Encyclopedia of Gerontology and Population Aging

Living Edition
| Editors: Danan Gu, Matthew E. Dupre

Myocardial Infarction

  • Li Lin
  • Cuntai ZhangEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-69892-2_1065-1



Myocardial infarction (MI) is defined by the presence of myocardial necrosis, formerly known as a heart attack (Ibanez et al. 2018; Ojha and Dhamoon 2019; Roffi et al. 2016; Saleh and Ambrose 2018). Acute myocardial infarction (AMI) is a condition characterized by ischemic injury and necrosis of the myocardial cells which usually occurs on the basis of coronary artery lesions. A sharp decrease or interruption in coronary blood supply triggers severe and persistent myocardial ischemia. After 6–8 weeks of AMI, chronic myocardial infarction is formed by scar tissue after gradual resorption of the necrotic myocardial tissue (Ibanez et al. 2018).


In 1910, Obraztsov and Strazhesko described the clinical features of AMI (Muller 1977). In 1966, Constantinitis et al. performed an autopsy on 16 AMI patients, showing that thrombosis was attributed to the plaque rupture site. Thrombosis formation was thus considered as the main cause of myocardial infarction (Saleh and Ambrose 2018). Since then, whether MI is caused by thrombosis has long been controversial. In 1980, DeWood et al. performed coronary angiography within 4 h after AMI. The results showed that 84% of patients showed complete occlusion of a coronary artery branch, finally validating that thrombus formation is the main cause of myocardial infarction (DeWood et al. 1980; Saleh and Ambrose 2018). An intensive understanding of the pathogenesis of MI has been achieved over the past 40 years. It has been found that thrombosis is not the only mechanism for the development of MI, Inflammation also contributes to the pathogenesis of acute coronary syndromes (Libby et al. 2014).

The etiology, diagnosis, classification, and treatment of MI have been constantly updated. The incidence of MI has changed with the increase in per capita income, average life expectancy, and the aging of the population. Several studies have shown that the incidence of STEMI has decreased and that of NSTEMI has increased (Roffi et al. 2016). However, the disease burden of MI is still high. In developed countries, more than one-third of all-cause deaths are attributed to cardiovascular disease each year (Yeh et al. 2010). MI causes approximately 2.4 million deaths/year in the United States and more than 1.48 million deaths/year in Europe (Nichols et al. 2014). In China, the number of MI patients increases by about 1.4 million/year (Zhou et al. 2016), and the annual number of deaths attributed to MI is about 1 million (Li et al. 2015; Yang et al. 2013). The incidence of MI event also increases as age increasing, 35% or 10% of MI occurs in persons 75 or 80 and older (Davis 2014). Meanwhile, age is also an independent predictor for complications, including a higher risk of bleeding, mechanical complications, heart failure, and death following an acute coronary event (Alexander et al. 2007).

Key Research Findings

Causes and Classification

Since 1970, the classification of MI has been evolved with a thorough understanding of the etiology. Initially, atherosclerosis and secondary inflammatory response were considered as the driving factors for thrombosis (Saleh and Ambrose 2018). Large and medium-sized arterial endothelial cells deposit with a large amount of low-density lipoprotein (LDL) which oxidizes to cause the release of inflammatory factors, enzymes, and intercellular adhesion molecules, subsequently initiating cascade response. Inflammatory cells such as monocytes, macrophages, and T lymphocytes get aggregated. Macrophages phagocytize and oxidize LDL to form foam cells which deposit in the intima. The smooth muscle cells in the middle membrane migrate to the inner membrane under continuous low-grade chronic inflammation stimulation, forming a fibrous cap with collagen fibers to cover the surface of the lipid nucleus. The vulnerable plaque is usually a thin fibrous cap containing a large number of inflammatory cells, which can be broken with macrophage infiltration and degradation of fibrous matrix. The release of lipid nucleus activates platelets and coagulation cascades to form thrombus, block blood vessels, and cause AMI in the corresponding blood supply area (Ambrose 2008; Borissoff et al. 2011; Libby 2013; Ross 1993) (see “Atherosclerosis”). According to the extent of MI, MI is categorized into transmural myocardial infarction (endocardium, myocardium, and epicardium involved myocardial necrosis) and nontransmural myocardial infarction (not all three abovementioned layers of the heart muscle are affected simultaneously). According to the ECG manifestations, MI is divided into Q-wave MI (pathologic Q waves in two contiguous leads, usually indicative of transmural myocardial infarction) and non-Q-wave MI (Ibanez et al. 2018; Saleh and Ambrose 2018). Pathological findings later confirmed that not all Q-wave MIs are transmural lesions. In 1990, definition of ST-elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (non-STEMI, NSTEMI) were employed. STEMI refers to ST-segment elevated in two or more adjacent ECG leads. Standard STEMI criteria applied to leads has various thresholds for the different regions, usually indicates criminal coronary occluded completely. NSTEMI refers to the MI presenting with ST-segment depression or other manifestations of myocardial ischemia, usually indicative of small branch occlusion, short-term reperfusion following coronary vascular occlusion, or collateral circulation established due to stable plaque-induced long-term vascular stenosis (Saleh and Ambrose 2018).

MI secondary to other diseases was increasingly observed thereafter. For example, spontaneous coronary dissection, in situ thrombosis, Kawasaki’s syndrome, Takayasu’s arteritis, giant cell arteritis, etc. Therefore, in 2007, the American Heart Association and the European Society of Cardiology issued a joint statement, which classified MI into five types according to the etiology of MI: spontaneous type 1 MI is related to primary coronary events (coronary plaque rupture, ulcers, fissures, erosion, or dissection) with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequently myocardial necrosis; type 2 MI is secondary to myocardial ischemia resulting from increased oxygen demand or decreased supply (for example, coronary spasm, anemia, hyperthyroidism, and arrhythmia); type 3 MI is linked to sudden cardiac death (symptoms suggestive of myocardial ischemia accompanied by presumed new ischemic ECG changes or ventricular fibrillation, but die before blood samples for biomarkers can be obtained, or before increase in cardiac biomarkers can be identified, or MI is detected by autopsy examination); type 4a MI, Myocardial infarction associated with percutaneous coronary intervention; type 4b MI, stent/scaffold thrombosis associated with percutaneous coronary intervention; type 4c MI, restenosis associated with percutaneous coronary intervention; type 5 MI, Myocardial infarction associated with coronary artery bypass grafting (Ibanez et al. 2018; Saleh and Ambrose 2018; Thygesen et al. 2018, 2007). The evolution of MI classification also reflects the understanding of MI mechanism and the evolution of treatment strategies.

Clinical Manifestations and Diagnosis

Previous diagnosis of MI remains largely based on three manifestations including ischemic chest discomfort, ECG changes, and elevated levels of serum myocardial injury markers. The diagnosis can be done with at least two items. Ischemic chest discomfort is the most prominent clinical symptom in most MI patients. The discomfort characteristics vary in terms of properties, location, duration, frequency, and precipitating and alleviation factors. Typical ischemic pain most commonly occurs in the posterior middle-lower section of the sternum. It can also occur in other atypical regions including the left anterior region, left parasternal region, anterior cervical region, lower jaw, and upper abdomen, etc. The pain may radiate to the left arm, the fingertip, and the left neck to shoulder. Heavy, pressure or squeezing pain may last for hours to days without any obvious predisposing factors or not related to exercise. The pain is usually accompanied by nausea, vomiting, sweating, weakness, breathing difficulties, restless fears, and other symptoms and cannot be relievable by resting or nitroglycerin (see “Ischemic Heart Disease”). However, the above symptoms may be atypical in the elderly and diabetic patients who may present with a painless MI associated with a worse prognosis. Physical examination is usually unremarkable or shows altered blood pressure and gallop rhythm, etc. Middle and late-stage murmurs at the cardiac apex can be heard when mitral papillary muscle dysfunctions or ruptures. The anterior MI may be accompanied by sympathetic overactivity while parasympathetic hyperactivity is accompanied by the inferior MI (Ibanez et al. 2018; Roffi et al. 2016).

According to the 2015 European Society of Cardiology (ESC) NSTE-ACS guidelines and the 2017 ESC STEMI guidelines, the diagnosis of MI requires a combination of multiple criteria. The value of increased myocardial injury biomarkers (high-sensitivity troponin, hs-cTn) should at least above the 99th percentile of the upper reference limit, and include at least one of the following: (1) symptoms of ischemia; (2) new or presumed new significant ST-T wave changes or left bundle branch block on 12-lead ECG; (3) development of pathological Q waves on ECG; (4) imaging evidence of new or presumed new loss of viable myocardium or regional wall motion abnormality; (5) intracoronary thrombus detected on angiography or autopsy (Ibanez et al. 2018; Roffi et al. 2016).

Cardiac troponin isoforms I and T (cTnI/T) are highly sensitive and specific for myocardial injury and have become the preferred diagnostic marker. The emergence of high-sensitivity troponin T increases the diagnostic positive rate of NSTEMI by 20% and concurrently reduces the false-positive rates for the diagnosis of unstable angina. In the 2015 ESC NSTE-ACS guidelines, hs-cTn changes within 1 or 3 h are used to rule out NSTEMI. Combining hs-cTn measurements with ECG findings may be used to identify MI. In the clinical setting, two consecutive hs-cTn levels (at least 1-h interval) below the upper limit of normal range suggests a negative predictive value close to 98% and a positive predictive value of 75–80%. Creatine kinase isoenzyme (CK-MB) is similar to cTn. CK-MB/total CK ratio of 2.5% or more is a specific indicator of myocardial injury, but relatively insensitive for the detection of smaller myocardial infarct size. Moreover, cTn is the preferred biomarker for the diagnosis of AMI in both European and American guidelines. Metabolic circulatory clearance of cTn requires 7–10 days and maybe longer for those with renal insufficiency. Hence, early ischemic events may be missed unless initially declined cTn increases again. Although CK-MB can be used to detect recurrent myocardial injury. However, small-sized recurrent MI may be undetectable because CK-MB is not as sensitive as cTn (Ibanez et al. 2018; Jneid et al. 2012; Morrow et al. 2007; Roffi et al. 2016).

Patients with STEMI usually have dynamic ECG changes. In the hyperacute stage, peaked T-wave is asymmetrical. In the acute phase, there are at least two adjacent leads with ST-segment elevation in the absence of left ventricular hypertrophy or left bundle branch block, male (<40 years old) ≥2.5 mm, male (≥40 years old) ≥2 mm, female V2–V3 lead ≥1.5 mm and/or other leads ≥1 mm. For patients with anterior MI, it is recommended to record the right chest lead (V3R and V4R) to determine if the right ventricular MI exists. ST-segment depression in leads V1–V3 indicates myocardial ischemia, especially when the terminal T wave is positive. The V7–V9 lead should be recorded at the same time. Posterior MI should be considered if the ST-segment elevation is ≥0.5 mm. In the next few hours, the ST segment obviously rises and forms a monophasic arched-back curve with T wave, and pathologic Q wave appears within 2 days (Q wave width ≥0.04 s; Q wave amplitude >1/4 of the R wave in the same lead). The ST segment gradually falls back to the baseline within 2 weeks if no timely intervention is given. The T wave then becomes flatten or inverted. After a few months, the T wave is symmetrically inverted and may persistently exist. NSTEMI has no obvious dynamic ECG changes but may have transient abnormalities in ST-segment and T wave, which represents myocardial ischemia (Ibanez et al. 2018) (see “Electrocardiogram Abnormalities”).

Other imaging techniques such as echocardiography can be used to assess left ventricular function, wall motion, and related mechanical complications. Radionuclide examination (SPECT, PET), myocardial magnetic resonance can be used to assess myocardial metabolic changes and myocardial activity. Multiple auxiliary examinations are used in combination with the diagnosis of MI and differential diagnosis with related diseases (acute abdomen, aortic dissection, pulmonary embolism, etc.).

Most elderly patients present with dyspnea as the main symptom. For this subgroup, more attention should be paid to the presence of consciousness disturbance, hypotension, and other heart failure signs such as jugular vein engorgement and pulmonary edema. Caution should be taken for those with remarkable but relieved chest pain after oral nitroglycerin. Dynamic ECG in this condition is still necessary because the ST segment deviation is relatively low and atypical for the elderly. Hypersensitive cardiac troponin is sensitive for the diagnosis of early MI in the elderly, but its specificity is lower than that in younger patients, and elevated troponin levels are associated with other diseases except ACS (Alexander et al. 2007; Varghese and Wenger 2018).

Risk Stratification

The risk assessment for STEMI includes the degree of myocardial damage, successful reperfusion rates, and related clinical signs such as advanced age, increased heart rate, hypotension, Killip grade > Grade I, prior history of MI, increased serum creatinine levels, heart failure or peripheral arterial disease, etc. (Reed et al. 2017). The Global Registry of Acute Coronary Events (GRACE) risk score is widely used and is also applicable for NSTEMI (de Araujo Goncalves et al. 2005). The GRACE risk scoring includes age, heart rate, blood pressure, creatinine, Killip grade, and risk factors (cardiac arrest at admission, ST-segment changes, elevated myocardial markers, etc.). Patients are divided into three groups as follows: low risk ≤108 points; moderate risk = 109–140 points; high risk >140 points. The GRACE risk score is associated with hospital mortality.

NSTEMI risk stratification: (1) very high risk: hemodynamic instability or cardiogenic shock; recurrent or ongoing chest pain refractory to medical treatment; life-threatening arrhythmias or cardiac arrest; mechanical complications of MI (papillary muscle dysfunction, ventricular aneurysm, etc.); acute heart failure; recurrent dynamic ST-T wave changes (especially intermittent ST-segment elevation); (2) High risk: rise or fall in cardiac troponin compatible with MI; dynamic ST- or T-wave changes (with symptoms or asymptomatic); GRACE score >140; (3) Intermediate risk: diabetes mellitus; renal insufficiency (eGFR <60 mL/min/1.73 m2); LVEF <40% or congestive heart failure; early post-infarction angina; prior PCI; prior CABG; GRACE score 109–140; (4) Low risk: without any of the above characteristics (Roffi et al. 2016).

Treatment and Prognosis

NSTEMI patients with very high risk have dismal short-term and long-term prognosis. Invasive revascularization is recommended within 2 h of First Medical Contact (FMC) regardless of ECG or biomarker findings. For patients holding at least one high-risk factor, an early invasive strategy is recommended (i.e., coronary angiography within 24 h). For patients with at least one moderate risk factor, recurrent symptom, or confirmed myocardial ischemia by noninvasive examination, coronary angiography should be performed within 72 h to rule out acute cardiovascular events. Bleeding risk should be assessed based on the HAS-BLED score in patients undergoing PCI. Patients with low to moderate bleeding risk (HAS-BLED = 0–2) should receive triple antithrombotic therapy (aspirin, clopidogrel, and vitamin K antagonist/new oral anticoagulant), switch to dual antithrombotic therapy (aspirin/clopidogrel and vitamin K antagonist/new oral anticoagulant) after 6 months, and a year later maintain single drug the whole lifetime. For patients with high bleeding risk (HAS-BLED ≥3 points), triple antithrombotic therapy could be reduced to double antithrombotic therapy after 4 weeks of maintenance. The single drug should also remain for a lifetime after 1 year (Reed et al. 2017; Roffi et al. 2016).

For STEMI patients, an electrocardiogram should be performed within 10 min of FMC for a definite diagnosis of MI. Reperfusion therapy is recommended if the patient’s symptoms occur within 12 h. If the patient could be transferred to a cardiac center with qualified PCI surgery necessities within 2 h, PCI is preferred, and reperfusion should be completed within 90 min. If the patient cannot reach the cardiac center within 2 h, the preferred thrombolytic strategy is recommended, and a loading dose of thrombolytic drugs should be given within 10 min (half dose of tenecteplase recommended for those ≥75 years). After transferring to the cardiac center, assessment of whether a rescue or elective PCI is necessary should be carried out. For post-PCI patients, unless presence of high-risk of bleeding, triple antithrombotic therapy is recommended for at least 6 months followed by double antithrombotic therapy for at least 12 months, and then a single drug for life-long time. For those with high bleeding risk, a combination with PPI (proton pump inhibitor) is suggested. For patients with high ischemic risk and absence of obvious bleeding, double antithrombotic therapy can be extended to 3 years before single drug maintenance (Ibanez et al. 2018; Reed et al. 2017; Windecker et al. 2014).

Emergent coronary artery bypass grafting (CABG) is suitable for patients with life-threatening extensive myocardial lesions or cardiac shock patients whose criminal arteries have been identified but difficult to access by PCI access. Emergent CABG is usually not recommended for STEMI patients with failed PCI or complete coronary occlusion that is unsuitable for PCI. In this condition, the benefit of surgical revascularization is uncertain. The myocardial salvage rate is relatively low, and the risk of surgery is relatively high because of the delayed reperfusion. Studies have shown that patients who underwent surgery on the day of MI have the highest mortality. However, high-risk patients with hemodynamic deterioration or recurrent ischemic events (extensive MI or recurrent ischemia caused by key coronary stenosis) should be operated as soon as possible. For other patients with stable status, an acute phase of at least 3–7 days (tigril discontinued for at least 3 days; clopidogrel discontinued for at least 5 days; prasugrel discontinued for at least 7 days) should wait before surgery. Persistent oral aspirin without suspension is recommended (Ibanez et al. 2018).

In addition to reperfusion therapy and antithrombotic therapy, daily lifestyle intervention (smoking cessation, weight loss, exercise, etc.), controls of blood glucose, serum lipids and blood pressure, and regular drugs which could improve symptoms and prognosis (beta-blockers, angiotensin-converting enzymes inhibitors/ACEI, angiotensin II receptor antagonist/ARB, aldosterone receptor antagonist/MRA) should also attract enough attention. Oral beta-blockers are recommended for patients with heart failure and/or LVEF ≤40% with long-term use unless contradictive. It is recommended to initiate high-intensity statin therapy as soon as possible and maintain a long-term application unless there are contraindications. The therapeutic goal of LDL-C is <1.8 mmol/L (70 mg/dL), or at least 50% lower than baseline if the baseline LDL-C is between 1.8 and 3.5 mmol/L. In the absence of contraindications, ACEI/ARB should be considered within the first 24 h to all STEMI patients with evidence of heart failure, LV systolic dysfunction, diabetes, or an anterior infarct. MRAs are recommended for patients who have been treated with ACEI/ARBs and beta-blockers, but still accompanied by LVEF ≤40%, heart failure, or diabetes without renal insufficiency or hyperkalemia (Ibanez et al. 2018; Reed et al. 2017; Roffi et al. 2016).

It is noteworthy that there is no age limit for reperfusion therapy (Ibanez et al. 2018). The invasive strategy is more commonly seen in younger patients compared to the elderly. Studies showed that 67% of patients younger than 70 years old underwent coronary angiography and only 33% of those older than 80 years received invasive intervention. Life expectancy, comorbidity, quality of life, physical fitness, patient values, and potential risks should all be carefully assessed for patients older than 80 years before revascularization. The elderly usually take excessive antithrombotic drugs for a long-term, antithrombotic regimen for the elderly should be settled based on the patient’s weight and renal function. Meanwhile, dose of beta-blockers, ACEI/ARBs, and statins should be adjusted to prevent side effects (Alexander et al. 2007; Varghese and Wenger 2018). Studies have shown that age is a major predictor of 6-month hospitalization and mortality for NSTEMI patients, and debilitation is a strong independent predictor of hospital stay and 30-day mortality for elderly NSTEMI patients (Roffi et al. 2016).

Future Perspectives of Research

Substantial progress was made in the study of pathogenesis and treatment of MI over the past 50 years. Early intervention has become a global consensus. The treatment of myocardial infarction is constantly improving. For STEMI patients, the most effective treatment for preventing heart failure and reducing the size of MI is to perform timely reperfusion. New cardiac protection therapy is also constantly updated. Inhibiting mitochondrial permeability transition pores, therapeutic hypothermia, and intravenous metoprolol before PCI may reduce MI size (Bulluck et al. 2016; Koutsoukis and Kanakakis 2019; Papageorgiou et al. 2018). Therefore, other cardioprotective treatments needed to explore for reducing post-intervention complications such as reperfusion injury and no-reflow. The formation of atherosclerosis is also a chronic inflammatory process. Related studies have found anti-inflammatory therapy that interleukin-1β inhibitor Canakinumab has a cardiovascular protective effect. A moderate dose of Canakinumab can reduce secondary cardiovascular endpoint events (Ridker et al. 2017). Anti-inflammatory therapy as a novel target for cardiovascular disease treatment spurs more researchers to explore the role of inflammatory mechanisms in the development of cardiovascular disease, and more clinical evidence is needed to support the effectiveness of anti-inflammatory treatments in acute coronary syndromes. Advances in new drug development have shown that ARB and enkephalinase inhibitor/ARNi complex preparation LCZ696 (Sacubitril-Valsartan) ameliorated MI size and decreased serum cTnI levels in animal experiments. Similar effects have been shown in clinical trials, including reduction of hospitalization rate and cardiovascular deaths in patients with heart failure (Ishii et al. 2017; Jarcho 2019; Mapelli et al. 2019). The development of atherosclerosis involves autoimmune factors and immunotherapy such as vaccination may curb the formation of atherosclerosis. Several candidate antigens have been identified and validated in animal models (Kobiyama et al. 2019). In addition, gene therapy and stem cell therapy are promising for improving the prognosis of MI and reducing the mortality rate of AMI (Marotta et al. 2018; Parviz et al. 2018).

Billions of dollars are spent annually on new drug development and treatment strategies for cardiovascular disease. However, primary prevention has been largely under-recognized, even if timely and effective secondary prevention has been achieved, health education and nursing care are also crucial for improving prognosis and reducing morbidity. We should recognize the importance of the asymptomatic phase prior to the MI event. Attention should be drawn towards early identification and treatment of high blood pressure, smoking cessation, and LDL level control. Primary prevention especially health education cannot be ignored. Therefore, research on interventions or drugs related to primary prevention of coronary heart disease should also attract more attention of researchers.


Despite the continuous improvement in MI management strategies, MI remains a major cause of disease morbidity and mortality worldwide. Prompt diagnosis and risk stratification, reconstruction of myocardial perfusion, adjuvant treatment, establishment of secondary prevention, and monitoring of complications are the main contents of MI treatment. Guideline-obeyed treatment strategies and cooperation between medical staff and institutions contribute to the life-saving and improved prognosis for patients with MI (Frampton et al. 2018). For elderly patients, individualized treatment and nursing care based on a comprehensive assessment are recommended because of their unique psychological and social factors.



  1. Alexander KP, Newby LK, Cannon CP, Armstrong PW, Gibler WB, Rich MW, … Society of Geriatric Cardiology (2007) Acute coronary care in the elderly, part I: non-ST-segment-elevation acute coronary syndromes: a scientific statement for healthcare professionals from the American Heart Association Council on Clinical Cardiology: in collaboration with the Society of Geriatric Cardiology. Circulation 115(19):2549–2569.  https://doi.org/10.1161/CIRCULATIONAHA.107.182615
  2. Ambrose JA (2008) In search of the “vulnerable plaque”: can it be localized and will focal regional therapy ever be an option for cardiac prevention? J Am Coll Cardiol 51(16):1539–1542.  https://doi.org/10.1016/j.jacc.2007.12.041CrossRefGoogle Scholar
  3. Borissoff JI, Spronk HM, ten Cate H (2011) The hemostatic system as a modulator of atherosclerosis. N Engl J Med 364(18):1746–1760.  https://doi.org/10.1056/NEJMra1011670CrossRefGoogle Scholar
  4. Bulluck H, Yellon DM, Hausenloy DJ (2016) Reducing myocardial infarct size: challenges and future opportunities. Heart 102(5):341–348.  https://doi.org/10.1136/heartjnl-2015-307855CrossRefGoogle Scholar
  5. Davis LL (2014) Cardiovascular issues in older adults. Crit Care Nurs Clin North Am 26(1):61–89.  https://doi.org/10.1016/j.ccell.2013.10.004CrossRefGoogle Scholar
  6. de Araujo Goncalves P, Ferreira J, Aguiar C, Seabra-Gomes R (2005) TIMI, PURSUIT, and GRACE risk scores: sustained prognostic value and interaction with revascularization in NSTE-ACS. Eur Heart J 26(9):865–872.  https://doi.org/10.1093/eurheartj/ehi187CrossRefGoogle Scholar
  7. DeWood MA, Spores J, Notske R, Mouser LT, Burroughs R, Golden MS, Lang HT (1980) Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 303(16):897–902.  https://doi.org/10.1056/NEJM198010163031601CrossRefGoogle Scholar
  8. Frampton J, Devries JT, Welch TD, Gersh BJ (2018) Modern management of ST-segment elevation myocardial infarction. Curr Probl Cardiol.  https://doi.org/10.1016/j.cpcardiol.2018.08.005
  9. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, … ESC Scientific Document Group (2018) 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: the Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 39(2):119–177.  https://doi.org/10.1093/eurheartj/ehx393
  10. Ishii M, Kaikita K, Sato K, Sueta D, Fujisue K, Arima Y, … Tsujita K (2017). Cardioprotective effects of LCZ696 (sacubitril/valsartan) after experimental acute myocardial infarction. JACC Basic Transl Sci 2(6):655–668.  https://doi.org/10.1016/j.jacbts.2017.08.001
  11. Jarcho J (2019) PIONEERing the in-hospital initiation of sacubitril–valsartan. N Engl J Med 380(6):590–591.  https://doi.org/10.1056/NEJMe1900139CrossRefGoogle Scholar
  12. Jneid H, Anderson JL, Wright RS, Adams CD, Bridges CR, Casey DE Jr, … Zidar JP (2012) 2012 ACCF/AHA focused update of the guideline for the management of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 focused update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 60(7):645–681.  https://doi.org/10.1016/j.jacc.2012.06.004
  13. Kobiyama K, Saigusa R, Ley K (2019) Vaccination against atherosclerosis. Curr Opin Immunol 59:15–24.  https://doi.org/10.1016/j.coi.2019.02.008CrossRefGoogle Scholar
  14. Koutsoukis A, Kanakakis I (2019) Challenges and unanswered questions in STEMI management. Hell J Cardiol.  https://doi.org/10.1016/j.hjc.2019.01.001
  15. Li J, Li X, Wang Q, Hu S, Wang Y, Masoudi FA, … China PCG (2015) ST-segment elevation myocardial infarction in China from 2001 to 2011 (the China PEACE-Retrospective Acute Myocardial Infarction Study): a retrospective analysis of hospital data. Lancet 385(9966):441–451.  https://doi.org/10.1016/S0140-6736(14)60921-1
  16. Libby P (2013) Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med 368(21):2004–2013.  https://doi.org/10.1056/NEJMra1216063CrossRefGoogle Scholar
  17. Libby P, Tabas I, Fredman G, Fisher EA (2014) Inflammation and its resolution as determinants of acute coronary syndromes. Circ Res 114(12):1867–1879.  https://doi.org/10.1161/CIRCRESAHA.114.302699CrossRefGoogle Scholar
  18. Mapelli M, Vignati C, Paolillo S, De Martino F, Righini F, Agostoni P (2019) Sacubitril/valsartan can improve exercise performance in systolic chronic heart failure patients: a case report. Curr Med Res Opin 35(Suppl 1):3–5.  https://doi.org/10.1080/03007995.2019.1576480CrossRefGoogle Scholar
  19. Marotta P, Cianflone E, Aquila I, Vicinanza C, Scalise M, Marino F, … Torella D (2018). Combining cell and gene therapy to advance cardiac regeneration. Expert Opin Biol Ther 18(4):409–423.  https://doi.org/10.1080/14712598.2018.1430762
  20. Morrow DA, Cannon CP, Jesse RL, Newby LK, Ravkilde J, Storrow AB, … National Academy of Clinical Biochemistry (2007) National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: clinical characteristics and utilization of biochemical markers in acute coronary syndromes. Circulation 115(13):e356–375.  https://doi.org/10.1161/CIRCULATIONAHA.107.182882
  21. Muller JE (1977) Diagnosis of myocardial infarction: historical notes from the Soviet Union and the United States. Am J Cardiol 40(2):269–271CrossRefGoogle Scholar
  22. Nichols M, Townsend N, Scarborough P, Rayner M (2014) Cardiovascular disease in Europe 2014: epidemiological update. Eur Heart J 35(42):2929.  https://doi.org/10.1093/eurheartj/ehu378CrossRefGoogle Scholar
  23. Ojha N, Dhamoon AS (2019) Myocardial infarction. StatPearls, Treasure IslandGoogle Scholar
  24. Papageorgiou N, Briasoulis A, Tousoulis D (2018) Ischemia–reperfusion injury: complex pathophysiology with elusive treatment. Hell J Cardiol 59(6):329–330.  https://doi.org/10.1016/j.hjc.2018.11.002CrossRefGoogle Scholar
  25. Parviz Y, Waleed M, Vijayan S, Adlam D, Lavi S, Al Nooryani A, … Stone GW (2018) Cellular and molecular approaches to enhance myocardial recovery after myocardial infarction. Cardiovasc Revasc Med.  https://doi.org/10.1016/j.carrev.2018.05.021
  26. Reed GW, Rossi JE, Cannon CP (2017) Acute myocardial infarction. Lancet 389(10065):197–210.  https://doi.org/10.1016/S0140-6736(16)30677-8CrossRefGoogle Scholar
  27. Ridker PM, MacFadyen JG, Thuren T, Everett BM, Libby P, Glynn RJ, Cantos Trial Group (2017) Effect of interleukin-1beta inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial. Lancet 390(10105):1833–1842.  https://doi.org/10.1016/S0140-6736(17)32247-XCrossRefGoogle Scholar
  28. Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F, … ESC Scientific Document Group (2016) 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J 37(3):267–315.  https://doi.org/10.1093/eurheartj/ehv320
  29. Ross R (1993) The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 362(6423):801–809.  https://doi.org/10.1038/362801a0CrossRefGoogle Scholar
  30. Saleh M, Ambrose JA (2018) Understanding myocardial infarction. F1000Res 7.  https://doi.org/10.12688/f1000research.15096.1
  31. Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction, Jaffe AS, Apple FS, … Al-Attar N (2007) Universal definition of myocardial infarction. Circulation 116(22):2634–2653.  https://doi.org/10.1161/CIRCULATIONAHA.107.187397
  32. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, … Executive Group on behalf of the Joint European Society of Cardiology/American College of Cardiology/American Heart Association/World Heart Federation Task Force for the Universal Definition of Myocardial Infarction (2018) Fourth universal definition of myocardial infarction (2018). Circulation 138(20):e618–651.  https://doi.org/10.1161/CIR.0000000000000617
  33. Varghese T, Wenger NK (2018) Non-ST elevation acute coronary syndrome in women and the elderly: recent updates and stones still left unturned. F1000Res 7.  https://doi.org/10.12688/f1000research.16492.1
  34. Windecker S, Hernandez-Antolin RA, Stefanini GG, Wijns W, Zamorano JL (2014) Management of ST-elevation myocardial infarction according to European and American guidelines. EuroIntervention 10(Suppl T):T23–T31.  https://doi.org/10.4244/EIJV10STA5CrossRefGoogle Scholar
  35. Yang G, Wang Y, Zeng Y, Gao GF, Liang X, Zhou M, … Murray CJ (2013) Rapid health transition in China, 1990–2010: findings from the Global Burden of Disease Study 2010. Lancet 381(9882):1987–2015.  https://doi.org/10.1016/S0140-6736(13)61097-1
  36. Yeh RW, Sidney S, Chandra M, Sorel M, Selby JV, Go AS (2010) Population trends in the incidence and outcomes of acute myocardial infarction. N Engl J Med 362(23):2155–2165.  https://doi.org/10.1056/NEJMoa0908610CrossRefGoogle Scholar
  37. Zhou M, Wang H, Zhu J, Chen W, Wang L, Liu S, … Liang X (2016) Cause-specific mortality for 240 causes in China during 1990–2013: a systematic subnational analysis for the Global Burden of Disease Study 2013. Lancet 387(10015):251–272.  https://doi.org/10.1016/S0140-6736(15)00551-6

Copyright information

© Springer Nature Switzerland AG 2020

Authors and Affiliations

  1. 1.Division of Cardiology, Department of Internal MedicineTongji Medical College, Tongji Hospital, Huazhong University of Science and TechnologyWuhanChina

Section editors and affiliations

  • Xiao-Li Tian
    • 1
  1. 1.Human Aging Research Institute (HARI), School of Life ScienceNanchang UniversityNanchangChina