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Year : 2021  |  Volume : 6  |  Issue : 1  |  Page : 4-20

2020 expert consensus on the prevention and treatment of heart failure after myocardial infarction

Branch of Cardiovascular Physicians, Chinese Medical Doctor Association, Chinese Cardiovascular Association, The Expert Consensus Working Group on the Prevention and Treatment of Heart Failure after Myocardial Infarction, China

Date of Submission25-Nov-2020
Date of Acceptance15-Jan-2020
Date of Web Publication30-Mar-2021

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2470-7511.312595

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Myocardial infarction (MI) is one of the most common and important causes of heart failure (HF). In China, HF after MI has a high incidence, and the prognosis is poor. In recent years, although China has successively issued guidelines for the diagnosis and treatment of MI and HF, respectively, there remains a lack of unified guidance for the diagnosis, treatment, and prevention strategies of HF after MI. Experts from the Branch of Cardiovascular Physicians, Chinese Medical Doctor Association, and the Chinese Cardiovascular Association compiled this consensus, covering the epidemiology, pathogenesis, diagnosis, treatment, prevention, and management of HF after MI. It aims to promote and optimize standardized clinical strategies for the disease management and improve patient outcome.

Keywords: Consensus; Diagnosis; Heart failure; Myocardial infarction; Prevention; Treatment

How to cite this article:
. 2020 expert consensus on the prevention and treatment of heart failure after myocardial infarction. Cardiol Plus 2021;6:4-20

How to cite this URL:
. 2020 expert consensus on the prevention and treatment of heart failure after myocardial infarction. Cardiol Plus [serial online] 2021 [cited 2021 Jul 30];6:4-20. Available from:

The Chinese edition of this article is published in the December 2020 issue (Vol.35, No. 12, Page 1166-1180) of Chinese Circulation Journal.

Heart failure (HF) is a serious and terminal stage of all cardiovascular diseases, with a high disability and fatality rate. With population aging, the prevalence of HF is rising, which is increasingly becoming an important public health problem worldwide.[1] Myocardial infarction (MI) is currently one of the most common and important causes of HF in the world. In China, epidemiological data have shown that the incidence of HF after MI is high. Although the development of drug and nondrug therapies has improved the outcome of patients with HF after MI, the all-cause mortality, cardiovascular event incidence, and readmission rate of patients remain high.[2],[3] This is related to the severity of the disease, the promptness and appropriateness of treatment, and the cardiologist's concepts of disease prevention and treatment.

In recent years, although China has successively issued guidelines for the diagnosis and treatment of MI and HF,[4],[5],[6] there remains a lack of unified guidance for HF after MI. To make the clinical diagnosis and treatment and prevention strategies of HF after MI more rational and standardized and to further optimize the whole-course management of HF after MI, the experts from the Branch of Cardiovascular Physicians, Chinese Medical Doctor Association, and the Chinese Cardiovascular Association compiled this consensus by combining evidence-based medicine both at home and abroad and referring to the latest guidelines.[4],[5],[6],[7],[8],[9],[10],[11],[12] This consensus includes seven major sections of HF after MI: definition and classification, epidemiology and prognosis, pathogenesis, diagnosis and evaluation, prevention measures, treatment of acute and chronic HF after MI, and patient management.

This consensus follows an internationally accepted approach for the presentation of grades of recommendations and sources of evidence:

  • Grade I: Procedures or treatments that have been proven and/or consistently recognized as beneficial, useful, and effective.
  • Grade II: Procedures or treatments in which useful and/or effective evidence is inconsistent or differing views exist.
  • Grade IIa: The application of these procedures or treatments is justified as the relevant evidence/views tend to be useful and/or effective.
  • Grade IIb: The application of these procedures or treatments may be considered as the relevant evidence/views have not been sufficiently proven to be useful and/or effective.
  • Grade III: Procedures or treatments that have been proven and/or consistently recognized as useless and/or ineffective and may be harmful in some cases; thus, they are not recommended.
  • Level of evidence A: Data derived from multiple randomized clinical trials or meta-analyses.
  • Level of evidence B: Data derived from a single randomized clinical trial or multiple nonrandomized controlled studies.
  • Level of evidence C: Expert consensus opinion and/or small clinical trials, retrospective studies, or registry studies only.

  Definition and Classification of Heart Failure after Myocardial Infraction Top

Definition of heart failure after myocardial infarction

HF is a group of clinical syndromes that occur as the results of any structural and/or functional cardiac disorder that causes decreased cardiac output and/or increased intracardiac pressure at rest or under stress. HF after MI is a complication that occurs after MI (including STEMI and NSTEMI) during hospitalization or after discharge.

Classification of heart failure after myocardial infarction

According to the time of onset, HF can be divided into early-onset (HF that is present on admission or occurs during hospitalization for MI) and late-onset (HF that occurs after discharge) after MI. According to the acuteness of onset, it can be divided into acute HF after MI and chronic HF after MI. Furthermore, according to the location and extent of infarction, acute HF can be divided into acute left HF, acute right HF, and acute global HF. The symptoms of most patients with acute HF after MI can be relieved by treatment in the hospital before developing into chronic HF. Chronic HF after MI can be decompensated by various inducing factors and results in acute exacerbations that require hospitalization. The type, location, and size of MI and the promptness and effectiveness of treatment are all determinants of the occurrence and severity of HF.

According to the left ventricular ejection fraction (LVEF), it can be divided into HFrEF (LVEF <40%), HFmrEF (LVEF 40%–49%), and HFpEF (LVEF ≥50%) [Table 1].
Table 1: Classification of post-MI HF by ejection fraction and diagnostic criteria

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  Epidemiology and Prognosis Top

Incidence and prognosis of heart failure after myocardial infarction

Data from Europe and the United States showed that the incidence of HF between 30 days and 6.7 years after MI is 13.1%–37.5%.[13],[14],[15],[16] The Framingham Heart Study[13] showed that the incidence of HF within 30 days after MI increased from 10% to 23.1% and the mortality decreased from 12.2% to 4.1% during 1970–1979 and 1990–1999, respectively; the incidence of HF within 5 years after MI increased from 27.6% to 31.9% and the mortality decreased from 41.1% to 17.3%. Hence, the mortality of MI showed a decreasing trend, while the incidence of HF after MI showed an increasing trend.

HF after MI significantly increases the risk of short- and long-term mortality. The France FAST-MI Registry[16] found that MI patients who developed HF had a significantly higher risk of in-hospital mortality (12.2%) and mortality 1 year after discharge (26.6%) than those without HF (3.0% and 5.2%, respectively). A Canadian Registry[17] also showed that both in-hospital mortality (3.6%) and 1-year mortality after discharge (14.6%) were higher in patients with NSTEMI who developed HF than in those without HF (1.1% and 4.4%, respectively). In a Norway Study involving 86,771 patients with first-onset acute MI from 2001 to 2009 (follow-up to the end of 2009), the mortality rate of male MI patients with HF was 61.4%, while the mortality rate of male MI patients without HF was 28.3%; for female MI patients (with or without HF), the mortality rate was 70.0% and 39.2%, respectively.[18]

Currently, epidemiological data on HF after MI in China are limited. The China CREATE Study from 2001 to 2004[19] found that the incidence of HF within 7 days after MI in patients with STEMI was 19.3%. The BRIGHT Study[3] found that acute MI patients (88% were STEMI) receiving emergency PCI had a 14.3% incidence of HF on admission. The 10-year data from the China PEACE Study[2] showed that during 2001–2011, the incidence of early-onset (in-hospital) HF after MI (LVEF ≤40%) in patients with STEMI presented a decreasing trend (2001: 17.4%, 2006: 17.9%, and 2011: 12.7%).

In terms of prognosis, the Japan AMI Registry[20] found that among patients with STEMI who had received PCI, the readmission rate in the 1st year was 4.4%. The 5-year cumulative risk of all-cause mortality (36.3%), risk of HF hospitalization (40.4%), and risk of cardiovascular death (19.1%) were higher in patients developing HF in the 1st year after discharge than in those without HF in the 1st year (10.1%, 4.3%, and 3.3%, respectively).

Risk factors for heart failure after myocardial infarction

The occurrence of HF after MI is related to multiple factors. A study based on the Myocardial Infarction Data Acquisition System found that hypertension, diabetes, and a history of renal and pulmonary disease were risk factors for HF after MI, while the implementation of revascularization (including PCI and coronary artery bypass grafting [CABG]) was associated with reduced readmission rates in patients with HF.[21] Another study[14] found that the incidence of HF in patients with zero to single-, double-, and triple-vessel disease was 10.7%, 14.6%, and 23.0%, respectively, within 30 days after MI and 14.7%, 20.6%, and 29.8%, respectively, within 5 years after MI. It is suggested that the larger the number of diseased coronary vessels in MI patients, the greater the possibility of HF in the future. In addition, patients with anterior MI, chronic total occlusion, and valvular regurgitation are also at high risk of HF after MI.

  Pathogenesis of Heart Failure after Myocardial Infarction Top

Cardiomyocyte loss

Cardiomyocyte loss is an essential cause of cardiac remodeling and HF after MI and mainly includes necrosis and apoptosis of cardiomyocytes. After acute coronary occlusion, cardiomyocytes are exposed to acute ischemia and hypoxia, resulting in ischemic necrosis. Necrotic cardiomyocytes release damage factors such as troponin, creatine kinase, and lactate dehydrogenase, aggravating damage to the cardiomyocytes.[22],[23] The apoptotic signaling pathway of cardiomyocytes in ischemic and nonischemic regions can also be activated by damage factors such as neurohumoral activation, oxidative stress, calcium overload, and the inflammatory response, which further mediate cardiomyocyte apoptosis.[24]
Figure 1: Pathogenesis of heart failure after myocardial infarction.
MI: Myocardial infarction, SNS: Sympathetic nervous system, RAAS: Renin-angiotensin-aldosterone system, NPS: Natriuretic peptide system, ECM: Extracellular matrix

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Cardiac remodeling

As a basic pathological process of HF after MI, cardiac remodeling refers to maladaptive changes in cardiomyocytes, noncardiomyocytes, and the extracellular matrix (ECM), which leads to pathological changes in ventricular geometry, causing increased stiffness and decreased contractility of the heart.[25] The main mechanisms of cardiac remodeling include (1) hypertrophy and loss of cardiomyocytes; (2) stretch-induced or compensatory hypertrophy of viable cardiomyocytes due to volume or pressure overload, accompanied by apoptosis; (3) changes in the cardiomyocyte phenotype: embryonic changes in gene expressions of ventricular myosin and troponin cause decreased contractility of cardiomyocytes;[26] and (4) changes in noncardiomyocytes and the ECM. The production of a large amount of ECM increases the stiffness of the ventricular wall and affects the diastolic function and coronary reserve capacity of the heart, leading to ischemia and hypoxia in cardiomyocytes.[27]

Immune injury and inflammation mediation

Damage-associated molecular patterns released by apoptotic and necrotic cardiomyocytes after MI activate the innate immune system and trigger a severe inflammatory response. The hyperactive long-term inflammatory response can cause expansion of the scope of damage, aggravate tissue function damage, and ultimately lead to HF.[28]

Neuroendocrine activation

The reduced cardiac output after MI can elicit reflex activation of the SNS and increase the secretion of norepinephrine and epinephrine, resulting in increased myocardial contractility, heart rate, and myocardial oxygen consumption.[29] Toxic effects of long-term high concentrations of catecholamines on cardiomyocytes (mitochondrial dysfunction of cardiomyocytes, increased production of reactive oxygen species, calcium overload, inducing apoptosis) promote cardiac remodeling.[30]

The reduced cardiac output after MI can also elicit reflex activation of the RAAS. The binding of angiotensin II to angiotensin II type 1 (AT1) receptors can cause increased aldosterone secretion, vasoconstriction, cardiomyocyte hypertrophy, and apoptosis, thereby leading to sodium and water retention and myocardial fibrosis to cause symptoms of HF and aggravate cardiac remodeling.[31],[32],[33]

In addition, the reduced cardiac output can elicit the activation of the natriuretic peptide system (NPS), which plays a favorable compensatory role in HF after MI. Natriuretic peptides specifically bind to receptors to dilate arteries and veins and reduce pulmonary capillary wedge pressure, systemic arterial pressure, and right atrial pressure, thereby reducing cardiac preload and afterload to improve cardiac remodeling.[34]

  Diagnosis of Heart Failure after Myocardial Infarction Top

Clinical diagnosis of heart failure after myocardial infarction

Diagnosis of HF after MI mainly depends on medical history, symptoms, signs, and auxiliary examination. First, patients should have a clear history of MI or definite radiographic evidence to support the presence of MI; second, symptoms, signs, chest X-ray, natriuretic peptide testing,[35] and echocardiography confirm the presence of HF. Echocardiography is the preferred method for assessing cardiac structure and function. It provides information on atrioventricular volume, left and right ventricular systolic and diastolic function, ventricular wall thickness, valvular function, and pulmonary arterial hypertension.[36] Cardiac magnetic resonance (CMR) is an alternative imaging method when echocardiography fails to make a diagnosis.[4]

Assessment of heart failure after myocardial infarction

B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) measurements are recommended for the diagnosis of HF after MI and the assessment of severity and outcome of the disease (I, A).[4] Diagnosis of acute HF can usually be excluded if BNP is <100 ng/L and NT-proBNP is <300 ng/L. In the diagnosis of acute HF, different NT-proBNP diagnostic cutoff points should be set according to different stratifications of age and renal function: NT-proBNP >450 ng/L for patients <50 years of age, >900 ng/L for patients >50 years of age, >1800 ng/L for patients >75 years of age, and >1200 ng/L for patients with renal insufficiency (glomerular filtration rate <60 mL/min).[37] For chronic HF, diagnosis is usually excluded if BNP is <35 ng/L and NT-proBNP is <125 ng/L.

The severity of HF following acute MI can be assessed using the Killip classification[5] [Table 2].
Table 2: Killip classification

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Hemodynamic changes in HF are characterized by decreased cardiac output and congestion in the pulmonary or systemic circulation, and their severity is often consistent with the symptoms and signs of HF. Acute HF or an acute attack of chronic HF after MI can also be categorized by the Forrester hemodynamic classification according to the invasive hemodynamic monitoring index[38],[39] [Table 3].
Table 3: Forrester classification

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Killip or Forrester class ≥II can be classified as HF, and the severity of HF is consistent with the increase of mortality.

Acute HF is usually divided into four types in clinical practice: “dry-warm,” “wet-warm,” “wet-cold,” and “dry-cold” according to the clinical manifestations of “blood stasis” ("wet"/"dry") and “hypoperfusion” ("cold"/"warm") in the peripheral tissues.

Chronic HF can be divided into four classes according to the patient's self-perceived limitation to perform daily life activities using the NYHA classification method [Table 4].[4]
Table 4: New York Heart Association Classification

Click here to view

In addition, the application of CMR examination in the assessment and grading of cardiac function after acute MI has also been proposed by some Chinese scholars and has been shown to be associated with prognosis.[40]

  Prevention of Heart Failure after Myocardial Infarction Top

Early myocardial reperfusion

Early opening of the infarct-related coronary artery can save moribund myocardium and reduce infarct size and cardiomyocyte loss, playing an important role in preventing or delaying the occurrence of HF. Despite the increased use of direct PCI in China during 2001–2010 (10.6%–28.1%, P < 0.0001),[2] the proportion of patients not receiving reperfusion therapy showed no significant change (45.3% in 2001 and 44.8% in 2011, P = 0.82), and over half of STEMI patients missed the optimal time for reperfusion due to delayed treatment. On the other hand, the in-hospital mortality of STEMI patients in China showed no significant decrease during the 10-year period. Early drug or mechanical reperfusion therapy has a definite clinical benefit in STEMI patients with sustained ST-segment elevation or new-onset left bundle branch block (LBBB) within 12 h of onset. Hospitals eligible for PCI should complete balloon dilation within 90 min as far as possible (I, A). If a patient is admitted to an ambulance but cannot be transferred to a PCI center to complete reperfusion therapy within 120 min, it is better to initiate thrombolytic therapy in the ambulance (I, A). If a patient is first admitted at hospital where PCI is unfeasible and can be transferred to a PCI center and complete reperfusion therapy within 120 min after first medical contact (FMC), the patient should be transferred to the PCI hospital for direct PCI (I, B) within 30 min; thrombolysis should be initiated within 30 min after FMC if the time from FMC to guidewire passing through the infarct-related artery is >120 min (I, A).[5] If a STEMI patient experiences hemodynamic instability and/or cardiogenic shock (CS) due to mechanical complications, IABP can be used as an adjunctive treatment (IIa, C).[5]

Prevention of cardiac remodeling

Blocking or delaying cardiac remodeling is an essential step in preventing HF after MI. If there are no contraindications, all patients with MI should take β-blockers and ACEIs for the rest of their lives (I, B);[6] for patients intolerant to ACEIs, ARBs may be used. Currently, routine combinations of ACEIs and ARBs are not recommended.[5] For MI patients with asymptomatic left ventricular systolic dysfunction (including decreased LVEF and/or regional wall motion abnormalities), ACEIs and β-blockers are recommended to prevent and delay the onset of HF and prolong survival.[4] Recently, studies have found that sacubitril/valsartan (an angiotensin receptor neprilysin inhibitor [ARNI]) can effectively reverse cardiac remodeling, with an effect superior to ACEIs and ARBs. Animal studies have shown that sacubitril/valsartan can ameliorate the level of myocardial fibrosis, inhibit the activity of the proinflammatory cytokine matrix metalloproteinase-9 and the production of aldosterone, increase the level of the natriuretic peptide in the blood, and alleviate pulmonary congestion, thereby delaying the progress of cardiac remodeling after MI.[41],[42],[43] Based on the above evidence for the reversal of cardiac remodeling, the administration of sacubitril/valsartan can be considered to prevent or delay cardiac remodeling in patients with MI. In the ongoing PARADISE-MI Study, acute MI patients with left ventricular systolic dysfunction and/or pulmonary congestion and without a known history of chronic HF were randomized to receive sacubitril/valsartan or ramipril, which will be able to clarify the efficacy of sacubitril/valsartan in the treatment of HF after MI.[44]{Figure 2}

Prevention and control of high-risk factors for heart failure after myocardial infarction

Low LVEF, previous medical history of MI, atrial fibrillation, hypertension, diabetes, dyslipidemia, stroke, chronic kidney disease, chronic obstructive pulmonary disease, and alcoholism are all associated with an increased risk of acute HF after MI.[45],[46] Active control of risk factors, such as lifestyle intervention, smoking cessation, and control of blood pressure, blood lipids, and blood glucose, can delay the onset of HF and prolong survival.

  Treatment of Heart Failure after Myocardial Infarction Top

For patients with acute HF after MI, it is necessary to improve and stabilize hemodynamics and relieve symptoms, while for patients with chronic HF after MI, standardized drug therapy is needed to delay cardiac remodeling and ameliorate the long-term prognosis.

Treatment of acute heart failure after myocardial infarction

Treatment goals

The treatment goals of acute HF after MI are to stabilize the hemodynamic state, correct hypoxia, relieve symptoms of HF, and maintain organ perfusion and function. Attention should be paid to improve the quality of life, as well as the short-term and long-term prognosis of patients.

Active treatment of etiology and inducing factors

  1. Patients with acute HF after MI eligible for emergency revascularization should be evaluated and undergo early revascularization (I, C).[4],[5]
  2. For acute exacerbation of chronic HF after MI, the inducing factors of HF should be identified and treated accordingly.

General treatment

Posture selection (semi-reclined or orthopneic position), oxygen inhalation, and use of sedatives are included. Different oxygen inhalation modes should be selected according to the severity of dyspnea in patients (the details are shown in “Nondrug Therapies"). Sedatives should be used with caution in patients with acute pulmonary edema and should be contraindicated in patients with persistent hypotension, shock, disturbance of consciousness, hypoxia, and severe chronic obstructive pulmonary disease.[4],[10],[11]

Drug therapies

  1. Diuretics: Intravenous diuretics, such as furosemide, torsemide, and bumetanide, are preferred, and hydrochlorothiazide or potassium-sparing diuretics may be combined if necessary.[4]
  2. Vasodilators (IIa, B): These mainly include nitrates, sodium nitroprusside, recombinant B-type brain natriuretic peptide, and urapidil. Blood pressure should be noted before and during the use of vasodilators, which are not recommended for patients with systolic blood pressure <90 mmHg.[4],[34]
  3. Positive inotropic drugs (IIb, C): Commonly used drugs include β-receptor agonists (dopamine and dobutamine), digitalis (cedilanid and lanatoside C), phosphodiesterase inhibitors (milrinone), and calcium sensitizers (levosimendan).[4] Positive inotropic agents should be used with caution in patients with HF during acute MI. Levosimendan can improve myocardial contraction and is well tolerated without aggravating arrhythmia in patients with acute HF after STEMI treated with PCI.[48] For patients with acute MI with CS, a meta-analysis has shown that levosimendan can improve cardiac function and hemodynamic parameters, but the benefit for survival is not clear.[47] Digitalis is not recommended within 24 h of acute MI.[4]
  4. Vasoconstrictors (IIb, B): Based on supplementing an effective blood volume, when blood pressure drops sharply or hypoperfusion occurs, vasoconstrictors can be used to increase blood pressure temporarily. Once the symptoms are relieved, the dose should be reduced immediately or even discontinued. Improper use of vasoconstrictors may lead to arrhythmia and even aggravate myocardial ischemia. Norepinephrine (IIb, B) is preferred in CS.[4]
  5. Drugs improving outcome: These drugs should be administered as early as possible after hemodynamic stability, which include β-blockers, ACEIs/ARBs/ARNIs, and aldosterone receptor antagonists; the dosage should be adjusted according to the patient's condition.[4] In patients with a medical history of chronic HF, ARNIs may be initiated in place of ACEIs or ARBs[4] as early as possible after hemodynamic stability.

Management of mechanical complications after myocardial infarction

  1. Free wall rupture: Free wall rupture is more common from 24 h to 1 week after MI and is characterized by a sudden loss of consciousness, shock, electromechanical dissociation, and acute cardiac tamponade. In case of doubt, a bedside echocardiogram should be performed immediately for confirmation and surgery should be performed as soon as possible for treatment. The goal of preoperative medical treatment is to stabilize the patient's hemodynamic status, and if necessary, mechanical circulatory support can be used.[5]
  2. Ventricular septal rupture: Ventricular septal rupture can be observed as early as within 24 h after MI and is manifested by a sudden deterioration of clinical conditions, such as the development of HF or CS. Vasodilators combined with IABP may improve symptoms. Patients with unstable hemodynamics should undergo surgery as soon as possible (within 1 week), and CABG should be performed at the same time as repair of the ventricular septal defect. However, early surgery has a high fatality rate; therefore, patients with stable hemodynamics should be treated surgically after 3–4 weeks.[5]
  3. Rupture of papillary muscle or chordae tendineae: This complication usually occurs 2–7 days after MI, often leads to acute mitral regurgitation, and is manifested by sudden acute left cardiac failure, pulmonary edema, and even CS. Diuretics, vasodilators, and IABP may be used to reduce left ventricular afterload, and positive inotropic agents may be used if necessary. Surgery should be performed as soon as possible for such patients.[5]

Treatment of chronic heart failure after myocardial infarction

Treatment goals

The treatment goals of chronic HF after MI mainly include improving clinical symptoms and quality of life, slowing down or reversing cardiac remodeling, reducing readmission, and decreasing mortality.

Drug therapies


Patients with signs of fluid retention should be treated with diuretics (I, C),[4] often oral diuretics, including loop diuretics (e.g., furosemide, torsemide), thiazide diuretics (e.g., hydrochlorothiazide, indapamide), and potassium-sparing diuretics (amiloride, triamterene).[11] Long-term use of diuretics at relatively high doses may cause RAAS activation and electrolyte disturbances. Hence, maintenance doses are recommended, i.e., the minimum dose for long-term maintenance of the “dry-weight state” in patients.


Unless contraindicated, all patients with HF after MI should be treated with β-blockers (I, A).[4] In HFrEF patients with LVEF <40%, β-blockers should generally be administered at a low starting dose and escalated every 2–4 weeks to the target dose or maximum tolerated dose.[4],[8],[49]

Currently, metoprolol succinate,[50],[51] bisoprolol,[52] and carvedilol[52] are three drugs recommended by the guidelines for the treatment of HF, which can reduce mortality and/or hospitalization rates in HF patients.

Angiotensin-converting enzyme inhibitors

ACEIs are the backbone therapy of HFrEF. To investigate the efficacy of ACEIs in HF after MI, the AIRE Study included 2006 patients with HF after acute MI who were followed up for a mean of 15 months. The results showed that patients taking ramipril had a significant lower mortality and a 27% reduction in relative risk compared with those in the placebo control group. Analysis of secondary end points showed a 19% reduction in the risk of the composite end point of death, severe/refractory HF, MI, or stroke.[53] This study establishes the position of ACEI in the treatment of HF after MI. ACEIs (I, A) should be administered to all patients with HFrEF after MI unless contraindicated or intolerable.[4] For the application of ACEIs in patients with HF after MI, it is usually recommended to administer at a low starting dose and escalate gradually during follow-up to the target dose or maximum tolerated dose.

Angiotensin II receptor blockers

Patients intolerant to ACEIs therapy may be treated with ARBs instead (I, A).[4] Commonly used drugs include valsartan,[54] losartan,[55] and candesartan.[56] The OPTIMAAL Study[55] included 5477 patients with acute MI with HF or patients with Q-wave acute anterior wall infarction or re-infarction who were followed up for a mean of 2.7 ± 0.9 years. The results showed that there were no significant differences in the primary end point (all-cause mortality) and secondary end points (sudden death, fatal or nonfatal re-infarction, and all-cause hospitalization rate) between the losartan group and the captopril group, but losartan was better tolerated than captopril, with fewer discontinuations due to adverse drug reactions. The VALIANT Study[57] showed that valsartan was as effective as captopril in reducing mortality in patients with HF after MI. It is recommended to administer ARBs at a low starting dose and gradually increase to the recommended dose or maximum tolerated dose.

Angiotensin receptor neprilysin inhibitors

Sacubitril/valsartan was the first ARNI to block AT1 receptors and enhance the NPS by inhibiting angiotensin receptors and neprilysin.[58],[59] PARADIGM-HF[60] included 8399 patients with HF (NYHA class II–IV, LVEF ≤35%). Among them, 43.4% of the patients in the sacubitril/valsartan group and 43.1% in the enalapril group had a history of MI. At a mean follow-up of 27 months, compared with enalapril, sacubitril/valsartan further significantly reduced the risks of the primary end point (composite end point of cardiovascular death or hospitalization for HF) (hazard ratio [HR] = 0.80; 95% confidence interval [CI], 0.73–0.87; P < 0.001), predefined broader composite end points (including MI, stroke, and sudden death after cardiac resuscitation) (HR = 0.83; 95% CI, 0.76–0.90, P < 0.001), and post hoc coronary composite end point (including cardiovascular death, nonfatal MI, hospitalization for angina pectoris, or coronary revascularization) (HR = 0.83; 95% CI: 0.75–0.92, P < 0.001). The TRANSITION Study[61] further demonstrated good feasibility and safety of early application of sacubitril/valsartan in patients with acute HF after achieving relatively stable hemodynamics. Based on these data, sacubitril/valsartan should be preferred and used early in the treatment of HF after MI. For patients with symptomatic HFrEF after MI in NYHA functional class II–III, if ACEIs/ARBs can be tolerated, ARNIs may be considered to replace ACEIs/ARBs to further improve prognosis (I, B).[4] Depending on patient tolerability, the dose of sacubitril/valsartan should be doubled every 2–4 weeks until the target maintenance dose of 200 mg twice daily is reached.

Aldosterone receptor antagonists

During the long-term use of ACEIs or ARBs, there is an “escape phenomenon” of aldosterone. Thus, the administration of aldosterone receptor antagonists (commonly used are eplerenone[62] and spironolactone[63]) on top of RAAS inhibitors contributes to further inhibition of the adverse effects of aldosterone. The EPHESUS Study compared the effects of eplerenone and placebo on clinical outcomes of HF after MI.[62] After a mean follow-up of 16 months, the incidence rates of all-cause mortality, sudden cardiac death, and hospitalization for HF were significantly lower in the eplerenone group than in the control group. For all patients with LVEF ≤35% in NYHA functional class II–IV who have been treated with ACEIs (or ARBs or ARNIs) and β-receptor blockers and remain symptomatic, aldosterone receptor antagonists can be added (I, A).[4]


The SHIFT Study showed that the use of ivabradine improved left ventricular function and quality of life in patients with HFrEF, reducing the relative risk of cardiovascular death and hospitalization for worsening HF by 18%.[64] A subgroup analysis of Chinese patients showed a 44% reduction in this risk.[65] In patients with sinus rhythm and LVEF ≤35% in NYHA functional class II–IV, ivabradine (IIa, C) is recommended for patients with a heart rate ≥70 beats/min (IIa, B) after standard treatment with ACEIs/ARBs/ARNIs and β-blockers or patients with heart rate ≥70 beats/min and contraindications or intolerance to β-blockers.[4]

Other drugs

As a novel hypoglycemic agent, sodium-dependent glucose transporter 2 inhibitors have been proven to have cardiovascular protective effects. The DAPA-HF Study included 4744 patients with HFrEF (45% with diabetes and 44% with MI)[66],[67] who were randomized to receive dapagliflozin (10 mg qd) or placebo treatment. The primary end point was the composite end point of cardiovascular death, hospitalization for HF, and emergency treatment for HF. The study results showed that dapagliflozin could significantly reduce the incidence of the primary end point events, the risk of all-cause mortality, and the risk of cardiovascular death in patients with HFrEF.

Vericiguat is an orally administered soluble activator of guanylate cyclase. The VICTORIA Study included 5050 patients with chronic HFrEF who had a recent episode of decompensation. The patients were randomized to receive either vericiguat (target dose: 10 mg qd) or placebo on top of their standard treatment, with a median follow-up of 10.8 months. Vericiguat significantly reduced the risk of the composite endpoint of cardiovascular death or first hospitalization for HF by 10%, suggesting a benefit for patients with HFrEF.[68]

CK-1827452, a novel agent that directly activates myosin, also has the potential to improve cardiac function.[69],[70] The efficacy and safety of these agents in the treatment of HF after MI need further investigation. Other drugs such as digitalis, vasodilators (nitrates, hydralazine), drugs for improving energy metabolism (such as trimetazidine, coenzyme Q10, levocarnitine, and creatine phosphate), and qiliqiangxin capsules can improve clinical symptoms, cardiac function, and quality of life in patients with chronic HF,[8] but there is no conclusive evidence for the effects on the long-term and short-term clinical outcomes in patients with chronic HF after MI.

Nondrug therapies

  1. Mechanical ventilation, including noninvasive ventilator-assisted ventilation, endotracheal intubation, and artificial mechanical ventilation: This is indicated for patients undergoing cardiopulmonary resuscitation after cardiopulmonary arrest and those with concomitant type I or II respiratory failure. When the effect of conventional oxygen therapy (nasal catheter and mask) is unsatisfactory (respiratory rate >25 times/min, SpO2 <90%), noninvasive positive pressure ventilation (NIPPV) (II a, B) should be used as early as possible.[4] For patients whose conditions continue to deteriorate after active treatment (with disturbance of consciousness, abnormalities of respiratory rhythm, or respiratory rate <8 times/min, weak or disappearance of spontaneous breathing, a progressive increase of PaCO2) or those intolerant to NIPPV or contraindicatory to NIPPV treatment, invasive positive pressure ventilation (I, C) should be performed promptly with endotracheal intubation.[4]
  2. Blood purification therapy: Hemofiltration alone is indicated for patients with acute pulmonary edema who are resistant to loop diuretics and thiazide diuretics or those with serum sodium <110 mmol/L. Purification treatment such as hemodialysis is indicated for patients with a concomitant progressive decline in renal function and serum creatinine >500 μmol/L.
  3. IABP: IABP (I, A) can be given when acute MI leads to acute HF with hemodynamic disturbance and severe myocardial ischemia with CS, which cannot be corrected by drugs (I, A).[4],[72],[73]
  4. Ventricular mechanical-assist devices: Short-term ECMO or a ventricular assist pump can be used in patients without obvious remission after conventional treatment[4],[71]
  5. CRT: If there are the following indications in patients with HF after MI, at least 3 months after standard treatment, CRT is recommended (I, A): sinus rhythm, QRS duration ≥150 ms, LBBB, LVEF ≤35%, and HF symptoms.[4]
  6. ICD: For patients with ischemic heart disease, at least 40 days after MI and at least 90 days after revascularization, with expected survival time >1 year, with the cardiac function still at class II–III after more than 3 months of optimized drug treatment directed by guidelines, with LVEF ≤35%, and in good condition, ICD implantation is recommended to prevent sudden death and to reduce mortality (I, A).[4],[74]
  7. Revascularization: Compared with drug therapy alone, coronary revascularization has advantages in improving the survival rate of patients with ischemic HF.[75] However, the best revascularization strategy has not been determined. The cardiac team should carefully evaluate the patient's clinical condition, coronary anatomy, expected completeness of revascularization, myocardial viability, coexisting valvular disease, and comorbidities and determine whether to choose CABG or PCI.
  8. Treatment of ventricular aneurysm: Patients with refractory HF combined with ventricular aneurysm can be treated with ventricular aneurysm resection to remove the ventricular wall with contradictory motion and restore the left ventricular shape as much as possible.[76] PVR is a new technique for the treatment of patients with left ventricular aneurysm complicated with HF. It uses a novel left ventricular septal device (also known as a parachute device) to reduce the left ventricular diastolic and end systolic volumes and the systolic ventricular shunt to increase left ventricular ejection volume and improve cardiac function and clinical symptoms;[77],[78] however, its value in clinical application needs to be further tested.
  9. Heart transplantation: Heart transplantation is the last option for patients with severe HF who have severely impaired cardiac function and are unresponsive to other therapies.

  Management of Patients with Heart Failure after Myocardial Infarction Top

The management of patients with HF after MI is a complex and arduous task that involves multiple aspects of daily life. Standardized treatment and management for the population with a high risk of chronic HF can delay the progress of HF and the deterioration of cardiac function, resulting in an improved survival rate and quality of life.

Frequency and content of follow-up

Patients are recommended to be followed up every 2 weeks after discharge and every 1–2 months after the condition is stable for the measurement of blood pressure and heart rate and a clinical evaluation of cardiac function. Routine blood tests, renal function, electrolytes, natriuretic peptide, electrocardiogram, and echocardiography are recommended to be performed when necessary; it is best to review echocardiography every 3 months. Doctors need to adjust the treatment plan according to the inspection results and pay attention to the management of comorbidities.

Multidisciplinary management scheme

Patients should follow medical protocols, follow dietary and exercise recommendations, use medications according to their physician's advice, and change their lifestyle to obtain more benefits.

Lifestyle management

Rational diet: adhere to a low-sodium diet. Daily salt intake of 2–3 g is recommended for patients with mild HF and <2 g for those with moderate-to-severe HF. Furthermore, a maximum of 1.5–2 L of water per day is recommended for patients with severe HF. Patients are recommended to pay attention to maintaining smooth stools, weigh daily and monitor blood pressure and heart rate, quit smoking, pay attention to rest and not get tired, and avoid infection. At the same time, patients with a stable condition are encouraged to exercise appropriately, mainly based on daily physical activities, and exercise that would not induce HF symptoms is preferred; control hypertension, diabetes, and other risk factors for cardiovascular disorders.[79]

Health education

Popularize relevant medical knowledge, including diet, exercise, early detection and treatment of HF symptoms, and drug therapy. Teach HF patients and their families how to recognize HF symptoms and deterioration signs and improve patients' participation in self-management and treatment compliance.

Psychological education

It is conducive to relieve the conditions and reduce the frequency of acute HF attacks by guiding the patients to conduct psychological counseling in a planned manner, avoiding and coping with various psychosocial and behavioral problems in the course of the disease, and keeping a good mental state.

Exercise rehabilitation

Bed rest is the basic principle of treatment in the exacerbation of HF; however, long-term bed rest can lead to a series of complications. Patients should be encouraged to exercise properly after HF symptoms are improved. The indication of exercise rehabilitation is stable HF of NYHA functional class I–III. Contraindications include early acute coronary syndrome, malignant arrhythmia, high-grade atrioventricular block, acute myocarditis, infective endocarditis, acute HF, uncontrolled hypertension, severe aortic valve stenosis, hypertrophic obstructive cardiomyopathy, and intracardiac thrombus.

Exercise rehabilitation of patients with chronic HF is still in the developing stage in China. Clinicians should help patients establish confidence in long-term exercise through education, guide patients to exercise step by step, record the exercise plan and actual situation in detail, and gradually cultivate patients' habit of regular exercise training. Strenuous exercise and exercise after a heavy meal are prohibited. If any discomfort occurs during exercise (such as chest pain and dyspnea), the exercise should be stopped immediately. If the above symptoms are not significantly relieved after rest or administration of the drug, immediate medical consultation should be sought. Special attention should be paid to blood glucose monitoring in patients with HF complicated with diabetes.[37],[80]

Remote monitoring

Remote monitoring is more and more important for out-of-hospital management of patients with HF after MI, including remote home monitoring, an implantable hemodynamic monitoring system, mobile health technology, and a diary for patients with HF. Remote monitoring facilitates doctors in knowing changes in patients' conditions in time and directs adjustment of the out-of-hospital treatment regimen.[7] At present, remote home monitoring has been shown to significantly improve the quality of life of patients,[81] but its long-term clinical benefit still needs to be confirmed by large clinical studies. Patients can select the corresponding remote monitoring modes according to their medical conditions and their own wishes to participate in the disease management.

Role of heart failure centers

In 2017, China began a nationwide development and certification program of HF centers and successively promulgated the “Certification Standards of China Heart Failure Center” for standard and primary hospitals, which aims to promote the standardized diagnosis, treatment, and management of HF through the establishment of regional HF centers. The long-term follow-up of patients with HF after MI is an important part of the development of HF centers. With the help of HF centers, patients with HF after MI can be better managed both in-hospital and out of hospital, and quality of life and outcomes can then be improved.

HF is a common complication after MI. The occurrence of HF after MI significantly increases the mortality and readmission rate, seriously affects patients' quality of life, and brings a huge socioeconomic burden. At present, the disease burden of HF after MI is severe in China. The clinical outcomes of patients can be improved only by continuously strengthening the clinicians' awareness of prevention, diagnosis, treatment, and management of HF after MI. In this paper, key clinical topics of HF after MI are discussed and summarized, and the clinical diagnosis and treatment regimens, as well as management modes, are recommended. The above data should be verified and further optimized in future clinical practice.

Expert Group Members (sorted by the first letter of surname)

Jian An (Shanxi Cardiovascular Hospital, China), Jun Bu (Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, China), Ji-Yan Chen (Guangdong Provincial People's Hospital, China), Liang-Long Chen (Fujian Medical University Union Hospital, China), Yun-Dai Chen (Chinese People's Liberation Army General Hospital, China), Xiang Cheng (Union Hospital affiliated to Tongji Medical College of Huazhong University of Science and Technology, China), Hong-Liang Cong (Tianjin Chest Hospital, China), Xiao-Tong Cui (Zhongshan Hospital Fudan University, China), Wei Dong (Chinese People's Liberation Army General Hospital, China), Yu-Gang Dong (The First Affiliated Hospital of Sun Yat-sen University, China), Zhi-Min Du (The First Affiliated Hospital of Sun Yat-sen University, China), Wei-Yi Fang (Shanghai Chest Hospital, China), Guo-Sheng Fu (Sir Run Run Shaw Hospital Affiliated to Zhejiang University School of Medicine, China), Chuan-Yu Gao (Fuwai Central China Cardiovascular Hospital, China), Jun-Bo Ge (Zhongshan Hospital Fudan University, China), Ning Guo (First Affiliated Hospital of Xi'an Jiaotong University, China), Xiao-Gang Guo (The First Affiliated Hospital of Zhejiang University School of Medicine, China), Ben He (Shanghai Chest Hospital, China), Yong He (West China Hospital Sichuan University, China), Lang Hong (Jiangxi Provincial People's Hospital, China), Yu-Qing Hou (Southern Hospital of Southern Medical University, China), Lan Huang (Xinqiao Hospital Army Medical University, China), Yong Huo (Peking University First Hospital, China), Shao-Bin Jia (General Hospital of Ningxia Medical University, China), Jun Jiang (The Second Affiliated Hospital of Zhejiang University School of Medicine, China), Wei Jin (Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, China), Ze-Ning Jin (Beijing Tiantan Hospital Affiliated to Capital Medical University), China, Jun Jin (Xinqiao Hospital Affiliated to Army Medical University, China), Li-Wen Li (Guangdong Provincial People's Hospital, China), Bao Li (Second Hospital of Shanxi Medical University, China), Chun-Jian Li (Jiangsu Provincial People's Hospital, China), Jian-Ping Li (Peking University People's Hospital, China), Lang Li (The First Affiliated Hospital of Guangxi Medical University, China), Wei-Min Li (The First Affiliated Hospital of Harbin Medical University, China), Xin-Li Li (Jiangsu Provincial People's Hospital, China), Yan Li (Tangdu Hospital of Air Force Medical University, China), Chun Liang (Shanghai Changzheng Hospital, China), Hui-Liang Liu (Beijing Electric Power Hospital, China), Qiang Liu (Shenzhen Traditional Chinese Medicine Hospital, China), Shi-Ming Liu (The Second Affiliated Hospital of Guangzhou Medical University, China), Xue-Bo Liu (Tongji Hospital of Tongji University, China), Jing-Hua Liu (Beijing Anzhen Hospital Affiliated to Capital Medical University, China), Cheng-Zhi Lu (Tianjin First Central Hospital, China), Jian-Fang Luo (Guangdong Provincial People's Hospital, China), Shu-Zheng Lv (Beijing Anzhen Hospital Affiliated to Capital Medical University, China), Gen-Shan Ma (Zhongda Hospital Affiliated to Southeast University, China), Li-Kun Ma (Anhui Provincial Hospital, China), Yi-Tong Ma (The First Affiliated Hospital of Xinjiang Medical University, China), Sato Naoki (Kawaguchi Cardiovascular and Respiratory Hospital, Japan, China), Shao-Ping Nie (Beijing Anzhen Hospital Affiliated to Capital Medical University, China), Ju-Ying Qian (Zhongshan Hospital Fudan University, China), Chao-Hui Qiu (Tong Ren Hospital Shanghai Jiao Tong University School of Medicine, China), Chun-Guang Qiu (The First Affiliated Hospital of Zhengzhou University, China), Xin-Kai Qu (Huadong Hospital Affiliated to Fudan University, China) Yoshihiko Saito (Nara Medical University Hospital, Japan), Cheng-Xing Shen (Shanghai Sixth People's Hospital, China), Guo-Hai Su (Jinan Central Hospital Affiliated to Shandong University, China), Xi Su (Wuhan Asia Heart Hospital, China), Yi-Da Tang (Peking University Third Hospital, China), Jian-Hong Tao (Sichuan Provincial People's Hospital, China), Ling Tao (Xijing Hospital of Air Force Medical University, China), Hua Wang (Beijing Hospital, China), Jian-An Wang (The Second Affiliated Hospital of Zhejiang University School of Medicine, China), Jing-Feng Wang (Sun Yat-sen Memorial Hospital, Sun Yat-sen University, China), Le-Feng Wang (Beijing Chao-Yang Hospital, Capital Medical University, China), Li-Xia Wang (Henan Provincial People's Hospital, China), Lian-Sheng Wang (Jiangsu Provincial People's Hospital, China), Zhen-Xing Wang (Jiangsu Province Hospital of Chinese Medicine, China), Qiang Wu (Guizhou Provincial People's Hospital, China), Yong-Jian Wu (Fuwai Hospital, Chinese Academy of Medical Sciences, China), Ding-Cheng Xiang (General Hospital of the Southern Theater of the Chinese People's Liberation Army, China), Biao Xu (Drum Tower Hospital Affiliated to Nanjing University Medical School, China), Ya-Wei Xu (Shanghai Tenth People's Hospital, China), Jie-Fu Yang (Beijing Hospital, China), Qing Yang (Tianjin Medical University General Hospital, China), Zhu-Hua Yao (Tianjin People's Hospital, China), Bo Yu (The Second Affiliated Hospital of Harbin Medical University, China), Zai-Xin Yu (Xiangya Hospital Central South University, China), Zu-Yi Yuan (First Affiliated Hospital of Xi'an Jiaotong University, China), Hai-Tao Yuan (Shandong Provincial Hospital, China), Wei-Xian Yin (Cheng Hsin General Hospital, China), Chun-Yu Zeng (Army Characteristic Medical Center, China), He-Song Zeng (Tongji Hospital Affiliated to Tongji Medical College Huazhong University of Science and Technology, China), Hong Zhang (The First People's Hospital of Yunnan Province, China), Jin-Ying Zhang (The First Affiliated Hospital of Zhengzhou University, China), Jun-Jie Zhang (Nanjing First Hospital, China), Rui-Yan Zhang (Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, China), Zheng Zhang (The First Hospital of Lanzhou University, China), Zhi-Hui Zhang (The Southwest Hospital of Army Medical University, China), Jin-Gang Zheng (China-Japan Friendship Hospital, China), Jing-Min Zhou (Zhongshan Hospital Fudan University, China), Sheng-Hua Zhou (The Second Xiangya Hospital of Central South University, China), Yu-Jie Zhou (Beijing Anzhen Hospital Affiliated to Capital Medical University, China), Ye Zhu (West China Hospital of Sichuan University, China)

Academic Secretary

Jing-Min Zhou (Zhongshan Hospital Fudan University, China), Xiao-Tong Cui (Zhongshan Hospital Fudan University, China)

Financial support and sponsorship


Conflicts of interest

Jun-Bo Ge is the Editorial Board member of the journal.

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