We reported here 280 hospitalized patients with clinical or laboratory-confirmed COVID-19. There were no significant clinical manifestation differences between the hypertensive and non-hypertensive group. The majority of patients presented with fever, cough, and dyspnea in this case control study. However, manifestations of the upper respiratory tract and gastrointestinal symptoms have been uncommon, indicating distinct viral tropism compared to severe acute respiratory coronavirus syndrome (SARS-CoV) and coronavirus syndrome of the Middle East (MERS-CoV)(21, 22). The common clinical manifestations of COVID-19 patients are fever, cough, and sputum.6 it may manifest as normal body temperature when the patient's immune response is low. Breath shortening or dyspnea indicates impaired lung function and loss of oxygen. Therefore, if the patient is observed to be in trouble breathing with no fever, the patient's health needs to be monitored for possible worsening (23).
Our findings show that male patients over the age of 65 and smoking may pose a higher risk of progressing to a serious or fatal condition and that comorbidities such as obesity, diabetes, cardiovascular disease or respiratory disease may also have a major impact on the prognosis of COVID-19.
Women are less vulnerable to viral infection than males, likely due to the protection of X chromosomes and sex hormones, which play an important role in both innate and adaptive immunity(24). At the same time, men thought to be associated with poor lifestyle behaviors such as smoking and underlying diseases. Therefore, most critical or fatal patients are male. As the body's immunity decreases with age, older patients are more likely to develop or even die of a critical illness. As a result, the patient is at higher risk of developing critical illness or death when the patient is male, over 65 years of age and smoking. Among those 280 patients in baseline isolation ward, 232 (82.6%) patients were discharged and 48 (17.4%) worsened. Those patients with poor prognosis were older male patients with more comorbidities, dyspnea, and lower counts of lymphocytes, and increased numbers of pulmonary lobes involvement from CT images of the chest. We have observed that patients with bad prognosis on admission often had elevated levels of CRP for further multivariate analysis of these risk factors, the major predictors of poor prognosis in COVID-19 patients were male sex, lymphopenia and obviously elevated CRP.
CRP is an acute-phase, downstream protein of the innate immune response(25). It is produced to activate the immune response, due to the increased synthesis of pro-inflammatory cytokines(26). Consequently, the serum CRP level has also been used as an inflammatory marker in the laboratory(25, 26). A range of studies suggested that CRP is a predictive factor for the progression of disease in patients diagnosed with MERS-CoV and H1N1(27, 28). They first stated in this analysis that CRP could also be the marker for COVID-19 progression.
When patients are combined with basic diseases such as diabetes and hypertension, the body is in a long-term state of discomfort and the immunity appears to be weak. In addition, the long-term history of diabetes and hypertension will damage the vascular structure, and the risk of developing into critical disease in infection is greater. Chronic heart disease patients are more likely to get infected because of their weakened heart function and low immunity. They are more likely to experience serious coronary problems when diagnosed with SARS-CoV-2, and to evolve into extreme diseases (23).
Coronavirus is a single-stranded, enveloped, non-segmented RNA virus(29). Six human coronaviruses have currently been identified. And the SARS-CoV-2 is identified as the seventh human coronavirus, isolated from the lower respiratory tract of pneumonia patients with unknown causes in Wuhan(30). SARS-CoV-2 attacks the alveolar epithelial cells through angiotensin-converting enzyme 2 (ACE2). ACE2 is the ACE of isozyme, expressed primarily in gastrointestinal, liver, test, lung and colon, and other organizations(31). ACE2's key function is to incise Ang II to produce Ang 1–7, which mediates the defensive effects of vasodilatation, anti-inflammatory and anti-proliferation, vascular smooth muscle contraction, cell proliferation, promotion of fibrosis and vascular inflammation(32–34). When SARS-CoV-2 binds to the ACE2 receptor on the surface of alveolar epithelial cells, mechanisms such as internalization, shedding, and viral replication down-regulate the expression of ACE2 in alveolar epithelial cells. Then the elevated accumulation of Ang II contributes to inflammatory response and exudation of neutrophils, macrophages and fibrins, resulting in loss of function of the pulmonary ventilation and difficulties in maintaining oxygenation(35). At the same time, viral infection triggers the imbalance between T-helper-1 and T-helper-2 responses which induces an inflammatory storm by increasing the levels of inflammatory factors such as interleukin-4, interleukin-10 and interleukin-6(36). Cytokines released by inflammatory storm in critical patients, inducing systemic immune dysfunction, which may be a major cause of multiple organ failure and even death (37).
previous studies have identified the prevalence of common comorbidities as rising the risk of COVID-19 patients (1). Additionally, some scholars believe that the presence of any coexisting disease was more common among patients with severe illness than among those with non-severe illness(2). It has been found that the most serious and lethal cases of COVID-19 occurred in the elderly or in patients with underlying comorbidity, in particular CVDs, diabetes mellitus, chronic lung and renal disease, hypertension, and cancer (2, 38–40). One Chinese meta-analysis involving 1,527 patients found that hypertension and cardiovascular disease accompanied by diabetes were the most prevalent cardiovascular metabolic comorbidities with COVID-19, consistent with our study. In their study, patients with diabetes or hypertension had a 2-fold increase in risk of serious illness or requiring intensive care (ICU) admission, whereas those with cardiovascular disease had a 3-fold increase(12). In a subset of 355 COVID-19 patients who died in Italy, the mean number of pre-existing underlying conditions was 2.7, and only 3 subjects had no comorbidity(41).
Our findings revealed the importance of the early detection of COVID-19 high risk patients, especially in hypertensive patients in primary hospitals.
having a control group was the strength point of our investigation. However, there are some limitation to the report. First, this was a single-center study with a small sample size. Second, that was a retrospective study, and the results need to be further verified by prospective studies. Third, we missed asymptomatic and mild cases managed at home, and hence it may have affected the outcome of the study.
Due to the rapidly evolving outbreak internationally, ongoing studies with the inclusion of more patients would be required to increase statistical power and support group analyzes stratified by specific comorbidities in particular, hypertension and association with death risk.
as explained, hypertension is one of the most common risk-associated comorbidities, but age co-founded this association. It's not clear if hypertension is an age-independent risk factor consistent with COVID-19 outcomes. It is necessary that hypertension stays tightly controlled as a precaution.