ST-Elevation Myocardial Infarction



ST-Elevation Myocardial Infarction


Ranjan Dahal

Debabrata Mukherjee



INTRODUCTION

Acute myocardial infarction (AMI) is defined as an acute myocardial injury with detection of a rise and/or fall of cardiac troponin (cTn) values with at least one value greater than 99th percentile of the upper reference limit of normal along with symptoms consistent with myocardial ischemia; or new ischemic changes in the electrocardiogram (ECG); or development of pathological Q waves; or imaging evidence of ischemic wall motion abnormalities or new loss of viable myocardium; or identification of a coronary thrombus by angiography or autopsy.1

ST-elevation myocardial infarction (STEMI) is defined as a clinical syndrome characterized by symptoms of myocardial ischemia along with persistent ST-segment elevation in ECG and subsequent release of cardiac biomarkers of myocardial injury. The ECG criteria for STEMI are listed in Table 6.1. Considering immediate reperfusion strategies and mortality benefit, it is imperative to designate patients with symptoms suggestive of myocardial ischemia and ST elevations in two contiguous ECG leads as STEMI.


Epidemiology

Ischemic heart disease remains a major public health problem with an estimated prevalence of around 153 million globally. Approximately 1.3 million hospital discharges from the US hospitals in 2014 had an acute coronary syndrome (ACS) listed as a primary or secondary diagnosis.2 There have been changing patterns in the incidence of ischemic heart disease. The overall incidence of STEMI visits has declined significantly whereas non-STEMI has increased. The trends of yearly STEMI incidence of emergency department visits have decreased by more than 60% from 2005-2007 to 2014-2015.3 Women have a later presentation and longer reperfusion (door-to-balloon and door-to-fibrinolysis) time even without contraindications to reperfusion therapy compared to men.4 There is a decreasing mortality trend following STEMI, which is likely from increased reperfusion strategy using primary percutaneous coronary intervention (PCI), newer generation stents, potent antiplatelet therapy, and aggressive secondary risk factors reduction.5 But overall mortality from STEMI is still substantial, accounting for 6.4% of total STEMI cases, with mortality influenced by advanced age, higher Killip class at presentation, time delay to treatment, treatment strategies, left ventricular dysfunction, higher number of diseased coronary arteries, unstable hemodynamics, anterior infarction, and comorbid conditions such as diabetes mellitus and renal failure.6


Risk Factors

The traditional modifiable risk factors for coronary artery disease are tobacco exposure, diabetes mellitus, hyperlipidemia, hypertension, metabolic syndrome, obesity, and physical inactivity. Nonmodifiable risk factors include a family history of premature cardiovascular diseases (first cardiovascular event at age <55 years for men and <65 years for women), genetics, and chronic kidney diseases. Nontraditional risk factors include socioeconomic and psychosocial stress, autoimmune diseases, malignancy, and its therapies, infections, sleep apnea, and pregnancy-related complications.

A substantial proportion of STEMI patients without prior cardiovascular diseases are noted to have no history of standard modifiable cardiovascular risk factors. These patients have higher in-hospital mortality compared to patients with traditional modifiable risk factors.7


PATHOGENESIS

Coronary artery atherosclerosis, nonatherosclerotic causes, and coronary vasospasm can all lead to coronary artery occlusion and STEMI. The most common cause is acute total or subtotal coronary artery occlusion by thrombus from the rupture or ulceration or erosion of atherosclerotic plaque.8 Nonatherosclerotic causes of STEMI include air emboli and emboli from the left ventricle, left atrial appendage, atrial myxomas, and infective endocarditis. Chest trauma, thoracic aortic dissection, spontaneous coronary artery dissection, collagen vascular diseases, and arteritis are other nonatherosclerotic causes. Drugs like cocaine or serotonin receptor agonists (triptans) and Prinzmetal angina can cause severe coronary vasospasm and STEMI.

The atherosclerotic plaque rich in lipids with necrotic core and thin fibrous cap are considered vulnerable plaques. The progression of plaques with the expansion of lipid core and macrophage accumulation causes plaques to rupture. Partial occlusion of the blood vessel lumen leads to myocardial ischemia and non-STEMI, whereas complete occlusion leads to transmural infarction and STEMI. The size of infarction depends on the duration of blood vessel occlusion, the presence of collateral blood supply, the level of occlusion, and microvascular circulation. However, the development of Q waves in ECG depends on the infarct size, not on the depth of myocardial involvement.










CLINICAL PRESENTATION

The most common symptom is retrosternal chest pain or discomfort radiating to the jaw, neck, left arm, or shoulder. The chest pain is usually diffuse, nonpositional, and dull aching or heavy pressure in nature, lasting more than 20 minutes. Other symptoms may be epigastric pain, neck pain, jaw pain, shortness of breath, nausea, vomiting, fatigue, diaphoresis, and generalized weakness. Occasionally, patients may present with sudden cardiac arrest.








The physical signs at presentation may mostly be unremarkable. It may vary depending on the extent and anatomy of myocardial infarction. Hypotension, tachycardia, cool skin, rales, an S3 gallop, and diminished pedal pulses are signs of left ventricular dysfunction and carry a worse prognosis. A new systolic murmur is indicative of mitral regurgitation or ventricular septal rupture. Thoracic ascending aortic dissection is a life-threatening condition that can involve coronaries and present as a STEMI. Myocarditis, pericarditis, and pneumo-mediastinum may all have STEMI-like presentations. A high index of clinical suspicion is required for the diagnosis of myocardial infarction as some patients may have atypical presentations.




DIAGNOSIS


Emergent Electrocardiogram

An ECG should be performed within 10 minutes of first medical contact (FMC) if an ACS is suspected.5 ECG criteria for STEMI are defined in Table 6.1, anatomic location of myocardial injury based on ST changes in ECG in Table 6.2, and Stillshot 6.1, 6.2, 6.3, 6.4, showing coronary artery occlusions and respective ECG changes. Standard ECG calibration is 10 mm/mV and 0.1 mV is equal to 1 mm square on the vertical axis.

A new or presumably new left bundle branch block (LBBB) is considered STEMI equivalent but should not be considered AMI in isolation. Inferior myocardial infarction is commonly associated with concomitant right ventricular infarction. However, a paced rhythm, Brugada syndrome, and left ventricular hypertrophy (LVH) make interpretation of ST segments challenging. The ECG should be repeated if the diagnosis is unclear. A complete resolution of the ST-segment elevation and symptoms after nitroglycerine administration is suggestive of coronary spasm. It is imperative to understand other causes of ST-segment elevation to manage accordingly. ST-segment elevations can be present in left ventricular aneurysm, ventricular-paced rhythm, early repolarization pattern, pneumo-mediastinum, LBBB, myocarditis, pericarditis, takotsubo cardiomyopathy, hemorrhagic cerebrovascular accident and can be a normal variant in young patients.



























Emergent Bedside Echocardiogram and Other Possible Diagnostic Testing

A bedside echocardiogram can be performed emergently if the diagnosis is uncertain to identify regional wall motion abnormalities and mechanical complications related to STEMI. It may also provide an alternate diagnosis such as ascending aortic dissection, pericardial effusion, and massive pulmonary embolism. A chest x-ray may be useful to detect features of aortic dissection. However, routine echocardiogram and chest x-ray delaying emergent coronary angiography are not recommended. (See image Video 6.1d&e and image Video 6.2b&c)

Cardiac magnetic resonance imaging (MRI) and coronary computed tomography (CT) have limited roles in STEMI. Routine blood tests for the cardiac serum marker cTn are indicated but should not delay reperfusion strategy. Other laboratory tests augmenting patient care may include complete blood count, coagulation profile, renal function test, liver function test, serum lipids, hemoglobin A1c, and serum glucose.

Thrombolysis in myocardial infarction (TIMI) and Global Registry of Acute Coronary Events (GRACE) risk scores can be used for early risk assessment of patients presenting with an ACS.9,10 Risk assessment should be repeated during hospitalization and at the time of discharge. These risk scores will provide an overall estimate of the patient’s prognosis, guide the treatment strategy, and inform family members of the potential outcomes.


MANAGEMENT

Appropriate management strategy begins with community awareness about anginal symptoms and preparedness to deliver reperfusion therapy expeditiously and effectively with efforts to make primary PCI the primary reperfusion strategy (Algorithm 6.1). Regional systems of STEMI care should be created and maintained for quality checks.

The optimal management begins at the scene before reaching the hospital. Patients with suspected ACS should be transported by ambulance rather than private vehicles owing to the small risk of cardiac arrest en route to the hospital. A prehospital ECG performed by trained personnel facilitates early reperfusion times and improved outcomes.11 If STEMI is suspected, devices with defibrillator capacity and continuous ECG monitor should be attached to the patient.5 Aspirin (162-325 mg loading dose) should be given orally en route to the hospital if not contraindicated. Sublingual nitroglycerine can also be given for chest pain if tolerated by hemodynamics. The facility receiving the patient should be alerted so that preparation for reperfusion therapy can be initiated. Some facilities even bypass emergency departments to achieve early reperfusion. Ambulances in European countries are well-equipped to administer prehospital fibrinolytic therapy, but are not currently available in the United States.12


Immediate Therapies



  • Oxygen: Oxygen should be given only if SaO2 less than 90% or PaO2 less than 60 mm Hg. Routine oxygen therapy in STEMI patients with normal oxygen saturation is not recommended because it increases the risk of myocardial injury and recurrent myocardial infarction (MI).13


  • Nitroglycerine: Sublingual tablets 0.3 to 0.6 mg and nitro sprays 0.4 to 0.8 mg can be administered every 5 minutes, up to three doses as needed for angina. Intravenous nitroglycerine can be administered for hypertensive and heart failure patients with ongoing ischemia. It should be used cautiously in patients with hypotension, right ventricular infarction, and recent phosphodiesterase inhibitor use.


  • Analgesics: Intravenous opioids can be used for pain control with dose titration based on symptoms and hemodynamics. However, it should be used cautiously in opioid naive, elderly, and patients with borderline hemodynamics. Nonsteroidal anti-inflammatory drugs other than aspirin should be avoided in STEMI patients.


Reperfusion Strategies


Primary Percutaneous Coronary Intervention

Reperfusion therapy should be administered to all STEMI patients with symptoms onset of fewer than 12 hours and no contraindications. Primary PCI is the preferred reperfusion therapy with the greatest survival benefit in high-risk patients.4 It has shown superior outcomes in reducing mortality, reinfarction, or stroke compared to fibrinolysis with similar treatment delays in high volume centers with an experienced operator and skilled staff. It also has lower rates of recurrent ischemia, emergency repeat revascularization, and intracranial hemorrhage.14 Patients should be considered for fibrinolysis therapy if they cannot be transferred to PCI-capable hospital with the goal of FMC to device time of 120 minutes.4,5 As per the catheterization laboratory registry in 2014, the median door-to-balloon time for primary PCI at presenting hospitals was 59 and 105 minutes if transferred from another facility.6

The 2017 European guidelines have started using the term door-to-reperfusion time.5 Both the American College of Cardiology (ACC) and the European Society of Cardiology (ESC) recommend primary PCI in patients with contraindications to fibrinolytic therapy, cardiogenic shock or acute severe heart failure, or life-threatening arrhythmias from STEMI irrespective of symptoms onset. ACC recommends primary PCI for up to 12 to 24 hours after symptoms onset whereas ESC recommends PCI for up to 48 hours.4,5 Early angiography within 24 hours is recommended if symptoms are completely relieved along with the complete resolution of ST spontaneously or after nitroglycerine administration. A routine coronary angiography can be performed in patients presenting 48 hours of symptom onset. However, routine PCI of the culprit artery is not recommended in asymptomatic STEMI patients presenting greater than 48 hours after symptom onset.5

The Minimizing Adverse hemorrhagic events by TRansradial access site and systemic Implementation of angioX (MATRIX) showed radial access was associated with lower risks of access site bleeding, vascular complications, and need for the blood transfusion compared to femoral access. The radial first

approach is the preferred technique depending on operator skills.15 (See image Videos 6.7-6.10.)