Cardiac Hypertension I Was Tested Three Yesrs Ago Do I Need Ti Get Testef Again

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Open Access

Peer-reviewed

Inquiry Article

Hypertension every bit a sequela in patients of SARS-CoV-2 infection

• Ganxiao Chen,
• Xun Li,
• Zuojiong Gong,
• Hao Xia,
• Yao Wang,
• Xuefen Wang,
• Yan Huang,
• Hector Barajas-Martinez,
• Dan Hu

x

• Published: April 28, 2021
• https://doi.org/x.1371/journal.pone.0250815

Figures

Abstract

Background

COVID-19 is a respiratory communicable diseases caused past SARS-CoV-2, and cardiovascular damage is commonly observed in affected patients. Nosotros sought to investigate the effect of SARS-CoV-2 infection on cardiac injury and hypertension during the current coronavirus pandemic.

Report design and methods

The clinical data of 366 hospitalized COVID-xix-confirmed patients were analyzed. The clinical signs and laboratory findings were extracted from electronic medical records. Two contained, experienced clinicians reviewed and analyzed the information.

Results

Cardiac injury was found in eleven.nineteen% (30/268) of enrolled patients. 93.33% (28/30) of cardiac injury cases were in the astringent group. The laboratory findings indicated that white blood cells, neutrophils, procalcitonin, C-reactive poly peptide, lactate, and lactic dehydrogenase were positively associated with cardiac injury marker. Compared with healthy controls, the 190 patients without prior hypertension have college AngⅡ level, of which 16 (8.42%) patients had a rise in claret pressure to the diagnostic criteria of hypertension during hospitalization, with a significantly increased level of the cTnI, procalcitonin, angiotensin-2 (AngⅡ) than those normal blood force per unit area ones. Multivariate assay indicated that elevated age, cTnI, the history of hypertension, and diabetes were independent predictors for illness severity. The predictive model, based on the four parameters and gender, has a skillful ability to identify the clinical severity of COVID-19 in hospitalized patients (area under the curve: 0.932, sensitivity: 98.67%, specificity: 75.68%).

Determination

Hypertension, sometimes accompanied past elevated cTnI, may occur in COVID-xix patients and get a sequela. Enhancing Ang Ii signaling, driven by SARS-CoV-two infection, might play an important part in the renin-angiotensin system, and consequently lead to the evolution of hypertension in COVID-nineteen.

Citation: Chen G, Li Ten, Gong Z, Xia H, Wang Y, Wang X, et al. (2021) Hypertension as a sequela in patients of SARS-CoV-2 infection. PLoS 1 16(iv): e0250815. https://doi.org/10.1371/journal.pone.0250815

Editor: Bhagwan Dass, University of Florida, United states of america

Received: Jan 25, 2021; Accepted: April 14, 2021; Published: April 28, 2021

Copyright: © 2022 Chen et al. This is an open admission article distributed under the terms of the Artistic Commons Attribution License, which permits unrestricted use, distribution, and reproduction in whatever medium, provided the original author and source are credited.

Data Availability: Data cannot be shared publicly because of the contents including data that could compromise research participant privacy/consent. Data are bachelor from the Renmin Hospital of Wuhan University Ethics Committee (contact via whdxrmyy@126.com) for researchers who run into the criteria for admission to confidential data.

Funding: The current work was supported past the National Natural Science Foundation Projection of China (Grant No. 81670304, D.H.).

Competing interests: The authors report no relationships that could be construed as a conflict of involvement.

Abbreviations: ACE2, angiotensin converting enzyme II; Ang II, Angiotensin II; AT1R, Angiotensin 2 type-ane receptor; COVID-19, coronavirus disease 2019; cTnI, cardiac troponin I; MERS, middle e respiratory syndrome; RAS, renin-angiotensin system; SARS, astringent astute respiratory syndrome

Introduction

In December 2019, an acute respiratory infectious disease known equally "coronavirus disease 2022 (COVID-19)" caused past a novel coronavirus occurred in Wuhan, China [i, 2]. Whole-genome sequencing and systematic analysis showed that this novel. Coronavirus is a distinct clade from beta coronavirus associated with human severe acute respiratory syndrome (SARS) and Heart East respiratory syndrome (MERS) [3], and was now officially named "SARS-CoV-ii" by World Health Organization. Both SARS-CoV and SARS-CoV-2 have been identified to employ the angiotensin converting enzyme II (ACE2) receptor equally the portal of entry into the afflicted cell [4, v]. ACE2, a membrane-bound aminopeptidase, is highly expressed in the center and lung [6, 7]. Although the principal clinical features of COVID-19 are dominated by respiratory symptoms, many patients with severe cardiovascular damage accept been reported by our squad and others [8, nine]. Besides, patients with underlying cardiovascular diseases might take an increased risk of expiry [8]. So, understanding the damage to the cardiovascular system caused past SARS-CoV-2 and the underlying mechanisms is of groovy importance so that these patients can be treated timely, and the mortality tin can be reduced. In this retrospective cohort study, the clinical data of hospitalized COVID-19-confirmed patients were analyzed to explore the consequences of SARS-CoV-two infection on the cardiovascular organisation.

Materials and methods

Study setting and population

There were 366 COVID-19-confirmed patients enrolled in this study, who were hospitalized in the Section of Infectious Diseases, Renmin Hospital of Wuhan University, from Feb 1 to May ane, 2020. Clinical severity was defined for all enrolled COVID-nineteen patients according to the guidelines of the National Health Commission of China, including four types as mild, moderate, severe, and critical types [10]. We divided the patients into the not-astringent group (mild and moderate types) and the severe group (astringent and disquisitional type). Mild type is divers as mild clinical symptoms and no pneumonia manifestation found in imaging. Moderate cases refer to those who present with fever and respiratory tract symptoms, etc. And take pneumonia manifestations found in imaging. Patients considered severe had 1 of the post-obit three conditions: respiratory distress and respiratory rate college than 30 times per minute; fingertip blood oxygen saturation less than 93% at rest; fractional arterial oxygen pressure (PaO2) / fraction of inspiration oxygen (FiO2) less than 300mmHg. Patients in critical type met one of the following criteria: respiratory failure, requiring mechanical ventilation; stupor; multiple organ failure, requiring intensive care management. This study was reviewed and approved by the Medical Ethical Commission of Renmin Infirmary of Wuhan Academy. All participants provided written informed consent and agreed to use their medical records for enquiry purposes.

Data collection

The clinical signs and laboratory findings were extracted from electronic medical records (Donghua Hospital Information Arrangement). Two independent, experienced clinicians reviewed and abstracted the data. The recorded information includes demographic data, potential comorbidities, symptoms, signs, laboratory examination results. The serum level of hypersensitive troponin I (cTnI) exceeding >xl pg/mL was considered cardiac injury [xi]. Blood pressures were obtained 3 fixed times in the morning time using standard measurement. History of hypertension was defined equally brachial blood pressure ≥ 140/90 mmHg or cocky-reported hypertension medication use before hospitalization. For patients without prior hypertension, elevated blood pressure was defined as claret force per unit area ≥ 140/ninety mmHg more than iii times during hospitalization.

The processes of patient screening

The screening process for evaluating the event of SARS-CoV-2 on the cardiovascular system is shown in Fig 1. Serum level of cardiac troponin I (cTnI) was tested in 276 of the 366 patients during hospitalization, among which 8 patients had a history of chronic middle disease (including ischemic heart affliction, arrhythmia, valvular disease, and heart failure) and were therefore excluded. Thus, 268 patients were enrolled to evaluate the result of SARS-CoV-2 on cardiac injury. Of the 366 patients, 278 had consummate blood pressure level data. Among these, 88 patients had a history of hypertension before hospitalization and were excluded; therefore, 190 patients were grouped to evaluate the event of SARS-CoV-2 on blood pressure. Among all 366 subjects, 194 subjects had data bachelor on serum level of cTnI and complete blood pressure data. After the exclusion of the case with a history of chronic centre disease, 186 cases were included to evaluate the association between cTnI, blood pressure, and clinical severity of COVID-19.

Statistical assay

Student'due south t-test or the Mann-Whitney test was used to compare the mean of continuous variables, Fisher's verbal test was used with limited data, the χ2 test was used to compare the proportion of chiselled variables. Spearman correlation assay was used to analyze the correlation between variables. The logistic regression model was used to decide factors associated with the clinical severity of COVID-19, and the analysis of receiver operating feature (ROC) curves was constructed according to standard procedures. The Youden index, defined as (sensitivity + specificity)– 1, was used to derive a reasonable cutting-off value. Scale of the risk prediction model, comparing the observed and predicted probability, was performed via a visual calibration plot in the R program. A P-value of < 0.05 was considered statistically significant. Statistical assay was carried out using SPSS software version 21.0 and R version 3.0.

Results

The result of SARS-CoV-2 on cardiac injury

The results showed that the median historic period of patients with or without cardiac injury was 74 y/o and 49 y/o with statistical significance (median [interquartile range]: 74 [73–86] vs. 49 [40–66] y/o, p < 0.001). Males were dominant in the cardiac injury group (86.67%). The cardiac injury was institute in 11.19% (30/268) of patients, only 93.33% (28/xxx) of them were in the astringent grouping. The proportion of cardiac injury was significantly lower in the non-astringent group (1.75% vs. 18.eighteen%, p < 0.001). Moreover, 66.67% (xx/30) of cardiac injury patients in the astringent grouping somewhen died. The most frequent symptom of patients was fever, followed by cough, fatigue, dyspnea, and chest stuffiness. The incidences of coughing, dyspnea, and breast stuffiness were significantly different between the patients with or without cardiac injury (93.33% vs. 68.91%, p = 0.005; 93.33% vs. 38.66%, p < 0.001; 86.67% vs. 36.97%, p < 0.001; respectively). Hypertension was the most frequent comorbidity, while the incidence of diabetes was significantly dissimilar between the 2 groups (33.33% vs. 14.29%, p = 0.017; Table 1). The laboratory findings indicated that the patients who suffered from cardiac injury had a higher level of white blood cells, neutrophils, monocytes, procalcitonin, C-reactive protein, lactate, and lactic dehydrogenase compared with the patients without cardiac injury (median [interquartile range]: 9.67 [v.62–13.73] vs. 5.93 [iv.45–7.06] cells/Fifty, p < 0.001; 5.52 [3.83–xi.62] vs. 3.72 [2.95–5.47] cells/L, p < 0.001; 0.62 [0.42–0.76] vs. 0.44 [0.25–0.69] cells/Fifty, p = 0.037; 630 [47.00–2750.00] vs. threescore [32.00–121.00] pg/mL, p < 0.001; 81.10 [fourteen.20–142.80] vs. 41.forty [5.00–74.xl] mg/L, p < 0.001; two.ten [1.95–iii.05] vs. 1.seventy [i.15–2.00] mmol/L, p<0.001; 428 [325.00–765.00] vs. 275 [218.00–375.00] U/50, p < 0.001; respectively). Correlation analysis showed that white blood cells, neutrophils procalcitonin, C-reactive protein, lactate and lactic dehydrogenase were significantly associated with cTnI, the r values were 0.515 [95% CI, 0.394–0.632], 0.486 [95% CI, 0.358–0.591], 0.477 [95% CI, 0.352–0.581], 0.459 [95% CI, 0.338–0.566], 0.424 [95% CI, 0.273–0.559] and 0.438 [95% CI, 0.291–0.561], respectively (Table 2).

The effect of SARS-CoV-two on claret pressure

Of the 190 qualified patients, sixteen (viii.42%) patients had a rise in blood force per unit area during hospitalization, among which six patients were male person, and 10 patients were female. As shown in Table three, no pregnant differences were found when comparing the baseline demographics, including age, gender, clinical category, symptoms, and comorbidities between patients with or without elevated blood pressure. Compared with the patients without elevated blood force per unit area, the level of cTnI and procalcitonin in the 16 patients rose significantly (median [interquartile range]: 22.00 [18.20–30.00] vs. 3.86 [ii.49–5.15], p < 0.001; 82 [53–430] vs. 49 [28–73], p = 0.023; Table 4). Elevated systolic blood pressure was observed in virtually of the patients, while diastolic blood pressure level was in the normal range. The median values of blood force per unit area and plasma cTnI levels changes of the sixteen patients are shown in Fig 2A. Systolic blood pressure and cTnI levels had a similar trend with the treatment fourth dimension. In improver, the blood pressure, cTnI, and white claret cells were continuously monitored in one alphabetize case (Fig 2B). With effective treatment, the patient'south condition improved with regards to symptoms and as evident on breast CT. Meanwhile, the systolic blood pressure and white claret cells reverted to the normal range, and the concentrations of cTnI were likewise gradually decreased. Among the 190 patients without prior hypertension, the serum levels of components in the renin-angiotensin system, including adrenocorticotrophic hormone, renin, angiotensin Ⅱ (Ang Ⅱ), and aldosterone, were detected in 28 patients. Comparing with salubrious controls showed that AngⅡ were significantly elevated in both the normal and elevated blood pressure groups (median [interquartile range]: 137.12 [123.63–161.67] vs. 87.90 [48.23–107.39] pg/mL, p < 0.001; 169.25 [142.17–186.98] vs. 87.90 [48.23–107.39] pg/mL, p < 0.001; respectively; Tabular array 5). When comparing the RAS between the normal and elevated claret pressure level groups, Ang Ⅱ levels were significantly college in the latter grouping (median [interquartile range]: 169.25 [142.17–186.98] vs. 137.12 [123.63–161.67] pg/mL, p = 0.020; Table 6).

Fig 2.

A. The systolic blood pressure and cTnI change of patients with elevated blood pressure level. B. The systolic blood force per unit area, cTnI, white claret cells, and chest computed tomography changes of i patient with elevated blood pressure. Tardily follow-up: The 4^th week afterward discharge from the hospital.

https://doi.org/10.1371/journal.pone.0250815.g002

The association between cardiac injury, claret pressure, and clinical severity of COVID-19

Results of demographic and laboratory findings betwixt the severe and non-severe group, based on guidelines of the National Health Commission of China, are shown in Tabular array vii. Patients in the severe group were significantly older, with a greater proportion of males (median [interquartile range]: 66 [57–76] vs. 42 [33–51] y/o, p < 0.001; 60.00% vs. xl.54%, p = 0.009; respectively). In addition, the cTnI, white claret cells, neutrophils, procalcitonin, C-reactive protein, and lactic dehydrogenase of the severe group were significantly higher than those of the non-astringent group (median [interquartile range]: seven.00 [5.78–27.00] vs. 5.68 [4.62–6.45] pg/mL, p < 0.001; five.98 [four.60–10.00] vs. 5.07 [3.65–6.00] ×10⁹cells/mL, p = 0.004; 3.85 [3.02–8.27] vs. 2.67 [ii.15–three.92] ×10^ix cells/mL, p < 0.001; 67.50 [32.00–288.00] vs. 36.00 [23.00–57.00] pg/mL, p = 0.005; 48.55 [vii.xl–81.50] vs. 6.xx [0.50–28.00] pg/mL, p <0.001; 316.00 [235.00–454.00] vs. 233.50 [187.fifty–292.00], p < 0.001; respectively). In contrast, patients in the severe grouping had a significantly lower level of lymphocytes median [interquartile range]: 0.78 [0.48–1.29] vs. one.27 [0.96–1.73], ×10^nine cells/mL, p < 0.001). Farther univariate assay revealed that the age, sexual activity, cTnI, white blood cells, neutrophils, lymphocytes, C-reactive poly peptide, lactic dehydrogenase, and history of hypertension and diabetes were significantly associated with the clinical severity of COVID-19. In the multivariate analysis, the age, cTnI and history of hypertension and diabetes remained significant independent predictors (OR = 1.11, 95% CI: i.07–1.16, p < 0.001; OR = 1.08, 95% CI: 1.01–i.15, p = 0.018; OR = 7.19, 95% CI: 2.55–xx.31, p < 0.001; OR = iv.28, 95% CI: 1.41–12.97, p = 0.010; Tabular array viii). The receiver operating characteristic curve of the 4 independent predictors and gender for clinical severity of COVID-19 is shown in Fig 3A (AUC: 0.932, sensitivity: 98.67%, specificity: 75.68%). The calibration indicated that the model was well-calibrated (Fig 3B).

Fig 3.

A. ROC curves of the age, cTnI, gender, and the presence of hypertension and diabetes for the identification of the severity of COVID-19. B. The scale plot for the comparison of the predicted and bodily probability. The Ten-axis and Y-axis correspond the model-predicted and actual probability of MAE, respectively. The red line: perfect prediction. The blackness line: predictive performance of the model after bootstrapping (B = 1000 repetitions).

https://doi.org/10.1371/journal.pone.0250815.g003

Discussion

SARS-CoV-2 has been identified as a single-stranded enveloped 39 RNA virus belonging to the beta-coronavirus genus of the coronaviridae family [3]. These coronaviruses accept a 3-dimensional spike protein construction protein, which can closely bind the human ACE2 receptor. Therefore, the cells with ACE2 expression may act as target cells and exist susceptible to SARS-CoV-ii infection [12]. ACE2 is a membrane-jump aminopeptidase with a vital role in the cardiovascular system [13, 14]. Information technology is, therefore, reasonable to speculate that SARS-CoV-2 will act on the heart and blood vessels, with resultant changes in the cardiovascular system.

Serum cardiac troponin assays have been proposed as the recommended marker of cardiac injury in COVID-19 patients [15]. Huang and colleagues discover that cTnI is increased essentially in 12.20% (5/41) Wuhan COVID-xix patients, in whom the diagnosis of the virus-related cardiac injury is made [eight]. Some other previous research also reported that patients with cardiac injury had higher levels of leukocyte counts, C-reactive protein, procalcitonin [16]. In this retrospective study, older patients with diabetes are more likely to suffer from cardiac injury. Our further assay shows that the level of white blood cells, neutrophils, procalcitonin, C-reactive protein, lactate, and lactic dehydrogenase were positively associated with cardiac injury. Besides, the cardiac injury occurred mostly in severe patients. Consequently, nosotros hypothesize that the astringent type of COVID-19 characterized past acute inflammation response might exist more decumbent to cardiac injury, especially in patients with preexisting cardiovascular disease. Chronic myocardial injury, acute nonischemic injury, and acute myocardial infarction accept all been proposed as causes of cTnI acme in COVID-19 patients [17]. I instance written report suggested that direct myopericardial involvement may be a complication of COVID-19 infection [18].

Understanding of the pathogenesis and complications of COVID-xix is still limited. Due to the lack of viral load quantification results in the literature, it is unclear whether the cardiac injury is directly related to viral load. The contempo literature review has shown that although cTnI concentration is only marginally increased in all patients with COVID-nineteen, (values in a higher place the 99^thursday percentile upper reference limit in only viii–12% of positive patients), they are significantly increased in patients with severe disease [19]. Our study further suggests that cardiac injury is an independent risk gene for astringent COVID-nineteen and in combination with age and other statistically significant comorbidities tin can be used to construct a logistic regression model of COVID-19 severity in hospitalized patients.

Sixteen patients without prior hypertension had a ascension in blood pressure during hospitalization, and higher systolic blood pressure was observed in almost of the patients. Except for lymphocytes and procalcitonin, no significant differences are establish in patients with and without elevated claret pressure. This suggests that abnormal claret pressure may be caused independently of the inflammatory response. The RAS plays a disquisitional role in the cardiovascular organisation, which includes a classical RAS axis (ACE-Ang Ii-AT1R pathway) and a not-classical RAS centrality (ACE2-Ang 1-seven-MasR-based pathway), counter-balancing role of the ii axes regulates cardiovascular physiology and disease [20, 21]. ACE2 cleaves Ang II into the Ang 1–vii, thus limiting substrate availability in the adverse ACE/Ang 2/AT1 receptor axis [22, 23]. Keidar and colleagues found that ACE2 antihypertensive properties may be due to the deposition of angiotensin II [24]. In this study, the laboratory results of RAS show that Ang II level is elevated in the bulk of patients without prior hypertension. Compared with normal blood pressure and good for you command groups, Ang Ⅱ levels were significantly higher in elevated blood pressure groups. A possible mechanism may be the binding of SARS-CoV-2 to ACE2 thereby inhibiting degradation of angiotensin II leading to elevated blood pressure. Another hypothesis is that over activation of the RAS organization promotes inflammatory response and cytokine tempest, which stimulates the NADH/NADPH oxidase system and triggers cell contraction and vasoconstriction, which then leads to COVID-19 related lung injury. Though the underlying machinery remains to exist elucidated, it is becoming evident that RAS plays a major role in hypertension and COVID-xix infection, equally observed in our written report. It has been noticed that recombinant human ACE2 is considered as a handling for patients with COVID-19 (ClinicalTrials.gov ID: NCT04287686). This finding probably shades of import implications for time to come treatment strategies. A recent long-term observational follow-upwardly study of patients with COVID-19 reported nearly 1-8th of patients without previous renal dysfunction developed a reduction in glomerular filtration rate at follow-up. In improver, COVID-19 survivors endure from relatively higher levels of depression, feet, and somatic symptoms (including fatigue or muscle weakness). Severe cases are more susceptible to the evolution of reduced pulmonary improvidence capacities [25]. Multiple above factors are capable of inducing hypertension in nonhypertensive patients. In improver, the median ages of these patients were 66.5 y/o. It seems that SARS-CoV-2 infection is just a trigger, and age plays a more than important role.

On the other hand, sixteen patients with elevated blood pressure level show significantly college levels of cTnI than those normal blood pressure patients. Several studies take demonstrated Ang Two straight or indirect effects on cardiomyocytes, some of which were related to pro-inflammatory and pro-hypertrophic responses [26]. Especially when the rest betwixt the ACE and ACE2 was disrupted in COVID-19 patients, the increase in Ang Two deportment could lead to myocardial inflammation, oxidative stress, and myocyte apoptosis. This hypothesis explains why elevated blood pressure level could occur in parallel with balmy cardiac injury of COVID-19 patients.

Study forcefulness and limitations

In the nowadays study, we propose that hypertension is probably a sequela of SARS-CoV-2 infection. Although a number of studies of COVID-19 have been reported, there are few reports about the sequela of the disease likely due to lack of long-term clinical follow-up, which also applies to our nowadays research. Next, it is difficult to analyze whether the claret pressure of COVID-19 patients with preexisting hypertension is further increased. Consequently, many patients could non be incorporated in the analysis because of the history of hypertension, which results in a relatively low sample size. As well, the present report uncovered rising Ang II as one possible mechanism that might outcome in hypertension in COVID-nineteen. Still, due to a lack of detection about ACE2 levels and other components, therefore, we cannot gain a comprehensive view of virus-induced imbalance of the RAS pathway.

Conclusion

In summary, SARS-CoV-2 may impair cardiomyocytes by systemic acute inflammation response, and the cTnI is correlated with the severity of the infection. Accompanied by mild height in cTnI, spontaneous hypertension may occur in patients during hospitalization, and could become a sequela of SARS-CoV-2 infection, which may be associated with markedly elevated Ang II levels.

Acknowledgments

We gratefully acknowledge contributions from all enrolled patients and related medical staff.

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Source: https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0250815