key: cord-0834235-g07awnc3 authors: Li, Ni; Zhu, Linwen; Sun, Lebo; Shao, Guofeng title: The effects of novel coronavirus (SARS-CoV-2) infection on cardiovascular diseases and cardiopulmonary injuries date: 2021-01-12 journal: Stem Cell Res DOI: 10.1016/j.scr.2021.102168 sha: 9b64ff5e9c11c2dbbb530d801cf1904fb5893958 doc_id: 834235 cord_uid: g07awnc3 COVID-19 caused by a novel coronavirus named SARS-CoV-2, can elites severe acute respiratory syndrome, severe lung injury, cardiac injury, and even death and became a worldwide pandemic. SARS-CoV-2 infection may result in cardiac injury via several mechanisms, including the expression of angiotensin-converting enzyme 2 (ACE2) receptor and leading to a cytokine storm, can elicit an exaggerated host immune response. This response contributes to multi-organ dysfunction. As an emerging infectious disease, there are limited data on the effects of this infection on patients with with underlying cardiovascular comorbidities. In this review, we summarize the early-stage clinical experiences with COVID-19, with particular focus on patients with cardiovascular diseases and cardiopulmonary injuries, and explores potential available evidence regarding the association between COVID-19, and cardiovascular complications. with particular focus on patients with cardiovascular disease. We provided evidence for further understanding of the pathogenesis of COVID-19 so as to provide a basis for designing cardiac-protective strategies. The clinical classification of novel coronavirus infection is mainly light, normal, heavy and severe. There may be various manifestations of cardiac injuries in different clinical types. Mild and ordinary patients usually have a lower probability of cardiac injury [9] . ECG changes occur in individual cases. 2%-4% of mild patients have myocardial necrosis markers damage, while severe patients have a higher risk of cardiac injury, which is 22.2% -31%. The risk of cardiac injury in dead patients is higher than that in survivors, which is 28%-88.9% [10] . In addition, the follow-up chronic damage caused by virus infection is also worthy of attention. Many cases including high-grade artioventricular block, artial filbrillation, polymorphic ventricular trachycardia, cardiogenic shock and pulseless electrical activity arrest were highlight the spectrum of arrhythmias observed in patients with infection [10] . The prognosis of covid-19 patients should be followed up in time. When making decisions regarding choice of antiarrhythmics, ionotropes, and vasopressors, clinicians need to keep in mind potential proarrhythmic effects of antimalarial and antibiotic therapies currently being investigated as therapeutic agents against COVID-19 [11] . We classified and summarized the cardiac manifestations of patients with different clinical types after infection. Shown in table 1. Early diagnosis and treatment are critical to prevent the spread of the disease and to improve the cure rate. These includes nucleic acid detection and serological diagnosis technologies [1] .The SARS-CoV-2 infection in suspected cases is currently confirmed according to the following evidence: 1) real-time fluorescence RT-PCR detection of SARS-CoV-2 nucleic acid，with clinical symptoms and epidemiological features [12] ， including oral swabs, throat swabs, nasal swabs, saliva, bronchoalveolar lavage fluid, blood, urine and fecal or rectal swabs. The SARS-CoV-2 nucleic acid diagnostic kit include a fluorescent PCR method, a joint probe anchoring polymerization sequencing method and an isothermal amplification method [13] ; 2) viral gene sequencing, highly homologous with the new coronavirus; 3) serological positivity of specific IgM antibody and IgG antibody to SARS-CoV-2.Common methods include immunoassay, colloidal gold strip, indirect immunofluorescence and pathogen isolation, electrochemiluminescence ELISA [14] ; 4) SARS-CoV-2 specific IgG antibody turned increased from negative to 4-fold acute phase levels. 5) High-resolution computed tomography (CT) of the chest has been considered a complementary diagnostic modality [15] . Thin-slice CT of the is simple and fast; combined with epidemiological history and clinical manifestations, it aids early isolation and intervention of suspected or confirmed cases. CT also evaluate the severity of the disease and dynamically monitor the disease process, so as to guide timely decision-making and provide prognostic information. The appearance of lungs on CT are described in various stages: stage I (0-4 d), stage II (5-9 d), stage III (10-14 d) , and stage IV (>14 d). In patients with COVID-19, bilateral lung involvement occurs in all stages (I, III, IV: 100.00%, II: 87.50%); the lesions are mainly peripherally distributed (subpleural distribution) (stage I: 50.00%, stage II: 62.50%, stage III: 60.00%, and stage IV: 90.00%), most commonly among those with stage IV. According to the limited autopsy and biopsy histopathological findings, the following pathophysiology is a summary. Pathophysiology on the heart and blood vessels: Degeneration and necrosis were seen in myocardial cells, and a few mononuclear cells, lymphocytes and/or neutrophils were seen in the stroma. There was some vascular endothelium exfoliation, intimal inflammation and thrombosis. It is reported that patients with congenital heart disease could be considered at higher risk for complications from COVID-19 [16] . Certain congenital heart disease patients in adults are likely at higher risk than others， includes the following conditions:double-outlet ventricle cyanotic heart defects, double-outlet ventricle, Fontan procedure, interrupted aortic arch, mitral atresia, single ventricle, pulmonary stresia, transposition of the great arteries, truncus arteriosus, other abnormalities of atrioventricular and ventriculoarterial connection. These symptoms could be considered high risk for complications related to COVID-19 infection on the basis of decreased functional reserve. Pathophysiology on the lung:The lung shows consolidation to varying degrees. Serous, fibrinous exudate and hyaline membrane were found in alveolar cavities. Focal hemorrhage and necrosis of lung tissue have been found, and hemorrhagic infarctions. Some alveolar exudates appear organized, associated with interstitial fibrosis [17] . Under electron microscope, coronavirus particles were found in the cytoplasm of bronchial mucosa epithelium and type II alveolar epithelial cells. The novel coronavirus antigen novel coronavirus antigen was positive in some alveolar epithelial cells and macrophages, and RT-PCR detected positive for new coronavirus DNA. Pathophysiology on other organs including spleen, hilar lymph nodes and bone marrow, kidney, brain etc.The spleen was obviously reduced. The number of lymphocytes was significantly reduced, focal hemorrhage and necrosis, macrophages proliferation and phagocytosis were observed in spleen, while the number of lymphocytes in lymph nodes was less and necrosis was seen.The number of three lineage cells in bone marrow decreased. The liver might dark red, the gallbladder is highly filled. Liver cell degeneration, focal necrosis with neutrophil infiltration, congestion of hepatic sinuses, infiltration of lymphocytes and monocytes in portal area, and microthrombosis. With the kidney, protein exudate was found in the glomerular balloon cavity, and the renal tubular epithelium degenerated and fell off, and transparent tubular type was seen. Interstitial congestion, microthrombosis and focal fibrosis were observed.The brain tissue was congested and edematous, and some neurons degenerated. Focal necrosis of adrenal gland was found. The mucosal epithelium of esophagus, stomach and intestine was denatured, necrotic and exfoliated. Respiratory droplets and close contact are currently the known transmission routes. In relatively closed environments, the virus propagates through aerosols at high concentrations for long periods of time [18] . Because SARS-CoV-2 can be isolated from feces and urine, attention should be paid to the spread of aerosols or contacts caused by environmental pollution by feces and urine. The transmission of tears and mother-to-child transmission remains to be confirmed [19] . There are no effective drugs and vaccines, and active participation of the entire population in self-protection and self-isolation has become the key to cutting off transmission routes and effectively controlling the epidemic. Novel coronavirus infection is typically characterized by respiratory symptoms, and some patients have viral infection related heart injuries. Cardiac function may be the decisive factor affecting the development of severe infection with cardiovascular disease.At the same time, it was found that the prognosis of patients with cardiovascular disease was more serious than that of common patients. We divided SARS-CoV-2 caused cardiopulmonary injuries into two situations:1)The cardiovascular injuries caused by COVID-19;2)underlying cardiovascular disease complicated with COVID-19 infection aggravates the injury.One is cardiovascular injuries caused by SARS-CoV-2. It might cause cardiovascular injures in COVID-19 patients by targeting many genes specifific to endothelium in the heart, lungs and vessels, which can increase vulnerability to cardiac injury via inhibition of cardioprotective proteins or activate pathways for systemic immune-mediated cardiovascular injuries.One of the proposed mechanisms might direct injury to myocardial cells due to viral invasion of the vascular endothelium and myocardium. The second presumption is the impact of tissue hypoxia, destabilization of coronary plaque, and micro-thrombogenesis caused by the systematic inflflammation associated with cytokine storm.The other situation is that cardiovascular basic diseases may accelerate the progress of COVID-19 disease. Case fatality rate of COVID-19 patients without associated disease is relatively low. While if the COVID-19 patients are underlying cardiovascular disease complicated, it can be classified as high risk patients, and the clinical prognosis of these patients is worse than that of ordinary patients.The gross mortality of patients with underlying diseases is much higher, with crude fatality rate was 10.5%.The fatality is even higher than those with cancer, those with diabetes, chronic respiratory diseases, and hypertension. Zhong Nanshan team sampled 1099 patients with covid-19 from 30 provinces and cities in China, of which 14.9% were complicated with hypertension, and hypertension patients were more likely to develop into severe cases, with a high incidence of composite endpoint events. 2.5% of patients with coronary heart disease were also more likely to develop into severe cases. 5 (12%) of the 41 patients with covid-19 were diagnosed with virus-related heart injury, mainly manifested as the increase of high-sensitivity troponin (>28 ng/L) [20] . Four of the five patients were admitted to intensive care unit (ICU), accounting for 31% of the total number of ICU patients. 2 patients had no cardiovascular basic diseases, but obvious cardiac injury occurred in the process of disease progression. One case showed persistent abnormal myocardial enzyme spectrum and ST segment change of ECG, and one case showed sudden progressive decrease of heart rate and no heart sound was heard. It was also reported that 2% of patients had chest pain during hospitalization. The levels of serum myocardial necrosis markers were increased in both mild and severe patients, but the risk of cardiac injury was higher in severe patients (22.2% -31%) and mild patients (2%-4%). The risk of cardiac injury in dead patients was higher than that in survivors (28%-88.9%). In addition, chronic damage is worthy of attention. The prognosis of covid-19 patients should be followed up in time. The novel coronavirus infection induced acute myocardial injury, and chronic myocardial damage caused by new coronavirus infection.,and the covid-19 patients patitents whose combined with underlying cardiovascular diseases usually aggravated intrinsic myocardial injury,which might getting worse. In addition to active antiviral therapy, attention should be paid to the control and treatment of cardiovascular disease for such patients. Many studies have found abnormal myocardial enzymes and myocardial injury markers in patients with COVID-19. Myocardial infarction is more common in these patients. This outcome is closely related to the severity of the disease and the increased risk of death in the hospital [21] . The abnormal degree of myocardial injury markers is related to the severity of the patient's condition. In 22%-58.1% of severe SARS-CoV-2 patients, the myocardial damage markers are elevated [22] . Studies also found that the levels of troponin, C-reactive protein, and procalcitonin in patients with COVID-19 were also significantly elevated [23] . It is suggested that for older patients with COVID-19 (especially men) with abnormal myocardial enzymes, myocardial injury markers and imaging indicators, caregivers should pay more attention to heart injury, so as to make interventional treatment decisions and improve outcomes [24, 25] . However, there remain many problems and bottlenecks in the current understanding, research, and treatment of COVID-19, including whether abnormal increases in levels of myocardial enzyme and myocardial damage markers are caused by viral infection, by septic shock, liver Injury, kidney injury, or by other comorbidities; more basic research and autopsy studies are needed. Myocarditis is increasingly recognized as a complication of COVID-19 and may result from direct viral injury or from exaggerated host immune response. Myocardial injury in patients with COVID-19 can be diagnosed by increasing the number of dynamic or routine ECG examinations and the examination of myocardial enzymes and inflammatory factors. For patients with suspected myocarditis, there should be early use of sufficient doses of steroids and intravenous immunoglobulin, and antiviral therapy, as well as ventilatory and circulatory support. It showed that C-reactive protein and procalcitonin increased in all children, which were higher than 94 mg/L and 1.6 ng/mL, respectively.. Patients with COVID-19 and acute myocarditis need to be diagnosed early after infection and be referred to expert centers for treatment. In April 2020, of four children and adolescents who were admitted to the intensive care due to multiple system inflammatory syndrome and Kawasaki disease-like features associated with the SARS-CoV-2 were found to have acute myocarditis symptoms within one week of admission [26] . SARS-CoV-2 was negative for qPCR in nasopharyngeal, respiratory tract and fecal specimens; however, there was positive serology. Cardiac MRI showed symptoms of diffuse myocardial edema.Endomyocardial biopsy may be performed if the diagnosis remains uncertain. These modalities are helpful for the diagnosis of myocarditis after SARS-CoV-2 infection in children and adolescents [26] . Vasoactive drugs and invasive mechanical ventilation are current management. In the setting of cardiogenic shock and refractory, life-threatening arrhythmias that persist despite medical therapy, advanced mechanical circulatory support devices should be considered. Besides,it is mainly supportive with the potential addition of interventions recommended for severe COVID-19 disease, such as remdesivir, steroids, and convalescent plasma. Studies found that heart failure was one of the main causes of death in patients with COVID-19. A wide range of factors can result in HF including coronary artery disease (CAD), hypertension, cardiomyopathy, atrial fifibrillation, or HF due to obesity. It is possibly related to renin-angiotensin-system (RAS) and ACE2 receptors [27, 28] , besides in patients who are more susceptible to heart failure, such as obese patients, the systemic inflflammation that results from COVID-19 infection may further increase the risk for heart failure. RAS is closely related to the occurrence and development of cardiovascular diseases; it plays an important role in regulating and maintaining the balance of blood pressure, water and electrolyte balance, and homeostasis [29] . ACE2 has high homology to ACE. ACE2 converts extracellular Ang I and Ang II into Ang-(1-7). Both ACE2 and Ang-(1-7) inhibit cardiomyocyte hypertrophy, inflammatory reactions, and oxidative stress caused by Ang II [30] . Relevant animal studies showed that ACE2 and Ang-(1-7) inhibited ventricular remodeling [31, 32] . Crackower et al. reported that ACE2 gene knockout mice had elevated levels of Ang II, decreased levels of Ang-(1-7) expression, and severe heart failure [33, 34] . The results of these animal experiments show that, after knocking out the expression of ACE2 in rat myocardium, the response of inflammatory factors and oxidative stress was enhanced, resulting in enhanced myocardial damage. It is speculated that the pathogenic mechanism in patients with COVID-19 may involve the binding of SARS-CoV-2 virus to ACE2, resulting in decreased ACE2 expression and increased Ang II expression in plasma and myocardial tissues. Decreased expression levels of Ang-(1-7), inflammatory responses and oxidative stress induce myocardial damage that turn leads to decreased myocardial contractility and heart failure [35] . SARS-CoV-2 infection can result in oxidative stress, fifibrosis, diastolic dysfunction, and subsequent systolic heart failure,mainly due to increased ROS production, low baseline levels of cytoprotective autocoids, uncoupling of mitochondrial enzymes etc. The [37, 38] . Once a patient with underlying disease is more easier to be infected, the lungs show obvious signs, and the proportion of cough symptoms increases [39, 40] . Patients with underlying diseases are more likely to evolve critical illness. The proportion of symptoms of chest tightness and shortness of breath was 32.14%, which is higher than that of the group without underlying diseases [41] .The pathophysiology of SARS-CoV-2 causing lung injury includes its binding to ACE2, resulting in a series of lung injuries. This also includes cytokine storms. The cytokines involved to "cytokine storms" include interferons, interleukins, chemokines, and tumor necrosis factors. The virus may activate nuclear transcription factor, activator protein-1 and activator-2 [42] . It can cause the recruitment of specific inflammatory cytokines and neutrophils, and it can also lead to the excessive production of chemokines, all of which ultimately lead to respiratory failure and death. All patients with COVID-19 should be treated with various antiviral drugs (such as α-interferon, lopinavir/ritonavir, ribavirin, chloroquine phosphate, and ridacive) to improve lung function. Simultaneously, attention should be paid to the adverse reactions of drugs, contraindications, and interactions with other drugs. There should be treatments with appropriate combinations of antibacterial drugs [43] .For patients with ARDS, more in-depth treatment plans should be adopted. Many hospitals regard noninvasive positive pressure ventilation (NPPV) as the main treatment for patients with ARDS. Nevertheless, the effect is not ideal, and some patients die of respiratory failure; therefore, NPPV should be used with caution. In addition, we must pay close attention to the patient's respiratory rate, tidal volume, oxygen saturation and other indicators [44, 45] . If the patient's respiratory distress does not improve after NPPV treatment, then regardless of oxygen saturation, noninvasive ventilation should be terminated and changed to endotracheal intubation. NPPV should also be monitored in terms of patient tolerance. If the patient develops anxiety, abdominal distension, difficulty sleeping, or even consciousness disturbances during the treatment, failure of NPPV should be considered, and tracheal intubation may be an option [46] . Extracorporeal membrane oxygenation is often used as a rescue measure to treat critically ill patients and is regarded as a guarantee for lung-protective ventilation [47] . As are often lymphopenic, thereby further contributing to organ injury. We summarized detailedly the most important mechanisms of novel coronavirus-related pathology below. ACE2 is expressed in lung, heart, kidney, and the gastrointestinal tract, localized in cardiomyocytes, cardiac fibroblasts, pericytes, vascular endothelium, and vascular smooth cells [51] . Zou et al. analyzed the distribution of ACE2 in human respiratory, cardiovascular, digestive and urinary systems using single cell RNA sequencing data [52] . They found that ACE2 was expressed not only in type II alveolar epithelial cells and lower respiratory tract epithelial cells, but also in cardiac muscle, vascular endothelium, esophageal epithelium, renal proximal convoluted tubule, and bladder epithelial cells. These findings suggest that these organs should be regarded as high-risk organs for SARS-CoV-2 infection. The cardiovascular system is a potential target organ of cardiovascular SARS-CoV-2 [53, 54] . The ACE2-related signaling pathway may play a key role in myocardial injury. SARS-CoV-2 can affect the regulation of the renin angiotensin system (RAS) system by downregulating the expression of ACE2, thereby causing or aggravating cardiac damage [55, 56] . RAS is one of the most important body fluid regulation systems. It can regulate blood pressure, water and electrolyte balance, and maintain homeostasis, playing important roles in the regulation of cardiovascular activities. Under physiological conditions, the ACE angiotensin II and ACE2 ang (1-7) axes maintain dynamic balance [57, 58] . However, in COVID-19 patients, expression of ACE2 is downregulated, leading to decreased Ang (1-7) levels, thereby weakening vasodilation and blood pressure reduction, as well as anti-inflammatory, anti-proliferation, anti-fibrotic, and anti-apoptotic effects in alveolar epithelial cells. The abnormal increase of AngII levels aggravates vasoconstriction, blood pressure, inflammatory reactions, apoptosis and pathogen proliferation, resulting in de novo heart damage or aggravation of pre-existing chronic cardiovascular disease ( Figure 1 ). As for the treatment plan for this mechanism, the key to prevention and Over-production of inflammatory cytokines and chemokines was common in COVID-19 patients, when acute heart and lung injury was diagnosed. Further There are many drug method including ILs receptor antagonists, TNF-α antagonist,Anti-VEGF agents etc from the mechanism on cytokine storms. It is worth mentioning that chloroquine should not be used together with moxifloxacin. The combination of macrolides and fluoroquinolones can prolong QT interval.Cytokine Storm Induced by SARS-CoV-2 and the Drug Therapy methods are shown in Table 2 [61-84]. The underlying cause of respiratory failure and organ dysfunction is essentially thrombosis, inflammation and endothelial dysfunction in COVID-19 patients. Disfunction of the endothelium turns into a disastrous battlefield of the complex interaction between "cytokine and coagulative storms" can be irreparably Severe hypoxia from acute respiratory damage caused by the virus may result in oxidative stress and myocardial injury from increased myocardial oxygen demand in the presence of severe hypoxia due to ARDS. Persistent spasm of pulmonary capillaries can cause pulmonary hypertension, in turn leading to left ventricular ejection dysfunction [85] . Myocardial cell damage and necrosis may occur in the context of long-term hypoxia, and the function of the center of gravity will be damaged. Patients with severe COVID-19 may suffer from embolism due to long-term bedrest, malnutrition, and abnormal coagulation function, all of which may have adverse effects on the heart. In addition to viral infection directly causing myocardial cell damage, virus-induced systemic inflammatory responses, and immune system disorders, imbalance of oxygen supply and demand, including hypoxemia, respiratory failure, shock, hypotension, persistent tachycardia, severe bradycardia, and anemia, can cause heart damage [86] . Drug-related myocardial injury may also occur. Table 2 ). Some patients with cardiovascular comorbidities (including coronary artery disease, hypertension) often have a poor outcomes of SARS-CoV-2 infections, and there may be complications such as ARDS [90] . The mortality rate of patients with COVID-19 and cardiovascular complications was also significantly elevated. Patients with cardiovascular comorbidities have weak vascular functional reserves. worsening sequelae of myocardial infarction and leading to heart failure [91] . The exact mechanisms of heart injury in patients with COVID-19 remain unclear. Some investigators believe that myocardial involvement is mediated by angiotensin converting enzyme-2 (ACE2) [92] . A mouse model showed that lung infections in patients with SARS-CoV-2 infection also caused ACE2-dependent myocardial infection [93] . Among SARS-CoV-2 patients in Toronto, 35% of autopsy results showed the presence of SARS coronavirus RNA in the heart [94] . Other studies showed that SARS-CoV-2-related cardiac involvement was characterized by cytokine storm mediated by an imbalance in responses between T helper cell subtypes, as well as hypoxia-induced intracellular calcium excess, leading to cardiomyocyte apoptosis. It may be that cardiovascular comorbidities are more common in the elderly, those with compromised immune systems, and those with elevated ACE2 levels, or that people with cardiovascular comorbidities are more sensitive to SARS-CoV-2 infection [95] . Compared with adult patients with COVID-19, children appear to suffer milder illnesses. Most are moderate or mild, and there are also asymptomatic patients [96] . From the reported newborns born in perinatal COVID-19 infected women, Symptoms of abnormal heart rate and pneumothorax [97] .Children appeared to be particularly vulnerable to other coronaviruses that may make them at least partially immune to SARS-CoV-2 infection [98] . The mechanisms and causes are unclear. It is speculated that the function of ACE2 protein in adults is stronger than that of children; therefore, SARS-CoV-2 is more infectious in adults [99] . Other studies reported that maternal antibodies can protect infants and young children from microbes immunized by the mother, so children are completely new to all microbes that have not been immunized by the mother [100] . New memory T and B cell pools can be established in the immune system of infants and young children, and reinfection of common pathogens can also be controlled. For these reasons, compared with adults, children's immune systems are typically able to respond to new microorganisms. By contrast, these functions may be weakened in adults and the elderly, and they may even be ineffective in patients over 70 years old [101] . were positive, and one patient was negative for both SARS-CoV-2 qPCR and serology, however, chest CT findings were typical of SARS-CoV-2 symptoms [104] . In the end, all children survived, and left ventricular function was completely restored when the patients were discharged from the pediatric intensive care unit, and there was no fever. In children, the US Centers for Disease Control defined severe COVID-19 disease as multisystem inflammatory syndrome in children (MIS-C). Children with MIS-C may have acute cardiac decompensation. Another study found that 20 children admitted to the pediatric intensive care unit in four academic tertiary care centers in Paris suffered from fever and symptoms of suspected SARS-CoV-2 infection. Therefore, a child's immune response system may have a dual function, namely to protect and to reduce immune-mediated lung tissue damage [105] . A study found that none of the nine pregnant women (all with caesarean section) who were infected with viruses during the second trimester passed the virus to their babies. Pregnancy suppresses the immune system, all babies had health scores higher than the Apgar scale for newborns [105] . Pregnancy suppresses the immune system (so that it does not attack the fetus). Pregnant women are particularly susceptible to respiratory pathogens and severe pneumonia; and the cardiovascular system of pregnant women is unbalanced during pregnancy, in addition, pregnant women's extra demand for oxygen and blood at the end of pregnancy increases the pressure on the cardiovascular system. [106] . Although pregnant women are more susceptible to respiratory pathogens than non-pregnant women, none of the nine women suffered from severe COVID-19. Some of the most severe symptoms of COVID-19 are due to cytokine storm, which causes immune cells and the substances they produce to spread throughout the tissue and aggravate the condition [101] . However, pregnancy is a state of immunosuppression, possibly explaining why these women did not become severely ill [107] . There is no evidence of vertical transmission in pregnant women during the third trimester. It was found that most pregnant women admitted to the hospital for SARS-CoV-2 infection were in the second trimester or the third trimester. Most patients had a good prognosis, and the transmission of SARS-CoV-2 to infants was not common. Studies have also found that there is poor perfusion in the maternal blood vessels, but it is good in the fetus, and there is no placental vascular disease after pregnancy [108] . At present, the precise mechanisms of myocardial injury caused by SARS-CoV-2 infection are not completely clear; nevertheless, the clinical and basic science studies reviewed here suggest that SARS-CoV-2 infection can lead to myocardial injury, and it is closely related to the disease progression and prognosis. We suggest that we should pay close attention to cardiovascular related indicators in patients with COVID-19, including myocardial markers and ECG changes. Lungs may not be the only target organ of SARS-CoV-2. Cardiovascular system damage should not be ignored and should be detected and treated as soon as possible. If acute heart injury occurs during treatment, cardiac protective drugs can be used as appropriate. Appropriate myocardial protection treatment may help reduce the mortality associated with COVID-19. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. 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During the period of submission and revision, new data on SARS-CoV-2 continued to emerge. The authors regret that they cannot cite those valuable work done afterwards. This work was supported by the Clinical features Inciden The clinical symptoms were mild and no pneumonia was found on imaging. Dear reviews, in this review, we summarize the early-stage clinical experiences with COVID-19, with particular focus on patients with cardiovascular diseases and cardiopulmonary injuries, and explores potential available evidence regarding the association between COVID-19, and cardiovascular complications.