NSTEMI is a shorthand medical term for non-ST segment elevation myocardial infarction. It is one type of myocardial infarction also called heart attack. It may be defined as a development of heart muscle necrosis (a form of cell death) without the ECG (electrocardiography) change of ST-segment elevation, resulting from an acute interruption of blood supply to a part of the heart and can be demonstrated by an elevation of cardiac markers (CK-MB or troponin) in the blood.
ST-segment is a portion of ECG; its elevation indicates full thickness injury of heart muscle. Absence of ST-segment elevation in NSTEMI is understood to involve less than full thickness (partial thickness) damage of heart muscle. Therefore, NSTEMI is less severe type of heart attack compared to STEMI (ST-segment elevation myocardial infarction) in which full thickness damage of heart muscle develpos.
Certain factors increase the risk of developing NSTEMI. Some of these are major and others are minor.
Major risk factors:
- High serum cholesterol level
- Diabetes mellitus
- Cigarette smoking
Minor risk factors:
- Increasing age
- Male gender
- Family history
- Physical inactivity
- Excess alcohol consumption
- Excess carbohydrates intake
- Social deprivation
- Competitive and stressful lifestyle with type A personality
- Diets deficient in fresh vegetables, fruit and polyunsaturated fatty acids.
NSTEMI usually occurs by developing a partial occlusion of a major coronary artery or a complete occlusion of a minor coronary artery previously affected by atherosclerosis. Atherosclerosis is a disease of artery in which mainly cholesterol deposition occur within the wall of the artery. This deposited cholesterol ultimately forms a plaque called atherosclerotic plaque. Many years are required to establish an atherosclerotic plaque. The most common mechanism of NSTEMI is rupture or erosion of an atherosclerotic plaque that triggers platelet aggregation, which lead to formation of a thrombus (blood clot) in a coronary artery. This arterial thrombus causes interruption of blood supply to part of the heart muscle; profound changes take place in the heart muscle that lead to irreversible changes and death of myocardial cells. Usually, partial thickness damage of heart muscle occurs.
(1) Chest pain: Chest pain is the main symptom. It is constricting, tightening, choking or heavy in character, usually located in the center of the chest, but may radiate to neck, jaw, shoulder, back, and arms (most commonly left arms). Occasionally, pain may be felt only at the sites of radiation. In older patients or those with diabetes mellitus, painless attack may occur (pain conducting autonomic nerve of the heart are degenerated in old age and in diabetes).
(2) Difficulty in breathing: Breathing difficulty occur when the damage to the heart muscle limits the pumping action of the left ventricle, causing acute left heart failure and consequent lung congestion.
(3) Nausea, vomiting, and sweating: These are due to autonomic nervous system upset.
(4) Palpitation: It is due to sympathetic nervous system activation.
(5) Cardiogenic shock: If NSTEMI involve a large territory of heart, patients may present with shock due to impaired myocardial function.
Initially, patients with suspected NSTEMI, ECG and cardiac markers estimation are mandatory.
The usual ECG findings of NSTEMI are ST-segment depression or T-wave inversion.
Cardiospecific isoenzyme CK-MB (creatine kinase myocardial band), and cardiospecific proteins troponin T and troponin I are rises in blood in NSTEMI. These are released from damaged heart muscle cells during and after attack. CK-MB starts to rise at 4-6 hours and falls to normal within 48-72 hours. Troponin T and troponin I start to rise at 4-6 hours and remain high for up to two weeks.
Full blood count:
WBC (white blood cell) count is usually elevated. ESR (Erythrocyte sedimentation rate) and CRP (C-reactive protein) may also elevate.
Assess for signs of lung edema.
Echocardiography uses sound waves to produce images of the heart. It is done for assessing the function of heart chamber and for detecting important complications.
NSTEMI can lead to several complications immediately following an attack or later in recovery. Usually, complications depend on what part of the heart is damaged and the extent of damage.
(A) Heart arrhythmia – Heart arrhythmia is a disturbance of the electrical rhythm of the heart. In NSTEMI, damaged heart muscle disrupts electrical signals and produces arrhythmia in which heartbeat may be too fast, too slow or irregular. It is the most common complication following an attack. The following types of arrhythmia may develop:
- Ventricular fibrillation
- Ventricular tachycardia
- Ventricular ectopics
- Accelerated idioventricular rhythm
- Atrial fibrillation
- Atrial tachycardia
- Atrioventricular block
- Sinus bradicardia
In majority of cases arrhythmia is mild and transient. It is controlled by rest, pain relief and medication. But, life threatening arrhythmia may develop that is the major cause of death during the first 24 hours after an attack.
(B) Acute heart failure – It may develop when the damage area of the heart muscle is large. Suddenly, this damaged heart cannot pump enough blood to meet the body’s demand and developed acute heart failure.
(C) Cardiogenic shock – It may develop after the large territory heart muscle damage. It leads to failure of the pumping action of the heart. The end results are very low blood pressure with an inadequate supply of oxygen rich blood to the tissues of the body.
(D) Mitral regurgitation – Papillary muscle damage sometimes causes mitral regurgitation.
(A) Dressler’s syndrome – This syndrome is characterized by fever, pleuritis and percarditis. It is caused by an autoimmune reaction to damage heart muscle. It occurs a few weeks or even months after an NSTEMI.
(B) Chronic heart failure – It occurs slowly over time after an attack in which the heart cannot pump enough blood to meet the body’s demand.
Patients should be admitted immediately to hospital, preferably to a cardiac care unit because there is a significant risk of death.
(1) Bed rest with continuous monitoring by ECG.
(2) Inhaled oxygen therapy.
(3) Relief of pain by opiate analgegic:
Intravenous morphine 10 mg or diamorphine 5 mg is usually used and may have to be repeated to relieve severe pain.
(4) Antiplatelet therapy:
Antiplatelet drugs prevent platelet aggregation within coronary artery. A 300 mg tablet of aspirin should be given orally as early as possible then 75 mg daily should be continued indefinitely if there are no side effects occur. Aspirin reduces the mortality rate of NSTEMI by approximately 25%. In combination of aspirin, clopidogrel 600 mg should be given orally as early as possible, followed by 150 mg daily for 7 days and 75 mg daily thereafter, gives a further reduction in mortality. Ticagrelor 150 mg followed by 90 mg two times daily is more effective than clopidegrol. High risk patients, especially patients with diabetes mellitus or patients who undergo percutaneous coronary intervention (PCI), should also be considered for intake of glycoprotein IIb/IIIa receptor blocker (block the final common pathway of platelet aggregation), such as tirofiban, abciximab, or eptifibatide.
(5) Anticoagulant therapy:
Anticoagulant drugs prevent reinfarction, and reduces the risk of thromboembolic complications. Anticoagulation can be achieved by using unfractionated heparin, low molecular weight heparin (also called fractionated heparin and includes enoxaparin, dalteparin) or a pentasaccharide (fondaparinux). Comparatively low molecular weight heparin is more safety and efficacious than unfractionated heparin, and pentasaccharide is more safety and efficacious than low molecular weight heparin. The dose regimens are:
- Enoxaparin: 1 mg/kg body weight two times daily usually for 8 days by subcutaneous injection.
- Dalteparin: 120 units/kg body weight two times daily usually for 8 days by subcutaneous injection.
- Fondaparinux: 2.5 mg daily usually for 8 days by subcutaneous injection.
Beta-blockers reduce arrhythmias, heart rate, blood pressure and myocardial oxygen demand, and relive pain. Oral beta-blocker atenolol 25-50 mg twice daily, metoprolol 25-50 mg twice daily, or bisoprolol 5 mg once daily are usually adequate. Patients with heart rate more than 90 beats/minute or patients with hypertension (systolic blood pressure more than 150 mmHg or diastolic more than 90 mmHg), intravenous beta-blockers (atenolol 5-10 mg or metoprolol 5-15 mg over 5 minutes) can be given. Beta-blockers should be avoided if there is heart failure, heart block, hypotension, or bradycardia.
Nitrates act as a vasodilator and relief pain. Nitrates should first be given buccally or by sublingual (under tongue) spray. If the patient experiencing persistent ischemic chest pain after 3 doses given 5 minutes apart, then intravenous glyceryl trinitrate 0.6-1.2 mg/hour or isosorbide dinitrate 1-2 mg/hour can be given until pain relieved or systolic blood pressure falls to less than 100 mgHg. Oral or sublingual nitrates can be used once the pain has resolved.
Irrespective of serum cholesterol level, all patients should receive statin such as atorvastatin, simvastatin, or rosuvastatin after NSTEMI.
(9) ACE (angiotensin converting enzyme) inhibitors or ARBs (angiotensive receptor blockers):
An ACE inhibitor such as ramipril, enalapril, captopril, or lisinopril is started 1 or 2 days after NSTEMI. ACE inhibitor therapy reduces ventricular remodeling, prevent the onset of heart failure, and reduce recurrent infarction. An ARB (valsartan, candesartan, losartan or olmesartan) is suitable alternatives in patients who are intolerant of ACE inhibitors (ACE inhibitors can cause dry cough).
(10) Coronary angiography and revascularization:
Before giving revascularization treatment, risk analysis in patients with NSTEMI should be done immediately after hospital admission. Several systems are available for risk stratification, but TIMI score and GRACE score are the best. These systems categorized the patients into low, medium and high risk groups.
Medium to high risk patients should be considered for early coronary angiography and revascularization, either by PCI (percutaneous coronary intervention) or by CABG (coronary artery bypass grafting). Early medical treatment is appropriate in low risk patients, and coronary angiography and revascularization are reserved for those who fail to settle with medical treatment.
Lifestyle after nstemi:
► Restrict physical activities for four to six weeks after attack – death tissue in damage heart muscle takes 4-6 weeks to be healed with fibrous tissue.
► Cessation of cigarette smoking.
► Maintaining an ideal body weight.
► Eating a Mediterranean style diet (diet rich in monounsaturated fatty acids and omega-3 fatty acids, but low in saturated fatty acids).
► Achieving well control of high pressure and diabetes mellitus if present.
► Taking regular exercise up to, but not beyond, the point of chest discomfort.
► Continue secondary prevention drugs therapy including aspirin, clopidogrel, beta-blocker, ACE inhibitor, and statin.
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Early death in NSTEMI is usually due to an arrhythmia. Long term mortality is high in those who have extensive damage of heart muscle, poor left ventricular function and persistent ventricular arrhythmia. Depression, social isolation and old age are also associated with a higher mortality. According to GRACE score, in-hospital death is less than 1% in low risk, 1-9% in medium risk and more than 9% in high risk patients with non-ST segment elevation myocardial infarction (Click here to learn more about in-hospital death rate). After hospital discharge, more than 80% patients survive for a further year, approximately 75% for 5 years, 50% for 10 years and 25% for 20 years.