Myocarditis nursing: troponin elevation, cardiac MRI, and arrhythmia monitoring

Introduction

Myocarditis is inflammation of the myocardium – the muscular wall of the heart. Unlike pericarditis, which affects the outer sac surrounding the heart, myocarditis directly damages cardiomyocytes, impairing the heart’s ability to contract and conduct electrical signals. The condition disproportionately affects young, previously healthy individuals, making it a high-stakes diagnosis nursing students must understand thoroughly.

The clinical spectrum ranges from subclinical disease (mild chest discomfort that resolves spontaneously) to fulminant myocarditis with rapid-onset cardiogenic shock requiring mechanical circulatory support. Sudden cardiac death in young athletes is one of the most feared outcomes. For nurses, early recognition, continuous cardiac monitoring, and strict activity management are the pillars of care.

Quick reference table

Pathophysiology

Myocarditis begins with a trigger – most often a viral infection – that initiates a cascade of immune-mediated myocardial injury. The process unfolds in three overlapping phases.

Acute phase (days 1–14): The pathogen directly invades cardiomyocytes, triggering innate immune activation. Natural killer cells and macrophages are recruited. In viral disease, the virus itself causes cytotoxic injury – Coxsackievirus B, for example, uses the coxsackievirus-adenovirus receptor (CAR) to enter cardiomyocytes and replicate, directly lysing cells.

Subacute phase (weeks 2–4): Adaptive immunity takes over. T-lymphocytes recognize myocardial antigens – sometimes including self-antigens due to molecular mimicry – and mount a cytotoxic attack on cardiomyocytes. This autoimmune amplification is why myocardial damage often peaks after the initial infection has cleared. Inflammatory cytokines (TNF-α, IL-1β, IL-6) suppress myocardial contractility independently of structural damage.

Chronic phase (months to years): In many patients, the immune response resolves and the myocardium recovers. In others – particularly those with extensive necrosis or ongoing autoimmune activity – progressive fibrosis and ventricular remodeling lead to dilated cardiomyopathy (DCM). Fibrotic tissue creates substrate for re-entrant arrhythmias and sudden cardiac death.

Fulminant myocarditis is a distinct, severe presentation characterized by abrupt onset (often following a clear viral prodrome) and hemodynamic compromise requiring vasopressors or mechanical circulatory support. Older teaching held that fulminant myocarditis carried a better long-term prognosis than nonfulminant disease if the patient survived the acute phase – a claim from a small 2000 NEJM cohort. Larger contemporary data (Ammirati et al, JACC 2019) found the opposite: fulminant presentation was associated with worse outcomes, including higher rates of death and transplantation, and the finding held even when the analysis was restricted to lymphocytic myocarditis to match the older study’s population. Treat fulminant myocarditis as the high-risk presentation it is.

The Dallas criteria define the histological diagnosis: active myocarditis requires inflammatory infiltrate with adjacent myocyte necrosis on endomyocardial biopsy. Borderline myocarditis shows infiltrate without necrosis. The diagnostic yield of biopsy is low (~20–35%) due to sampling error, which is why cardiac MRI has become the preferred non-invasive diagnostic standard.

Causes and risk factors

Etiology table

Key risk factors: Male sex (2:1 predominance), age 15–45 years, recent viral illness (1–4 weeks prior), immunosuppression, residence in or travel to Chagas-endemic areas.

Clinical presentation

Myocarditis presents along a spectrum – from incidental ECG findings after a “flu-like” illness to fulminant hemodynamic collapse. The preceding viral illness, typically 1–4 weeks before cardiac symptoms, is a critical historical detail.

Chest pain is the most common presenting complaint. It is often pleuritic (worsening with inspiration or position) when pericarditis co-exists (myopericarditis), but can also be pressure-type, mimicking acute coronary syndrome – particularly because troponin is elevated in both.

Dyspnea reflects ventricular dysfunction and reduced cardiac output. Orthopnea (dyspnea when lying flat) and paroxysmal nocturnal dyspnea indicate worsening heart failure.

Palpitations and syncope result from arrhythmias – both supraventricular and ventricular. New onset ventricular tachycardia in a young patient with a recent viral illness should immediately raise suspicion for myocarditis.

Constitutional symptoms – fever, malaise, myalgias, and fatigue – are common and reflect the underlying inflammatory process. Fatigue is often disproportionate to the degree of cardiac dysfunction, an important clinical clue.

Fulminant myocarditis presents dramatically: cardiogenic shock, rapid deterioration over hours to days, severely reduced ejection fraction, and hemodynamic instability requiring vasopressors or mechanical support. Contemporary cohort data associate fulminant presentation with worse outcomes – higher in-hospital mortality and higher rates of death or heart transplantation at follow-up – reversing the older “paradoxically better prognosis” teaching that came from a small 2000 series. Some patients do recover ventricular function completely, but that possibility does not make the fulminant presentation lower-risk.

The classic demographic – a young, previously healthy male presenting with chest pain and dyspnea following a respiratory or GI illness – should always trigger myocarditis on the differential, particularly if initial workup rules out ACS.

Diagnostics

Lake Louise criteria (2018 update): Cardiac MRI diagnoses myocarditis when at least one T2-based criterion (myocardial edema) AND at least one T1-based criterion (myocardial injury/fibrosis, including LGE) are present. LGE in a non-ischemic pattern (subepicardial or mid-myocardial, sparing the subendocardium) distinguishes myocarditis from infarction.

Medical management

Most patients with acute myocarditis receive supportive care; immunosuppression is reserved for specific histological subtypes. The 2025 ESC guidelines for myocarditis and pericarditis (the first ESC guideline to cover myocarditis) group both conditions under the umbrella term inflammatory myopericardial syndrome (IMPS) and note that in biopsy-proven acute myocarditis up to 50% of patients recover spontaneously, while 10–25% develop progressive ventricular dysfunction.

Activity restriction during the acute inflammatory phase is non-negotiable and is one of the most important nursing teaching points. Premature return to exercise while the myocardium is still inflamed is a recognized trigger for fatal arrhythmias and sudden cardiac death in young athletes.

The guidance on how long that restriction lasts changed in 2025, and this is a point where older study resources are now out of date. The 2015 AHA/ACC Task Force recommended a fixed 3–6 month period away from competitive sports for all patients. The 2025 AHA/ACC sports participation statement (Kim et al.) replaced that fixed interval with an individualized, criteria-based approach: an athlete may resume participation after roughly 4–6 weeks provided symptoms have resolved, inflammation has resolved on cardiac MRI, and there is no relevant arrhythmia on ambulatory monitoring. The emphasis moved from time elapsed to documented recovery plus shared decision-making between clinician and athlete. The 2024 ACC expert consensus decision pathway on myocarditis takes the same criteria-driven position, and so do the 2025 ESC guidelines: restriction of physical exercise until clinical remission, for at least 1 month, is a class I recommendation for athletes and non-athletes alike. ESC defines remission as resolved symptoms plus normalized markers (CRP, troponin) and investigations (ECG, effusion, CMR evidence of active inflammation).

For nursing practice the teaching point is unchanged in substance: no competitive sport or strenuous exercise until the cardiology team clears the patient on the basis of repeat imaging and rhythm monitoring, never on the basis of feeling better.

Heart failure management: Patients with LV systolic dysfunction or HF receive guideline-directed medical therapy (ESC 2025, class I). Once the patient is hemodynamically stable, that means the standard HFrEF regimen: an ARNI (sacubitril/valsartan), ACE inhibitor, or ARB; an evidence-based beta-blocker; a mineralocorticoid receptor antagonist (spironolactone, eplerenone); and an SGLT2 inhibitor (dapagliflozin, empagliflozin), plus loop diuretics for volume overload. ESC 2025 suggests continuing beta-blockers for at least 6 months after acute myocarditis with troponin elevation, and continuing HF therapy for at least 6 months after LV function fully recovers.

NSAIDs – a limited role: Older teaching labels NSAIDs as contraindicated in myocarditis, based on mouse models of Coxsackievirus myocarditis in which NSAIDs increased viral replication and myocardial injury. The 2025 ESC guidelines take a narrower position: NSAIDs (with a proton pump inhibitor) should be considered to relieve symptoms when pericarditis features accompany the myocarditis (class IIa), uncomplicated cases with chest pain may be treated empirically with aspirin or an NSAID if needed, and colchicine should be considered in myopericarditis to reduce recurrences. NSAIDs are not a treatment for myocarditis itself, and they are best avoided in patients with reduced LVEF or heart failure, where they promote sodium and fluid retention. In pericarditis, by contrast, aspirin or an NSAID plus colchicine is first-line.

Immunosuppression:

• Giant cell myocarditis: Requires aggressive immunosuppression – typically high-dose corticosteroids combined with azathioprine, mycophenolate, or cyclosporine, with antithymocyte globulin as a second-line option (ESC 2025). In the landmark multicenter registry (Cooper et al., NEJM 1997), median survival across the whole cohort was 5.5 months from symptom onset, and 89% died or required transplantation. Immunosuppression changed that trajectory materially: patients given corticosteroids plus cyclosporine, azathioprine, or both averaged 12.3 months of survival, against 3.0 months for those receiving no immunosuppressive therapy.
• Autoimmune / immune-mediated myocarditis (SLE, sarcoidosis): Treat the underlying condition; corticosteroids are standard.
• Checkpoint inhibitor myocarditis: Immediate cessation of the offending agent and high-dose corticosteroids, started within 24 hours (ESC 2025, class I). Up to half of patients are steroid-refractory; if there is no response in 24–48 hours, second-line options include mycophenolate, antithymocyte globulin, abatacept, or alemtuzumab.
• Lymphocytic myocarditis: Routine immunosuppression is not recommended in acute myocarditis with preserved LV function (ESC 2025, class III). Corticosteroids should be considered in fulminant, non-infectious myocarditis (class IIa) and may be considered when LVEF is impaired and refractory to standard HF therapy (class IIb). ESC’s immunosuppressive regimens apply to virus-negative disease, which is one reason biopsy with viral testing usually comes first.

IVIG: Commonly prescribed for children with acute myocarditis, but the evidence rests on case series and retrospective analyses, and ESC 2025 states that randomized studies are still needed before IVIG can be advised for adults.

Mechanical circulatory support (MCS): Fulminant myocarditis with cardiogenic shock may require:

• Intra-aortic balloon pump (IABP) – reduces afterload and augments diastolic perfusion
• Impella (axial flow pump) – provides higher degree of hemodynamic support
• Veno-arterial ECMO (VA-ECMO) – for severe biventricular failure; allows cardiac rest and recovery

These patients require ICU-level nursing care. The goal is to “bridge” the patient through the acute inflammatory phase, after which the myocardium may recover substantially.

Heart transplantation: Reserved for patients with refractory, progressive disease who are not MCS candidates or do not recover on support.

Nursing assessment and interventions

Hemodynamic and cardiac monitoring

Continuous telemetry is mandatory in all patients with confirmed or suspected myocarditis. The primary nursing concern is life-threatening arrhythmia – ventricular tachycardia and ventricular fibrillation occur without warning and are the leading cause of sudden death in this population. Report any new PVCs, VT runs, heart block, or rate changes immediately to the provider.

Monitor vital signs with particular attention to:

• Heart rate: Tachycardia is common and expected with systemic inflammation and reduced stroke volume. New bradycardia suggests conduction system involvement (heart block).
• Blood pressure: Hypotension signals hemodynamic compromise; prompt escalation is required.
• SpO2: Continuous pulse oximetry; supplemental oxygen for saturation below 94%.
• Temperature: Fever elevates myocardial oxygen demand – give antipyretics per order (acetaminophen is the usual choice; do not substitute an NSAID unless it has been specifically ordered).

Fluid and volume management

Myocarditis with reduced EF carries significant risk of fluid overload and progression to acute decompensated heart failure.

• Strict intake and output monitoring every 4–8 hours (hourly for unstable patients)
• Daily weights at the same time each morning, before eating, after voiding
• Assess for JVD, peripheral edema, adventitious breath sounds (crackles), and orthopnea at each assessment
• Report weight gains of >2 lbs overnight or >5 lbs in a week immediately
• Fluid restriction may be ordered for patients with significant LV dysfunction

Activity restriction and positioning

Rest is the rule in the acute phase: ESC 2025 advises complete rest during acute myocarditis and no physical activity beyond sedentary activities until symptoms resolve and inflammation settles. Explain the rationale clearly to patients – particularly young athletes who feel “not that sick” and struggle to understand why they cannot exercise. Physical activity during active myocardial inflammation dramatically increases arrhythmia risk and can precipitate sudden cardiac death.

• Elevate the head of bed to 30–45 degrees for orthopnea and to reduce preload
• Assist with all activities of daily living during the acute phase
• Implement a graduated activity protocol only after provider authorization and documented hemodynamic stability

Pain and symptom management

Chest pain should be assessed with each set of vital signs. Use a standardized scale (0–10 NRS). Differentiate between pleuritic chest pain (pericarditis component) and pressure-type chest pain (myocardial ischemia) – report changes in character or severity. Acetaminophen is the usual first analgesic. NSAIDs are given only when the provider orders them, typically for pericarditis-type pain with preserved LV function, and should be questioned in a patient with heart failure or reduced EF.

Medication monitoring

• Beta-blockers: Monitor for symptomatic bradycardia and hypotension before each dose; hold for HR <50 bpm or SBP <90 mmHg per protocol.
• ACE inhibitors/ARBs: Monitor renal function and potassium; watch for first-dose hypotension.
• Diuretics: Monitor electrolytes – hypokalemia increases arrhythmia risk.
• Anticoagulation: Patients with documented intracardiac thrombus or atrial fibrillation may be anticoagulated; monitor for bleeding.

Patient and family education

• Activity restriction is the most critical teaching point. No competitive sports, heavy lifting, or vigorous exercise until the cardiology team grants clearance based on repeat cardiac MRI and rhythm monitoring – not on symptom resolution alone.
• Return precautions: chest pain, palpitations, syncope, worsening dyspnea, or leg swelling – return to ED immediately.
• Importance of follow-up cardiac MRI and Holter monitoring before return to exercise.
• Medication adherence – especially beta-blockers and ACE inhibitors, which must not be stopped abruptly.
• Alcohol avoidance – alcohol is cardiotoxic and can worsen LV dysfunction.

Complications

Risk stratification for SCD: Patients with persistent LV dysfunction, extensive LGE on cardiac MRI, or non-sustained VT on ambulatory monitoring need close follow-up. Under ESC 2025, an ICD is recommended after the acute phase for sustained VT that was not hemodynamically tolerated (class I) and should be considered for tolerated sustained VT (class IIa). A primary-prevention ICD may be considered once the acute phase has passed (3–6 months) if risk factors for ventricular arrhythmia persist (class IIb). Because inflammation can resolve, a wearable cardioverter-defibrillator is sometimes used as a bridge in selected patients.

Myocarditis vs pericarditis

These conditions share features – chest pain, ECG changes, elevated inflammatory markers, young patient demographics – but differ in important ways that affect management.

When both layers are involved, the 2025 ESC guidelines define myopericarditis as predominant pericarditis with some myocardial involvement, and perimyocarditis as predominant myocarditis with some pericardial involvement. Both sit under the umbrella term inflammatory myopericardial syndrome (IMPS). The distinction matters because the leading process guides management: myopericarditis is treated much like pericarditis (anti-inflammatory therapy plus colchicine) and generally carries a good prognosis, while perimyocarditis is managed as myocarditis.

See the full comparison in the pericarditis nursing reference.

NCLEX tips

• Coxsackievirus B is the most common cause of viral myocarditis – the single most tested fact about myocarditis etiology.
• NSAIDs have a limited role in myocarditis – in pericarditis, aspirin or an NSAID plus colchicine is first-line, while in myocarditis NSAIDs are limited to pericarditis-type chest pain (ESC 2025, class IIa) and are avoided in heart failure or reduced EF. Many question banks still teach “NSAIDs are contraindicated in myocarditis,” and an answer that withholds an NSAID from a myocarditis patient with low EF remains the safe choice.
• Activity restriction until documented recovery – the 2025 AHA/ACC statement replaced the old fixed 3–6 month period with criteria-based clearance (symptoms resolved, inflammation resolved on cardiac MRI, no relevant arrhythmia), possible from about 4–6 weeks. The 2025 ESC guidelines likewise recommend restricting exercise until remission, for at least 1 month (class I). Older question banks and textbooks still teach “3–6 months,” so note which version a question is testing. Either way, patients who “feel better” are not cleared to exercise without cardiac imaging follow-up.
• Giant cell myocarditis has the worst prognosis of all subtypes – median survival was 5.5 months in the landmark registry cohort, and immunosuppression is what extends it. This is the subtype where endomyocardial biopsy changes management.
• Cardiac MRI with late gadolinium enhancement (LGE) is the gold-standard non-invasive diagnostic test. LGE in a subepicardial or mid-myocardial pattern (not subendocardial) differentiates myocarditis from myocardial infarction.
• Troponin is elevated in myocarditis – this differentiates it from pure pericarditis. Elevated troponin in a young patient with chest pain and recent viral illness = think myocarditis.
• Fulminant myocarditis presents with rapid cardiogenic shock and carries worse outcomes than nonfulminant disease in contemporary data. Older sources teach a “paradoxically better prognosis” – that claim came from a small 2000 cohort and was reversed by larger 2019 data, so be alert to which version a question is testing.
• VA-ECMO or Impella may be required for fulminant myocarditis with cardiogenic shock – mechanical support is a bridge to recovery.
• Young athlete + chest pain + viral prodrome 1–4 weeks prior = classic myocarditis presentation. Know this clinical picture.
• Telemetry is mandatory – VT and VF occur without warning; continuous monitoring is a nursing priority.
• Myopericarditis vs perimyocarditis – myopericarditis is predominantly pericarditis (managed like pericarditis); perimyocarditis is predominantly myocarditis (managed like myocarditis). The first half of the word is the minor partner.
• IVIG is commonly given to children with acute myocarditis, but the evidence is observational; ESC 2025 says adult use still needs randomized trials.
• Checkpoint inhibitor myocarditis (from cancer immunotherapy drugs like pembrolizumab) affects about 1% of treated patients but carries mortality of up to 50% – stop the drug immediately and start high-dose corticosteroids within 24 hours.
• Chagas disease (Trypanosoma cruzi) is a major cause of myocarditis and DCM in Latin America – important for NCLEX questions with travel history or immigrant populations.
• Daily weights – weight gain of >2 lbs overnight signals fluid retention and worsening heart failure; report immediately.

Internal links

• Heart failure nursing: assessment, interventions, and NCLEX review – myocarditis frequently progresses to acute decompensated heart failure; review HF management in parallel
• Pericarditis nursing: assessment, interventions, and NCLEX review – often co-exists with myocarditis as myopericarditis; key comparison for NCLEX
• Infective endocarditis nursing: assessment, interventions, and NCLEX review – another infectious cardiac condition with overlapping inflammatory mechanisms
• Atrial fibrillation nursing: assessment, interventions, and NCLEX review – myocarditis-associated atrial arrhythmias and rate control management
• EKG interpretation cheat sheet for nurses – interpreting the ST changes, T-wave inversions, and arrhythmias associated with myocarditis
• Sepsis nursing: assessment, interventions, and NCLEX review – fulminant myocarditis with cardiogenic shock shares hemodynamic monitoring priorities with septic shock

References

1. Caforio ALP, Pankuweit S, Arbustini E, et al. (2013). Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. European Heart Journal. 34(33):2636–2648. doi:10.1093/eurheartj/eht210

2. Ammirati E, Frigerio M, Adler ED, et al. (2020). Management of acute myocarditis and chronic inflammatory cardiomyopathy: an expert consensus document. Circulation: Heart Failure. 13(11):e007405. doi:10.1161/CIRCHEARTFAILURE.120.007405

3. Ferreira VM, Schulz-Menger J, Holmvang G, et al. (2018). Cardiovascular magnetic resonance in nonischemic myocardial inflammation: expert recommendations. Journal of the American College of Cardiology. 72(24):3158–3176. doi:10.1016/j.jacc.2018.09.072

4. Cooper LT Jr. (2009). Myocarditis. New England Journal of Medicine. 360(15):1526–1538. doi:10.1056/NEJMra0800028

5. McCarthy RE 3rd, Boehmer JP, Hruban RH, et al. (2000). Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis. New England Journal of Medicine. 342(10):690–695. doi:10.1056/NEJM200003093421003

6. Kindermann I, Barth C, Mahfoud F, et al. (2012). Update on myocarditis. Journal of the American College of Cardiology. 59(9):779–792. doi:10.1016/j.jacc.2011.09.074

7. Schultz JC, Hilliard AA, Cooper LT Jr, Rihal CS. (2009). Diagnosis and treatment of viral myocarditis. Mayo Clinic Proceedings. 84(11):1001–1009. doi:10.4065/84.11.1001

8. Frustaci A, Chimenti C, Calabrese F, Pieroni M, Thiene G, Maseri A. (2003). Immunosuppressive therapy for active lymphocytic myocarditis: virological and immunologic profile of responders versus nonresponders. Circulation. 107(6):857–863. doi:10.1161/01.CIR.0000048147.15962.31

9. Blauwet LA, Cooper LT. (2010). Myocarditis. Progress in Cardiovascular Diseases. 52(4):274–288. doi:10.1016/j.pcad.2009.11.006

10. Maron BJ, Udelson JE, Bonow RO, et al. (2015). Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 3: hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and other cardiomyopathies, and myocarditis. Circulation. 132(22):e273–e280. doi:10.1161/CIR.0000000000000239

11. Caforio ALP, Adler Y, Agostini C, et al. (2017). Diagnosis and management of myocardial involvement in systemic immune-mediated diseases: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Disease. European Heart Journal. 38(35):2649–2662. doi:10.1093/eurheartj/ehx321

12. Peretto G, Sala S, Rizzo S, et al. (2020). Ventricular arrhythmias in myocarditis: characterization and relationships with myocardial inflammation. Journal of the American College of Cardiology. 75(9):1046–1057. doi:10.1016/j.jacc.2020.01.036

13. Imazio M, Brucato A, Barbieri A, et al. (2013). Good prognosis for pericarditis with and without myocardial involvement: results from a multicenter, prospective cohort study. Circulation. 128(1):42–49. doi:10.1161/CIRCULATIONAHA.113.001531

14. Ammirati E, Veronese G, Brambatti M, et al. (2019). Fulminant versus acute nonfulminant myocarditis in patients with left ventricular systolic dysfunction. Journal of the American College of Cardiology. 74(3):299–311. doi:10.1016/j.jacc.2019.04.063

15. Moslehi JJ, Salem JE, Sosman JA, Lebrun-Vignes B, Johnson DB. (2018). Increased reporting of fatal immune checkpoint inhibitor-associated myocarditis. Lancet. 391(10124):933. doi:10.1016/S0140-6736(18)30533-6

16. Cooper LT Jr, Berry GJ, Shabetai R. (1997). Idiopathic giant-cell myocarditis – natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators. New England Journal of Medicine. 336(26):1860–1866. doi:10.1056/NEJM199706263362603

17. Kim JH, Baggish AL, Levine BD, et al. (2025). Clinical considerations for competitive sports participation for athletes with cardiovascular abnormalities: a scientific statement from the American Heart Association and American College of Cardiology. Journal of the American College of Cardiology. 85(10):1059–1108. doi:10.1016/j.jacc.2024.12.025

18. Drazner MH, Bozkurt B, Cooper LT Jr, et al. (2025). 2024 ACC expert consensus decision pathway on strategies and criteria for the diagnosis and management of myocarditis. Journal of the American College of Cardiology. 85(4):391–431. doi:10.1016/j.jacc.2024.10.080

19. Schulz-Menger J, Collini V, Gröschel J, Adler Y, et al. (2025). 2025 ESC Guidelines for the management of myocarditis and pericarditis. European Heart Journal. 46(40):3952–4041. doi:10.1093/eurheartj/ehaf192

20. Pfizer Laboratories Div Pfizer Inc. COMIRNATY (COVID-19 vaccine, mRNA) injection: prescribing information, Warnings and precautions – myocarditis and pericarditis. DailyMed, US National Library of Medicine (setid 48c86164-de07-4041-b9dc-f2b5744714e5). Accessed October 10, 2026. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=48c86164-de07-4041-b9dc-f2b5744714e5

21. Heidenreich PA, Bozkurt B, Aguilar D, et al. (2022). 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 145(18):e895–e1032. doi:10.1161/CIR.0000000000001063