NSTEMI stands for Non-ST-elevation myocardial infarction, or non-STEMI.
ST refers to the ST segment, which is part of the EKG heart tracing used to diagnose a heart attack.
A heart attack is diagnosed as chest pain, with blood tests that show elevated markers of heart damage such as cardiac troponin and EKG changes.
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.
If there is a pattern of ST-elevation on the EKG, this is called a STEMI, short for ST elevation myocardial infarction.
With elevation of the blood markers suggesting heart damage, but no ST elevation seen on the EKG tracing, this is known as a NSTEMI.
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.
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.
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.
NSTEMI has a higher sustained mortality than in patients with STEMI myocardial infarction (D’Souza M et al).
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
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.
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.
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.
NSTEMI is treated Initially with aspirin and anticoagulants, which improve outcomes.
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.
Other medicines such as a beta-blocker or nitrates may be given.
Many patients undergo cardiac angiography to determine the degree of
arterial blockages.
With severe blockages stents or coronary artery bypass surgery will be advised.
Management of Non ST-Segment Myocardial Infarction:
Aspirin
An antiplatelet agent: Plavix (Clopidogrel) or Effient (Prasugrel) or Brilinta (Ticagrelor)
These antiplatelet agents are often given for a year or sometimes longer after NSTEMI.
If a stent is placed, these medicines are required to prevent clotting inside the stent.
Beta-Blockers slow the heart rate and reduce the amount of work the heart has to do.
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.
ACE-Inhibitors reduce enlargement of the heart, and control blood pressure and improve prognosis.
Statins help prevent recurrent CV events and are currently recommended as a lifelong treatment.
Statins lower cholesterol and help to stabilize the vulnerable plaques that are responsible for heart attacks.
Spironolactone may be added to help prevent further deterioration and to strengthen the muscle.
With persistent chest pain after the attack and initial treatment drugs nitrates may be added.
STEMI is more of an immediate emergency than NSTEMI, because of a known total occlusion of a heart vessel that needs opening back up urgently.
In terms of long-term outcomes, STEMI and NSTEMI have equal health implications.
Patients with NSTEMI often have other illnesses such as ongoing critical illness, diabetes, kidney disease, and they have a generally high risk over the long term.
33% with confirmed MI have no chest pain on presentation, especially those who are older, female, or have DM, or CHF.
5% of NSTEMI will develop cardiogenic shock with 60% mortality.
Keeping the hematocrit above 30% in patients with acute acute myocardial infarction and anemia, results in a 33% reduction and 30 day mortality withe use of transfusion.
Clinical factors that increase likelihood of acute coronary syndrome/AMI
Chest pain radiating to both arms
Chest pain associated with diaphoresis
Chest pain associated with nausea/vomiting
Chest pain with exertion
Evaluation
Non-STEMI ECG + positive troponin
Angiography indicated for:
Recurrent angina/ischemia with or with out symptoms of CHF
Elevated troponins
New or presumably new ST-segment depression
High-risk findings on noninvasive stress testing
Depressed LV function
Hemodynamic instability
Sustained V-tach
PCI within previous 6 mo
Prior CABG
Treatment:dual antiplatelet therapy and antithrombotic therapy is mainstay of treatment.
Aspirin is recommended dose is 325 mg/d.
Aspirin reduces death from MI by 12.5 → 6.4%.
Should be used in all ACS unless contraindicated.
In pts with true ASA allergies, substitute P2y12 inhibitors.
GPIIb/IIIa Inhibitors eptifibatide, abciximab, tirofiban benefit only for patients undergoing PCI.
Heparin or enoxaparin along with ASA are given.
ESSENCE trial showed 20% decrease in death, MI or urgent revascularization with LMWH
Oxygen used only if SpO2 <90%
Administer sublingual nitroglycerin every 5 min x3 for continuing ischemic pain and then assess need for IV nitroglycerin.
Nitroglycerin is used cautiously in inferior MI or if patient is on sildenafil.
NSAIDs other than ASA can be harmful.
β-blockers are started within 24 hours, with a heart rate of 50-60.
β-blockers are contraindicated if HR<50 or SBP<90, acute CHF, low flow state, or PR interval >240ms.
β-blockers decrease inotropic and chronotropic response to catecholamines.
If beta-blockers cannot be used
diltiazem is considered, as nifedipine is harmful.
ACE inhibitor started within 24 hours
reduces 30 day mortality by 7%, and
those with recent MI and LV dysfunction benefit most.
Transfuse to keep hemoglobin >10gms.
Thrombolytics are not indicated in Non-STEMI.
TIMI Risks
points % risk of mortality, MI, or need for revascularization
0 5%
1 5%
2 8%
3 13%
4 20%
5 26%
6 41%