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Table of Contents
Year : 2019  |  Volume : 2  |  Issue : 4  |  Page : 98-104

Diagnosis and management of acute myocardial infarction: An overview

1 Department of Cardiology, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang Province, China
2 Department of Cardiology, The First Teaching Hospital of China Three Gorges University, Yichang, Hubei Province, China
3 Department of Physiology, Basic Medical College of Jiamusi University, Jiamusi, Heilongjiang Province, China

Date of Submission12-Oct-2019
Date of Decision05-Nov-2019
Date of Acceptance08-Nov-2019
Date of Web Publication25-Feb-2020

Correspondence Address:
Dr. Lin-Lin Jia
Department of Physiology, Basic Medical College of Jiamusi University, Jiamusi, Heilongjiang Province, 154002
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/VIT.VIT_1_20

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Acute myocardial infarction (AMI) occurs when there is acute disruption of coronary blood flow, resulting in a sudden imbalance between myocardial oxygen demand and supply, which causes ischemia and necrosis. AMI accounts for the highest mortality rate of approximately 15% worldwide. The acute complications of AMI, including cardiac arrhythmias, tolls almost 50% deaths, which may occur on the way to the hospital. The effective treatment modalities for AMI include antianginal medications and reperfusion with thrombolytics (tissue plasminogen activator) or percutaneous coronary intervention (PCI). PCI is the established and widely used reperfusion technique in the management of AMI as thrombolytics are contraindicated in many patients. PCI is superior to thrombolytics with a higher reperfusion rate of approximately 90%, shorter hospital stay, and lowering the mortality rate. The intervention performed within 90 min of hospital arrival improves the clinical outcomes significantly. In this article, major updates in diagnosis and treatment modalities of AMI have been summarized, mainly focusing on the efficacy of PCI in improving the clinical outcomes.

Keywords: Acute myocardial infarction, clinical outcomes, percutaneous coronary intervention, thrombolytics (tissue plasminogen activator)

How to cite this article:
Dilip D, Lokendra K, Jia LL. Diagnosis and management of acute myocardial infarction: An overview. Vasc Invest Ther 2019;2:98-104

How to cite this URL:
Dilip D, Lokendra K, Jia LL. Diagnosis and management of acute myocardial infarction: An overview. Vasc Invest Ther [serial online] 2019 [cited 2021 Jan 18];2:98-104. Available from: https://www.vitonline.org/text.asp?2019/2/4/98/279225

  Introduction Top

Acute myocardial infarction (AMI) is a fatal urgent condition, in which there is sudden and decreased blood flow in coronary arteries causing abnormality in myocardial perfusion activity. AMI is a part of the spectrum called acute coronary syndrome (ACS), which includes unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).[1] AMI has a considerable impact on global health, affecting around 7.5 million persons each year with a mortality rate of around 15% worldwide.[2] The prevalence of AMI is three times more common in males than in females; however, many new cases of AMI are increasing in postmenopausal women. The prevalence also increases in elderly patients >70 years' age with a mortality rate of four times higher than in younger patients.[3],[4] The most common cause of death following AMI is ventricular fibrillation, which causes about 50% of deaths before reaching the hospital.[5] A significant increase in the incidence of AMI and related mortality is reported in many developing countries, mainly because of changes in dietary habits, sedentary lifestyle, smoking, and reduction in physical exercise.[6]

  Etiology Top

The significant risk factors for AMI include hypertension, hyperlipidemia, diabetes mellitus, tobacco smoking, and nonmodifiable risk factors such as age, gender, and family history of coronary artery disease.[7] The uncontrolled blood sugar level is the only risk factor with the worst outcomes and leads to an increase in cardiovascular-related mortality rate by 2- to 4-folds.[8],[9] High body mass index, high low-density lipoprotein with low high-density lipoprotein levels, and cigarette smoking correlate with acute coronary events and mortality.[10] The other emerging risk factors include metabolic syndrome, apoprotein B, lipoprotein (a), homocysteine, prothrombotic factor (fibrinogen), and pro-inflammatory factor (C-reactive protein) which are associated for developing myocardial infarction (MI).[11],[12] Psychological factors also correlate with the early precipitation of AMI. Acute anxiety states, anger, and depression have been shown to have negative impacts on cardiovascular outcomes.[13]

  Pathophysiology Top

Atherosclerosis is the major underlying cause for MI seen in more than 90% of cases. The risk of atheroma formation and pathogenesis is 40%–50% higher in the anterior descending branch of the left coronary artery (LAD). Similarly, 30%–40% atherosclerosis may occur in the right coronary artery and 15%–20% in the left circumflex artery.[14] Atherosclerosis results in a decrease in myocardial perfusion sufficient to cause the death of myocardial cells. The mismatch between myocardial oxygen demand and supply is often a result of the rupture of the fibrous cap of coronary atheroma. This exposes the underlying subendothelial tissue, leading to the thrombus formation and causing occlusion of the involved coronary artery.[15] The atherosclerotic plague with rich lipid core and thin fibrous cap easily gets ruptured, exposing the blood to thrombogenic factors, and activation of platelet and coagulation cascade. All these events initiate the inflammatory process within the myocardium, thereby precipitating the acute coronary episodes.[16],[17] Other conditions that cause this imbalance include coronary vasospasm, hypotension, valvular heart disease, and cardiomyopathy. AMI usually occurs in the morning time within few hours after awakening. The increased release of cortisol and catecholamines in morning hours causes sympathetic overactivity leading to an imbalance between myocardial oxygen demand and supply, ultimately infarction.[18]

  Clinical Presentation Top

The meticulous history taking from the patient may provide diagnostic clues during the initial phase of the presentation. Patients with typical AMI present with retrosternal chest pain described as heavy, squeezing, tightness, crushing in nature. This pain lasts for 30–60 min and often radiating to the left arm, neck, and lower jaw.[19] In addition, some patients have palpitation, sweating, nausea, and feeling of impending doom. Severe epigastric pain or discomfort may be seen in patients with inferior wall MI.[20] About 20% of patients may have silent MI in elderly or diabetic or postoperative patients and are asymptomatic misleading in diagnosis.[21] On examination, patients with AMI appear pale, sweaty with mild fever and cold peripheries. There may be no specific physical signs noted unless complications develop. Sinus tachycardia, S4 heart sound, and a raised JVP are the typical findings in AMI patients. About 25% of patients with anterior wall MI have features of sympathetic hyperactivity as tachycardia or hypertension. Similarly, about 50% of patients with inferior wall MI have manifestations of parasympathetic hyperactivity as bradycardia or hypotension.[22]

  Diagnosis Top

The initial evaluation for AMI includes history taking, clinical examination, and diagnostic tests. The initial investigation is ECG which can easily detect AMI based on ST-segment elevation (>1 mm elevation in two or more contiguous limb leads and >2 mm elevation in two or more contiguous precordial leads). This is also associated with ST-segment depression in reciprocal leads.[23] The electrocardiogram (ECG) is the only test that can distinguish between STEMI and NSTEMI as both have raised cardiac markers. Hyperacute symmetrical T waves are the early ECG findings of AMI. ST-segment depression in the anteroseptal precordial leads V1–V4 with R/S wave ratio greater than 1 in leads V1 or V2 predicts posterior wall MI. Thus, posterior leads V7–V9 must be used for detecting ST-segment elevation in the posterior leads.[24] STEMI can be considered when a new left bundle branch block without any secondary cause is seen.[25] Some patients with AMI also develop pathological Q-waves after a few days of infarction. Pathological Q wave is characterized by 0.04s in duration, >4 mm deep and ¼ of R-wave, which represents fully evolved MI.[26] Because of the increasing incidence of silent MI, ECG should be done in all patients older than 45 years and having any form of chest discomfort or new epigastric pain. A special notation is given for diffuse ST-segment depression in the precordial and limb leads along with ST-segment elevation more than 1 mm in aVR. There may be stenosis of LCA or proximal part of LAD with such findings.[27]

Cardiac biomarkers frequently used in the diagnosis of AMI include myoglobin, creatine kinase-myocardial band (CK-MB) and cardiac-specific troponin T, I. Myoglobin is the earliest biomarker to rise in AMI with no cardiac specificity. CK-MB, which is less specific for AMI than troponins tend to rise within 4–8 h, peak at 24 h and return to baseline by 48–72 h. CK-MB, however, is considered specific for reinfarcted cases. Troponins are competent biomarkers with higher specificity and prognostic values. They begin to rise in 4–6 h after MI, peak at 18–24 h and last for 7–10 days, which aids in diagnosis.[28],[29] The estimation of cardiac biomarkers at different periods like at presentation, 6–9 h later, and then at 12–24 h provides an appropriate treatment approach for AMI. In recent years, ischemia modified albumin (IMA) is considered as a reliable cardiac marker for the early detection of an ACS. IMA is produced by the alteration of human albumin due to ischemia. IMA become elevated within 6–10 min after ischemia, remains elevated up to 6–12 h, and returns to normal within 12–24 h. The main advantage of measuring IMA is that it provides us appropriate time in deciding treatment modality to halt the progression from ischemia to infarction.[30],[31] Furthermore, the use of IMA and troponins constitute an excellent combination to provide maximum benefits in the early diagnosis of ACS and its treatment.[32],[33]

Two-dimensional echocardiography detects infarct-associated regional wall motion abnormalities. However, it cannot distinguish STEMI from an old myocardial scar or severe ischemia.[34] It is particularly used in detecting complications of AMI like acute mitral insufficiency, ventricular septal rupture, thrombus or other valvular abnormalities, and guides in treatment modality.[35]

  Management Top

The preliminary management for patients with AMI aims in relieving pain, restoration of oxygen supply with the prevention and treatment of complications. As soon as AMI is diagnosed, supplemental oxygen is administered by nasal cannula to maintain the saturation >90%. Analgesics such as morphine sulfate and nitrates are given for pain relief. The loading dose of aspirin, clopidogrel, metoprolol, atorvastatin, enalapril is given immediately as they significantly lower the mortality rate.[36] Aspirin and clopidogrel are used as antiplatelet drugs that inhibit platelet aggregation. Several guidelines emphasized the marked decline in mortality with the combined use of antiplatelet medications as compared with aspirin alone.[37] Cardioselective beta-blockers are equally effective in lowering mortality by decreasing cardiac oxygen consumption and limiting the infarct size. ACEI/ARBS works by reducing preload and post-MI cardiac remodeling. They are primarily used for lowering mortality in patients with anterior wall MI or with ejection fraction <40%. Lipid-lowering drugs or statins inhibit the HMG CoA reductase enzyme and used in the acute setting of AMI. They promote plaque stabilization, reverse endothelial dysfunction, and decrease thrombogenicity.[38]

Reperfusion therapy with percutaneous coronary intervention (PCI) or thrombolytic (fibrinolytic) should be done in patients with STEMI or a new Left bundle branch block (LBBB) within 12 h of symptoms onset. Fibrinolysis has been a vital reperfusion strategy for decades. They are preferred, especially where PCI is unavailable or cannot be initiated within the recommended timeframe. The core element in fibrinolytic therapy is a door-to-needle time of <30 min, which has a direct impact on outcomes. The patients treated within 1–3 h also gets benefit from an approximately 3% reduction in mortality and can still be useful for up to 12 h.[39] Although fibrinolytic therapy is readily available, it provides reperfusion in a maximum of 80% of cases only. It is associated with high rates of recurrent ischemia and vascular reocclusion.[40] It cannot be administered in many patients because of several contraindications such as prior intracranial hemorrhage, intracranial malignancy, active bleeding, or bleeding diathesis. Other contraindications include ischemic stroke or head trauma in the past 3 months, severe uncontrolled hypertension, aortic dissection, and pregnancy. The main complications following fibrinolytic therapy include bleeding and reperfusion arrhythmias. Similarly, fibrinolysis is associated with a high risk of hemorrhagic stroke in elderly patients or with a history of hypertension and cerebrovascular disease.[41]

Anticoagulants like unfractionated heparin (UFH), low molecular-weight heparin (LMWH) are the adjuvant drugs used in patients undergoing PCI or fibrinolysis therapy. The rational use of anticoagulants has shown to decrease reinfarction and reocclusion following reperfusion therapy. UFH-bivalirudin or LMWH-enoxaparin can be used along with PCI, whereas LMWH is the best to be used with fibrinolytic.[42] Furthermore, patients receiving fibrinolytic should be administered with anticoagulation until PCI is done. If PCI is not available, anticoagulants should be continued for at least 2 days or the duration of admission up to 8 days.

GP IIb/IIIa inhibitors like abciximab, tirofiban are the most potent antiplatelets used as adjuvants in AMI undergoing PCI. These drugs have antagonist action on GP IIb/IIIa receptors and exhibit a negative effect on common pathways resulting in decreased platelet aggregation. The synergistic use of GP IIb/IIIa inhibitors with dual antiplatelet drugs and anticoagulants is found to be beneficial only at the time of PCI.[43] Patients receiving fibrinolytic are not benefitted with GP IIb/IIIa inhibitors.

The management of NSTEMI includes stabilization with oxygen and maintaining saturation above 90%. Medications used are morphine for pain control, aspirin, and clopidogrel to prevent clot propagation. Beta-blockers and nitrates are used as anti-ischemic drugs and LMWH as an anticoagulant. Studies have shown that GP IIb/IIIa inhibitors tend to reduce mortality in NSTEMI cases requiring coronary angioplasty. The management of NSTEMI differs from STEMI in that emergent reperfusion with fibrinolysis or PCI is not effective in NSTEMI patients. Reperfusion is considered only if pain persists despite medical treatment or hemodynamic deterioration occurs. Those patients with higher risk assessment calculations need to undergo early coronary intervention for better outcomes.[44]

In addition, a detailed history should be taken about the concomitant use of phosphodiesterase inhibitors like sildenafil within the last 24 h and tadalafil within the last 48 h. As the use of those drugs along with nitrates can cause severe fall in blood pressure that can be life-threatening.[45] Similarly, patients with inferior wall MI may also have hypotension due to right ventricular infarction.[46] For them, intravenous fluids are given along with above MI medications. Moreover, NSAIDs are not included in the AMI treatment protocol, as they have shown certain cardiac adverse effects.[47]

  Revascularization With Percutaneous Coronary Intervention Top

PCI is the most effective reperfusion technique widely used in the treatment of ACS, including STEMI. Andreas Gruentzig was the first scientist to introduce the concept of PCI in 1977 for revascularization of occluded coronary arteries as a replacement for cardiac bypass surgery.[48] Since then, PCI had gained wide popularity in reconstituting myocardial perfusion for obstructive coronary artery disease and treating complex lesions in unstable conditions.[49] This intervention involves advancing a balloon-tipped catheter at an intracoronary lesion site followed by balloon dilatation and stent implantation. Cardiac intervention has undergone remarkable progress in the last two decades.[50] The innovative idea of using coronary stents since 1994 has been reported to reduce the acute complications following PCI.

In addition, the further development of drug-eluting stents (DESs) in 2003 has substantially reduced the problem of restenosis, increasing the success rates of recanalization. These DESs slowly release anti-proliferative drugs directly into the plaque over a few months. In recent days, DESs are used in >90% of coronary angioplasty procedures.[51] With the advancement in catheter technique, PCI has now become superior to conventional medical treatment, including thrombolytic. PCI remains the cornerstone treatment modality for AMI in maximum cases.[52]

Trans-radial PCI has more indications as compared with femoral access PCI because of the reduced risk of vascular complications with a decrease in mortality.[53] Coronary angioplasty leads to a high reperfusion rate of approximately 90% and has only a few contraindications. The use of local anesthesia as a sedative has shortened the hospital stay up to 1 day of short duration.[54] The door-to-balloon time has been a promising element that is directly related to clinical outcomes and quality of care.[55] With the same baseline characteristics, patients in whom the intervention is done within 90 min is found to have better clinical outcomes. The longer door-to-balloon time has a direct association with a decline in quality of life, regardless of symptom onset to door time and regardless of associated risk factors.[56]

The intervention performed within 90 min of hospital arrival improves the clinical outcomes and reduces the mortality to <5% in the first 30 days.[57] Rates of rehospitalization are lower for recurrent UA after an early invasive approach. The death rate in admitted patients following PCI is found to be low regardless of age, gender, presence of ST elevation, diabetes, or renal failure.[58] The positive clinical outcome following PCI is reported to be higher even in elderly patients despite the higher mortality and complication rates.[59],[60] As a result of advanced reperfusion strategy, PCI has a better prognosis, improves the health-related quality of life over that provided by optimal medical therapy.[61],[62]

The main clinical indications for PCI include Acute STEMI, NSTEMI, unstable, and stable angina with hemodynamic deterioration. Various adjuvant drugs are used in AMI patients undergoing PCI to reduce the infarct size. These drugs promote the recanalization of coronary arteries and reperfusion of the coronary microcirculation. Antiplatelet drugs such as aspirin, clopidogrel or prasugrel, UFH, and GP IIb/IIIa inhibitors are the recommended drugs.[63]

PCI is not done in those patients who cannot tolerate antiplatelet therapy or have certain comorbid conditions that severely limit the lifespan. Both interventional cardiologists and cardiac surgeons should be jointly involved for CABG in patients with diabetes and complicated multivessel coronary artery diseases.[64] Complications following PCI are not frequently observed and tolls mortality rate of around 0.1%–0.3%. The possible complications following PCI include bleeding, procedure-related immediate complications, and contrast-induced nephropathy.[65] Complications such as reinfarction and stent thrombosis after the intervention may be seen in STEMI cases. Similarly, elderly patients >65 years, undergoing an emergency procedure or with ESRD have a higher risk of having complications following PCI.[66]

  Complications of Acute Myocardial Infarction Top

The most common complication of AMI is related to conduction abnormalities occurring in more than 90% of patients. Ventricular tachycardia and fibrillation may occur within the first hour, causing 50% deaths.[67] Amiodarone and lidocaine are generally used in the management of post-MI arrhythmias.[68] Another highly fatal complication is a cardiogenic shock that may occur in 7% of cases. Early PCI or CABG is the baseline treatment approach to reduce mortality.[69] Other complications include Dressler syndrome, papillary muscle rupture, mitral regurgitation, ventricular aneurysms, and ventricular septal rupture.[70] Early detection of these complications is very crucial for prompt medical or surgical management.

  Summary Top

AMI is the single emergent condition with the highest mortality rates worldwide. The mortality rate occurring within 1 year of AMI is about 10%. The effective treatment modalities for AMI include reperfusion with thrombolytics or PCI. PCI is the recommended strategy for achieving durable reperfusion in patients with STEMI as compared with fibrinolytic therapy. With the combination of catheter techniques and the development of new devices, the procedural outcomes of PCI have improved even in elderly patients, resulting in a lower occurrence of adverse cardiac events. As the guidelines for PCI highlights the door-to-balloon time of <90 min supported by various strengths of evidence, every heart care center and cardiologist need to rectify their treatment strategy. As a result, we can achieve maximum goals in reducing mortality and morbidity, which can be significant progress in the field of cardiac intervention.

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