Acute myocardial infarction
Last updated date: 30-Mar-2023
Originally Written in English
Acute Myocardial Infarction
In the industrialized world, acute myocardial infarction (MI) is one of the major causes of death. The disease affects quite three million individuals globally, with quite a million people dying annually in the United States. Non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI) are the two types of acute myocardial infarction. NSTEMI is similar to unstable angina. Cardiac markers, on the other hand, are not elevated in unstable angina.
Leading to a lack of oxygen, a MI causes permanent damage to the heart muscle. An MI can decrease diastolic and systolic function, making the patient vulnerable to arrhythmias. Furthermore, a MI can result in a variety of significant consequences. The aim is to maintain blood flow and reperfuse the heart. A better prognosis comes with the earlier treatment (less than 6 hours after symptoms beginning).
When two of the following criteria are met, a MI is diagnosed:
- Ischemia signs and symptoms
- A left bundle branch block (LBBB) or new ST-segment alterations
- On the ECG, there are pathogenic Q waves (a late sign of MI).
- A new regional wall motion abnormalities were discovered in imaging analysis.
- An intracoronary thrombus found after autopsy or angiography
Acute Myocardial Infarction Definition
The pathological definition of myocardial infarction (MI), sometimes known as a heart attack, is the permanent loss of myocardial cells induced by ischemia. In terms of clinical diagnosis, MI is a syndrome characterized by a set of symptoms, the most common of which is chest pain, which is accompanied by biochemical laboratory changes, electrocardiographic (ECG) changes, or findings on imaging modalities capable of detecting myocardial injury and necrosis.
According to American Heart Association (AHA), acute myocardial infarction is diagnosed when either of the following criteria:
- At least one value of cardiac biomarker readings (ideally utilizing cardiac troponin [cTn]) is above the 99th percentile of the upper reference limit and at least one of the following findings is required.
- Ischemia signs and symptoms
- Significant ST-segment-T wave changes that are new or considered to be new, or a new left bundle branch block (LBBB)
- On the ECG, pathologic Q waves develop.
- New evidence of viable myocardial loss or a new regional wall motion abnormality on imaging
- Angiography or autopsy detecting an intracoronary thrombus.
- Cardiac muscle loss with symptoms suggestive of myocardial ischemia and probable new ischemic changes or new BBB on ECG.
Types of Acute Myocardial Infarction
- Type 1: Caused by atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection in one or more coronary arteries with intraluminal thrombus, resulting in reduced myocardial blood supply or distal platelet emboli, and resulting in myocyte necrosis. There may or may not be underlying obstructive coronary artery disease in the patient.
- Type 2: MI caused by an increase in oxygen demand or a reduction in supply (e.g., coronary endothelial dysfunction, coronary artery spasm, coronary artery embolus, anemia, tachyarrhythmias, respiratory failure, hypertension, or hypotension).
- Type 3: Sudden, unexpected cardiac death before blood samples for biomarkers could be taken or before they appear in the circulation.
- Type 4a: Caused by primary coronary intervention. Biomarker values (cTn is recommended) that are more than 5 times the 99th percentile of the upper reference limit. Additionally, one or more of the following is required: angiographic loss of patency of a major coronary artery or a side branch or chronic sluggish flow or no flow or embolization; or proof of recent loss of viable myocardium or new regional wall motion abnormality by cardiac imaging.
- Type 4b: MI related to stent thrombosis as revealed by coronary angiography or autopsy in the presence of myocardial ischemia in combination with a rise and/or decline of cardiac biomarkers.
- Type 5: Related to open-heart surgery. Patients have cardiac biomarker values that are greater than 10 times the 99th percentile the upper normal limit. In addition, either
- New development of pathologic Q waves or new bundle branch block
- New graft or native coronary artery blockage that is angiographic-documented
- Recent loss of viable cardiac muscle or new regional wall motion abnormalities.
According to a WHO database review of death certificates, coronary artery disease (CAD) mortality in Japan was much lower than in the United States and Europe, and it had decreased by roughly 30% by the mid-1990s.
A considerable increase in CAD-related mortality has been observed in China, which is most likely due to an increase in cardiovascular disease risk factors, particularly smoking and dyslipidemia.
Other developing countries, such as India, Latin America, the Middle East, and Sub-Saharan Africa, are likely to have a major increase in the prevalence of CAD and related mortality, with an estimated 80 percent increase from about 9 million in 1990 to a predicted 20 million by 2020.
Acute Myocardial Infarction Pathophysiology
Myocardial Cell Death
The normal heart requires a steady supply of oxygen and nutrients, which is mostly delivered by the coronary circulation, in order to continue to function and properly pump blood to meet the demands of the body. If the blood flow to the myocardium does not meet demand, a condition known as myocardial ischemia occurs. If the imbalance persists, it sets off a chain reaction of cellular, inflammatory, and metabolic responses that eventually end in the irreversible death of heart muscle cells and MI.
Evolution of Myocardial Infarction
The severity of the myocardial injury is determined by the duration and level of metabolic demand at the time of the event, as well as the severity of compromised myocardial perfusion. Within 60 seconds, a severe loss of the cardiac muscle cell's capacity to contract can be noticed. If oxygen deprivation to the myocardium continues due to a lack of blood supply, permanent myocardial injury can occur in as little as 20 minutes and as long as several hours, depending on many factors such as the body's metabolic status and the availability of coronary collateral blood flow.
The restoration of blood flow to the damaged myocardium can sometimes result in further hypoxic cellular damage, a phenomenon known as reperfusion injury. A complicated interaction between oxygen free radicals and intracellular calcium causes myocardial damage and death, as well as a microvascular malfunction and lethal arrhythmias. The role of nitric oxide (an endothelium-derived relaxing factor) as a cardioprotective agent against reperfusion injury has been established, since nitric oxide helps to inactivate oxygen free radicals, thus alleviating the reperfusion injury process.
[H3] Stunning and Hibernation of Myocardium
Following an acute event to the myocardium, stunned myocardium is a situation of transitory left ventricular dysfunction. It happens when coronary blood flow is obstructed for a short period (5 to 15 minutes). Following the re-establishment of coronary blood flow, shocked myocardium usually lasts for hours or days. However, persistent ischemia causes a loss of contractile activity in the myocardium, which can be partial or complete. This is known as myocardial hibernation, and it can be reversed with revascularization.
The atheromatous plaque that causes acute MI forms in a multi-stage dynamic process. This process begins with artery intimal thickening, which is made up of vascular smooth muscles with very few or no inflammatory cells and can be seen shortly after birth. The creation of fibrous cap atheroma, which has a lipid-rich necrotic core surrounded by fibrous tissue, occurs as a result. A thin-cap fibroatheroma, also known as a vulnerable plaque, develops over time and is made up mostly of a massive necrotic core separated from the vascular lumen by a thin fibrous cap infiltrated by inflammatory cells and missing in smooth muscle cells, making it sensitive to rupture.
Acute Myocardial Infarction Etiology
The condition that causes the majority of acute myocardial infarction cases is atherosclerosis. An acute thrombus that obstructs atherosclerotic coronary. Coronary thrombosis is thought to be caused mostly by plaque rupture and erosion. Platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur as a result of plaque erosion or rupture, leading to coronary thrombosis and occlusion.
Flow dynamics and endothelial shear stress are implicated in the etiology of vulnerable plaque deposition inside the coronary vasculature. A considerable body of evidence suggests that the causative lesions in many cases are stenoses with a diameter of less than 70% and are located proximally within the coronary tree. Coronary atherosclerosis is most noticeable near artery branching points. Atheroma with a big lipid-rich core surrounded by a thinning fibrous cap is the causative lesions that are more prone to rupture.
Acute Myocardial Infarction Risk Factors
Non-modifiable Risk Factors
- Family history of early coronary artery disease
- Male-pattern baldness
Modifiable Risk Factors
- Smoking or other tobacco use
- Elevated cholesterol and triglycerides, including hereditary lipoprotein disorders
- Diabetes mellitus
- Obesity (abdominal obesity)
- Psychosocial stress
- Sedentary lifestyle and/or lack of exercise
- Reduced consumption of fruits and vegetables
- Poor oral hygiene
- Type A personality
- Elevated homocysteine levels
- Presence of peripheral vascular disease
Acute Myocardial Infarction Symptoms
In the days or even weeks leading up to a MI, patients may experience the following symptoms:
- Tight chest
The following are the hallmarks of typical pain in acute MI:
- For approximately half to one hour, severe and non-resolving
- Substernal pain and radiates to the neck, shoulder, and jaw, as well as down the left arm.
- A squeezing, hurting, burning, or even stabbing sensation is commonly described as a substernal pressure sensation.
- The symptom in some people is epigastric, with a sense of indigestion or fullness, as well as gas.
How to Diagnose Acute Myocardial Infarction?
Acute Myocardial Infarction ECG
The most critical test is an ECG, which should be performed within 10 minutes after the presentation.
The presence of ST-segment elevation of less than 1 mm in two or more consecutive leads subtending the damaged area is usually diagnostic for STEMI.
The presence of pathologic Q waves is not required for the diagnosis. Because ST-segment elevation can be modest, especially in the inferior leads (II, III, aVF), the ECG must be examined carefully. Sometimes the reader's attention is wrongly focused on leads with ST-segment depression. ST-segment elevation on ECG has a specificity of 90 percent and a sensitivity of 45 percent for identifying myocardial infarction if the symptoms are typical. Serial tracings (every 8 hours for 1 day, then daily) that demonstrate a slow evolution toward a stable, more typical pattern or the development of aberrant Q waves over several days tend to support the diagnosis.
After myocardial cell necrosis, cardiac enzymes (e.g., creatine kinase-MB isoenzyme [CK-MB]) and cell contents (e.g., troponin I, troponin T, myoglobin) are released into the bloodstream as cardiac markers (serum markers of myocardial cell injury). After an injury, the markers appear at different times and their levels decline at varying rates. The sensitivity and specificity of these markers for myocardial cell injury vary greatly, although troponins (cTn) are the most sensitive and specific, and are now the markers of choice. Several new, very sensitive, and accurate tests for cardiac troponin (hs-cTn) have recently become available.
A hs-cTn level should be measured on presentation and three hours later in patients suspected of developing a myocardial infarction (at presentation and 6 hours if using a standard cTn assay).
All laboratory tests should be evaluated in light of the disease probability at the time of the test. This is especially important for the hs-cTn assay because of its high sensitivity but also applies to all cTn assays.
The combination of coronary angiography and percutaneous coronary intervention is usually diagnostic. Urgent coronary angiography and PCI (primary PCI) are performed as soon as possible after the beginning of acute myocardial infarction. This method has reduced morbidity and mortality and improved long-term survival. When the time between pain and primary PCI is short (three to four hours), the infarction is frequently terminated.
Angiography is obtained urgently for patients with ST-elevation myocardial infarction, patients with persistent pain despite maximal medical therapy, and patients with complications (e.g., markedly elevated cardiac markers, presence of shock, acute mitral regurgitation, ventricular septal defect, unstable arrhythmias). Patients with uncomplicated NSTEMI whose symptoms have resolved typically undergo angiography within the earlier 24 to 48 hours of hospitalization to detect lesions which will require treatment.
Coronary angiography may be utilized after initial examination and therapy in patients who have signs of persistent ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias, or other abnormalities that imply ischemic episodes are recurring.
Acute Myocardial Infarction Treatment
Unless there is convincing proof to the contrary, all patients being transferred for chest pain should be treated as if the pain is ischemic in nature. Patients with hemodynamic instability or breathing difficulty should be transported by advanced cardiac life support–trained team if available.
The following are examples of particular prehospital care:
- Intravenous access, supplementary oxygen if oxygen saturation is less than 90%, and pulse oximetry.
- Immediate non-enteric-coated chewable aspirin administration on the way
- Nitroglycerin, taken sublingually or as a spray, for active chest discomfort.
- If available, telemetry and prehospital electrocardiography (ECG)
The majority of MI-related deaths occur early and are caused by primary ventricular fibrillation (VF). As a result, quick ECG monitoring, electric cardioversion in situations of VF, and rapid transport of the patient to allow for prompt coronary evaluation are the priorities.
Emergency Department and In-hospital Management
A targeted history and focused physical examination should be performed on all patients arriving at the emergency room with symptoms suggestive of acute myocardial infarction (MI). In addition to obtaining intravenous (IV) access, a 12-lead electrocardiogram (ECG) assessed by an experienced physician should be conducted within 10 minutes of arrival.
Supplemental oxygen is indicated only for patients who are breathless, hypoxic (oxygen saturation < 90%), or who present with heart failure.
Unless there’s a proven history of aspirin allergy, all patients with ACS should use non-enteric-coated chewable aspirin in a dose of at least 162 to 325 mg. Patients who have aspirin intolerance should still be given aspirin at the time of hospital admission.
Nitrates are powerful vasodilators that work primarily to relax the veins. Reduced venous blood return to the heart (i.e., lower ventricular preload) is the outcome of systemic venodilation, which reduces the workload of the heart, lowers oxygen demand, and lowers ischemic symptoms.
- Analgesics (painkillers)
Symptomatic IV morphine should be used to treat refractory or severe pain.
For patients with a clinical manifestation of STEMI within 12 hours of symptom initiation and prolonged ST-segment elevation or new or suspected new left bundle branch block (LBBB), early mechanical intervention (percutaneous coronary angioplasty) or pharmacologic reperfusion should be performed as soon as possible. Additionally, if there’s clinical and/or ECG evidence of continuous ischemia, it’s fair to think about an early reperfusion strategy for patients who come after quite 12 hours, with primary PCI being the preferable technique for this group.
1. Percutaneous coronary angioplasty
PCI is described as an emergency percutaneous coronary intervention without prior fibrinolytic treatment in the setting of STEMI. It is the recommended reperfusion approach in STEMI patients if it can be done quickly, within clinical practice guidelines–mandated periods (90 minutes of presentation), and in high-volume centers with experienced interventional cardiologists and professional support staff.
Fibrinolysis is an important reperfusion method, especially in situations where primary PCI is not possible within the recommended time frames for STEMI patients. The effectiveness of fibrinolytic therapy in STEMI patients is well established, with the greatest benefit found when given early (within 12 hours of symptom onset) and to patients with the highest cardiovascular risk, such as those over 75 years old.
3. Coronary artery bypass surgery (CABG)
CABG has a limited function in the acute therapy of STEMI, despite significant improvements in intraoperative myocardial protection. CABG is still used to treat cardiogenic shock, failed PCI, high-risk anatomy, and surgical correction of mechanical STEMI adverse effects.
Regardless of the technique used, anticoagulant medications are an important supplementary therapy for reperfusion therapy (i.e., whether it is primary PCI or fibrinolysis therapy). Different anticoagulant medications are available; the utility of each drug varies depending on the clinical situation and reperfusion procedure.
Unfractionated heparin (UFH), bivalirudin, and low molecular weight heparin (LMWH) are all choices for primary PCI. Because of the increased risk of catheter thrombosis, fondaparinux is not used in this situation.
Anticoagulation should be administered to patients receiving fibrinolytic therapy until revascularization is done.
Other Measures of Management
1. Angiotensin-converting enzyme inhibitors (ACEi)
Unless they are contraindicated, start angiotensin-converting enzyme (ACE) inhibitors and continue them forever in all patients with a left ventricular ejection fraction of less than 40%, hypertension, diabetes mellitus, or stable chronic kidney disease.
After a MI, all patients should take a beta-blocker for the rest of their life. Current clinical practice guidelines advocate using one of three beta-blocker drugs: metoprolol, carvedilol, or bisoprolol, all of which have been shown to lower mortality in patients with heart failure after myocardial infarction.
3. Lipid-lowering agents
High-potency statin medication should be initiated and continued permanently for all individuals with an acute MI. High-potency statins like atorvastatin 40 mg or 80 mg, or rosuvastatin 20 mg, are indicated by current clinical practice guidelines.
Any patient experiencing acute symptoms of acute myocardial infarction should be instructed to call the ambulance and be transferred by emergency medical personnel rather than by themselves, family, or friends. If suspicious acute myocardial infarction symptoms persist longer than 20 minutes at rest or are coupled with near syncope/syncope or hemodynamic instability, patients should be instructed to go to the emergency room very away.
Acute myocardial infarction is caused by a combination of factors, one of which is diet. Educate individuals who have had a myocardial infarction (MI) about the importance of a low-cholesterol, low-salt diet. Before discharge from the hospital, all patients should see and be evaluated by a dietician. Exercise training should also be emphasized because current research shows that cardiac rehabilitation after a MI reduces the risk of recurrent cardiovascular events.
All patients should be informed about the importance of quitting smoking in the development of coronary artery disease. To assist patients in quitting smoking after a MI, smoking cessation classes should be made available.
Acute myocardial infarction has a significant death rate outside of the hospital. According to statistics, at least one-third of patients die before arriving at the hospital, and another 40 to 50 percent die there. Within the first 12 months after myocardial infarction, another 5% to 10% of people will die. Within the first 12 months after a MI, roughly half of all patients will need to be readmitted.
The prognosis is determined by the ejection fraction, age, and other comorbidities. Patients who do not have any revascularization will have a worse prognosis than those who get revascularization. Patients with early and effective reperfusion and intact left ventricular function have the best prognosis.