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International Medical Scientific Journal     Issue-2 

10.5281/zenodo.5080427 

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Art of Medicine          Volume-1 

International Medical Scientific Journal     Issue-2 

10.5281/zenodo.5080427 

4 

Art of Medicine 
International Medical Scientific journal 

 

Founder and Publisher Pascual Izquierdo-Egea 

Published science may 2021 year. Issued Quarterly. 

Internet address: http://artofmedicineimsj.us 
E-mail: info@artofmedicineimsj.us 

11931 Barlow Pl Philadelphia, PA 19116, USA +1 (929) 266-0862 

 

 

 

 

 

 

 

 



Art of Medicine          Volume-1 

International Medical Scientific Journal     Issue-2 

10.5281/zenodo.5080427 

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Coronavirus infection and cardiovascular diseases 
Abdukodirova N.M., Tulaboeva G.M., Saidov Kh.Kh., Fazilbekova Z.N. 

Development Center of Professional Qualifications of Medical Workers under the 

Ministry of Health of the Republic of Uzbekistan 

 

Abstract: Coronavirus pandemic the recently emerged ongoing coronavirus 
infection (COVID-19) pandemic has spread to almost the entire world.  With all the 

severity of the COVID-19 problem, mortality rates from this disease cannot be 

compared with mortality rates from cardiovascular diseases (CVD), which remain the 
main cause of death of the population.   

Keywords: COVID-19, various CC3, CHF, AH. 

 

Literary review 

COVID-19 is especially difficult for older people, most likely because it is they 

who, as a rule, suffer from various CC3: arterial hypertension (AH), coronary heart 

disease (IHD), chronic heart failure (CHF).  Therefore, there is reason to believe that the 
COVID-19 pandemic may further increase mortality from CC3.  Coronary Virus 

Infection Vascular Diseases It has now become apparent that the so-called severe acute 

respiratory syndrome (SARS acute respiratory syndrome), cardiovascular pneumonia 

associated with it, is the main complication of COVID-19, and they are believed to be 
the cause of death of such patients.  This feature has been noted for other viral diseases 

as well.  Pneumonia itself can cause a number of cardiovascular complications, even in 

individuals without CVD [2].  It should be emphasized that in patients with pre-existing 

CVD, this risk will be significantly higher.  Unfortunately, to date, there is no clear 
statistical data on what kind of sick causes COVID-19 die, but individual clinical 

observations indicate that the immediate cause of death may be not only acute 

respiratory failure, but cardiovascular complications. 
A meta-analysis of eight studies and> 46,000 patients in China showed that 

hypertension, diabetes and cardiovascular disease were the most common comorbidities.  

Underlying cardiovascular disease gave the highest chances of any comorbidity to 

develop severe versus moderate COVID-19.  Hypertension and respiratory illness also 
increased the risk of developing severe COVID-19.  Patients with CVD had high pre-

existing mortality rates.  Mortality rates of COVID-19 patients by selected 

comorbidities.  Patients with cardiovascular disease are at increased risk of developing 
COVID-19 and should take extra precautions.  Acute heart damage in COVID-19 is 

manifested by left ventricular (LV) dysfunction, heart failure, ventricular arrhythmias, 

ECG, increased changes in B-type natriuretic peptide (BNP) and troponin (2,21-23).  In 

the first 41 cases with confirmed COVID-19 in Chinese patients, acute heart damage, 



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defined as elevated heart biomarkers with altered dysfunction, was observed in 12% of 

patients.  In a later ECG and left ventricular study, the study found acute heart damage 
in 19.7% of patients, while in the USA, conducted in 21 as an intensive care patient 

study; cardiomyopathy was described in 33%. Acute heart injury has been independently 

associated with mortality in hospitalized COVID-19 patients in China.  

Pathophysiological theories for heart damage include direct myocardial infection with 
SARS-Co-2, myocardial inflammation, Takotsubo syndrome, or overwhelming multiple 

organ disease.  While direct transmission of the virus via ACE-2 receptors has been 

postulated, COVID-19 myocardium has been histopathological examination of an 

associated direct infection with SARS-CoV-2.  Instead, cardiomyopathies have not been 
observed, infiltrates with LV dysfunction ACE-1 / ARB and beta-blockers are shown as 

the putative pathophysiology of renin-COVID-19 imbalance, inflammatory 

myocardium. For patients of the angiotensin system, indicating their potential 
therapeutic role.  However, much more research is needed to determine the underlying 

pathophysiology and optimal treatment.  The increase in troponin is reflective (MI).  The 

diagnostic value is unclear, as it may be associated with non-coronary conditions, a 

prognostic marker and may be myocarditis or myocardial infarction, respiratory 
infections and myocardial infarction type 2. 

Myocardial injury in including acute COVID-19 patients may present with ST 

elevations in the absence of obstructive coronary artery disease (CAD).  Whether this is 
due to microvascular injury or myocarditis is unclear.  To avoid unnecessary coronary 

angiography of the disease, during the acute period, hemodynamically stable patients 

with COVID-19 and possible MI of the patient are best managed conservatively, with 

invasive procedures delayed until recovery from COVID-19. 
Previously, it was shown that viral diseases can destabilize the course of ТНЕС, in 

particular, in patients with IHD and CHF, ruptures of atherosclerotic plaques are 

observed under the influence of systemic inflammation caused by the virus [3].  That is 
why it has long been proposed to stabilize drugs capable of atherosclerotic plaques in the 

complex treatment of patients with a viral infection complicated by SARS.  These drugs 

included aspirin, statins, beta-blockers, angiotensin-converting enzyme (ACE inhibitor) 

[3]. Systemic inhibitors of inflammation caused by a viral infection also have a 
procoagulant effect, increasing the likelihood of thrombosis; therefore, treatment with 

antiplatelet agents was  also considered necessary, especially in those patients with 

coronary artery disease who had previously undergone angioplasty with stenting [4]).  
All of the above theoretically creates the prerequisites for active cardiovascular drugs in 

patients with SARS caused by a viral infection.  However, scientific data on the 

effectiveness of such treatment is extremely limited.  However, it should be mentioned 

that in 2014, during Africa, there was an outbreak of Ebola, an attempt was made to treat 
SARS with angiotensin I receptor antagonists (ARA) and statins.  Generics were sent to 

the epidemic focus of Sierra Leone. About 100 patients with Ebola fever received a 



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combination of these drugs, after which the doctors of the above drugs were  given.  

Noted a significant improvement in their condition.  Despite the fact that a rigorous 
controlled study has not been conducted, these data have been published as clinical 

observations [5].    

It has been suggested that blockers of the aldosterone system (PAAS) may be very 

promising in the treatment of the current COVID-19 pandemic [6].  Therefore, the 
publication of the Medical Journal, which appeared at the end of February 2020, the 

authors of which, turning the obvious data on the increased mortality of patients with 

COVID-19 in patients with concomitant drugs, renin-angiotensin-unexpected British 

attention to CVD, concluded that one of the reasons for this  may be taking an ACE 
inhibitor and ARA [7].  The cause of the coronavirus is angiotensin-converting enzyme 

2 (ACE2) to enter the cell.  Since it has been shown that the use of both ACE inhibitors 

and ARBs can significantly increase the production of ACE2, these drugs can contribute 
to a more severe course of COVID-19. The   authors, however, were rather cautious in 

the named use, it was concluded that the Conclusions recognized that their  the 

assumption about the relationship of coronavirus infection with the intake of ACE 

inhibitors and ARBs is only a hypothesis that needs to be confirmed by specially 
planned studies, and only after that it can be recommended to limit ACE inhibitors and 

ARBs for the  period of COVID-19 disease and replace them with drugs of a different 

mechanism of action [7].  Soon, another publication appeared Ј.  Diaz [8], in which the 
author, based on the results of a small study of 1099 patients conducted in China [9], 

indicates that the most severe outcomes of COVID-19 were observed in patients with 

hypertension, coronary artery disease, diabetes mellitus and chronic kidney disease.  It is 

these patients, as Ј points out.  Diaz, have indications for the appointment of ACEI and 
ARA.  Note that the original publication does not contain the therapy received with an 

ACE inhibitor and ARB.  However, Ј.  Diaz concludes that taking ACE inhibitors and 

ARBs is one of the risk factors for severe outcomes of COVID-19 [8]. 
Unfortunately, the above publications received a wide response both in the media 

and among practitioners.  We already have separate (so far, however, not documented) 

reports of cancellation of ACE inhibitors and ARBs in elderly patients with CC3.  It is  

surprising that some communities that, according to evidence, the Center for Evidence-
Based  Oxford Medicine, University Medicine, hastened to adopt very ambiguous 

documents, on the one hand, recognizing that there is no real evidence of the harm of  

ACE inhibitors and ARBs in patients at risk of getting COVID-19, but on the other  - 
calling for the abolition of these drugs where CC3 is not very difficult [10].  Even a 

special algorithm has been proposed that determines when and in which patients should 

be canceled an ACE inhibitor or ARA in COVID-19.  If the application is to objectively 

assess the degree of evidence of the proposed algorithm from the standpoint of 
evidence-based medicine, then it should be classified as recommendation class I (the 

proposed algorithm can do more harm than good), and its level of evidence should be 



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regarded as "C" (expert opinion).  Ironically, the position expressed by the University of 

Oxford Center for Evidence-Based Medicine has just been endorsed in an editorial that 
appeared in the British Medical Journal [11].  This article has re-published the algorithm 

for applying or canceling ARA in COVID-19.  It should be noted by the ACEI that the 

above position has just been criticized by the well-known expert in evidence-based 

medicine G. FitzGerald in an interview with the President of the European Society of 
Cardiology V. Casadei, where the recommendations were called contradictory.  It should 

also be noted that the publications mentioned above and their positions are a serious 

criticism of published works.  R. Sarzani expressed the opinion that "Hasty speculations 

can be dangerous" | 12 |, believing that the binding of the virus to ACE2 will result in 
hyper activation of the RAAS and an increase in the damaging effect of coronavirus, 

respectively, on the lungs.  Drugs that reduce the activity of the RAAS will weaken this 

effect.  Therefore, according to R. Sarzani, there is no reason to restrict the use of the 
above drugs in patients with COVID-19. D. Gurwitz believes that the competition for 

receptors between coronavirus and ARA has no clinical significance at all lags behind 

the tactics of using ARA in COVID-19 as   one attempt to improve the condition of 

patients [13].  The European Journal of Cardiology has just dedicated a special 
publication to the topic of whether IZ COVID-19 inhibitors are needed [14).  

The main conclusion of the article: based on the existing data, as well as on the 

proven effect of ACE inhibitors and ARBs in patients with CVD, including those with 
comorbid pathology, on mortality rates, therapy with these drugs should be continued in 

CHF, AH, myocardial infarction in modern recommendations, regardless   from the 

presence of COVID-19. Cancellation of drugs blocking the RAAS or transfer of patients 

to drugs of other groups in accordance with clinical requirements is undesirable, since 
this can increase cardiovascular mortality in patients with severe COVID-19.  The most 

fully and objectively, from our point of view, the discussed problem is estimated in the 

publication of M. Vaduganathan et al. [15].  The article notes that the hypothesis on the 
relationship between the activation of RAAS by ACE inhibitors and ARA and the 

increased risk of COVID-19 disease and its complicated course has no clinical evidence.  

The paper also states that Clinical Safety Effects of Drugs Affecting the RAAS in 

Patients with COVID-19 are currently underway.  Cancellation of ACE inhibitors and 
ARBs in CVD patients with COVID-19, according to the authors, can destabilize their 

studies. To assess, lead to an unfavorable outcome.    

The main conclusion of the article: based on the existing data, as well as on the 
proven effect of ACE inhibitors and ARBs in patients with CVD, including those with 

comorbid pathology, on mortality rates, therapy with these drugs should be continued in 

CHF, AH, myocardial infarction in modern recommendations, regardless from the 

presence of COVID-19. Cancellation of drugs blocking the RAAS or transfer of patients 
to drugs of other groups in accordance with clinical requirements is undesirable, since 

this can increase cardiovascular mortality in patients with severe COVID-19.  The most 



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fully and objectively, from our point of view, the discussed problem is estimated in the 

publication of M. Vaduganathan et al. [15].  The article notes that the hypothesis on the 
relationship between the activation of RAAS by ACE inhibitors and ARA and the 

increased risk of COVID-19 disease and its complicated course has no clinical evidence.  

The paper also states that Clinical Safety Effects of Drugs Affecting the RAAS in 

Patients with COVID-19 are currently underway.  Cancellation of ACE inhibitors and 
ARBs in CVD patients with COVID-19, according to the authors, can destabilize their 

studies. To assess, lead to an unfavorable outcome 

Until reliable clinical status and clinical data are obtained, the authors believe, 

there is no reason to change CVD therapy in patients with COVID-19, and even more so 
in commas in patients at risk of this disease.  The professional communities did not 

remain aloof from the discussed problem.  Thus, the Council of the European Society of 

Certain Medical Cardiologists on Hypertension issued a special statement in which it 
noted that hypertensive patients are strongly advised to continue taking their usual 

antihypertensive therapy, since there is no clinical evidence, an ACE inhibitor or that 

ARA treatment should be discontinued due to COVID-  19 [15). 

Thus, we note that medicine has more than once encountered the fact that 
hypotheses based on pathophysiological data, speculating on separate, not always well-

studied mechanisms of action that do not have strict CLINICAL confirmation, lead to 

erroneous conclusions.  Attempts to introduce unproven hypotheses into medical 
practice can have unpredictable consequences.  All this may fully be related to calls to 

cancel ACE inhibitors and ARAs when they show signs of COVID-19, drugs that have 

saved the lives of millions of people with CVD.  Cancellation of these drugs in patients 

with severe CC3 under conditions of increased load on the heart caused by infectious 
diseases, from our point of view, can lead to catastrophic consequences. 

 

  



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References  

1. Russian statistical yearbook.  Moscow: Rosstat;  2019 (In Russ.) [Russian 
statistical yearbook.  M: Rosstat;  2019].   

2. Yu C.M.  Cardiovascular complications of severe аcute respiratory syndrome.  

Postgrad Med J. 2006; 82: 140-4.  DOI: 10.1136 / pgmj.2005.037515.   

3. Xiong T.Y., Redwood S., Prendergast B., Chen M. Coronaviruses and 
cardiovascular system: acute and long-term complications.  Eur DOI: 10.1093 / 

eurheartjehaa231.   

4. Libby P., Simon D.L.  Inflammation and thrombosis: the clot thickens.  

Circulation.  2001; 103: 1718-20. Heart J. 2020;  DOI: 10.1161 / 01.cir.103.13.1718.   
5. Fedson D.S., Rordam O.M.  Testing Ebola patients: a "bottom up" approach 

using generic statins and angiotensin receptor blockers.  Int J Infect Dis.  2015: 36: 80-4.   

6. Fedson D.S., Opal S., Rordam O.M.  Hiding in plain sight: an approach to 
treating patients with severe COVID-10 infection.  mBio.  11: e00398-20.  DOI: 

10.1128 / mBio.00398-20.   

7. Sommerstein R., Grani C. Rapid response: re: preventing a covid-19 pandemic: 

ACE inhibitors as a potential risk factor for fatal Covid-19.  VM.  2020; 368: m810.   
8. Diaz J.H.  Hurothesis: angiotensin-converting enzyme inhibitors and 

angiotensin receptor blockers may increase the risk of severe COVID-19.  J Travel Med.  

2020 Mar 18.pi: taaa041.  DOI: 10.1093 / jtm / taaa041.  9. Guan W., Ni Z., Liang W., et 
al.  Clinical characteristics of coronavirus disease in China.  N Engl Med.  2020, 

February 28. DOI: 10.1056 / MEЈMoa2002032.  10. Aronson J.K., Ferner R.E.  

Angiotensin converting enzyme inhibitors and angiotensin receptor blockers in COVID-

19 [cited by April 14, 2020].  Available from: https://www.cebm.net/covid-
19/angiotensin-converting-enzyme-ace-inhibitors-and-angiotensin-receptor-blockers-in-

covid-19 /.  

11. Aronson J.A., Ferner R.E.  Drugs and the renin-angiotensin 2020; 369: 
m1313.  Doi: 10.1136 / bmj.m1313.   

12. Sarzani R. Relationship between COVID-19 and rennin-angiotensin-

aldosterone-system blockers: hasty speculations may be dangerous.  BMJ.  2020; 368: 

m810.   
13. Gurwitz D. Angiotensin receptor blockers as tentative SARS-CoV-2 

therapeutics.  Drug Disc Res.  system in covid-19.  2020. DOI: 10.1002 / ddr.21656.   

14. Kuster G., Pfister O., Burkard T., et al.  SARS- COV2: should inhibitors of the 
renin-angiotensin system be withdrawn in patients with COVID-19?  Eur 20. Нeart 2020 

Mar pi: ehaa235.  DOI: 10.1093 / eurheartj / ehaa235.  15. Vaduganathan M., Vardeny 

O., Michel T., et al.  Renin-Angiotensin-Aldosterone System Inhibitors in Patients with 

Covid-19.  N Engl J Med.  2020 Mar 30. DOI: 10.1056 / NEJMSI2005760. 


