STEMI

ST-Elevation Myocardial Infarction (STEMI)

I. What every physician needs to know.

ST-segment elevation myocardial infarction (formerly known as Q-wave myocardial infarction) is an acute coronary syndrome caused by myocardial ischemia which results clinically in angina (or its equivalent), ST segment elevations on electrocardiogram (EKG), and subsequent elevation of cardiac biomarkers indicating myocardial necrosis. Myocardial injury develops as a result of an imbalance between myocardial oxygen supply and demand and is most commonly due to disruption of an atherosclerotic plaque with persistent thrombotic occlusion of a coronary artery.

STEMI results from total occlusion of the involved coronary artery as opposed to a subtotal thrombosis, which causes a non ST-segment elevation MI (NSTEMI).

II. Diagnostic Confirmation: Are you sure your patient has ST-segment elevation myocardial infarction?

N/A

A. History Part I: Pattern Recognition:

Patients typically present with a substernal, pressure-like pain radiating to the shoulder, neck, jaw, or left arm. However, pain can be felt isolated to any one of these areas or sometimes no pain is felt at all. Most often occurring at rest, the pain is more intense or prolonged than any previously experienced episodes of unstable angina, usually lasting more than 20 minutes. Associated symptoms include diaphoresis, nausea/vomiting (especially with inferior wall involvement), or lightheadedness. Occasionally location of pain may be epigastric and easily confused for gastrointestinal illnesses.

In the absence of chest pain, unexplained dyspnea is worrisome and should be considered an anginal equivalent, particularly in patients with risk factors for atherosclerotic cardiovascular disease (ASCVD).

Atypical presentations or “silent myocardial infarctions” (MIs) more commonly occur in females, elderly, diabetics, and patients with prior heart failure. Up to 33% of patients having a myocardial infarction present with symptoms other than chest pain.

B. History Part 2: Prevalence:

Risk factors for coronary heart disease

Hypertension: Blood pressure (BP) greater than 140/90 mmHG (millimeters mercury) or use of antihypertensive meds.
Family history in a first degree relative of premature coronary artery disease (men < 55 years old or women < 65 years old).
Dyslipidemia: elevations in non-High density lipoprotein (HDL) cholesterol and low levels of HDL cholesterol.
Age: Males ≥55 years old and females ≥ 65 years old.
Diabetes mellitus (DM).
Microalbuminuria or estimated glomerular filtration rate (GFR) below 60mL/min (milliliters/minute).
Lifestyle factors such as tobacco smoking alcohol intake, obesity (Body mass index [BMI] > 30 kilograms/meter² [kg/m²]), physical inactivity and diet.
A HDL greater than 60 mg/dl (milligrams/deciliter) is a negative risk factor for ASCVD.

Coronary heart disease risk equivalents

Non-coronary atherosclerotic disease – carotid artery disease, cerebral vascular disease, abdominal aortic aneurysm, and peripheral arterial disease.
DM
Chronic kidney disease.

The risk of having a cardiovascular event in these patients is equivalent to persons with prior history of coronary artery disease (CAD).

C. History Part 3: Competing diagnoses that can mimic ST-segment elevation myocardial infarction.

Cardiac chest pain

NSTEMI – ST depressions or T wave inversions noted on EKG with elevated cardiac biomarkers.
Unstable angina – normal cardiac biomarkers; EKG changes (ST depressions or T wave inversions) are usually transient.
Acute pericarditis – concomittant symptoms of viral illness; positional changes in chest pain; diffuse ST-elevation on EKG with PR depressions.
Vasospasm (Prinzmetal’s angina or cocaine-induced).
Myocarditis – chest pain may be sharp, +/- fever, may describe recent symptoms consistent with a viral infection.
Coronary artery dissection (associated with acute coronary syndromes (ACS) in peripartum women).
Aortic dissection – sharp, tearing chest pain without ST elevation on EKG (unless coronary artery dissection occurs). Widened mediastinum on chest X-ray (CXR).
Takotsubo or stress-induced cardiomyopathy – brought on by an emotional or physical stressor.

Non-cardiac chest pain

Gastrointestinal: gastroesophageal reflux disease (GERD), esophageal spasm, esophageal rupture, pancreatitis, cholecystitis, choledocholithiasis, peptic ulcer disease (PUD).
Pulmonary: pneumonia, pulmonary emboli, tension pneumothorax.
Costochondritis: reproducible chest wall tenderness.

D. Physical Examination Findings.

Presentation can vary widely from a completely normal exam to sudden death resulting from a ventricular arrhythmia.
Tachycardia and/or hypertension can result from reflex activation of the sympathetic nervous system in response to myocardial ischemia. Bradycardia may be present in setting of an an inferior wall myocardial infarction due to parasympathetic activation. Multiple other forms of conduction abnormalities such as varying forms of heart block may be present due to an ischemic insult involving the arterial supply to the electrical system of the heart.
A paradoxically split second heart sound or presence of a 3rd or 4th heart sound may be audible.
Pre-existing murmurs may change in intensity or timing. A new murmur of mitral regurgitation could indicate papillary muscle dysfunction.
In large territory infarcts, there may be signs of acute heart failure (e.g., hypotension , pulmonary edema). Hypotension and elevated jugular venous pressure in the absence of pulmonary edema is indicative of a right ventricular infarct.

E. What diagnostic tests should be performed?

In addition to prompt assessment of hemodynamic stability and obtaining a focused history, an EKG should be done ideally within 10 minutes of arrival to ED and is usually sufficient to make the diagnosis of STEMI. Cardiac biomarkers may initially be normal if the patient presents early after symptom onset.

1. What diagnostic studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Electrocardiogram

An electrocardiogram reveals new ST segment elevations at the J point in 2 contiguous leads of ≥ 2mm (millimeters) in men or ≥ 1.5mm in women in leads V2, V3 and or ≥ 1mm in any other leads. The presence of a new (or presumably new) left bundle branch block (LBBB) has been considered to be a STEMI equivalent. However, this finding is rare and should not be considered to be a STEMI equivalent without other evidence of an evolving myocardial infarction. The initial EKG may reveal hyperacute (peaked) T wave with subsequent evolution to J-point elevation and ST-segment elevation, and finally development of pathologic Q waves and T wave inversions. These changes usually progress over a period of 2 weeks but may be more accelerated depending on the infarct size and rapidity of reperfusion.

The area of infarction can usually be localized on the EKG using the following anatomic lead groups:

Inferior wall (supplied by the right coronary artery (RCA) in 90% of cases and the left circumflex (LCX) artery in the remainder): II, III, aVF;
Anterior wall (left anterior descending (LAD) artery): V2, V3, V4;
Lateral wall (nondominant (LCX) artery): I and aVL, V5 and V6;
Septal (LAD): V1 to V2.

ST changes in inferior leads should prompt placement of right-sided leads (V4R, V5R, V6R) to evaluate for right ventricular infarction. ST depression in ≥2 precordial leads (V1-V4) should prompt an evaluation for a posterior wall infarction with placement of posterior leads (V7, V8, V9). The presence of ST depressions in multiple leads with a concomitant STE in aVF can indicate left main or proximal LAD.

If the initial EKG is nondiagnostic in a patient with ongoing chest pain with a high index of suspicion for an acute MI, the EKG should be repeated every 20 minutes to evaluate for dynamic EKG changes.

Echocardiogram

An echocardiogram is used to assess for segmental wall motion abnormalities, left ventricle function and for any valvular abnormalities.

2. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

The general approach to biochemical diagnosis of acute MI is measurement of troponin I or T at 0 hours and 6-8 hours of presentation. If first two values are negative and high index of suspicion for STEMI exists, then repeat at 12 to 24 hours. If troponin assay is unavailable, then a less specific and sensitive alternative is to serially measure CK-MB (creatinine kinase myocardial band).

CK-MB

A CK-MB is less specific for myocardial injury than cardiac troponins. Elevated CK-MB with normal troponin more often indicates release of MB isoenzyme from noncardiac tissue. The utility of CK-MB is greater than troponins in the diagnosis of post-procedural MIs.

Cardiac troponin (I and T)

A cardiac troponin is more specific and sensitive than CK-MB for diagnosis of myocardial injury, but can be elevated in other conditions (e.g., sepsis, chronic kidney disease, heart failure, pulmonary embolism, rapid atrial fibrillation). A negative troponin does not exclude MI, especially if done soon after symptom onset. Eighty percent of patients with STEMI will rule in within 2-3 hours. Serial monitoring of troponin can exclude most acute MIs within 6-8 hours of symptom onset. Levels can stay elevated for 1-2 weeks after an acute myocardial infarction (AMI) but do not rapidly rise or fall. Reinfarction can be diagnosed if there is a 20% or greater increase in a repeated sample.

III. Default Management.

Prompt diagnosis of STEMI with an EKG is the first step in management, as reperfusion therapy has greatest benefit in mortality when performed early after presentation.

A. Immediate management.

For any patient suspected to have STEMI, immediately (ideally within 10 minutes of arrival) establish IV access, initiate continuous EKG monitoring and obtain 12-lead EKG, obtain blood tests (cardiac biomarkers, complete blood count [CBC], basic metabolic panel [BMP], and a coagulation profile; prothrombin time [PT], partial thromboplastin time [PTT] and international normalized ratio [INR]), and assess for and maintain hemodynamic stability.

Early interventions

Should be initiated immediately while assessing patient for fibrinolysis or percutaneous coronary intervention (PCI).

Give oral, chewed or crushed aspirin 162 to 325 mg (milligrams) (non-enteric coated). This medication can be given rectally if oral administration is not possible.
Give a high intensity statin (atorvastatin 40-80 mg or rosuvastatin 20-40 mg) as early as possible (preferably before PCI).
If not contraindicated, start an oral cardioselective beta-blocker within the first 24 hours – to prevent recurrent ischemia (by treating hypertension and tachycardia, both of which place increased demands on an already ischemic myocardium). Rate control also helps prevent ventricular arrhythmias. Verapamil or diltiazem are acceptable alternatives when beta-blockers are contraindicated, but should be avoided in significant left ventricular (LV) systolic dysfunction.
Oral angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) should be given within 24 hours to STEMI patients with LV ejection fraction (EF) less than 40%.
Sublingal (SL) nitroglycerin (NTG) 0.4 mg every 5 minutes for 3 occurrences, then given intravenous (IV) for persistent pain, hypertension or heart failure. NTG is contraindicated if phosphodiesterase inhibitor was used within previous 24-48 hours, in hypotensive patients, those with right ventricular infarcts and those with brady or tachycardia.
Morphine 2 to 4 mg IV for relief of chest pain that is not relieved by NTG.
Supplemental oxygen for patients with cyanosis, respiratory distress or hypoxemia (arterial saturation < 90%).
Discontinue all nonsteroidal anti-inflammatories (NSAIDs) at time of presentation.

Reperfusion of coronary arteries, if achieved immediately after presentation, can result in rapid restoration of myocardial blood flow and reduction in the mortality associated with STEMI. The method of reperfusion (fibrinolysis vs. percutaneous coronary intervention) will depend on the duration of symptom onset and the estimated “door-to-balloon” (DTBT) and “door-to-needle” times. These times measure the delay from time of presentation to an emergency department, to the time needed to achieve first balloon inflation with PCI (“door-to-balloon” time) or time to initiation of fibrinolytic infusion (“door-to-needle” time). Either method of reperfusion should be offered to all patients with STEMI presenting within the first 12 hours of symptom onset. Significant evidence exists that improved outcomes occur when PCI is chosen over fibrinolysis in most patients with STEMI. When available, PCI is the reperfusion strategy of choice as it’s associated with lower risks of recurrent MI and intracranial hemorrhage compared to fibrinolysis. The goal “door-to-balloon” time is within 90 minutes. Patients that initially present to a non-PCI-capable hospital should be transferred to a PCI-capable hospital if the time from first medical contact to PCI will not exceed 120 minutes.

If prompt performance of PCI with a door-to-balloon time within 90 minutes in a PCI-capable facility, or transfer to a PCI-capable facility is unavailable, fibrinolysis is recommended in STEMI patients presenting within 12 hours of symptom onset. Alternatively, if patients present 12-24 hours after symptom onset and no PCI is available, fibrinolysis should be performed if the patients have hemodynamic instability or a large region of myocardium at risk. The goal “door-to-needle time” is within 30 minutes of arrival. Because of the possibility of reocclusion or failure after fibrinolysis, patients treated with this strategy should be immediately transferred to a PCI-capable facility.

Reperfusion in patients presenting 12-24 hours after symptom onset, is reasonable if the patient continues to have clinical or eletrocardiographic evidence of ongoing ischemia. In this instance PCI is preferred. Regardless of the duration from symptom onset to presentation PCI is preferred if the patient has evidence of severe systolic heart failure or cardiogenic shock.

Due to the increased risk of mortality associated with it, coronary artery bypass graft (CABG) should be deferred for 3-7 days post-STEMI (unless absolutely necessary) to allow for myocardial recovery.

If no reperfusion therapy is to be initiated, dual antiplatelet therapy should be initiated.

Antiplatelet and anticoagulant therapy

All STEMI patients should receive aspirin and a second antiplatelet agent, namely a P2Y12 receptor antagonist. The choice of second antiplatelet depends on the method of reperfusion undertaken. Clopidogrel should be used if fibrinolysis is the treatment method of choice. If the reperfusion strategy is by PCI, clopidogrel, prasugrel, or ticagrelor can be utilized.

All patients should also receive anticoagulation with either unfractionated heparin (UFH), low molecular weight heparin, or bivalirudin.

In addition to dual antiplatelet therapy and anticoagulation, adjunctive therapy with a glycoprotein (GP) IIb/IIIa inhibitor may be beneficial if the clot burden is large or the patient wasn’t adequately loaded with a second antiplatelet agent.

Electrolyte balance

Maintaining potassium and magnesium concentrations above 4.0meq/L (milliequivalents/liter) and 2.0meq/L respectively is recommended as prophylaxis for life-threatening ventricular tachyarrhythmias.

Early risk stratification

With scoring systems like the TIMI (thrombolysis in myocardial infarction), risk score for STEMI is useful for predicting the risk of in-hospital mortality, but has little utility deciding on a treatment strategy as most patients with STEMI are diagnosed and rapidly reperfused.

High risk clinical presentations of STEMI

Those that warrant aggressive management with urgent PCI include:

Advanced age;
Heart failure;
Hemodynamic instability (hypotension, tachyacardia, ventricular arrhythmias);
Anterior wall MI.

TIMI risk score for acute STEMI

Predicts 30-day mortality after MI:

DM, history of hypertension or history of angina (1 point);
Systolic blood pressure less than 100mmHg (3 points);
Heart rate greater than 100 beats per minute (2 points);
Killip class II-IV (2 points);
Body weight less than 150lb (pounds) or 67kg (1 point);
Anterior lead ST elevation or LBBB (1 point);
Time to treat more than 4 hours (1 point);
Age: 75 years or older (3 points), 65-74 years old (2 points), Less than 65 (0 points).

Total points with associated risk of mortality:

– 0 Points = 0.8%
– 1 Point = 0.6%
– 2 Points = 2.2%
– 3 Points = 4.4%
– 4 Points = 7.3%
– 5 Points = 12%
– 6 Points = 16%
– 7 Points = 23%
– 8 Points = 27%
– 14 Points = 36%

B. Physical Examination Tips to Guide Management.

Vital signs should be checked frequently to assess for developing hemodynamic compromise (e.g., arrhythmias or hypotension). Patients should be placed on continuous telemetry monitoring.
Monitor heart and lung sounds for new murmurs or signs of heart failure.
A mitral regurgitation (MR) murmur may develop post-infarction. A new or worsening MR occurring concurrently with hypotension and signs of pulmonary edema is indicative of life-threatening papillary muscle rupture.
Presence of a pericardial friction rub heard on auscultation post-MI could represent peri-infarction pericarditis.

C. Laboratory Tests to Monitor Response to, and Adjustments in, Management.

Serial cardiac biomarkers should be measured until they peak and start to trend down. If recurrence of chest pain, repeat biomarkers to assess for re-infarction.
CBC: anemia can result in decreased oxygen supply to myocardium and subsequent ischemia. Although there are differing opinions about when to transfuse, it’s probably more beneficial than risky to give a packed red blood cell (pRBC) transfusion if the hemoglobin level is < 8 mg/dL. Monitor for decreases in hemoglobin/hematocrit while on fibrinolytics, antiplatelets or anticoagulation.
Monitor PT/INR/PTT while on warfarin or unfractionated heparin.
BMP: creatinine and potassium levels should be monitored after initiating ACE inhibitor. Potassium and magnesium should be replaced in order to prevent ventricular arrhythmias.
Blood glucose should be measured pre-meal to tailor insulin regimens to achieve adequate glycemic control. Ideally blood glucose levels should be kept below 180 mg/dL.

D. Long-term management.

Elective angiography should be performed prior to discharge in patients who underwent reperfusion with fibrinolysis.

An echocardiogram should be performed to assess left ventricular function in those who have not undergone angiography or left ventriculography.

Medication

Initiate or continue medications that have proven mortality benefits (recommendations below are based on absence of contraindications):

Antiplatelet agents

Medically managed patients treated with fibrinolysis: clopidogrel 75 mg daily (for up to 14 days and ideally up to 1 year) and aspirin 81 to 325 mg (indefinitely).

Patients who received a bare-metal stent (BMS) or a drug-eluting stent (DES): clopidogrel 75 mg daily, prasugrel 10 mg daily or ticagrelor 90 mg twice daily (for 1 year) and aspirin 81 to 325 mg daily indefinitely. Continuation of dual antiplatelet therapy past 12 months should be considered in patients that have not had adverse events. In patients with BMS who have had a bleeding complication consideration can be given to discontinuing the P2Y12 inhibitor after 1 month as the risk of stent thrombosis is the greatest in the first 14-30 days.
ACE inhibitor (or ARB) should be given within 24 hours of diagnosis and continued indefinitely (particularly if patient has hypertension (HTN), DM, heart failure, or LV dysfunction with EF 40% or less). Use should be avoided in patients with hypotension, hyperkalemia, bilateral renal artery stenosis or renal impairment.
Beta-blockers should be started ideally within 24 hours of the acute event and continued indefinitely. This medication class should be used with caution in patients with signs of heart failure, cardiogenic shock, conduction abnormalities or reactive airway disease.
Statins should be given to all post-STEMI patients regardless of low-density lipoprotein (LDL).

For patients ≤ 75 years a high intensity statin (atorvastatin 40-80 mg or rosuvastatin 20-40 mg) should be used.

For patients > 75 years or patients who are intolerant to a high intensity statin, moderate intensity statin should be used.
Aldosterone antagonists are recommended for use in STEMI patients who are already taking therapeutic doses of an ACEI, have DM, LV dysfunction (with an EF ≤40%), or have symptomatic heart failure. Use should be avoided in patients with hyperkalemia or renal impairment.

Control symptoms of ischemia with nitroglycerin and beta-blockers (or calcium channel blockers).

Oral anticoagulation with warfarin is recommended to prevent embolization in the setting of atrial fibrillation or presence of an LV thrombus. Anticoagulation with one of the novel oral anticoagulants (dabigatran, rivaroxaban, apixaban and edoxaban) may be considered for patients with atrial fibrillation.

Recommend lifestyle and risk factor modification

Encourage smoking cessation. If needed, start nicotine or non-nicotine replacement therapy.
HTN – “Joint National Committee 8” guidelines recommend goal BP less than 150/90mmHg in patients ≥ 60 years of age and less than140/90mmHg in patients with DM and chronic kidney disease (CKD) regardless of age as well as patients < 60 years old.
DM – dietary and medication regimens modified to achieve glycosylated hemoglobin (HgbA1c) below 7%.
Dyslipidemia – statin therapy is the mainstay of treatment.
Dietary – Reduce intake of saturated and trans fats, cholesterol, sodium, sweets, sugar-sweetened beverages and red meats. Increase intake of fruits, vegetables, whole grains, low-fat dairy, poultry, fish, legumes, nontropical vegetable oils and nuts.
Promote and average of 40 minutes of moderate to vigorous physical activity at least 3-4 days per week. Patients can usually start exercising 3 weeks after STEMI.
Weight recommendations: BMI 18.5 to 24.9kg/m² and waist circumference less than 40 inches for men and less than 35 inches for women.

IV. Management with Co-Morbidities

N/A

A. Renal Insufficiency.

Use of isosmolar contrast agents is indicated for patients with CKD who require angiography. Dose adjustments should be made for medications that are renally cleared.