiac diseases manifest themselves soon after birth, although symptoms do not appear until early childhood or adolescence. Adulthood is when some complications can arise, such as issues with heart and body growth and development, infections of the sinuses, respiratory tract, throat, lungs, and heart, endocarditis, pulmonary hypertension, high blood pressure, and a heart that cannot pump enough blood, which can result in heart failure [5].

In numerous experimental animal models, cardiac malformations have been created by disrupting specific molecules that act in the developmental pathways involved in myocyte specification, differentiation, or cardiac morphogenesis [1]. The precise genetic, epigenetic, and environmental causes of the many heart abnormalities are still not entirely understood. Researchers have made some progress in their understanding of unusual Mendelian CHD families through human genome analysis and DNA gene sequencing in patient cohorts with CHD throughout the past 40 years of genetic study into heart illnesses.

Although the discovery of disease gene mutations’ penetrance is well known, this research has yielded three noteworthy insights: first, human CHD mutations affect a heterogeneous set of molecules that orchestrate cardiac development; second, CHD mutations frequently alter gene-protein dosage; and third identical pathogenic CHD mutations cause a variety of distinct malformations, and this suggests that higher-order interactions are responsible for specific CHD phenotypes.

1.2. Types of Congenital Heart Diseases

There are very few misdiagnoses made nowadays since clinical and echocardiographic diagnoses are so precise, but there are still significant diagnostic challenges with the classification and, consequently, with the inclusion as specific lesions. These lesions comprise a range of different types and accordingly varying severities. CHD lesions include isolated ventricular septal defect, patent ductus arteriosus, atrial septal defects of the fossa ovalis (secundum) type, isolated partial anomalous pulmonary venous connection, atrioventricular septal defects, pulmonic stenosis, bicuspid aortic valves, coarctation of the aorta, and mitral incompetence [6].

The classification of numerous lesions is inconsistent, and hence the classification of CHD into three types of lesions based on severity is, therefore, highly helpful. The first category presents severe CHD that encompasses cyanotic and acyanotic heart diseases. Most patients who present extremely unwell during the newborn period or early infancy fall into this category (Figure 1). Cyanotic heart disease includes tetralogy of fallot including pulmonary atresia, absent pulmonary valve, and hypoplastic right or left heart. Although right-to-left shunting, insufficient pulmonary blood flow, or common mixing lesions can be used to categorize cyanotic heart lesions, many defects contain several physiologic problems [6]. The “five T’s” of cyanotic CHD which include transposition of the great arteries, tetralogy of fallot, truncus arteriosus (also known as “truncus”), total anomalous pulmonary venous connection, and anomalies of the tricuspid valve remain a helpful mnemonic [7]. Acyanotic heart diseases include atrioventricular septal defect, a large ventricular septal defect, and a large patent ductus arteriosus [6]. The second category presents moderate CHD which comprises mild or moderate aortic stenosis or aortic incompetence, pulmonic stenosis or incompetence, and complex forms of ventricular septal defect. The third category presents mild CHD, most patients fall within this category, and this is due to their lack of symptoms, potential lack of substantial murmurs, and frequent early spontaneous resolution of their lesions. This category includes small ventricular septal defect, small patent ductus arteriosus, mild pulmonic stenosis, and others [6].

1.3. Noncardiac Cyanosis-Inducing Etiologies

Some patients present as suspects of cyanotic heart defect as their presentation resembles that of Cyanotic heart disease; however, upon cardiological examinations, a heart defect is excluded. Serological markers reveal increased blood methemoglobin (MHb) levels and decreased activity of NADH-dependent MHb reductase which causes methemoglobinemia [8]. Methemoglobinemia, an uncommon yet easily detected condition, may resemble cyanotic CHD. A permanent or temporary enzyme shortage may be caused by toxic substances, particularly nitrate absorption. Methemoglobinemia with subsequent hemoglobin disorders or congenital enzyme deficiencies has a dismal prognosis. The preferred therapeutic and diagnostic tool is methylene blue [9]. As a matter of physiology, hemoglobin loses its capacity to transport molecular oxygen and carbon dioxide when the ferrous (Fe₂) iron component of hemoglobin is oxidized to the ferric (Fe₃) state to generate MHb. Cyanosis, compromised aerobic respiration, metabolic acidosis, and in extreme situations, mortality, are all effects of increased MHb levels. To convert MHb back to hemoglobin, erythrocytes contain reduced glutathione, reduced NADPH-MHb reductase, and cytochrome-b5-MHb reductase. When these enzyme systems are overworked, methemoglobinemia becomes fatal [10]. Individuals develop cyanosis as the MHb content rises. The typical symptoms include confusion and tachypnea, followed by anxiety, light-headedness, headache, and tachycardia. Patients may have acidosis, seizures, arrhythmias, and eventually coma and death if the MHb levels rise. For a given MHb concentration, patients with the underlying cardiac, pulmonary, or hematologic disease may have more severe symptoms [11].

2. COVID-19/SARS-CoV-2

2.1. Overview

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 outbreak, also known as COVID-19, which was initially discovered in China in December 2019 [12]. The COVID-19 pandemic was formally classified as a public health emergency of international concern by the World Health Organization in January 2020, as a result of the SARS-CoV-2 virus’ quick spread over the world. Coronaviruses belong to the Nidovirales order’s Coronaviridae family of enclosed, positive single-stranded RNA viruses with genomes that range in size from 26 to 32 kb [13]. There are currently four identified genera of the virus, namely, alpha (α), beta (β), gamma (γ), and delta (δ) [14]. The novel SARS-CoV-2, on the other hand, is a member of the genus coronavirus and has an RNA genome size of 29.9 kb [15]. Research has shown that the SARS-CoV-2 virus is primarily spread between humans by inhalation or contact with droplets that are infectious, with an incubation period of 2 to 14 days [16‐18]. A wide variety of clinical symptoms, ranging from asymptomatic to symptomatic, are associated with SARS-CoV-2 infection, including respiratory symptoms, fever, shortness of breath, cough, dyspnea, viral pneumonia, and in more severe cases, pneumonia, severe acute respiratory syndrome, heart failure, renal failure, and even death [19]. However, respiratory failure, septic shock, renal failure, hemorrhage, and heart failure are the leading causes of death associated with COVID-19.

Individual differences in the clinical presentation of new SARS-CoV-2 infection range from asymptomatic presentations to severe respiratory distress syndrome and multiorgan failure. Consequently, it is difficult to make an accurate COVID-19 diagnosis. The epidemiological history, clinical signs, and confirmation by a range of laboratory detection techniques are the main components of the usual clinical diagnosis of COVID-19 (Figure 2) [20].

Figure 2

Schematic presentation of analytical methods available for SARS-CoV-2 detection. A sample should be obtained from the patient by means of a long swab that is inserted into the nostrils and is adequately swept against the walls of the nasopharynx. Following sample collection, RNA extraction is performed followed by any of the analytical laboratory methods (RT-qPCR, RT-LAMP, NGS, CRISPR, and ddPCR). Alternatively, a sample can be collected from the patient’s serum. Blood is then treated to obtain antigens and/or antibodies present which then can be analyzed via ELISA, lateral flow of chemiluminescence immunoassay. Recreated from [20] via BioRender.

2.2. COVID-19 Pathophysiology

The three phases of COVID-19 represent its pathogenesis. Viral entry into the respiratory epithelium initiates the first phase, which is followed by cellular proliferation. The initial immune response is characterized by moderate symptoms and is characterized by the activation of monocytes and macrophages. Pulmonary vasodilatation and enhanced vascular permeability mark the start of the subsequent phase. Following leukocyte migration, fluid extravasation and pulmonary edema occur. Alveolar injury, hypoxia, heart damage, and stress are thus provoked. The excessive inflammatory response leads to a large cytokine storm in the last phase, which is its defining feature [21].

3. COVID-19 in Patients with Cyanotic Congenital Heart Disease

The SARS-CoV-2 infection may directly or indirectly affect the heart by affecting the respiratory system and other organs. In the context of COVID-19, there are three processes that result in cardiac involvement: (1) direct damage brought on by direct viral entry into cardiac cells, (2) hypoxia-induced myocardial ischemia, and (3) an exaggerated, heightened inflammatory response characterized by endothelial overactivation and microvascular thrombi [2, 22]. The effects of this infection on a heart that is pressure- or volume-overloaded in the context of CHD could theoretically be more severe. Furthermore, there are no established risk factors for COVID-19 severity in CHD patients [23]. Patients with CHD frequently exhibit genetic abnormalities, although it is unclear how these syndromes may affect the patient in this case. Physicians should prioritize emergency measures by learning how CHD affects the course and outcome of COVID-19 [23]. Patients with CHD are thought to be at a higher risk of mortality from COVID-19 infection or suffering worse complications. In a study conducted by Bromberg et al., adults with CHD had comparable COVID-19 mortality rates to the general population. While the anatomic complexity does not seem to predict the severity of infection, patients with worse physiological stages are more susceptible, such as cyanosis and pulmonary hypertension [24]. The study yielded a conclusion that male sex, diabetes, cyanosis, pulmonary hypertension, renal insufficiency, and prior hospital admission for heart failure were all risk factors for poor prognosis in COVID-19 and COVID infection-related mortalities [24, 25].

The most typical symptom in these patients is cough, followed by edema, fever, dyspnea, cyanosis, restlessness, and poor feeding in infants. Laboratory results show that some patients exhibit extremely increased C-reactive protein or erythrocyte sedimentation rate. Others develop mild lymphopenia, and some develop thrombocytopenia during their hospital stay. Low oxygen saturation levels also seem to be an alarming laboratory finding [23].

Clinicians are in constant search for an association between CHD patients’ contraction of COVID-19 and adverse outcomes of infection. For this sake, some researchers consider hospitalization for COVID-19 requiring noninvasive or invasive ventilation and/or inotropic support, as well as a death outcome to be defining features of a problematic and complicated disease course [26]. Cyanotic lesions, such as unrepaired cyanotic abnormalities or Eisenmenger syndrome, were among the congenital heart anomalies that posed a particularly high risk and are considered the most important predictors of a complicated disease course [26]. Due to a right-to-left shunt as well as severe aberrant pathobiology of the pulmonary tissue and pulmonary vascular bed, individuals with cyanotic heart disease, including those with Eisenmenger syndrome, exhibit persistent hypoxemia and frequently have much lower resting oxygen saturations. In the event of respiratory tract infections with reduced oxygenation, such patients hold a risk of rapidly deteriorating. An increase in right-to-left shunting caused by an increase in pulmonary vascular resistance and an inflammatory-mediated decrease in systemic vascular resistance exacerbates pre-existing hypoxemia in the case of a severe COVID-19 infection [27]. Additionally, the risk of paradoxical embolism is higher for these patients. A worse result in these individuals may also be caused by the potential increased prothrombotic risk brought on by pre-existing hemostatic problems, venous stasis, endothelial damage, and inflammatory response [28]. D-dimer may aid in the early identification of these high risk patients and assist in outcome prediction. Additionally, preliminary findings show that anticoagulant medication appears to be related to decreased mortality in the subgroup satisfying sepsis-induced coagulopathy criteria or with noticeably raised D-dimer levels in patients with severe COVID-19 [29]. The main risk factor is venous stasis, which is frequently visible in the cavopulmonary circuit due to the lack of a pump for both pulmonary blood flow and systemic venous return; therefore, these patients should be given long-term anticoagulation [30]. Even lesser levels of pulmonary involvement can be anticipated to cause the patients status to worsen. To avoid stroke from an air embolism, air filters should be installed on all venous cannulas in patients with (residual) right-to-left shunts [31].

Oxygen saturation levels of less than 90% at rest or during activity may be typical in adults with CHD patients with cyanotic heart disease. Cyanosis can be remarkable when the fingers and toes are clubbed. In addition to the present measurements, treatment decisions must be based on the pre-COVID-19 baseline oxygen saturation [31]. Instead of absolute values of oxygen saturation, thresholds for oxygen dosing or switching to mechanical ventilatory assistance must be based on variables such as respiratory rate and lactate levels. Venesections should not be performed since chronic cyanosis causes an adaptive increase in hemoglobin levels that are needed in this situation (Figure 3) [31].

3.1. Impact of COVID-19 on Pediatric Patients with Congenital Heart Disease

According to recent advances, the COVID-19 infection and the pandemic’s collateral damage present a burden on pediatric patients with CHD. Most infected pediatrics have mild to moderate illnesses, and laboratory and radiographic data show significant interindividual variation. However, cardiac involvement in children with COVID-19 who are healthy has been observed and is related to a number of factors [2]. Children can develop myocarditis, arrhythmias, cardiogenic shock, and catastrophic multisystem inflammatory syndrome. Children who have been infected have reported cases of asymptomatic, mild, moderate, severe, and critically sick cases. Patients with CHD, especially those with cyanotic abnormalities, are more likely to need intensive care unit (ICU) hospitalization and artificial respiratory assistance. COVID-19 may aggravate hypoxemia and impair tissue perfusion in these patients. Additionally, patients with complex CHD who also have pulmonary hypertension, immunodeficiencies (such as DiGeorge syndrome), and other concomitant diseases such as reduced myocardial contractility are at risk of developing severe and critical COVID-19 illness [2].

3.2. Vaccination for COVID-19 in Congenital Heart Disease Patients

Until today, there are not enough data on the COVID-19 vaccine’s acceptability, immunogenicity, and safety in adults with CHD. In a study conducted by Fusco et al. on COVID-19 vaccination in adults with CHD has revealed that COVID-19 vaccinations, had it been Pfizer-BioNTech BNT162b2 vaccine, Moderna, or AstraZeneca-ChAdOx1, have acceptable immunogenicity and seem safe in adults with CHD. However, the most susceptible patients in the study displayed a reduced antibody response. Patients in this study reported symptoms after the first and second doses. Symptoms duration was always limited, there were no allergic responses, and the most frequent symptoms were headaches, fever, muscle soreness, gastrointestinal disturbances, exhaustion, and dizziness [32]. To this end, studies provided comforting information about the vaccinations’ good safety profile, with the majority of side effects being brief and mild, similar to what has previously been documented in the general population worldwide [33]. It appears that vaccination avoidance based on worries about vulnerability due to the underlying heart disease is not justified. Vaccine administration is a low-risk action. As noted before, regardless of prior viral infection, adults with CHD patients with advanced physiological stages may have reduced antibody responses; however, this does not diminish the positive effect of these patients receiving COVID-19 vaccines [32].

3.3. Specific Considerations for Severely Affected Adults with Congenital Heart Disease Patients

When handling severely impacted adults with CHD patients with complicated underlying lesions, a detailed study of the underlying anatomy and pathophysiology is necessary, and they should be admitted to secondary or tertiary adults with CHD centers. Many adults with CHD patients are prone to developing arrhythmias, which frequently require immediate management to avoid decompensation [34]. Some concerns are relevant for adults with CHD patients who are hospitalized in critical care units. For instance, common prior surgical procedures (Blalock–Taussig–Thomas shunts and subclavian flap) can alter blood pressure readings, so measures should be performed from the contralateral side. Chronic arterial occlusion typically prevents central venous access because of prior critical care stays, numerous operations, and pacemaker leads. Large catheters, such as those used for hemofiltration, may have trouble fitting through a persistently tiny right superior vena cava due to a persistently small right superior vena cava.

Patients with Down syndrome are more likely to develop lung infections and acute respiratory distress syndrome which are frequently linked to CHD and immunological abnormalities (Figure 3) [35].

In a study conducted by Sachdeva et al. on the outcome of COVID-19-positive children with heart disease and grown-ups with CHD, researchers aimed at identifying risk factors that might be associated with mortality in those patients. A total of 94 patients were included, and they were presented with either symptomatic or asymptomatic COVID-19 infection. In this study, researchers classified the types of heart diseases into obstructive, acyanotic, and cyanotic CHD and acquired heart disease in children. 31 patients had acyanotic CHD, and 39 patients were cyanotic, with >80% of the patients being unoperated. Based on the occurrence of cyanotic episodes, refractory heart failure, persistent shock, or the need for ventilatory support, the degree of sickness upon presentation was divided into severe and nonsevere illness [36]. Children with CHD are known to have poorer prognosis with common respiratory viral and bacterial infections, and pneumonia are the most prevalent noncardiac cause of mortality in these children [36, 37]. Furthermore, COVID-19 pneumonia in a child with CHD can result in hypercapnic vasoconstriction, worsening /Q mismatch, embolic events, worsening pulmonary hypertension, and progressive hypoxia. According to this study, children with cyanotic CHD are probably more prone to experience this combined impact, which will decrease tissue oxygenation and perfusion, hence, making these patients face a fatal battle against COVID-19 infection. [38].

Literature has some studies that contradict the former findings. Some studies concluded that children and young adults with an underlying cardiac condition rarely had to be hospitalized for coronavirus illness. Cardiovascular risk factors were not linked to an increased chance of hospitalization; however, extracardiac comorbidities were linked. The severe acute respiratory syndrome of coronavirus did not seem to be associated with the traditional cardiac risk factors for more severe acute respiratory infections in children. For instance, in these studies, most patients who required treatment had ventricular dysfunction, or had persistent, substantial cardiac abnormalities that affected hemodynamics, reported having mild or asymptomatic infections [39]. The patients with palliated single ventricle CHD and those with residual cyanotic CHD who are among the people most at risk for developing severe respiratory infections did not require hospitalization for the severe acute respiratory syndrome of coronavirus infection during the study period. When comorbidities were examined individually as risk factors, only chronic lung disease and immune suppression showed statistically significant correlations with hospitalization. This conclusion may be partially explained by the limited sample size of these studies, which reduces the sensitivity to identifying possible risk factors in cardiac patients [39].

To this end, according to the anatomical and physiological stage classification, patients with complex CHD, such as Fontan patients, cyanotic congenital heart defects (unrepaired or palliated), single ventricles, and pulmonary atresia, should be regarded as having high risk of complications from COVID-19 infection because of a decreased functional reserve. When patients are admitted, the treatment plan should address indicators of end-organ damage, symptomatic support, and management of respiratory failure. Patients with mild illness can be handled with noninvasive measures of additional oxygen support [40]. However, patients with severe COVID-19 disease frequently require intubation to improve oxygenation and ventilation because they have symptoms resembling acute respiratory distress syndrome. This can be difficult for Fontan patients because increased intrathoracic pressure brought on by positive pressure ventilation has detrimental effects on intrapulmonary and intracardiac hemodynamics, resulting in lower preload and, ultimately, decreased systemic cardiac output. Positive end expiratory pressure (PEEP) should be kept within the range to maintain the lung’s functional residual capacity and prevent atelectasis and hypoxia-related vasoconstriction if intubation is necessary [40].

3.4. Hospitalization of Congenital Heart Disease Patients with COVID-19

When looking at the hospitalization of these patients, and according to recent research by the American Heart Association, people who were hospitalized with COVID-19 infection and had a congenital heart defect were more likely to experience serious sickness along with a complicated disease course or die than those who did not have a congenital heart problem. Individuals with congenital cardiac defects who contracted COVID-19 were also more likely to need ventilator support or treatment in an ICU [41]. Patients who had a heart defect and other medical issues were older than 50, or were male were among those who were most at risk for developing the most severe COVID-19 sickness [42]. In a study conducted by Diaz et al., the researchers attempted to describe patient characteristics in those with and without CHDs during hospitalization for COVID-19. At the time of the COVID-19 hospitalization, the results of the study revealed that patients with CHDs were considerably more likely to have obesity, acute pulmonary hypertension, venous thromboembolism, acute ischemic stroke, acute arrhythmia, myocardial damage, and heart failure but not respiratory failure. Patients with CHDs were much more likely to be admitted to the ICU and had a significantly longer median length of stay than patients without CHDs [43]. Furthermore, it is important to identify the risk factors associated with the increased mortality rates in these hospitalized patients. Studies had implied that physical symptoms such as anorexia, nausea, vomiting, diarrhea, chest discomfort, myalgia, and fever have no bearing on a patient’s mortality. However, the mortality rates of COVID-19 cardiovascular patients were significantly correlated to symptoms such as headache, loss of consciousness, oxygen saturation below 93%, and the requirement for mechanical ventilation [44].

4. Materials and Methods

We performed a comprehensive and updated search on the severity of SARS-CoV-2 infection in patients with cyanotic CHD. Our search included some studies and reports published in the literature. Our search relied mostly on PubMed, Medline, and Google Scholars. The keywords used for the search included congenital heart disease, cyanosis, COVID-19, and SARS-CoV-2. Upon our search, studies handling the association between COVID-19 and CHD were retrieved, and their conclusions were compiled in our review. The studies are tabulated (Table 1), which shows the objectives, methodologies, and results of each study. Additionally, many narrative reviews were also retrieved to complement and support the information presented in our review.

5. Discussion

According to the literature presented above, the comorbidities and the complexity of the heart defects were thought to be the main risk factors for poor outcomes in the case of COVID-19. Patients with cyanotic heart disease are at a particularly high risk when challenged with the infection. Upon infection with COVID-19, the existing cyanotic CHD manifests itself dramatically. Patients with cyanotic heart disease exhibit continuous hypoxemia and frequently have considerably lower resting oxygen saturations because of a right-to-left shunt as well as severe abnormal pathobiology of the pulmonary tissue [27]. These patients are at an increased risk for rapid health deterioration in the setting of respiratory tract infections with inadequate oxygenation [27]. Importantly, patients have a higher risk of paradoxical embolism [28]. This risk stems from the concomitant prothrombotic risk due to pre-existing hemostasis issues, venous stasis, endothelial damage, and inflammatory response may also result in a worse outcome [28]. Despite all these findings, a study conducted by Sabatino et al. aimed to evaluate the clinical traits and prognoses of COVID-19-affected CHD patients [45]. The cohort study showed that patients with CHD experienced a mild COVID-19 clinical course in contrary to the high case-fatality rates observed in earlier studies on patients with cardiovascular comorbidities [45]. However, this study had several limitations but was reassuring and comforting for CHD patients [45].

Along the course of COVID-19 pandemic, the approach to the vulnerable patients given their different presentations was problematic. Professionals in charge of particularly high risk groups, such as adult patients with CHD, were forced to make difficult choices during the initial onset of the COVID-19 pandemic [46]. During the early weeks of the pandemic, pre-existing cardiovascular illnesses were discovered to be a key indicator of a poor prognosis in cases of infection with the novel SARS-CoV-2 [46]. It was not known for a long time whether this link held true for the predominantly adult individuals with CHD. A prospective multicenter European registry published in March 2023 attempted to assess the changes in risk stratification of adults with CHD patients [46]. By contrasting the results of two surveys given to experts in the field of adults with CHD at two different points during the pandemic, at the start and soon after the first outcome data on adults with CHD patients with COVID-19 were available, they determined changes in risk stratification of adults with CHD patients during the pandemic [46]. The overall risk perception was lower in the second survey than it was in the first when assessing the significance of general and adults with CHD-specific risk factors for a complicated disease course in the case of COVID-19 among the patients [46]. This was true even for risk factors related to physiological stage, which have been linked to poor prognostic outcomes in adults with CHD patients with COVID-19 [24, 46].

This implies that the same risk factors that suggest poor outcomes in COVID-19 cases as are seen in the general population similarly influence the outcomes of adults with CHD patients [46]. Although COVID-19 individuals with cyanotic heart illnesses were at risk for a worst outcome in general, the anatomical complexity of CHD per se did not appear to be related to the increased mortalities and morbidities in case of COVID-19 infection [46]. The prognosis of patients in later waves of the pandemic was improved by the knowledge gathered during the first wave, and hence, approach to the patients has changed significantly along to pandemic [46].

6. Conclusion

The COVID-19 pandemic has acutely affected patients with the underlying medical conditions. However, the effects of this infection in the context of CHD could conceivably be more severe, particularly in patients with cyanotic CHD. Based on the anatomical and physiological stage classification of the cardiac status, physicians should have specific considerations when handling a cyanotic patient. However, more studies need to address the clinical presentation of cyanotic CHD patients in particular and investigate the changes of this presentation along the various waves of COVID-19 pandemic. This would allow for a better healthcare provision and better treatment outcomes.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Authors’ Contributions

Lama A Ammar and Joseph E Nassar have contributed equally to this work.

Acknowledgments

The authors appreciate Dr. Rana Zareef for her review of the paper and positive feedback.

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Copyright © 2023 Lama A Ammar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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