Vol 28, No 2 (2021)
Original Article
Published online: 2020-12-17

open access

Page views 3577
Article views/downloads 2459
Get Citation

Connect on Social Media

Connect on Social Media

Underlying heart diseases and acute COVID-19 outcomes

Iván J. Núñez-Gil1, Antonio Fernández-Ortiz1, Charbel Maroud Eid2, Jia Huang3, Rodolfo Romero4, Victor Manuel Becerra-Muñoz5, Aitor Uribarri6, Gisela Feltes7, Daniela Trabatoni8, Inmaculada Fernandez-Rozas9, Maria C. Viana-Llamas10, Martino Pepe11, Enrico Cerrato12, Maurizio Bertaina13, Thamar Capel Astrua14, Emilio Alfonso15, Alex F. Castro-Mejía16, Sergio Raposeiras-Roubin17, Fabrizio D'Ascenzo18, Carolina Espejo Paeres19, Jaime Signes-Costa20, Alfredo Bardaji21, Cristina Fernandez-Pérez1, Francisco Marin22, Oscar Fabregat-Andres23, Ibrahim Akin24, Vicente Estrada1, Carlos Macaya1
Pubmed: 33346365
Cardiol J 2021;28(2):202-214.

Abstract

Background: The presence of any underlying heart condition could influence outcomes during the coronavirus disease 2019 (COVID-19).


Methods: The registry HOPE-COVID-19 (Health Outcome Predictive Evaluation for COVID-19, NCT04334291) is an international ambispective study, enrolling COVID-19 patients discharged from hospital, dead or alive.

Results: HOPE enrolled 2798 patients from 35 centers in 7 countries. Median age was 67 years (IQR: 53.0–78.0), and most were male (59.5%). A relevant heart disease was present in 682 (24%) cases. These were older, more frequently male, with higher overall burden of cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus, smoking habit, obesity) and other comorbidities such renal failure, lung, cerebrovascular disease and oncologic antecedents (p < 0.01, for all). The heart cohort received more corticoids (28.9% vs. 20.4%, p < 0.001), antibiotics, but less hydroxychloroquine, antivirals or tocilizumab. Considering the epidemiologic profile, a previous heart condition was independently related with shortterm mortality in the Cox multivariate analysis (1.62; 95% CI 1.29–2.03; p < 0.001). Moreover, heart patients needed more respiratory, circulatory support, and presented more in-hospital events, such heart failure, renal failure, respiratory insufficiency, sepsis, systemic infammatory response syndrome and clinically relevant bleedings (all, p < 0.001), and mortality (39.7% vs. 15.5%; p < 0.001).

Conclusions: An underlying heart disease is an adverse prognostic factor for patients suffering COVID-19. Its presence could be related with different clinical drug management and would benefit from maintaining treatment with angiotensin converting enzyme inhibitors or angiotensin receptor blockers during in-hospital stay.

Article available in PDF format

View PDF Download PDF file

References

  1. WHO. WHO statement regarding cluster of pneumonia cases in Wuhan, China. https://www.who.int/china/news/detail/09-01-2020-who-statement-regarding-cluster-of-pneumonia-cases-in-wuhan-china (Accesed 3rd May 2020).
  2. WHO. http://www.euro.who.int/en/health-topics/health-emergencies/coronavirus-covid-19/news/news/2020/3/who-announces-covid-19-outbreak-a-pandemic (Accesed 3rd May 2020).
  3. Dong E, Du H, Gardner L. An interactive web-based dashboard to track COVID-19 in real time. Lancet Infect Dis. 2020; 20(5): 533–534.
  4. Hulot JS. COVID-19 in patients with cardiovascular diseases. Arch Cardiovasc Dis. 2020; 113(4): 225–226.
  5. Shi S, Qin Mu, Shen Bo, et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol. 2020; 5(7): 802–810.
  6. Centers for Disease Control and Prevention. Coronavirus disease 2019 (COVID19). https://www.cdc.gov/coronavirus/2019ncov/needextraprecautions/peopleathigherrisk.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2F2019‐ncov%2Fspecific‐groups% 2Fhigh‐riskcomplications.html (Accessed 22 April 2020).
  7. Madjid M, Solomon S, Vardeny O. Cardiac Implications of Novel Coronavirus (COVID-19). In: Committee ASaQ, editor. ACC Clinical Bulletin. USA: ACC; 2020.
  8. Wang D, Hu Bo, Hu C, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020; 323(11): 1061–1069.
  9. Zheng YY, Ma YT, Zhang JY, et al. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020; 17(5): 259–260.
  10. Bansal M. Cardiovascular disease and COVID-19. Diabetes Metab Syndr. 2020; 14(3): 247–250.
  11. Aghagoli G, Gallo Marin B, Soliman LB, et al. Cardiac involvement in COVID-19 patients: Risk factors, predictors, and complications: A review. J Card Surg. 2020; 35(6): 1302–1305.
  12. Holy EW, Jakob P, Manka R, et al. Impact of a nationwide COVID-19 lockdown on acute coronary syndrome referrals. Cardiol J. 2020; 27(5): 633–635.
  13. Núñez-Gil IJ, Estrada V, Fernández-Pérez C, et al. Health Outcome Predictive Evaluation for COVID 19 international registry (HOPE COVID-19), rationale and design. Contemp Clin Trials Commun. 2020; 20: 100654.
  14. Li Bo, Yang J, Zhao F, et al. Prevalence and impact of cardiovascular metabolic diseases on COVID-19 in China. Clin Res Cardiol. 2020; 109(5): 531–538.
  15. Zhu H, Rhee JW, Cheng P, et al. Correction to: cardiovascular complications in patients with COVID-19: consequences of viral toxicities and host immune response. Curr Cardiol Rep. 2020; 22(5): 36.
  16. Lorente-Ros A, Monteagudo Ruiz JM, Rincón LM, et al. Myocardial injury determination improves risk stratification and predicts mortality in COVID-19 patients. Cardiol J. 2020; 27(5): 489–496.
  17. Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020; 181(2): 271–280.e8.
  18. Chen Li, Hao G. The role of angiotensin-converting enzyme 2 in coronaviruses/influenza viruses and cardiovascular disease. Cardiovasc Res. 2020; 116(12): 1932–1936.
  19. Burrell LM, Risvanis J, Kubota E, et al. Myocardial infarction increases ACE2 expression in rat and humans. Eur Heart J. 2005; 26(4): 369–75; discussion 322.
  20. Soro-Paavonen A, Gordin D, Forsblom C, et al. FinnDiane Study Group. Circulating ACE2 activity is increased in patients with type 1 diabetes and vascular complications. J Hypertens. 2012; 30(2): 375–383.
  21. Oudit GY, Kassiri Z, Jiang C, et al. SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS. Eur J Clin Invest. 2009; 39(7): 618–625.
  22. Lu R, Zhao X, Li J, et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020; 395(10224): 565–574.
  23. Waxman DA, Kanzaria HK, Schriger DL. Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection. N Engl J Med. 2018; 378(26): 2538–2539.
  24. Shi S, Qin Mu, Shen Bo, et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol. 2020; 5(7): 802–810.
  25. Luo W, Hong Y, Gou J, et al. Clinical pathology of critical patient with coronavirus pneumonia (COVID-19). Pre-Prints. 2020: 1–14.
  26. Wu Z, McGoogan JM. Characteristics of and Important Lessons From the Coronavirus Disease 2019 (COVID-19) Outbreak in China: Summary of a Report of 72 314 Cases From the Chinese Center for Disease Control and Prevention. JAMA. 2020; 323(13): 1239–1242.
  27. Shi S, Qin Mu, Shen Bo, et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol. 2020; 5(7): 802–810.
  28. Duffy EY, Cainzos-Achirica M, Michos ED. Primary and secondary prevention of cardiovascular disease in the era of the coronavirus pandemic. Circulation. 2020; 141(24): 1943–1945.
  29. Huang Z, Jiang Y, Chen J, et al. Inhibitors of the renin-angiotensin system: The potential role in the pathogenesis of COVID-19. Cardiol J. 2020; 27(2): 171–174.
  30. Kowalik MM, Trzonkowski P, Łasińska-Kowara M, et al. COVID-19 - Toward a comprehensive understanding of the disease. Cardiol J. 2020; 27(2): 99–114.
  31. Dzieciatkowski T, Szarpak L, Filipiak KJ, et al. COVID-19 challenge for modern medicine. Cardiol J. 2020; 27(2): 175–183.