Published online Jul 25, 2022. doi: 10.5501/wjv.v11.i4.216
Peer-review started: March 7, 2022
First decision: April 8, 2022
Revised: June 15, 2022
Accepted: July 6, 2022
Article in press: July 6, 2022
Published online: July 25, 2022
Processing time: 136 Days and 23 Hours
Coronavirus disease 2019 (COVID-19) is associated with poor cardiovascular outcomes in patients with heart failure (HF) of all categories of ejection fraction (EF), but mainly in patients with HF with reduced EF. Moreover, cardiac transplant patients exhibit worse cardiovascular prognosis, high mortality, and more admissions to the intensive care unit. In general, COVID-19 seems to de-teriorate the clinical status of HF and favors the development of acute respiratory distress syndrome and multiorgan failure, especially in the presence of cardiovascular comorbidities such as diabetes mellitus, kidney dysfunction, and older age. COVID-19 may induce new-onset HF with complex mechanisms that involve myocardial injury. Indeed, myocardial injury comprises a large category of detrimental effects for the myocardium, such as myocardial infarction type 1 or type 2, Takotsubo cardiomyopathy, microvascular dysfunction and myocarditis, which are not easily distinguished by HF. The pathophysiologic mechanisms mainly involve direct myocardial damage by severe acute respiratory syndrome coronavirus 2, cytokine storm, hypercoagulation, inflammation, and endothelial dysfunction. The proper management of patients with COVID-19 involves careful patient evaluation and ongoing monitoring for complications such as HF.
Core Tip: Coronavirus disease 2019 poses a serious threat to patients with pre-existing heart failure (HF) and might induce new-onset HF in hospitalized patients, with complex mechanisms that involve myocardial injury. Cytokine storm, described as excessive inflammation and coagulation, results in microvascular dysfunction, myocardial ischemia and myocarditis, which might not be easily distinguishable from HF. Patients with advanced HF, such as those with reduced ejection fraction, exhibit worse cardiovascular outcomes. Treatment should take into consideration patient-specific characteristics and includes a thorough cardiologic assessment along with obtainment of evidence following published guidelines.
- Citation: Tsigkou V, Siasos G, Oikonomou E, Bletsa E, Vavuranakis M, Tousoulis D. “Heart failure in COVID-19 patients: Critical care experience”: A letter to the editor. World J Virol 2022; 11(4): 216-220
- URL: https://www.wjgnet.com/2220-3249/full/v11/i4/216.htm
- DOI: https://dx.doi.org/10.5501/wjv.v11.i4.216
We read with interest the systematic review of John et al[1], who presented the interaction between coronavirus disease 2019 (COVID-19) and heart failure (HF) from a critical care perspective. After discussing evidence from 26 observational studies, the authors concluded that patients with HF have higher mortality during hospitalization for COVID-19, as well as more complications and admissions to the intensive care unit (ICU)[1]. Furthermore, they found that patients with HF with reduced ejection fraction (HFrEF) exhibited worse outcomes in comparison to patients with HF with mildly reduced ejection fraction (HFmrEF) and with preserved EF (HFpEF)[1].
Patients with HF and COVID-19 develop serious complications, according to the literature; these include severe hypotension, acute respiratory distress syndrome (ARDS), and death[2]. This comes in accordance with the authors’ conclusions that HF is a risk factor for COVID-19 and that patients with HF might require hospitalization or develop more complications post hospitalization in ICU, possibly due to an additional organ injury[1]. Patients with HF often need mechanical ventilation and develop venous thromboembolism, sepsis, acute kidney injury, and stroke[3]. In clinically unstable patients with COVID-19 recommendations suggest the discontinuation of chronic cardioprotective medications, such as angiotensin-converting enzyme (ACE) inhibitors or the angiotensin receptor-neprilysin inhibitor due to hypotension[4]. Among the literature there is uncertainty about the safety of these drugs in patients with HF since severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the ACE2 receptor and administration of these regimens increase the expression of ACE2 in the heart[5,6]. Several clinical trials are under progress, nevertheless, the current recommendation is to continue these drugs in clinically stable patients and in infected patients at risk of complications[6].
Heart transplant patients with comorbidities exhibit poorer cardiovascular outcomes and a need for ICU therapeutic modalities[7]. John et al[1] have also resulted in this conclusion, although the prognosis of critically ill heart transplant patients was, according to them, somewhat similar to the critically ill non-heart transplant patients. As mentioned by the authors, patients with HFrEF and COVID-19 have a poorer overall prognosis[1]. Indeed, COVID-19 is linked to poor prognosis of patients with advanced HFrEF, which is reflected by the need for inotropes and/or an intra-aortic balloon pump, increased incidence of lethal arrhythmias and/or cardiogenic or septic shock, and the need for transplantation[8]. However, evidence from the literature indicates that HFpEF might also be a risk factor for adverse complications, as well as a consequence of COVID-19 due to direct myocardial damage, which hi-ghlights the need for proper follow-up care of the infected patients[9,10].
COVID-19 may worsen myocardial injury in patients with HF due to the release of pro-inflammatory cytokines, the so-called ‘cytokine storm’[11]. On the other hand, COVID-19 might ignite de novo left ventricular dysfunction posthospital admission[2]. Indeed, the risk of de novo HF post hospital admission, according to the authors, is greater, especially for patients who have been admitted to the ICU[1]. The diagnosis of de novo HF is challenging, since patients might suffer from subclinical myocarditis, sepsis-induced cardiomyopathy, Takotsubo cardiomyopathy, or subclinical ischemia[12,13]. According to the authors, in most of the studies cardiac injury was defined as the increase in cardiac troponin I > the 99th percentile upper reference limit or new electrocardiography/echocardiography findings; however, not all the studies reported strict definitions about chronic and de novo HF[1]. Actually, symptoms of COVID-19 might be similar to HF, and pneumonia and pulmonary edema might coexist, thereby complicating the diagnosis of both entities[14]. Interestingly, this comes in accordance with the authors conclusions about the diagnostic difficulties among patients with severe ARDS due to COVID-19 and acute decompensation of HF[1].
COVID-19 induces direct and indirect injury in the myocardium via various mechanisms that involve excessive inflammation, hypercoagulation, endothelial dysfunction, and sympathetic system activation[15]. Myocardial injury in patients with COVID-19 is mediated by ischemic and non-ischemic mechanisms, which lead to different clinical consequences and therapeutic implications[16]. SARS-CoV-2 binds to human cells on the ACE2 receptor, which is overexpressed in patients with cardiovascular diseases and exerts harmful effects through direct inoculation of the myocardium[17]. Moreover, the virus stimulates an immune response, which involves T lymphocytes and cell-mediated cytotoxicity; these mechanisms may be associated with the induction of myocarditis post-infection[18]. Myocarditis might present as acute HF in serious cases and diagnosis must be carried out with considerations of findings from medical history-taking, laboratory examinations, electrocardiograms, echocardiography, and cardiovascular magnetic resonance studies; however, a definite diagnosis also involves endomyocardial biopsy, which is not routinely performed[13].
On the other hand, SARS-CoV-2 has been implicated in cardiac ischemia of several types[19]. The imbalance between oxygen supply and demand is reflected by the increase in cardiac troponins and reflects type 2 myocardial infarction (MI) ischemia, which is a common characteristic of pneumonia due to hypotension and blood hypoxemia, especially in patients with pre-existing coronary heart disease[19]. Also, type 1 MI might be the result of pre-existing coronary plaques that become unstable due to the proinflammatory and procoagulant states of the infection[20]. Additionally, the virus induces microvascular dysfunction in patients through endothelial dysfunction; in fact, proinflammatory biomarkers and the development of microthrombi may induce endothelial dysfunction at the level of microcirculation[21]. Lastly, there is evidence that acute coronary microvascular dysfunction may result in Takotsubo syndrome in patients with COVID-19 and especially among those with pre-existing comorbidities, but the specific mechanisms are under investigation[22].
Great effort is needed in order to improve our understanding of the therapeutic needs of patients with HF and COVID-19[23]. Lockdown policies might have reduced visits to general practitioners and have led to lower rates of diagnosis of heart disease, which could then result in more de novo HF diagnoses[24]. Targeting the cytokine storm with anti-inflammatory medications such as corticosteroids has been linked to decreased morbidity and mortality from virus infection[25]. On-going inflammation is also present in survivors of COVID-19 infection and poses a great risk for the development of HF, indicating the need for novel therapeutic advances[25]. The development of myocardial injury following COVID-19 infection and specifically of de novo HF might result in more hospitalizations and higher mortality; therefore, understanding the pathophysiology of COVID-19 is the cornerstone for therapeutic success[26]. This comes in accordance with the authors conclusions about the need of future studies in order to elucidate the pathophysiology of the complex effects of COVID-19 in the heart[1]. The management of patients with COVID-19 and prior or de novo acute HF should be similar and identify at an early stage possible complications, along with the treatment of oxygenation abnormalities, bleeding events and arrhythmias[27]. A detailed cardiac assessment of the structural and functional characteristics of the infected patients should be performed in order to identify the acute or worsening function of the heart[27]. Moreover, guideline-directed treatment should be continued in patients with HF according to their clinical status, irrespectively of COVID-19[26]. The increase of our knowledge from the on-going studies as well as the course of the pandemic might provide a more robust evidence for the management of the patients[26].
Provenance and peer review: Unsolicited article; Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Cardiac and cardiovascular systems
Country/Territory of origin: Greece
Peer-review report’s scientific quality classification
Grade A (Excellent): 0
Grade B (Very good): B, B
Grade C (Good): C, C
Grade D (Fair): 0
Grade E (Poor): 0
P-Reviewer: Barone M, Italy; Lee S, South Korea; Papadopoulos K, Thailand; Wang MK, China S-Editor: Liu JH L-Editor: A P-Editor: Liu JH
1. | John KJ, Mishra AK, Ramasamy C, George AA, Selvaraj V, Lal A. Heart failure in COVID-19 patients: Critical care experience. World J Virol. 2022;11:1-19. [PubMed] [DOI] [Cited in This Article: ] [Cited by in CrossRef: 8] [Cited by in F6Publishing: 9] [Article Influence: 4.5] [Reference Citation Analysis (0)] |
2. | Arentz M, Yim E, Klaff L, Lokhandwala S, Riedo FX, Chong M, Lee M. Characteristics and Outcomes of 21 Critically Ill Patients With COVID-19 in Washington State. JAMA. 2020;323:1612-1614. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 1511] [Cited by in F6Publishing: 1590] [Article Influence: 397.5] [Reference Citation Analysis (0)] |
3. | Chen T, Wu D, Chen H, Yan W, Yang D, Chen G, Ma K, Xu D, Yu H, Wang H, Wang T, Guo W, Chen J, Ding C, Zhang X, Huang J, Han M, Li S, Luo X, Zhao J, Ning Q. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study. BMJ. 2020;368:m1091. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 2289] [Cited by in F6Publishing: 2447] [Article Influence: 611.8] [Reference Citation Analysis (2)] |
4. | Inciardi RM, Adamo M, Lupi L, Cani DS, Di Pasquale M, Tomasoni D, Italia L, Zaccone G, Tedino C, Fabbricatore D, Curnis A, Faggiano P, Gorga E, Lombardi CM, Milesi G, Vizzardi E, Volpini M, Nodari S, Specchia C, Maroldi R, Bezzi M, Metra M. Characteristics and outcomes of patients hospitalized for COVID-19 and cardiac disease in Northern Italy. Eur Heart J. 2020;41:1821-1829. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 332] [Cited by in F6Publishing: 361] [Article Influence: 90.3] [Reference Citation Analysis (0)] |
5. | Danser AHJ, Epstein M, Batlle D. Renin-Angiotensin System Blockers and the COVID-19 Pandemic: At Present There Is No Evidence to Abandon Renin-Angiotensin System Blockers. Hypertension. 2020;75:1382-1385. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 361] [Cited by in F6Publishing: 356] [Article Influence: 89.0] [Reference Citation Analysis (0)] |
6. | Vaduganathan M, Vardeny O, Michel T, McMurray JJV, Pfeffer MA, Solomon SD. Renin-Angiotensin-Aldosterone System Inhibitors in Patients with Covid-19. N Engl J Med. 2020;382:1653-1659. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 1484] [Cited by in F6Publishing: 1521] [Article Influence: 380.3] [Reference Citation Analysis (0)] |
7. | Bottio T, Bagozzi L, Fiocco A, Nadali M, Caraffa R, Bifulco O, Ponzoni M, Lombardi CM, Metra M, Russo CF, Frigerio M, Masciocco G, Potena L, Loforte A, Pacini D, Faggian G, Onorati F, Sponga S, Livi U, Iacovoni A, Terzi A, Senni M, Rinaldi M, Boffini M, Marro M, Jorgji V, Carrozzini M, Gerosa G. COVID-19 in Heart Transplant Recipients: A Multicenter Analysis of the Northern Italian Outbreak. JACC Heart Fail. 2021;9:52-61. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 57] [Cited by in F6Publishing: 57] [Article Influence: 19.0] [Reference Citation Analysis (0)] |
8. | Bocchi EA, Lima IGCV, Biselli B, Salemi VMC, Ferreira SMA, Chizzola PR, Munhoz RT, Pessoa RS, Cardoso FAM, Bello MVO, Hajjar LA, Gomes BR. Worsening of heart failure by coronavirus disease 2019 is associated with high mortality. ESC Heart Fail. 2021;8:943-952. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 11] [Cited by in F6Publishing: 8] [Article Influence: 2.7] [Reference Citation Analysis (0)] |
9. | Panagides V, Vincent F, Weizman O, Jonveaux M, Trimaille A, Pommier T, Cellier J, Geneste L, Marsou W, Deney A, Attou S, Delmotte T, Fauvel C, Ezzouhairi N, Perin B, Zakine C, Levasseur T, Ma I, Chavignier D, Noirclerc N, Darmon A, Mevelec M, Karsenty C, Duceau B, Sutter W, Mika D, Pezel T, Waldmann V, Ternacle J, Cohen A, Bonnet G; Critical COVID-19 France Investigators. History of heart failure in patients with coronavirus disease 2019: Insights from a French registry. Arch Cardiovasc Dis. 2021;114:415-425. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 5] [Cited by in F6Publishing: 6] [Article Influence: 2.0] [Reference Citation Analysis (0)] |
10. | Hadzibegovic S, Lena A, Churchill TW, Ho JE, Potthoff S, Denecke C, Rösnick L, Heim KM, Kleinschmidt M, Sander LE, Witzenrath M, Suttorp N, Krannich A, Porthun J, Friede T, Butler J, Wilkenshoff U, Pieske B, Landmesser U, Anker SD, Lewis GD, Tschöpe C, Anker MS. Heart failure with preserved ejection fraction according to the HFA-PEFF score in COVID-19 patients: clinical correlates and echocardiographic findings. Eur J Heart Fail. 2021; 23: 1891-1902. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 11] [Cited by in F6Publishing: 13] [Article Influence: 4.3] [Reference Citation Analysis (0)] |
11. | Madjid M, Safavi-Naeini P, Solomon SD, Vardeny O. Potential Effects of Coronaviruses on the Cardiovascular System: A Review. JAMA Cardiol. 2020;5:831-840. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 1095] [Cited by in F6Publishing: 1190] [Article Influence: 297.5] [Reference Citation Analysis (2)] |
12. | Mishra AK, Lal A, Sahu KK, Sargent J. Cardiovascular factors predicting poor outcome in COVID-19 patients. Cardiovasc Pathol. 2020;49:107246. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 13] [Cited by in F6Publishing: 16] [Article Influence: 4.0] [Reference Citation Analysis (0)] |
13. | Siripanthong B, Nazarian S, Muser D, Deo R, Santangeli P, Khanji MY, Cooper LT Jr, Chahal CAA. Recognizing COVID-19-related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management. Heart Rhythm. 2020;17:1463-1471. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 527] [Cited by in F6Publishing: 474] [Article Influence: 118.5] [Reference Citation Analysis (0)] |
14. | Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, Liu S, Zhao P, Liu H, Zhu L, Tai Y, Bai C, Gao T, Song J, Xia P, Dong J, Zhao J, Wang FS. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020;8:420-422. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 5228] [Cited by in F6Publishing: 5609] [Article Influence: 1402.3] [Reference Citation Analysis (2)] |
15. | Tomasoni D, Italia L, Adamo M, Inciardi RM, Lombardi CM, Solomon SD, Metra M. COVID-19 and heart failure: from infection to inflammation and angiotensin II stimulation. Searching for evidence from a new disease. Eur J Heart Fail. 2020;22:957-966. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 140] [Cited by in F6Publishing: 186] [Article Influence: 46.5] [Reference Citation Analysis (0)] |
16. | Shi S, Qin M, Shen B, Cai Y, Liu T, Yang F, Gong W, Liu X, Liang J, Zhao Q, Huang H, Yang B, Huang C. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol. 2020;5:802-810. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 2428] [Cited by in F6Publishing: 2918] [Article Influence: 729.5] [Reference Citation Analysis (1)] |
17. | Lindner D, Fitzek A, Bräuninger H, Aleshcheva G, Edler C, Meissner K, Scherschel K, Kirchhof P, Escher F, Schultheiss HP, Blankenberg S, Püschel K, Westermann D. Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases. JAMA Cardiol. 2020;5:1281-1285. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 428] [Cited by in F6Publishing: 556] [Article Influence: 139.0] [Reference Citation Analysis (0)] |
18. | Abdelnabi M, Eshak N, Saleh Y, Almaghraby A. Coronavirus Disease 2019 Myocarditis: Insights into Pathophysiology and Management. Eur Cardiol. 2020;15:e51. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 11] [Cited by in F6Publishing: 11] [Article Influence: 2.8] [Reference Citation Analysis (0)] |
19. | Wu C, Chen X, Cai Y, Xia J, Zhou X, Xu S, Huang H, Zhang L, Du C, Zhang Y, Song J, Wang S, Chao Y, Yang Z, Xu J, Chen D, Xiong W, Xu L, Zhou F, Jiang J, Bai C, Zheng J, Song Y. Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China. JAMA Intern Med. 2020;180:934-943. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 4960] [Cited by in F6Publishing: 5316] [Article Influence: 1329.0] [Reference Citation Analysis (1)] |
20. | Bikdeli B, Madhavan MV, Jimenez D, Chuich T, Dreyfus I, Driggin E, Nigoghossian C, Ageno W, Madjid M, Guo Y, Tang LV, Hu Y, Giri J, Cushman M, Quéré I, Dimakakos EP, Gibson CM, Lippi G, Favaloro EJ, Fareed J, Caprini JA, Tafur AJ, Burton JR, Francese DP, Wang EY, Falanga A, McLintock C, Hunt BJ, Spyropoulos AC, Barnes GD, Eikelboom JW, Weinberg I, Schulman S, Carrier M, Piazza G, Beckman JA, Steg PG, Stone GW, Rosenkranz S, Goldhaber SZ, Parikh SA, Monreal M, Krumholz HM, Konstantinides SV, Weitz JI, Lip GYH; Global COVID-19 Thrombosis Collaborative Group, Endorsed by the ISTH, NATF, ESVM, and the IUA, Supported by the ESC Working Group on Pulmonary Circulation and Right Ventricular Function. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75:2950-2973. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 2080] [Cited by in F6Publishing: 2114] [Article Influence: 528.5] [Reference Citation Analysis (0)] |
21. | Chen L, Li X, Chen M, Feng Y, Xiong C. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res. 2020;116:1097-1100. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 674] [Cited by in F6Publishing: 768] [Article Influence: 192.0] [Reference Citation Analysis (0)] |
22. | Minhas AS, Scheel P, Garibaldi B, Liu G, Horton M, Jennings M, Jones SR, Michos ED, Hays AG. Takotsubo Syndrome in the Setting of COVID-19. JACC Case Rep. 2020;2:1321-1325. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 90] [Cited by in F6Publishing: 102] [Article Influence: 25.5] [Reference Citation Analysis (0)] |
23. | Chieffo A, Stefanini GG, Price S, Barbato E, Tarantini G, Karam N, Moreno R, Buchanan GL, Gilard M, Halvorsen S, Huber K, James S, Neumann FJ, Möllmann H, Roffi M, Tavazzi G, Ferré JM, Windecker S, Dudek D, Baumbach A. EAPCI Position Statement on Invasive Management of Acute Coronary Syndromes during the COVID-19 pandemic. EuroIntervention. 2020;16:233-246. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 14] [Cited by in F6Publishing: 15] [Article Influence: 3.8] [Reference Citation Analysis (0)] |
24. | Andersson C, Gerds T, Fosbøl E, Phelps M, Andersen J, Lamberts M, Holt A, Butt JH, Madelaire C, Gislason G, Torp-Pedersen C, Køber L, Schou M. Incidence of New-Onset and Worsening Heart Failure Before and After the COVID-19 Epidemic Lockdown in Denmark: A Nationwide Cohort Study. Circ Heart Fail. 2020;13:e007274. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 63] [Cited by in F6Publishing: 70] [Article Influence: 17.5] [Reference Citation Analysis (0)] |
25. | Freaney PM, Shah SJ, Khan SS. COVID-19 and Heart Failure With Preserved Ejection Fraction. JAMA. 2020;324:1499-1500. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 62] [Cited by in F6Publishing: 55] [Article Influence: 13.8] [Reference Citation Analysis (0)] |
26. | Task Force for the management of COVID-19 of the European Society of Cardiology. Corrigendum to: European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis; and ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 2-care pathways, treatment, and follow-up. Eur Heart J. 2022;43:1776. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 5] [Cited by in F6Publishing: 20] [Article Influence: 6.7] [Reference Citation Analysis (0)] |
27. | Zhang Y, Coats AJS, Zheng Z, Adamo M, Ambrosio G, Anker SD, Butler J, Xu D, Mao J, Khan MS, Bai L, Mebazaa A, Ponikowski P, Tang Q, Ruschitzka F, Seferovic P, Tschöpe C, Zhang S, Gao C, Zhou S, Senni M, Zhang J, Metra M. Management of heart failure patients with COVID-19: a joint position paper of the Chinese Heart Failure Association & National Heart Failure Committee and the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2020;22:941-956. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 70] [Cited by in F6Publishing: 75] [Article Influence: 18.8] [Reference Citation Analysis (0)] |