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Non ST Elevation MI

Medical term for non-ST segment elevation myocardial infarction.

Defined as a development of heart muscle necrosis without the ECG change of ST-segment elevation, resulting from an acute interruption of blood supply to a part of the heart and demonstrated by an elevation of cardiac markers CK-MB or troponin in the blood.

ST-segment elevation indicates full thickness injury of heart muscle and its absence is understood to involve less than full thickness damage of heart muscle.

NSTEMI is less severe type of heart attack compared to STEMI.

TIMI risk score uses seven key risk factors to estimate

morbidity and mortality at 14 days.

GRACE score integrates age, heart rate, systolic blood pressure, Killip classification of acute heart failure, renal function, ST segment deviation, presence of cardiac arrest at presentation, elevated cardiac biomarkers.

GRACE School quick text the risk of my calories and repeated ECS during hospitalization work and it six months and can be used to guide therapeutic decisions.

Higher sustained mortality than in patients with STEMI myocardial infarction (D’Souza M et al).

Major risk factors:

High serum cholesterol level

Hypertension

Diabetes mellitus

Cigarette smoking

Minor risk factors:

Increasing age

Male gender

Family history

Physical inactivity

Obesity

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.

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.

Chest pain is the main symptom, and it may be constricting, tightening, choking or heavy in character.

Chest pain is usually located in the center of the chest, but may radiate to neck, jaw, shoulder, back, and arms.

In older patients or those with diabetes mellitus, painless attack may occur.

Dyspnea may 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.

Nausea, vomiting, and sweating may occur due to autonomic nervous system dysfunction.

Palpitation due to sympathetic nervous system activation may occur.

If a large segment of heart is involved patients may present with shock due to impaired myocardial function.

ECG findings of NSTEMI usually are ST-segment depression or T-wave inversion.

Cardiospecific isoenzyme CK-MB and proteins troponin T and troponin increase in NSTEMI.

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.

WBC is usually elevated.

ESR and CRP may also elevate.

Chest X-ray may show congestion, and cardiomegaly.

Echocardiography is done to assess the function of heart chambers and for detecting important complications.

Complications: Heart arrhythmias including

Ventricular fibrillation

Ventricular tachycardia

Ventricular ectopics

Accelerated idioventricular rhythm

Atrial fibrillation

Atrial tachycardia

Atrioventricular block

Sinus

In majority of cases arrhythmia is mild and transient, but life- threatening arrhythmia may develop during the first 24 hours after an attack.

Complication: Acute heart failure

Complication: Cardiogenic shock

Complication: Mitral regurgitation due to papillary muscle damage.

Late complications: Dressler’s syndrome, and chronic congestive heart failure.

Aspirin reduces the mortality rate of NSTEMI by approximately 25%.

Anticoagulant drugs prevent reinfarction, and reduces the risk of thromboembolic complications.

Anticoagulation can be achieved by using unfractionated heparin, low molecular weight heparin, or a pentasaccharide, fondaparinux.

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.

The use of 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 suggested.

In the presence of tachycardia or hypertension intravenous beta-blockers atenolol 5-10 mg or metoprolol 5-15 mg over 5 minutes can be given.

Beta-blockers avoided if there is heart failure, heart block, hypotension, or bradycardia.

Nitrates should first be given buccally or by sublingual spray if there is persistent ischemic chest pain.

Irrespective of serum cholesterol level, all patients should receive a statin agent after NSTEMI.

An ACE inhibitor is started 1 or 2 days after NSTEMI as it reduces ventricular remodeling, prevents the onset of heart failure, and reduces recurrent infarction.

ARBs are suitable alternatives in patients who are intolerant of ACE inhibitors because of dry cough.

Risk analysis in patients with NSTEMI is done immediately after hospitalization and TIMI score and GRACE scores are the best.

These systems risk categorized the patients into low, medium and high risk groups.

Medium to high risk patients are considered for early coronary angiography and revascularization, either by PCI (percutaneous coronary intervention) or by CABG (coronary artery bypass grafting).

In low risk patient’s medical treatment is appropriate reserving coronary angiography and revascularization are reserved for those who fail to medical treatment.

After NSTEMI physical activities are restricted for four to six weeks after attack.

Early death is usually due to an arrhythmia.

Long term mortality is high with extensive damage of heart muscle, poor left ventricular function and persistent ventricular arrhythmia.

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.

After hospital discharge, more than 80% patients with NSTEMI survive for a further year, approximately 75% for 5 years, 50% for 10 years and 25% for 20 years.

Very elderly are at high risk for death.

Re-hospitalization rates do not rise substantially when inventing advancing age.

Similar management of non-ST segment elevation MI in older patients as for younger patients, considering functional status, and comorbid health conditions.

Non-ST segment elevation myocardial infarction are more frequent than ST-segment elevation myocardial infarction in older patients.

More than half of older adults are rehospitalized within one year after a non–ST-segment elevation myocardial infarction, and the oldest patients experience a 2 fold higher mortality after discharge compared with younger adults.

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