Acute Myocardial Infarction

Acute myocardial infarction (AMI) ,colloquially referred to as a heart attack, is an irreversible death of a myocardial segment sequel to persistent occlusion and inadequacy of coronary blood flow to the heart. AMI typically presents with central chest pain which may radiate to the neck, left arm, jaw, and shoulders. Accompanying these symptoms are diaphoresis, dyspnea and presyncope.

The disease is related to the following processes:  vascular and has an incidence of about  260 / 100.000.

Overview

Acute myocardial infarction (AMI) refers to irreversible myocardial necrosis resulting from sustained myocardial ischemia [1] [2]. AMI is usually the complication of coronary artery disease in which an atherosclerotic plaque, mostly, occludes coronary blood flow. 

AMI may present with no symptoms at all. However, typical symptoms of AMI are a central chest pain which often radiates to the jaw, neck, left arms, and shoulders and which may be associated with dyspnea, palpitations and, presyncope.

Diagnosis of AMI is made by characteristic features on the ECG. However, coronary angiography presents an excellent modality for both diagnostic and therapeutic purposes in the management of AMI.

Treatment of AMI is achieved with fast institution of antiplatelet and thrombolytic therapy and, most importantly, anticoagulation. Percutaneous intervention and coronary artery bypass surgery may be necessary in cases unresponsive to medical treatment.

Etiology

The risk factors for AMI consist of diseases and lifestyle habits which predispose one to vascular damage and occlusion. These factors could be categorized as modifiable and nonmodifiable. The modifiable risk factors include diabetes mellitus, hyperlipidemia, hypertension, tobacco use, and substance abuse. The non modifiable risk factors include a male gender and a positive family history of vasculocclusive diseases.

High levels of total cholesterol, LDL, or triglycerides cause considerable increase in the risk of developing coronary artherosclerosis and AMI. Persistent reduction of HDL levels below 40mg/dl is also associated with a high risk of developing AMI [3]. Dyslipidemia may also be the indirect link between diabetes and coronary artery disease. Diabetes causes coronary artery diseases directly by causing endothelial damage.

Hypertension involving either or both systolic and diastolic pressures is a strong risk factor for coronary artery disease and AMI [4]. Tobacco use constitutes a significant risk factor of AMI and strokes. Constituents of tobacco impose toxic reactions to the endothelium of blood vessels. This injury, in turn, triggers an inflammatory response which results in atherosclerotic changes in the vessels [5].

Although, males are said to be at a higher risk of developing coronary artery disease than females, the incidence evens out with increasing age. A family history of atherosclerotic cardiovascular and cerebrovascular diseases are often associated with genetic links to these diseases, predisposing individuals with such family histories to developing coronary artery disease.

Coronary artery disease and AMI are not exclusively linked to atherosclerosis, other vascular and cardiac defects including vasculitis, valvular heart defects, coronary trauma, and congenital coronary defects may also predispose to AMI.

Epidemiology

Cardiovascular disease is the leading cause of death in the United States. As reported in the results of the 2005 Behavioral Risk Factor Surveillance System (BRFSS) survey, MI occurs more in men than women and the incidence of the disease significantly increases with age.

Sex distribution
Age distribution

Pathophysiology

Acute myocardial infarction is the terminal response of the heart to undercompensated and persistent myocardial ischemia. Most cases of AMI result from coronary artery disease involving atherosclerotic occlusion of the vessel [6]. This makes AMI a presentation of acute coronary syndromes.

An atherosclerotic plaque is made up of a lipid core and a fibromuscular outer layer. This outer layer is eroded with time by the actions of catalytic enzymes which include collagenases, proteases and matrix metalloproteases. This enzymatic breakdown coupled with hemodynamic forces in the blood vessel completely erode the fibromuscular layer and a consequent endothelial damage. The endothelial injury triggers the extrinsic coagulation pathway, eventually leading to thrombus formation. Occlusion of the coronary vessel is caused by the thrombus.

Persistent occlusion of the coronary vessel shifts changes from compensation to the occurrence of an acute myocardial infarction. Prolonged ischemia first leads to necrosis of the endocardium, then the myocardium before affecting the epicardium. After onset of AMI, failure to restore coronary blood flow within 8 hours leads to a significant myocardial loss. The severity of AMI is determined by the extent of myocardial necrosis, which in turn, is determined by the duration and level of coronary occlusion. The more proximal the coronary occlusion occurs, the greater the severity and complications of AMI.

Prognosis

AMI causes death in 30% of cases, over half of which occur before the patient arrives at the hospital. Generally, most of the deaths caused by AMI occur within the first 24 hours of onset of symptoms. Up to 10% of patients who get treatment for AMI die within the same year of treatment, and in up to 50% of cases, there is a recurrence of AMI.

Most of the deaths from AMI are due to ventricular arrhythmias. Deaths within a year of successful treatment of AMI results from ventricular arrhythmias, ventricular failure, or a recurrent AMI. Consequently, a stress ECG is recommended for all patients successfully treated for AMI. Poor stress ECG results strongly predicts imminent mortality.

By and large, prognosis of AMI depends largely on the extent of myocardial necrosis, the timing of initiating reperfusion measures, and the degree of ventricular dysfunction. Early reperfusion and revascularization ( initiation of thrombolytic therapy within 30 minutes of presentation or of percutaneous intervention within 90 minutes of presentation) with preserved ventricular function is associated with a better prognosis.

A high thrombolysis in Myocardial infarction score (TIMI) is strongly associated with a high mortality rate in AMI. Several indices are taken into account in calculating this score. The more indices present in the individual, the higher the score. These indices include [7]:

1. At least 65 years of age.

2. Presence of at least 3 risk factors for artherosclerotic cardiovascular disease.

3. Positive history of coronary artery disease.

4. Elevated cardiac enzymes.

5. Aspirin use within the last one week.

6. ST segment elevation by at least 0.5mm.

Presence of risk factors of atheroscleotic vascular diseases, late or unsuccessful reperfusion, severe ventricular failure, congestive cardiac failure, pulmonary edema all contribute to high mortality and bad outcome [8] [9]. Laboratory findings of elevated B-natiuretic peptide, C-reactive proteins levels and high secretory-associated  phospholipase A2 activity are also associated with high mortality in AMI [10] [11] [12] [13] [14].

Presentation

Presentation of acute MI may range from asymptomatic to sudden cardiac death. Asymptomatic AMIs occur most commonly in diabetics. Typical symptoms of acute MI include;

  • Chest pain, which could be experienced as pressure or a squeezing/choking sensation at the center of the chest which radiates to the jaw, shoulder, left arm and, occasionally, to the back.
  • Chest pain may, typically, be associated with the following; dyspnea, epigastric pain, palpitations, diaphoresis, syncope or presyncope and disorientation. AMIs occur most likely in the early hours of the morning and with exertion.

Workup

The ECG is the diagnostic test of choice and should be done within 10 minutes of presentation. Therapeutic interventions are guided by ECG results. Diagnosis is confirmed with serial ECG tracings done every 8 hours within the first 24 hours of presentation, then once daily. Gradual return to normal ECG findings or development of abnormal Q waves confirm the diagnosis.

An elevation of the ST segment by at least 1 mm on the adjacent leads opposite the diseased area on the ECG is diagnostic of an ST segment elevation myocardial infarction (STEMI). ST segment elevation has a 90% specificity and 45% sensitivity in diagnosing AMI. In STEMI, ECG shows ST-segment elevation ≥ 1 mm in at least 2 adjacent leads opposite the damaged area, which is diagnostic as supposed to its absence in non-ST segment elevation myocardial infarction (NSTEMI).

AMI often has similar ECG tracings as left bundle branch block, therefore, it is recommended that patients with symptoms in keeping with AMI and a provisional diagnosis of left bundle branch block should be treated for STEMI.

Assay of cardiac markers helps in the diagnosis of AMI. Cardiac markers include CK-MB, myoglobin, troponin I, and troponin T. These cardiac markers have varying sensitivities and specificities for AMI. However, the troponins are most sensitive and specific and are the cardiac markers of choice in the diagnosis of AMI.

Coronary angiography serves for both diagnostic evaluation and therautic intervention in the management of AMI. In emergency settings, coronary angiography is recommended. It is also recommended as a therapeutic modality in patients unresponsive to medical therapy and those which severe cardiac sequalae such as cardiogenic shock and unstable arrhythmias. In unstable angina or uncomplicated NSTEMI, diagnostic angiography is necessary posttreatment for detection of untreated lesions.

Adjunct investigations include erythrocyte sedimentation rate and complete blood count. A high ESR supports, but is a non-specific index in the diagnosis of AMI. Additionally, same day lipid profile should be done in all patients treated for AMI.

Treatment

Both STEMI and NSTEMI have different courses of treatment, therefore, the importance of an early ECG cannot be overemphasized. Nonetheless, the first step of treating all cases of MI is an urgent revascularizaton and reperfusion. Thereafter, relief of pain and prevention or treatment of complications are initiated.

En route the emergency room, the patient should have an intravenous line in place and concurrent administration of supplemental oxygen, aspirin, and nitroglycerin. If available, a prehospital ECG should be obtained.

At the emergency department, medical reperfusion strategies should be commenced immediately. These reperfusion treatments include: thrombolytic therapy, anticoagulation, and antlatelet therapy. Thrombolytic treatment should be administered within 30 minutes of the patient's presentation. Beyond 2 hours of presentation, use of thrombolytics show little effectiveness. Thrombolytic therapy has not proven to be of benefit in the treatment of STEMI.

Antiplatelet therapy is also vital in management of AMI. It is associated with high success if administered early even before arriving at the hospital. Clopidogrel is used in cases of aspirin allergy. As recommended in the Antiplatelet Therapy for Reduction of Myocardial Damage During Angioplasty-Myocardial Infarction (ARMYDA-6 MI) multicenter study, a stat dose of 600 mg clopidogrel, compared to a 300 mg stat dose, prior to primary PCI was associated with a smaller infarct size [15].

Anticoagulation is the most critical aspect of treatment of ACS. It should be instituted together with anti platelet therapy in all suspected or diagnosed cases of unstable angina or NSTEMI. Unfractionated heparin, enoxaparin, and bivalirudin are examples of potent anticoagulants for use in these cases, especially those for whom invasive interventions may be necessarily.

Other aspects of treatment in the management of AMI include pain relief, correction of complications, and cardioprotective treatment plans. Pain relief is best achieved with morphine sulphate in STEMI [16].

ACE inhibitors and beta-blockers also significantly reduce morbidity and mortality in AMI. However, these should be used only after excluding all contraindications to their use. Angiotensin-receptor blockers are alternatives to ACE inhibitors if there are any contraindications to the use of ACE inhibitors. Nondihydropyridine calcium channel blockers ( verapamil and diltiazem) are indicated if there are contraindications to the use of beta-blockers upon exclusion of left ventricular failure, pulmonary edema and AV block [17] [18].

Failure of the above medical intervention and percutaneous interventions are indications for coronary artery bypass surgery (CABG). CABG is also indicated if there are concomitant cardiac complications or defects.

Prevention

The modifiable risk factors for coronary artery disease can be prevented to forestall the occurrence or recurrence of AMI. Smoke cessation is associated with a 50% reduction in the risk of recurrence of AMI within the same year of quitting. This informs the recommendation of counselling and appropriate smoke cessation therapies for all patients with acute coronary syndrome who smoke.

Mild alcohol consumption has also been shown to reduce the risk of atherosclerotic vascular disease. However, there are no strict guildlines on alcohol use in the prevention of AMI and, therefore, should be based on the doctor's clinical discretion.

Patient Information

Overview.

Myocardial infarction is the medical term for a heart attack. A heart attack occurs when the blood flow to the heart is blocked for a long time. The heart muscle dies after a prolonged period of inadequate blood and oxygen supply. This death and sudden loss of action of the heart muscle is what is referred to as a heart attack. It presents suddenly, that's why its described as acute.

Etiology.

The obstruction of the blood supply is initiated by a fatty substance which attaches to the blood vessel wall, building up with time and trigerring the development of a clot which, ultimately, blocks the vessel. This deprivation of blood flow causes the heart muscle to die, becoming fatal in a few hours.The risk of having a heart attack increases with advancing age, tobacco smoking, diabetes and a family history of a heart attack, to name a few.

Presentation.

A heart attack , typically, presents with chest pain which radiates to the left arm, jaw, shoulders and neck. There could also be breathlessness, vomiting , and sweating. Patients also feel lightheaded and dizzy.

Work up.

An Electrocardiogram (ECG) is the diagnostic method of choice for AMI. Once your symptoms are typical of a heart attack, an urgent ECG would be ordered. Other laboratory tests such as cardiac enzyme levels may also be necessary to support the diagnosis. A coronary angiography is a form of X-ray of the blood vessels of the heart done after a dye is passed through them to make them more visible. This test may be ordered to view the coronary vessels and the site of the blockage and it could also be used to remove the blockage in emergency situations.

Treatment.

A heart attack requires an urgent treatment, which involves an urgent call to the paramedics who would initiate treatment to reopen the blood vessel even before reaching the hospital. The longer one stays without restoring the blood flow to the heart, the more likely the individual would die, even en route the hospital. In severe cases, surgery may be needed to repair the affected blood vessel.

Prognosis.

More than one-third of patients who develop a heart attack die, half of these people die before getting to the hospital. The key thing to note in AMI is that the longer the patient stays without treatment of the symptoms, the greater the extent of the heart muscle death and the higher the chances of death from this condition.

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