COVID-19-associated heart failure: Difference between revisions

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==Overview==
==Overview==
[[Corona virus disease 2019]] [[COVID-19]] caused by a novel enveloped, [[positively stranded RNA]] leading to not only [[respiratory]] [[disease]], but also [[multiorgan envolvement]]. [[Cardiac]] complication is one of the manifestation of [[COVID-19]] [[infection]] and [[patients]] may present with [[heart failure]] [[disease]] as a consequence of [[COVID-19]] or exacerbation of underlying [[heart failure ]] disease. History of [[heart failure]] [[disease]], regardless of [[left ventricular ejection fraction]], may be a risk factor of severity of [[COVID-19]] [[course]]. During the pandemic, [[heart failure hospitalization]] reduced about 45% leading to increased [[in-hospital]] [[mortality]] [[rates]]. In addition, evidence of [[myocardial injury]] ranging 10-40%  in critically ill [[COVID-19]] [[patients]] and [[cardiovascular complication]]s led to increased [[incidence]] of acute or chronic [[heart failure]] [[disease]]. Few cases of [[myocarditis]] and severe [[left ventricular systolic dysfunction]] associated [[COVID-19]] have been reported. However, studies addressed  both [[systolic]] and [[diastolic]] [[left ventricular]] dysfunction, [[left ventricular]] [[diastolic]] impairnment, [[pulmonary hypertension]], [[right ventricular]] [[dysfunction]] as the consequence of [[cardiac ]] involvement in [[COVID-19]] [[patients]].
Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in [[patients]] with [[COVID-19]]. [[Patients]] with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to advanced age and the presence of multiple [[Comorbidity|comorbidities]].


==Historical perspective==
==Historical perspective==
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==Pathophysiology==
==Pathophysiology==
* The [[pathogenesis]] of [[heart failure]] in [[COVID-19]] has been proposed by two mechanisms of the direct and indirect effect of [[COVID-19]].
*  Factors related to indirect mechanisms are:
* [[Fever]], [[sympathetic activity]] induced [[tachycardia]] and increased [[myocardial oxygen consumption]]
* [[Hypoxia]] induced [[oxidative stress]] and [[intracellular acidosis]] and [[mitocondrial damage]] and [[cell death]]<ref name="pmid30338885">{{cite journal |vauthors=van der Pol A, van Gilst WH, Voors AA, van der Meer P |title=Treating oxidative stress in heart failure: past, present and future |journal=Eur J Heart Fail |volume=21 |issue=4 |pages=425–435 |date=April 2019 |pmid=30338885 |pmc=6607515 |doi=10.1002/ejhf.1320 |url=}}</ref>
* Abnormal inflammatory response was ascribed about one week after [[viral disease]] and imbalance between T helper type 1 and 2 induced [[hyperinflammatory response]] and [[acute lung injury]] and [[ARDS]].<ref name="pmid32971105">{{cite journal |vauthors=Unudurthi SD, Luthra P, Bose RJC, McCarthy JR, Kontaridis MI |title=Cardiac inflammation in COVID-19: Lessons from heart failure |journal=Life Sci |volume=260 |issue= |pages=118482 |date=November 2020 |pmid=32971105 |pmc=7505073 |doi=10.1016/j.lfs.2020.118482 |url=}}</ref>
* It is thought that release of [[TNF]] and IL1B is associated with [[cardiac injury]] and [[myocardial cell depression]].<ref name="pmid8642298">{{cite journal |vauthors=Kumar A, Thota V, Dee L, Olson J, Uretz E, Parrillo JE |title=Tumor necrosis factor alpha and interleukin 1beta are responsible for in vitro myocardial cell depression induced by human septic shock serum |journal=J Exp Med |volume=183 |issue=3 |pages=949–58 |date=March 1996 |pmid=8642298 |pmc=2192364 |doi=10.1084/jem.183.3.949 |url=}}</ref>
* [[Cytokin storm]]  was associated with [[acute heart failure]] and [[oxidative stress]] and [[inflammation]].
* [[DIC]] and small vessel [[thrombosis]] as a consequence of [[pulmonary]] vascular [[endothelitis]] and [[cytokine storm]] has been seen in the course of [[COVID-19]] [[infection]].<ref name="pmid32437596">{{cite journal |vauthors=Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, Vanstapel A, Werlein C, Stark H, Tzankov A, Li WW, Li VW, Mentzer SJ, Jonigk D |title=Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19 |journal=N Engl J Med |volume=383 |issue=2 |pages=120–128 |date=July 2020 |pmid=32437596 |pmc=7412750 |doi=10.1056/NEJMoa2015432 |url=}}</ref>
* Use of some [[medication]]  for [[COVID-19]] caused  [[myocardial injury]] including some [[antiviral]] drugs, [[hydroxychloroquine]] and [[azithromycin]] with [[QT prolongation]] effect and increased risk of [[VT]], [[Torsades de pointes]] and [[death]].<ref name="pmid33031652">{{cite journal |vauthors=Horby P, Mafham M, Linsell L, Bell JL, Staplin N, Emberson JR, Wiselka M, Ustianowski A, Elmahi E, Prudon B, Whitehouse T, Felton T, Williams J, Faccenda J, Underwood J, Baillie JK, Chappell LC, Faust SN, Jaki T, Jeffery K, Lim WS, Montgomery A, Rowan K, Tarning J, Watson JA, White NJ, Juszczak E, Haynes R, Landray MJ |title=Effect of Hydroxychloroquine in Hospitalized Patients with Covid-19 |journal=N Engl J Med |volume=383 |issue=21 |pages=2030–2040 |date=November 2020 |pmid=33031652 |pmc=7556338 |doi=10.1056/NEJMoa2022926 |url=}}</ref><ref name="pmid32442023">{{cite journal |vauthors=Nguyen LS, Dolladille C, Drici MD, Fenioux C, Alexandre J, Mira JP, Moslehi JJ, Roden DM, Funck-Brentano C, Salem JE |title=Cardiovascular Toxicities Associated With Hydroxychloroquine and Azithromycin: An Analysis of the World Health Organization Pharmacovigilance Database |journal=Circulation |volume=142 |issue=3 |pages=303–305 |date=July 2020 |pmid=32442023 |pmc=7365677 |doi=10.1161/CIRCULATIONAHA.120.048238 |url=}}</ref>
* Direct mechanism of [[COVID-19]] on [[myocardium ]] is mediated by attachment of viral spike protients to [[ACE2]] receptor on the [[myocardium]] and increased risk of [[cytokine]] production, [[contractil deficit]], sarcomer disarray,  and [[cell death]].
* Attachment of [[COVID-19]] to [[ACE2]] receptors downregulate [[ACE2]] activity , increased production of [[angiotensin2]] , increased proinflammatory effect, [[increased]] [[proliferation]] and [[vasoconstriction]] and [[fibrosis]].<ref name="pmid33681537">{{cite journal |vauthors=Bailey AL, Dmytrenko O, Greenberg L, Bredemeyer AL, Ma P, Liu J, Penna V, Winkler ES, Sviben S, Brooks E, Nair AP, Heck KA, Rali AS, Simpson L, Saririan M, Hobohm D, Stump WT, Fitzpatrick JA, Xie X, Zhang X, Shi PY, Hinson JT, Gi WT, Schmidt C, Leuschner F, Lin CY, Diamond MS, Greenberg MJ, Lavine KJ |title=SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis |journal=JACC Basic Transl Sci |volume=6 |issue=4 |pages=331–345 |date=April 2021 |pmid=33681537 |pmc=7909907 |doi=10.1016/j.jacbts.2021.01.002 |url=}}</ref>


*Presumed pathophysiologic mechanisms for the development of new or [[Congestive heart failure|decompensated heart failure]] in [[patients]] with [[COVID-19]] include:<ref name="pmid322193572">{{cite journal| author=Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D | display-authors=etal| title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume=  | issue=  | pages=  | pmid=32219357 | doi=10.1001/jamacardio.2020.1096 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219357  }}</ref> <ref name="pmid323602422">{{cite journal| author=Mehra MR, Ruschitzka F| title=COVID-19 Illness and Heart Failure: A Missing Link? | journal=JACC Heart Fail | year= 2020 | volume= 8 | issue= 6 | pages= 512-514 | pmid=32360242 | doi=10.1016/j.jchf.2020.03.004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32360242  }}</ref> <ref name="pmid321863312">{{cite journal| author=Xiong TY, Redwood S, Prendergast B, Chen M| title=Coronaviruses and the cardiovascular system: acute and long-term implications. | journal=Eur Heart J | year= 2020 | volume= 41 | issue= 19 | pages= 1798-1800 | pmid=32186331 | doi=10.1093/eurheartj/ehaa231 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32186331  }}</ref> <ref name="pmid306250662">{{cite journal| author=Musher DM, Abers MS, Corrales-Medina VF| title=Acute Infection and Myocardial Infarction. | journal=N Engl J Med | year= 2019 | volume= 380 | issue= 2 | pages= 171-176 | pmid=30625066 | doi=10.1056/NEJMra1808137 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30625066  }}</ref> <ref name="pmid321407322">{{cite journal| author=Chen C, Zhou Y, Wang DW| title=SARS-CoV-2: a potential novel etiology of fulminant myocarditis. | journal=Herz | year= 2020 | volume= 45 | issue= 3 | pages= 230-232 | pmid=32140732 | doi=10.1007/s00059-020-04909-z | pmc=7080076 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32140732  }}</ref>
   
**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]]) <ref name="pmid32644140">{{cite journal |vauthors=Jabri A, Kalra A, Kumar A, Alameh A, Adroja S, Bashir H, Nowacki AS, Shah R, Khubber S, Kanaa'N A, Hedrick DP, Sleik KM, Mehta N, Chung MK, Khot UN, Kapadia SR, Puri R, Reed GW |title=Incidence of Stress Cardiomyopathy During the Coronavirus Disease 2019 Pandemic |journal=JAMA Netw Open |volume=3 |issue=7 |pages=e2014780 |date=July 2020 |pmid=32644140 |pmc=7348683 |doi=10.1001/jamanetworkopen.2020.14780 |url=}}</ref> <ref name="pmid32363351">{{cite journal |vauthors=Minhas AS, Scheel P, Garibaldi B, Liu G, Horton M, Jennings M, Jones SR, Michos ED, Hays AG |title=Takotsubo Syndrome in the Setting of COVID-19 Infection |journal=JACC Case Rep |volume= |issue= |pages= |date=May 2020 |pmid=32363351 |pmc=7194596 |doi=10.1016/j.jaccas.2020.04.023 |url=}}</ref>
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)




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==Epidemiology and Demographics==
==Epidemiology and Demographics==
* The [[prevalence]] of [[heart failure]] was approximately 10,000 per 100,000 [[SARS-COV-2]] [[infected]] [[patients]]. <ref name="pmid32517963">{{cite journal |vauthors=Lala A, Johnson KW, Januzzi JL, Russak AJ, Paranjpe I, Richter F, Zhao S, Somani S, Van Vleck T, Vaid A, Chaudhry F, De Freitas JK, Fayad ZA, Pinney SP, Levin M, Charney A, Bagiella E, Narula J, Glicksberg BS, Nadkarni G, Mancini DM, Fuster V |title=Prevalence and Impact of Myocardial Injury in Patients Hospitalized With COVID-19 Infection |journal=J Am Coll Cardiol |volume=76 |issue=5 |pages=533–546 |date=August 2020 |pmid=32517963 |pmc=7279721 |doi=10.1016/j.jacc.2020.06.007 |url=}}</ref>
*Data on [[incidence]] on acute [[heart failure]] in [[COVID-19]] patients is limited.
*In one study, [[acute heart failure]] was seen in 4.1% of patients with [[acute cardiac injury]]. <ref name="urlAssociation of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China | Global Health | JAMA Cardiology | JAMA Network">{{cite web |url=+https://doi.org/10.1001/jamacardio.2020.0950 |title=Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China &#124; Global Health &#124; JAMA Cardiology &#124; JAMA Network |format= |work= |accessdate=}}</ref>
*In a retrospective study on 191 [[COVID-19]] patients in Wuhan, China, the incidence of [[heart failure]] was 23% (52% in non-survivors vs 12% in survivors). <ref name="pmid32171076">{{cite journal |vauthors=Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, Xiang J, Wang Y, Song B, Gu X, Guan L, Wei Y, Li H, Wu X, Xu J, Tu S, Zhang Y, Chen H, Cao B |title=Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study |journal=Lancet |volume=395 |issue=10229 |pages=1054–1062 |date=March 2020 |pmid=32171076 |pmc=7270627 |doi=10.1016/S0140-6736(20)30566-3 |url=}}</ref>


=== Age ===
=== Age ===
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==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
* [[Disease]] may be ranged from [[asymptomatic]] , mild symptoms ([[fever]], [[dry cough]], [[fatigue]]), or severe [[disease]] (severe [[pneumonia]], [[ARDS]], fatal [[outcome]]).<ref name="pmid32502551">{{cite journal |vauthors=Li J, Gong X, Wang Z, Chen R, Li T, Zeng D, Li M |title=Clinical features of familial clustering in patients infected with 2019 novel coronavirus in Wuhan, China |journal=Virus Res |volume=286 |issue= |pages=198043 |date=September 2020 |pmid=32502551 |pmc=7265838 |doi=10.1016/j.virusres.2020.198043 |url=}}</ref>
*[[COVID-19]] patients with [[chronic heart failure]] are more likely to develop severe forms of the disease.
* In the presence of [[heart failure]] in [[COVID-19]] [[disease]], the course of the disease was much more severe and the risk of [[hospitalization]] was high.<ref name="pmid32444366">{{cite journal |vauthors=Petrilli CM, Jones SA, Yang J, Rajagopalan H, O'Donnell L, Chernyak Y, Tobin KA, Cerfolio RJ, Francois F, Horwitz LI |title=Factors associated with hospital admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study |journal=BMJ |volume=369 |issue= |pages=m1966 |date=May 2020 |pmid=32444366 |pmc=7243801 |doi=10.1136/bmj.m1966 |url=}}</ref>
*[[COVID-19]] patients who develop [[acute heart failure]] (either de novo acute heart failure or acute decompensated heart failure) generally have worse outcomes.
* The [[incidence]] of [[acute heart failure]] increased among [[COVID-19]] [[patients]] and was associated with high [[mortality rates]].<ref name="pmid33135851">{{cite journal |vauthors=König S, Hohenstein S, Meier-Hellmann A, Kuhlen R, Hindricks G, Bollmann A |title=In-hospital care in acute heart failure during the COVID-19 pandemic: insights from the German-wide Helios hospital network |journal=Eur J Heart Fail |volume=22 |issue=12 |pages=2190–2201 |date=December 2020 |pmid=33135851 |doi=10.1002/ejhf.2044 |url=}}</ref>
*[[Acute heart failure]] in [[COVID-19]] may progress to [[cardiogenic shock]].  
* [[Patients]] with [[chronic heart failure]] may progress to develop acute decompensated [[heart failure]] in the setting of [[COVID-19]].
 
* Discontinuation of [[guideline-directed medical  therapy]] was associated with higher [[mortality]] rate in such [[patients]]. <ref name="pmid32833283">{{cite journal |vauthors=Rey JR, Caro-Codón J, Rosillo SO, Iniesta ÁM, Castrejón-Castrejón S, Marco-Clement I, Martín-Polo L, Merino-Argos C, Rodríguez-Sotelo L, García-Veas JM, Martínez-Marín LA, Martínez-Cossiani M, Buño A, Gonzalez-Valle L, Herrero A, López-Sendón JL, Merino JL |title=Heart failure in COVID-19 patients: prevalence, incidence and prognostic implications |journal=Eur J Heart Fail |volume=22 |issue=12 |pages=2205–2215 |date=December 2020 |pmid=32833283 |pmc=7461427 |doi=10.1002/ejhf.1990 |url=}}</ref>
 
* [[Myocardial injury]] and high [[troponin]] level may be seen in [[heart failure]] associated [[COVID-19]].
* During the [[pandemic]] period, [[heart failure]] [[hospitalization ]] reduced ranging from 30% to 66% compared with parallel time due to fear of contracting the [[virus]] in hospital.<ref name="pmid32519793">{{cite journal |vauthors=Shah N, Ahmed I, Nazir T |title=Heart failure-related hospitalisation and management during the COVID-19 pandemic: a reflection. Letter regarding the article 'The impact of COVID-19 on heart failure hospitalization and management: report from a Heart Failure Unit in London during the peak of the pandemic' |journal=Eur J Heart Fail |volume=23 |issue=2 |pages=343–344 |date=February 2021 |pmid=32519793 |pmc=7300617 |doi=10.1002/ejhf.1931 |url=}}</ref>
* [[Patients]] with [[heart failure]] admitted in the hospital were sicker, presented with higher rates of [[NYHA]] 2-3 [[symptoms]], and severe [[peripheral edema]] which are the markers of [[in-hospital]] [[ mortality]].<ref name="pmid32519793">{{cite journal |vauthors=Shah N, Ahmed I, Nazir T |title=Heart failure-related hospitalisation and management during the COVID-19 pandemic: a reflection. Letter regarding the article 'The impact of COVID-19 on heart failure hospitalization and management: report from a Heart Failure Unit in London during the peak of the pandemic' |journal=Eur J Heart Fail |volume=23 |issue=2 |pages=343–344 |date=February 2021 |pmid=32519793 |pmc=7300617 |doi=10.1002/ejhf.1931 |url=}}</ref>
* Presence of [[comorbidities]]  including [[cardiovascular disease]], [[diabetes]], [[chronic respiratory disease]], [[hypertension]] were associated with fatal [[outcome]] in [[covid-19]] [[patients]]. <ref name="pmid32809274">{{cite journal |vauthors=Cannatà A, Bromage DI, Rind IA, Gregorio C, Bannister C, Albarjas M, Piper S, Shah AM, McDonagh TA |title=Temporal trends in decompensated heart failure and outcomes during COVID-19: a multisite report from heart failure referral centres in London |journal=Eur J Heart Fail |volume=22 |issue=12 |pages=2219–2224 |date=December 2020 |pmid=32809274 |pmc=7461082 |doi=10.1002/ejhf.1986 |url=}}</ref>
* Among [[hospitalized]] [[COVID-19]] [[patients]], presence of [[heart failure]] was correlated with higher risk of [[mechanical ventilation]] and [[mortality]], regardless of [[left ventricular ejection fraction]].<ref name="pmid33129663">{{cite journal |vauthors=Alvarez-Garcia J, Lee S, Gupta A, Cagliostro M, Joshi AA, Rivas-Lasarte M, Contreras J, Mitter SS, LaRocca G, Tlachi P, Brunjes D, Glicksberg BS, Levin MA, Nadkarni G, Fayad Z, Fuster V, Mancini D, Lala A |title=Prognostic Impact of Prior Heart Failure in Patients Hospitalized With COVID-19 |journal=J Am Coll Cardiol |volume=76 |issue=20 |pages=2334–2348 |date=November 2020 |pmid=33129663 |pmc=7598769 |doi=10.1016/j.jacc.2020.09.549 |url=}}</ref>
* Common complication of preexisting [[heart failure]] after diagnosis of  [[COVID-19]] are:<ref name="pmid33179839">{{cite journal |vauthors=Tomasoni D, Inciardi RM, Lombardi CM, Tedino C, Agostoni P, Ameri P, Barbieri L, Bellasi A, Camporotondo R, Canale C, Carubelli V, Carugo S, Catagnano F, Dalla Vecchia LA, Danzi GB, Di Pasquale M, Gaudenzi M, Giovinazzo S, Gnecchi M, Iorio A, La Rovere MT, Leonardi S, Maccagni G, Mapelli M, Margonato D, Merlo M, Monzo L, Mortara A, Nuzzi V, Piepoli M, Porto I, Pozzi A, Sarullo F, Sinagra G, Volterrani M, Zaccone G, Guazzi M, Senni M, Metra M |title=Impact of heart failure on the clinical course and outcomes of patients hospitalized for COVID-19. Results of the Cardio-COVID-Italy multicentre study |journal=Eur J Heart Fail |volume=22 |issue=12 |pages=2238–2247 |date=December 2020 |pmid=33179839 |doi=10.1002/ejhf.2052 |url=}}</ref>
*: [[Acute heart failure]]  
*: Acute [[renal failure]]
*: [[Multiorgan failure]]
* In [[COVID-19]] [[patients]] presence of underlying [[cardiovascular disease]] was associated with poor outcome, and [[case fatality rate]] of [[COVID-19]]  with [[cardiovascular comorbidities]] was 10.5%.<ref name="pmid33334865">{{cite journal |vauthors=Bae S, Kim SR, Kim MN, Shim WJ, Park SM |title=Impact of cardiovascular disease and risk factors on fatal outcomes in patients with COVID-19 according to age: a systematic review and meta-analysis |journal=Heart |volume=107 |issue=5 |pages=373–380 |date=March 2021 |pmid=33334865 |pmc=7747496 |doi=10.1136/heartjnl-2020-317901 |url=}}</ref>
 
==Diagnosis==
==Diagnosis==


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**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.
**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.  
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.  
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.


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===Echocardiography or Ultrasound===
===Echocardiography or Ultrasound===


* [[ Echocardiography]] is not recommended routinely in [[COVID-19]] [[ patients]]. However, [[Echocardiography]] may be useful in selected [[COVID-19]] [[patients]] (about 16% ) who have high level of [[D-dimer]] and [[troponin]] level for measurement of [[plmonary arterial pressure]], [[cardiac thrombus]],[[right ventricular function]].<ref name="pmid32963823">{{cite journal |vauthors=Benyounes N, Van Der Vynckt C, Tibi S, Iglesias A, Salomon L, Gout O, Tibi T |title=Echocardiography in Confirmed and Highly Suspected Symptomatic COVID-19 Patients and Its Impact on Treatment Change |journal=Cardiol Res Pract |volume=2020 |issue= |pages=4348598 |date=2020 |pmid=32963823 |pmc=7495215 |doi=10.1155/2020/4348598 |url=}}</ref>
*A complete standard [[transthoracicechocardiography]] [[(TTE)]] has not been recommended in [[COVID-19]] patients considering the limited [[personal protective equipment (PPE)]] and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{cite journal |vauthors=Cosyns B, Lochy S, Luchian ML, Gimelli A, Pontone G, Allard SD, de Mey J, Rosseel P, Dweck M, Petersen SE, Edvardsen T |title=The role of cardiovascular imaging for myocardial injury in hospitalized COVID-19 patients |journal=Eur Heart J Cardiovasc Imaging |volume=21 |issue=7 |pages=709–714 |date=July 2020 |pmid=32391912 |doi=10.1093/ehjci/jeaa136 |url=}}</ref>
* Among [[COVID-19]] [[patients]] with underlying [[cardiovascular disease]], [[left ventricular function]] commonly was normal. However, presence of [[right ventricular dilation]] and [[dysfunction]] were associated with poor outcome in such situation.<ref name="pmid33796573">{{cite journal |vauthors=Li Y, Fang L, Zhu S, Xie Y, Wang B, He L, Zhang D, Zhang Y, Yuan H, Wu C, Li H, Sun W, Zhang Y, Li M, Cui L, Cai Y, Wang J, Yang Y, Lv Q, Zhang L, Johri AM, Xie M |title=Echocardiographic Characteristics and Outcome in Patients With COVID-19 Infection and Underlying Cardiovascular Disease |journal=Front Cardiovasc Med |volume=8 |issue= |pages=642973 |date=2021 |pmid=33796573 |pmc=8008078 |doi=10.3389/fcvm.2021.642973 |url=}}</ref>
*To deal with limited resources (both [[personal protective equipment]] and personnel) and reducing the exposure time of personnel, a focused [[TTE]] to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] [[(POCUS)]]
**[[Focused cardiac ultrasound study]] [[(FoCUS)]]  
**[[Critical care echocardiography]]  
 
*Cardiac ultrasound can help in assessing the following parameters:
**[[Left ventricular systolic function]] [[(left ventricular ejection fraction, LVEF)]] to distinguish [[systolic dysfunction]] with a [[reduced ejection fraction]] (LVEF<40%) from [[diastolic dysfunction]] with a preserved ejection fraction (LVEF>40%)
**Left ventricular [[diastolic function]]
**Left ventricular structural abnormalities, including [[left ventricular size]] and [[left ventricular wall thickness]]
**[[Left atrial size]]
**[[Right ventricular]] size and function
**Detection and quantification of [[valvular abnormalities]]
**Measurement of [[systolic pulmonary artery pressure]]
**Detection and quantification of [[pericardial effusion]]
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].


===CT scan===
===CT scan===

Latest revision as of 17:25, 23 March 2022

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Main article: COVID-19

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]Mandana Chitsazan, M.D. [3]

Synonyms and keywords: Novel coronavirus, COVID-19, Wuhan coronavirus, coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, 2019-nCoV, 2019 novel coronavirus, heart failure, acute heart failure, de Novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with a preserved ejection fraction

Overview

Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19. Patients with chronic heart failure may be at higher risk of developing severe COVID-19 infection due to advanced age and the presence of multiple comorbidities.

Historical perspective

  • In late December 2019, the novel coronavirus, SARS-CoV-2, originated in Wuhan, China. [1]
  • The World Health Organization(WHO) declared the outbreak a Public Health Emergency of International Concern On January 30, 2020, [2] and a pandemic on March 12, 2020. [3]
  • On March 27, 2020, Inciardi et al. reported the first case of acute myopericarditis complicated by heart failure in an otherwise healthy 53-year-old woman one week after the onset of symptoms of COVID-19. [4]

Classification

  • Acute heart failure has two forms:
    • Newly-arisen (“de novo”) acute heart failure
    • Acutely decompensated chronic heart failure (ADCHF)

Pathophysiology



Common Precipitating factors in COVID-19 patients
Cardiac
Pressure overload
Volume overload
  • Renal dysfunction
Pulmonary
Increased systemic metabolic demand
Iatrogenic
  • Cardiovascular toxicity of medications
  • Aggressive fluid resuscitation
Others
  • Anemia

Causes

Acute heart failure in COVID-19 patients may be caused by: [10] [11]

Differentiating COVID-19 associated heart failure from other Diseases

  • For further information about the differential diagnosis, click here.

Epidemiology and Demographics

Age

Gender

Race

Risk Factors

To read more on the risk factors of congestive heart failure, click here.

Screening

  • There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
  • Routine measurement of natriuretic peptides and/or cardiac troponins has not been recommended in the absence of a high index of suspicion for heart failure on the clinical grounds.

Natural History, Complications, and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography or Ultrasound

CT scan

CMR

Other Imaging Findings

  • To view other imaging findings on COVID-19, click here.

Other Diagnostic Studies

  • To view other diagnostic studies for COVID-19, click here.

Treatment

Medical Therapy

Interventional therapy

Surgery

Primary Prevention

Secondary Prevention

References

  1. ↑ "WHO | Pneumonia of unknown cause – China".
  2. ↑ "Statement on the second meeting of the International Health Regulations (2005) Emergency Committee regarding the outbreak of novel coronavirus (2019-nCoV)".
  3. ↑ "WHO Director-General's opening remarks at the media briefing on COVID-19 - 11 March 2020".
  4. ↑ Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D, Cani DS, Cerini M, Farina D, Gavazzi E, Maroldi R, Adamo M, Ammirati E, Sinagra G, Lombardi CM, Metra M (March 2020). "Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiol. doi:10.1001/jamacardio.2020.1096. PMID 32219357 Check |pmid= value (help).
  5. ↑ Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D; et al. (2020). "Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiol. doi:10.1001/jamacardio.2020.1096. PMID 32219357 Check |pmid= value (help).
  6. ↑ Mehra MR, Ruschitzka F (2020). "COVID-19 Illness and Heart Failure: A Missing Link?". JACC Heart Fail. 8 (6): 512–514. doi:10.1016/j.jchf.2020.03.004. PMID 32360242 Check |pmid= value (help).
  7. ↑ Xiong TY, Redwood S, Prendergast B, Chen M (2020). "Coronaviruses and the cardiovascular system: acute and long-term implications". Eur Heart J. 41 (19): 1798–1800. doi:10.1093/eurheartj/ehaa231. PMID 32186331 Check |pmid= value (help).
  8. ↑ Musher DM, Abers MS, Corrales-Medina VF (2019). "Acute Infection and Myocardial Infarction". N Engl J Med. 380 (2): 171–176. doi:10.1056/NEJMra1808137. PMID 30625066.
  9. ↑ Chen C, Zhou Y, Wang DW (2020). "SARS-CoV-2: a potential novel etiology of fulminant myocarditis". Herz. 45 (3): 230–232. doi:10.1007/s00059-020-04909-z. PMC 7080076 Check |pmc= value (help). PMID 32140732 Check |pmid= value (help).
  10. ↑ 10.0 10.1 Jabri A, Kalra A, Kumar A, Alameh A, Adroja S, Bashir H, Nowacki AS, Shah R, Khubber S, Kanaa'N A, Hedrick DP, Sleik KM, Mehta N, Chung MK, Khot UN, Kapadia SR, Puri R, Reed GW (July 2020). "Incidence of Stress Cardiomyopathy During the Coronavirus Disease 2019 Pandemic". JAMA Netw Open. 3 (7): e2014780. doi:10.1001/jamanetworkopen.2020.14780. PMC 7348683 Check |pmc= value (help). PMID 32644140 Check |pmid= value (help).
  11. ↑ 11.0 11.1 Minhas AS, Scheel P, Garibaldi B, Liu G, Horton M, Jennings M, Jones SR, Michos ED, Hays AG (May 2020). "Takotsubo Syndrome in the Setting of COVID-19 Infection". JACC Case Rep. doi:10.1016/j.jaccas.2020.04.023. PMC 7194596 Check |pmc= value (help). PMID 32363351 Check |pmid= value (help).
  12. ↑ [+https://doi.org/10.1001/jamacardio.2020.0950 "Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China | Global Health | JAMA Cardiology | JAMA Network"] Check |url= value (help).
  13. ↑ Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, Xiang J, Wang Y, Song B, Gu X, Guan L, Wei Y, Li H, Wu X, Xu J, Tu S, Zhang Y, Chen H, Cao B (March 2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. PMC 7270627 Check |pmc= value (help). PMID 32171076 Check |pmid= value (help).
  14. ↑ Kociol RD, Pang PS, Gheorghiade M, Fonarow GC, O'Connor CM, Felker GM (2010). "Troponin elevation in heart failure prevalence, mechanisms, and clinical implications". J Am Coll Cardiol. 56 (14): 1071–8. doi:10.1016/j.jacc.2010.06.016. PMID 20863950.
  15. ↑ Saenger AK, Rodriguez-Fraga O, Ler R, Ordonez-Llanos J, Jaffe AS, Goetze JP; et al. (2017). "Specificity of B-Type Natriuretic Peptide Assays: Cross-Reactivity with Different BNP, NT-proBNP, and proBNP Peptides". Clin Chem. 63 (1): 351–358. doi:10.1373/clinchem.2016.263749. PMID 28062628.
  16. ↑ Gao L, Jiang D, Wen XS, Cheng XC, Sun M, He B; et al. (2020). "Prognostic value of NT-proBNP in patients with severe COVID-19". Respir Res. 21 (1): 83. doi:10.1186/s12931-020-01352-w. PMC 7156898 Check |pmc= value (help). PMID 32293449 Check |pmid= value (help).
  17. ↑ Han H, Xie L, Liu R, Yang J, Liu F, Wu K; et al. (2020). "Analysis of heart injury laboratory parameters in 273 COVID-19 patients in one hospital in Wuhan, China". J Med Virol. 92 (7): 819–823. doi:10.1002/jmv.25809. PMC 7228305 Check |pmc= value (help). PMID 32232979 Check |pmid= value (help).
  18. ↑ Christ-Crain M, Breidthardt T, Stolz D, Zobrist K, Bingisser R, Miedinger D, Leuppi J, Tamm M, Mueller B, Mueller C (August 2008). "Use of B-type natriuretic peptide in the risk stratification of community-acquired pneumonia". J. Intern. Med. 264 (2): 166–76. doi:10.1111/j.1365-2796.2008.01934.x. PMID 18298480.
  19. ↑ Mueller C, Laule-Kilian K, Frana B, Rodriguez D, Scholer A, Schindler C, Perruchoud AP (February 2006). "Use of B-type natriuretic peptide in the management of acute dyspnea in patients with pulmonary disease". Am. Heart J. 151 (2): 471–7. doi:10.1016/j.ahj.2005.03.036. PMID 16442916.
  20. ↑ Lai CC, Sung MI, Ho CH, Liu HH, Chen CM, Chiang SR, Chao CM, Liu WL, Hsing SC, Cheng KC (March 2017). "The prognostic value of N-terminal proB-type natriuretic peptide in patients with acute respiratory distress syndrome". Sci Rep. 7: 44784. doi:10.1038/srep44784. PMID 28322314.
  21. ↑ Determann RM, Royakkers AA, Schaefers J, de Boer AM, Binnekade JM, van Straalen JP, Schultz MJ (July 2013). "Serum levels of N-terminal proB-type natriuretic peptide in mechanically ventilated critically ill patients--relation to tidal volume size and development of acute respiratory distress syndrome". BMC Pulm Med. 13: 42. doi:10.1186/1471-2466-13-42. PMID 23837838.
  22. ↑ Park BH, Park MS, Kim YS, Kim SK, Kang YA, Jung JY, Lim JE, Kim EY, Chang J (August 2011). "Prognostic utility of changes in N-terminal pro-brain natriuretic Peptide combined with sequential organ failure assessment scores in patients with acute lung injury/acute respiratory distress syndrome concomitant with septic shock". Shock. 36 (2): 109–14. doi:10.1097/SHK.0b013e31821d8f2d. PMID 21478812.
  23. ↑ Cosyns B, Lochy S, Luchian ML, Gimelli A, Pontone G, Allard SD, de Mey J, Rosseel P, Dweck M, Petersen SE, Edvardsen T (July 2020). "The role of cardiovascular imaging for myocardial injury in hospitalized COVID-19 patients". Eur Heart J Cardiovasc Imaging. 21 (7): 709–714. doi:10.1093/ehjci/jeaa136. PMID 32391912 Check |pmid= value (help).
  24. ↑ Teerlink JR, Alburikan K, Metra M, Rodgers JE (2015). "Acute decompensated heart failure update". Curr Cardiol Rev. 11 (1): 53–62. doi:10.2174/1573403x09666131117174414. PMID 24251454.
  25. ↑ Seferovic PM, Ponikowski P, Anker SD, Bauersachs J, Chioncel O, Cleland J, de Boer RA, Drexel H, Ben Gal T, Hill L, Jaarsma T, Jankowska EA, Anker MS, Lainscak M, Lewis BS, McDonagh T, Metra M, Milicic D, Mullens W, Piepoli MF, Rosano G, Ruschitzka F, Volterrani M, Voors AA, Filippatos G, Coats A (October 2019). "Clinical practice update on heart failure 2019: pharmacotherapy, procedures, devices and patient management. An expert consensus meeting report of the Heart Failure Association of the European Society of Cardiology". Eur. J. Heart Fail. 21 (10): 1169–1186. doi:10.1002/ejhf.1531. PMID 31129923. Vancouver style error: initials (help)
  26. ↑ Bleumink GS, Feenstra J, Sturkenboom MC, Stricker BH (2003). "Nonsteroidal anti-inflammatory drugs and heart failure". Drugs. 63 (6): 525–34. doi:10.2165/00003495-200363060-00001. PMID 12656651.


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