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![RAAS and Bradykinin Systems in SAR-CoV-2 infection. SARS-CoV-2 infection results in interaction with transmembrane protease, serine 2 (TMPRSS2) and ACE2, leading to subsequent down regulation of ACE2 [27]. This loss of ACE2 function leads to decreased metabolism of Ang II](publication/353640291/figure/fig5/AS:1052341549674501@1627909185713/RAAS-and-Bradykinin-Systems-in-SAR-CoV-2-infection-SARS-CoV-2-infection-results-in.png)
RAAS and Bradykinin Systems in SAR-CoV-2 infection. SARS-CoV-2 infection results in interaction with transmembrane protease, serine 2 (TMPRSS2) and ACE2, leading to subsequent down regulation of ACE2 [27]. This loss of ACE2 function leads to decreased metabolism of Ang II
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Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the virus responsible for the COVID-19 pandemic. Patients may present as asymptomatic or demonstrate mild to severe and life-threatening symptoms. Although COVID-19 has a respiratory focus, there are major cardiovascular complications (CVCs) associated with infection. The reported CVCs...
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... detailed in Figure 5, within the RAAS, Ang II mediates some of the pathophysiological effects of SARS-CoV-2 through the binding to AT1Rs (Figure 5) [17,40]. These pathophysiological effects can increase AT2R expression. ...
Context 2
... detailed in Figure 5, within the RAAS, Ang II mediates some of the pathophysiological effects of SARS-CoV-2 through the binding to AT1Rs (Figure 5) [17,40]. These pathophysiological effects can increase AT2R expression. ...
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Citations
... The RAS is a fundamental regulatory pathway responsible for maintaining homeostasis in the body, governing critical processes, such as blood pressure control, electrolyte balance, and fluid equilibrium. Furthermore, the RAS is involved in regulating inflammation, immune responses, and vascular function, which are important factors in COVID-19 pathogenesis (Cooper et al. 2021;El-Arif et al. 2021;Cantero-Navarro et al. 2021;Khazaal et al. 2022). ...
Infection by the recent SARS-CoV-2 virus causes the COVID-19 disease with variable clinical manifestations ranging from asymptomatic or mild respiratory symptoms to severe respiratory distress and multiorgan failure. The renin-angiotensin system, responsible for maintaining homeostasis and governing several critical processes, has been considered the main system involved in the pathogenesis and progression of COVID-19. Here, we aimed to assess the possible association between variants in the RAS-related genes and COVID-19 susceptibility and severity in a sample of the Moroccan population. A total of 325 individuals were recruited in this study, with 102 outpatients, 105 hospitalized patients, and 118 healthy controls negative for SARS-CoV-2 infection, and subjected to NGS gene panel sequencing containing eleven RAS pathway genes. A total of 65 functional variants were identified, including 63 missenses, 1 splice, and 1 INDEL. Most of them were rare, with 47 (72%) found in a single individual. According to the common disease/common variant hypothesis, five common candidate variants with MAF > 10% were identified (ACE2 rs2285666, TMPRSS2 rs12329760, AGT rs699 genes, ACE rs4341, and ACE rs4343). Statistical analysis showed that the ACE rs4343 AA genotype was associated with a 2.5-fold increased risk of severe COVID-19 (p = 0.026), and the T genotype of the ACE2 rs2285666 variant showed a borderline association with susceptibility to SARS-CoV-2 in males (p = 0.097). In conclusion, our results showed that the RAS pathway genes are highly conserved among Moroccans, and most of the identified variants are rare. Among the common variants, the ACE rs4343 polymorphism would lead to a genetic predisposition for severe COVID-19.
... Vasilieva, N.G. Chopik, et al. in the expression of this important functional receptor and, consequently, the disruption of the renin-angiotensin-aldosterone and kallikrein-kinin systems (Cooper et al., 2021;Gupta, 2022). ...
COVID-19 is a dangerous disease with long-lasting consequences. Vaccination contributes to the accumulation of neutralizing anti-S IgG antibodies, reducing the incidence of COVID-19 and its complications. However, in some individuals, the inflammatory process can persist for an indefinite period and lead to a wide range of dysfunctions. The current task is to investigate molecular markers for their detection. The aim of this study is to examine the levels of anti-S IgG antibodies, lactate, glucose, lactate dehydrogenase, and C-reactive protein in the peripheral blood of individuals who have and have not been affected by COVID-19 after vaccination. The research subject is venous blood. Among 547 employees of the Neurosurgery Institute (481 vaccinated against COVID-19 and 66 unvaccinated individuals), levels of anti-S IgG antibodies were investigated, as well as levels of lactate, lactate dehydrogenase, glucose, and C-reactive protein. At the time of the study, among 372 individuals, 16 months had passed from the first vaccination, and 12 months had passed from the second vaccination; in 21 individuals, 12 months had passed after a single vaccination, and in 88 individuals, 16 months had passed from the first vaccination, 12 months from the second, and 6 months from the third vaccination. Methods. Quantitative determination of IgG antibodies to the S protein of the SARS-CoV-2 virus. Confirmation of COVID-19 using the RT-PCR method (Allplex 2019-nCoV kit, SeeGene, Korea). Levels of lactate, lactate dehydrogenase, glucose, and C-reactive protein were determined using reagents from BioSystems (Spain). Statistical analysis of the obtained data was performed using Jamovi software (USA) and the following criteria: χ2 ‒ Kruskal-Wallis, W ‒ Dwass-Steel-Critchlow-Fligner (DSCF), χ2 ‒ Pearson, t ‒ Student, rs ‒ Spearman, τb ‒ Kendall. A statistically significant difference was considered at p < 0.05. Results. The level of anti-S IgG antibodies to the SARS-CoV-2 virus was higher in vaccinated individuals compared to unvaccinated individuals (Kruskal-Wallis χ2=14.09; p < 0.001). A higher level of antibodies to the S protein of the virus was observed when using the Comirnaty vaccine compared to vaccination with Moderna, AstraZeneca, Pfizer, and CoronaVac (Dwass-Steel-Critchlow-Fligner (DSCF): W 4.26, p=0.002; W 4.62, p=0.010; W 4.84, p=0.006, respectively). Vaccination reduces the likelihood of contracting the disease by 1.84 times (Odds Ratio (OR) 1.84; 95% Confidence Interval (CI) 1.02‒3.30; χ2=4.129; p=0.043). However, no statistically significant dependence on the prevention of COVID-19 incidence based on the type of vaccines used was found (Kruskal-Wallis χ2=2.072; p=0.72). A statistically significant difference in C-reactive protein levels is observed between groups with early mild complications and early moderate-severity complications (DSCF: W=4.193, p=0.009). A statistically significant difference in LDH levels is noted between individuals without chronic diseases and those with chronic diseases at the time of the study (Kruskal-Wallis χ2=6.08, p=0.014). In individuals vaccinated against the SARS-CoV-2 virus, a positive correlation is found between the levels of C-reactive protein and lactate dehydrogenase (Kendall's τb 0.134, p < 0.001). The mean levels of lactate among individuals with mild, moderate, and severe forms of COVID-19 are higher than the reference mean; similarly, the mean levels of glucose in these same groups are higher than the reference mean. A positive correlation exists between the levels of lactate and glucose among individuals vaccinated against the SARS-CoV-2 virus (Kendall's τb 0.082, p < 0.01). Conclusions. Vaccination contributes to an increase in antibody levels. The level of antibodies after the third vaccination exceeded the levels after the first (Dwass-Steel-Critchlow-Fligner (DSCF): W 4.42, p=0.005) and second vaccinations (W 4.24, p=0.008). Vaccination reduces the likelihood of COVID-19 infection by 1.84 times (Odds Ratio ‒ 1.84; 95% Confidence Interval 1.02‒3.30; Pearson χ2=4.129; p=0.043). The frequency of COVID-19 incidence is not dependent on the type of vaccine used: AstraZeneca, Comirnaty, CoronaVac, Moderna, Pfizer (Kruskal-Wallis χ2=2.072; p=0.723), and the level of antibodies in the vaccinated individuals' serum. In the post-COVID-19 remote period, regardless of vaccination status, various complications are observed. However, among the vaccinated, the number of individuals without complications or with minimal complications is greater than in the unvaccinated group, while the number of individuals with early and severe complications is lower (Kruskal-Wallis χ2=6.127; p=0.047). A high level of C-reactive protein (DSCF: W=4.19, p=0.009), a tendency toward increased levels of lactate dehydrogenase (DSCF: W=3.27, p=0.054), elevated levels of lactate (2.17+1.23, t=3.34; p=0.002), and glucose (6.06+0.048, t=10.54; p < 0.001) indicate that after recovering from COVID-19, regardless the type of vaccines used, in individuals with distant symptoms there are metabolic changes that are signs of a chronic inflammatory process. Individuals with chronic diseasees show an increase in the level of lactate dehydrogenase (χ2=6.08; p=0.014) and a tendency toward increased levels of C-reactive protein (χ2=3.74; p=0.053). Molecular markers of inflammation such as increased levels of lactate, glucose, C-reactive protein, and lactate dehydrogenase are informative for identifying individuals with an inflammatory process in the post-COVID-19 remote period.
... Патофизиология этого состояния не до конца изучена. Вероятным механизмом взаимосвязи АГ и ПС является дисрегуляция ренин-ангиотензин-альдостероновой системы и калликреин-кининовой системы, а также имеющаяся при АГ эндотелиальная дисфункция, которая усиливает повреждающее действие вируса в отношении сосудистой стенки и его провоспалительную активность [14]. ...
Aim. To evaluate cardiovascular risk factors as predictors of the post-coronavirus disease 2019 (COVID-19) syndrome.
Material and methods. This prospective cohort study included adult patients admitted to a university hospital with a clinically or laboratory-confirmed diagnosis of COVID-19. A number of cardiovascular risk factors were assessed at admission, including the Cardio-Ankle Vascular Index (CAVI). After hospital discharge, patients were observed for 6 months. Then, data on the course of the post-COVID-19 period was collected from electronic medical records and discharge summaries. Two following outcomes were assessed: the development of post-COVID-19 syndrome and the development of newly diagnosed diseases or worsening of existing chronic diseases in the post-COVID-19 period.
Multivariable logistic regression was used to assess the association between potential predictors and outcomes, and odds ratios (OR) with 95% confidence intervals (95% CI) were calculated to assess the association strength. The statistical significance level was p<0,05.
Results. The final analysis included 125 patients (68 (54,4%) women). The median age was 59,0 [50,5, 71,0] years. Post-COVID-19 syndrome was diagnosed in 32,8% of patients. The most common symptoms were weakness (19,2%), headaches (11,2%) and shortness of breath (10,4%). In multivariate analysis, CAVI ≥9,5, increased systolic blood pressure (SBP) and glomerular filtration rate (GFR) on admission were associated with the post-COVID-19 syndrome, with an OR of 2,415 (95% CI 1,174-2,846), 1,045 (95% CI 1,010-1,082), 0,971 (95% CI 0,946-0,998), respectively. Age (OR 1,056, 95% CI 1,009-1,105) and body mass index (OR 1,132, 95% CI 1,027-1,248) were associated with newly diagnosed diseases or worsening of existing chronic diseases in the post-COVID-19 period.
Conclusion. Objective indicators such as SBP, CAVI and GFR may be predictors of post-COVID-19 syndrome, and age and body mass index are associated with the unfavorable course of chronic diseases in the post-COVID-19 period.
... However, this possibility does not modify the relevance of our conclusions since, by encompassing the entire years of follow-up, we can assume that the role of influenza in determining hypertension should be at least constant in the two periods, if not lower in the second triennium due to the use of masks and other measures implemented during the pandemic, which limited the incidence of influenza infection [29,30]. Second, we acknowledge that our results do not allow any speculation on the pathophysiologic mechanisms underlying the increased rate of incident hypertension in the pandemic period, which could include direct effects of SARS-CoV-2 infection on endothelial cells, and indirect effects like stress, changes in diet and exercise and in cardiovascular prevention strategies, and access to health system during pandemic; other possibilities include persistent activation of RAAS and endothelial injury which have been reported among patients with COVID-19 and both are associated with blood pressure elevation [31][32][33][34]. Besides, consequences of severe COVID-19 including systemic hypoxia, acute respiratory distress, hyper-coagulation, sepsis, inflammation, metabolic stress, and cytokine storm may stress the cardiovascular system, eventually leading to blood pressure dysregulation [35][36][37][38]. ...
Background: While the augmented incidence of diabetes after COVID-19 has been widely confirmed, controversial results are available on the risk of developing hypertension during the COVID-19 pandemic.
-Methods: We designed a longitudinal cohort study to analyze a closed cohort followed up over a 7-year period, i.e., 3 years before and 3 years during the COVID-19 pandemic, and during 2023, when the pandemic was declared to be over. We analyzed medical records of more than 200,000 adults obtained from a cooperative of primary physicians from January 1, 2017, to December 31, 2023. The main outcome was the new diagnosis of hypertension.
-Results: We evaluated 202,163 individuals in the pre-pandemic years and 190,743 in the pandemic years, totaling 206,857 when including 2023 data. The incidence rate of new hypertension was 2.11 (95% C.I. 2.08–2.15) per 100 person-years in the years 2017–2019, increasing to 5.20 (95% C.I. 5.14–5.26) in the period 2020–2022 (RR = 2.46), and to 6.76 (95% C.I. 6.64–6.88) in 2023. The marked difference in trends between the first and the two successive observation periods was substantiated by the fitted regression lines of two Poisson models conducted on the monthly log-incidence of hypertension.
-Conclusions: We detected a significant increase in new-onset hypertension during the COVID-19 pandemic, which at the end of the observation period affected ~ 20% of the studied cohort, a percentage higher than the diagnosis of COVID-19 infection within the same time frame. This observation suggests that increased attention to hypertension screening should not be limited to individuals who are aware of having contracted the infection but should be extended to the entire population.
... Він входить до складу ККС, пов'язаної із реакцією запалення і такої, що опосередковує різні функції проникності судин, такі як тромбоз і згортання крові. БK індукує вазодилатацію в системі периферичного кровообігу шляхом зниження тонусу гладкої мускулатури артерій та збільшення кровотоку [2][3][4]. Крім того, він ініціює екстравазацію плазми, через вплив на ендотелій капілярів і вазоконстрикцію шляхом індукції гладком'язових волокон вен. Під час запальних станів, таких як астма, він сприяє руху клітин від крові до тканин і активує тучні клітини, фібробласти, макрофаги та гладку мускулатуру органів [5]. ...
... Кініназа II або АСЕ інактивує ККС шляхом розкладання БК, KD, DAБК і DAKD на неактивні метаболіти. Подібним чином АПФ2 метаболізує DAБК до БК (1-7) і DAKD до KD (1-8) [2]. (Створено за допомогою Biorender.com). ...
... 1). Це вказує на інший прямий зв'язок між ККС і РААС [2,12]. ...
Огляд літератури присвячений участі брадикініну (БК) в розвитку коронавірусної хвороби (COVID-19), спричиненою вірусом SARS-CoV-2, та інших патологічних станів, а також можливості застосування деяких препаратів, які впливають на сигналінг вищезазначеного нанопептиду. БК є потужною короткоживучою вазоактивною сполукою, яка діє як вазодилататор і медіатор запалення в різних сигнальних каскадах. Він входить до складу калікреїн-кінінової системи (ККС), що входить до складу системи ренін-ангіотензин-альдостерон (РААС), яка відіграє ключову роль у патогенезі COVID-19. Як фактор ККС, БК залежить від інших компонентів, необхідних для його синтезу та підтримки. Наразі існує гіпотеза, яка свідчить про те, що шлях БК дерегульований у пацієнтів із COVID-19, що призводить до різних ускладнених респіраторних захворювань. Теорії шторму цитокінів і БК пропонують пояснення різноманітності симптомів і систем органів, уражених після інфекції SARS-CoV-2. Наведені в огляді дані свідчать, що БK є молекулою величезного терапевтичного потенціалу, яка заслужено потребує відповідної спрямованої уваги. Встановлено, що наслідком посилення утворення БK єважкі мультисимптомні патологічні зміни при інфекції COVID-19. Оскільки COVID-19 значною мірою впливає на ККС, існує багато медіаторів, які можуть посилювати тяжкість захворювання. Тому, важливим моментом терапії при COVID-19 є модуляція сигналінгу БК. Було показано, що ефекти БK компенсуються за допомогою деяких сполук, які є антагоністами B2R. Фактори БК-шляху та цитокіни, такі як інтерлейкін-6 (IL-6) та IL-1, можуть бутиключовими для використання блокаторів, навіть як допоміжних засобів. Таким чином, щоб запобігти тяжким ускладненням, викликаних COVID-19 та покращити результати лікування цього інфекційного захворювання необхідно проводити фармакологічне таргетування компонентів ККС, пов’язаних із БK, головним чином – кінінових рецепторів.
... The KKS controls vascular permeability, vasodilation, and cytokine release in tissue injury. 8,9 It consists of a system of enzymes, proteins, and peptides that regulate blood pressure, pain signaling, inflammation, and coagulation 10 and induces dilation and enhances permeability of vessels to help maintain normal blood pressure. The KKS also has a defensive role in protecting against pathogens. ...
... While COVID-19 binding of ACE2 has been speculated to activate both the RAS and KKS, 8 its presence directly activates the KKS as the virus binds to kininogen through its structural proteins 29 and secretes a cysteine protease to cleave kininogen into bradykinin. Additionally, the KKS and RAS recruit leukocytes 7 alongside cytokines to fight the COVID-19 virus at the site of infection. ...
... The RAS and KKS are connected to the inflammatory cytokines, 8 and it was expected that levels of the peptides may Figure S4 and Tables S4−S8). While no conclusion can be made on this result, we are pursuing an additional study on cytokines and COVID-19 severity.. ...
... Additionally, the oral anticoagulant apixaban is being trialed as a prophylactic anticoagulant since the high association between COVID-19 and consecutive thromboembolism and microangiopathy has been proven beforehand [3,84]. Another drug worthy of study in the context of LCS is an angiotensin receptor blocker, such as telmisartan, due to its ability to reestablish cardiovascular homeostasis by regulating the RAAS [3,85]. Therefore, Cooper et al. reviewed the association between LCS and cardiovascular complications and future implications for pharmacological therapies [85]. ...
... Another drug worthy of study in the context of LCS is an angiotensin receptor blocker, such as telmisartan, due to its ability to reestablish cardiovascular homeostasis by regulating the RAAS [3,85]. Therefore, Cooper et al. reviewed the association between LCS and cardiovascular complications and future implications for pharmacological therapies [85]. ...
Citation: Zimmermann, P.; Sourij, H.; Aberer, F.; Rilstone, S.; Schierbauer, J.; Moser, O. SGLT2 Inhibitors in Long COVID Syndrome: Is There a Potential Role? J. Cardiovasc. Dev. Abstract: The coronavirus disease (COVID)-19 has turned into a pandemic causing a global public health crisis. While acute COVID-19 mainly affects the respiratory system and can cause acute respiratory distress syndrome, an association with persistent inflammatory stress affecting different organ systems has been elucidated in long COVID syndrome (LCS). Increased severity and mortality rates have been reported due to cardiophysiological and metabolic systemic disorders as well as multiorgan failure in COVID-19, additionally accompanied by chronic dyspnea and fatigue in LCS. Hence, novel therapies have been tested to improve the outcomes of LCS of which one potential candidate might be sodium-glucose cotransporter 2 (SGLT2) inhibitors. The aim of this narrative review was to discuss rationales for investigating SGLT2 inhibitor therapy in people suffering from LCS. In this regard, we discuss their potential positive effects-next to the well described "cardio-renal-metabolic" conditions-with a focus on potential anti-inflammatory and beneficial systemic effects in LCS. However, potential beneficial as well as potential disadvantageous effects of SGLT2 inhibitors on the prevalence and long-term outcomes of COVID-19 will need to be established in ongoing research.
... Furthermore, binding the SARS-CoV-2 virus to angiotensin-converting enzyme 2 (ACE-2) receptors on the endothelium results in the release of angiotensin 2 and reduced nitric oxide (NO) production, causing damage to the endothelium through increased oxidative stress and mitochondrial dysfunction [13,30,31]. Finally, the importance of ACE-2 in the homeostasis of the Renin-Angiotensin-Aldosterone System (RAAS) is already known, and the viral binding through the viral spike protein can cause significant dysregulation and cardiovascular symptoms [32]. ...
Long COVID-19 is a recognized entity that affects millions of people worldwide. Its broad clinical symptoms include thrombotic events, brain fog, myocarditis, shortness of breath, fatigue, muscle pains, and others. Due to the binding of the virus with ACE-2 receptors, expressed in many organs, it can potentially affect any system; however, it most often affects the cardiovascular, central nervous, respiratory, and immune systems. Age, high body mass index, female sex, previous hospitalization, and smoking are some of its risk factors. Despite great efforts to define its pathophysiology, gaps remain to be explained. The main mechanisms described in the literature involve viral persistence, hypercoagulopathy, immune dysregulation, autoimmunity, hyperinflammation, or a combination of these. The exact mechanisms may differ from system to system, but some share the same pathways. This review aims to describe the most prevalent pathophysiological pathways explaining this syndrome.
... В постгоспитальный период в контрольной и основной группах регистрировалась разнонаправленная динамика большинства параметров ВРС: RMSSD, Var, LF, а также более выраженный прирост величины VLF и HF в основной группе, в то время как наибольший прирост SDANN отмечался в контрольной группе. Полученные результаты свидетельствуют о том, что перенесенный COVID-19 у пациентов с ОИМпST, оказывал влияние на характер ВРС при ОКС и развивающемся ОИМ, что, вероятно, обусловлено выраженным вегетативным дисбалансом с преобладанием симпатикотонии и снижением парасимпатического влияния, более значимой активацией гуморальных механизмов, включая ренин-ангиотензиновую систему [22]. Подтверждением симпатикотонии в этом случае служат более выраженные увеличения ВРС в ранний госпитальный период у пациентов с ОИМпST c перенесенным COVID-19: SDNN на 46%, LF на 59%. ...
Aim. To compare heart rate variability parameters in patients after a coronavirus disease 2019 (COVID-19) with acute ST elevation myocardial infarction (STEMI) during the inhospital and post-hospital periods.
Material and methods. A total of 140 patients with STEMI were divided into 2 groups: I — patients with STEMI who had COVID-19 (n=52) in the period of 1,5-6 months before acute coronary syndrome, II — comparison group (n=88), which included patients with STEMI without prior COVID-19. All patients underwent infarct-related artery stenting within the first 24 hours from the onset. Heart rate variability (HRV) parameters were determined for all patients on days 2-3 and days 9-11 and 6 months after the hospitalization for STEMI.
Results. Patients in group I showed more pronounced changes in HRV indicators on days 2-3 of STEMI: RMSSD (root square of successive RR intervals) by 21% (p=0,026), variations (Var) (the difference between the minimum and maximum RR intervals) by 33% (p=0,013), VLF (total very low-frequency HRV) by 7% (p=0,009) were higher, and HF (highfrequency HRV) by 40% (p=0,003), pNN50% (ratio of the number of consecutive RR interval pairs differing by >50 ms to the total number of RR intervals) by 66% (p=0,038) were lower than in the control group, respectively. On days 9-11 of the disease in patients with a history of STEMI and COVID-19, in contrast to the control group, there was a more pronounced increase in the SDNN (standard deviation of RR intervals) by 46% (p=0,005), VLF by 42% (p=0,031), whereas in the control group there were an increase of only 22% (p=0,004) and 11% (p=0,022), respectively. The HF value in the main group increased by 25% (p=0,007), while in the control group it decreased by 19% (p=0,030). Six months after STEMI in the main group, the RMSSD decreased by 19% (p=0,009), Var by 16% (p=0,041), VLF by 30% (p=0,025), LF (low-frequency component HRV) by 11% (p=0,005), while the control group these parameters decreased by 20% (p=0,006), 21% (p=0,001), 9% (p=0,011), and 7% (p=0,016), respectively.
Conclusion. In patients with STEMI and prior COVID-19, the initial HRV values differ from similar HRV parameters in patients with STEMI without prior COVID-19. In the hospital and post-hospital periods, the changes of HRV in patients with and without COVID-19 are multidirectional as follows: pronounced sympathetic hyperactivity predominates, and slower recovery of HRV in patients after COVID-19 predominates.
... The myocardial injury in patients with COVID-19 has been attributed to coronary spasm, microthrombi formation, plaque rupture, hypoxic injury or cytokine storm disposing the same pathophysiology with the three clinical variants of Kounis syndrome [5]. One of the main proposed mechanisms for development of cardiovascular complications and new onset hypertension is the ACE2 and its interactions with RAAS and KKS [6]. The ACE2 receptors are expressed throughout the human body located mainly in heart, blood vessels' endothelium, lungs, intestines, testes and neurons. ...
The novel severe acute respiratory coronavirus-2 (SARS-Cov-2) constitutes the causative agent of coronavirus disease-2019 (COVID-19). Several mechanisms have been proposed regarding the development of cardiovascular complications during and after acute COVID-19 infection. COVID-19, caused by SARS-CoV-2, has emerged as one of the deadliest pandemics in modern history. Several clinical and pathophysiologic mechanisms have been proposed for development of cardiovascular complications during and after acute COVID-19 infection. The myocardial injury in patients with COVID-19 has been attributed to coronary spasm, microthrombi formation, plaque rupture, hypoxic injury or cytokine storm disposing the same pathophysiology with the three clinical variants of Kounis syndrome. One of the main proposed mechanisms for development of cardiovascular complications is the angiotensin converting enzyme 2 (ACE2) and its interactions with the renin-aldosterone system (RAAS) and the kinin-kallikrein system (KKS). The ACE2 receptors are expressed throughout the human body located mainly in heart, blood vessels endothelium, lungs, intestines, testes and neurons. The SARS-CoV-2 directly invades the endothelial cells that contain ACE2 receptors and constitutes the main pathway through which the virus enters the endothelial cells. This leads to downregulation of the ACE2 receptors and causes angiotensin II accumulation leading to prothrombotic effects such as hemostatic imbalance via activation of the coagulation cascade, impaired fibrinolysis, thrombin generation, vasoconstriction, endothelial and platelet activation, and pro-inflammatory cytokine release. Indeed, angiotensin I exerts no direct biological function except that its high levels can stimulate catecholamine production. It is metabolized to its biologically active byproduct angiotensin II, a potent vasoconstrictor, by angiotensin converting enzyme (ACE) through cleavage of the two terminal amino acids. SARS-CoV-2 infection prevents the counterbalancing action of the KKS system that normally causes vasodilation and regulates tissue repair, inflammation, cell proliferation, and platelet aggregation. All this cascade leads to the following cardiovascular events: cardiac arrhythmias, cardiac arrest, cardiomyopathy, cytokine storm, heart failure, ischemic myocardial injuries and microvascular disease, Kounis syndrome, long COVID, myocardial fibrosis, myocarditis, new onset hypertension, pericarditis, postural orthostatic tachycardia syndrome (POTS), pulmonary hypertension, stroke, Takotsubo Syndrome, venous thromboembolism and thrombocytopenia. In this narrative review we describe and elucidate when and how the COVID-19 affects the human cardiovascular system, in various areas on the human body that are vulnerable in every category of patients including children and athletes.
