Acute ST-Elevation Myocardial Infarction

Continuing Education Activity

An acute ST-elevation myocardial infarction occurs due to occlusion of one or more coronary arteries, causing transmural myocardial ischemia which in turn results in myocardial injury or necrosis. This activity reviews the presentation, evaluation, and management of patients with with ST-elevation myocardial infarctions and highlights the role of the interprofessional team in caring for these patients.

Objectives:

• Describe the evaluation of a patient with a suspected myocardial infarction.
• Describe EKG findings in a patient with an ST-elevation myocardial infarction.
• List the treatment and management options available for an acute ST-elevation myocardial infarction.
• Employ interprofessional team strategies to improve outcomes for patients with ST-elevation myocardial infarctions.

Introduction

An acute ST-elevation myocardial infarction (STEMI) is an event in which transmural myocardial ischemia results in myocardial injury or necrosis.[1] The current 2018 clinical definition of myocardial infarction (MI) requires the confirmation of the myocardial ischemic injury with abnormal cardiac biomarkers.[2] It is a clinical syndrome involving myocardial ischemia, EKG changes and chest pain.

Etiology

An ST-elevation myocardial infarction occurs from occlusion of one or more of the coronary arteries that supply the heart with blood. The cause of this abrupt disruption of blood flow is usually plaque rupture, erosion, fissuring or dissection of coronary arteries that results in an obstructing thrombus. The major risk factors for ST-elevation myocardial infarction are dyslipidemia, diabetes mellitus, hypertension, smoking, and family history of coronary artery disease.[3][4] 

Myocardial infarction in general can be classified [5] from Type 1 to Type 5 MI based on the etiology and pathogenesis. Type 1 MI is due to acute coronary atherothrombotic myocardial injury with plaque rupture. Most patients with ST-segment elevation MI (STEMI) and many with non-ST-segment elevation MI (NSTEMI) comprise this category. Type 2 MI is the most common type of MI encountered in clinical settings in which is there is demand-supply mismatch resulting in myocardial ischemia. This demand supply mismatch can be due to multiple reasons including but not limited to presence of a fixed stable coronary obstruction, tachycardia, hypoxia or stress. However, the presence of fixed coronary obstruction is not necessary. Other potential etiologies include coronary asospasm, coronary embolus, and spontaneous coronary artery dissection ( SCAD). Sudden cardiac death patients who succumb before any troponin elevation comprise Type 3 MI. Types 4 and 5 MIs are related to coronary revascularization procedures like Percutaneous Coronry Intervention (PCI) or Coronary artery Bypass Grfting ( CABG).

Epidemiology

The estimated annual incidence of myocardial infarction (MI) in the United States is 550,000 new and 200,000 recurrent.[6] In 2013, 116,793 persons in the United States suffered a fatal MI with 57% occurring in men and 43% in women.[6] The average age of incidence of a first MI is 65.1 for men and 72 for women.[6] Approximately 38% of patients who present to the hospital with acute coronary syndrome have an ST-elevation myocardial infarction.[6]

Pathophysiology

For an acute thrombotic coronary event to cause ST-segment elevation on a surface ECG, there needs to be a complete and persistent occlusion of blood flow. Coronary athersclerosis and presence of high risk thin cap fibroatheroma (TCFA) can result in sudden onset plaque rupture[7]. This results in changes in vascular endothelium resulting in cascade of platelet adhesion , activation and aggregartion [8] resulting in thrombosis formation.

Coronary artery occlusion in animal models shows a "wave-front" of myocardial injury that spreads from the sub-endocardial myocardium to the sub-epicardial myocardium resulting in a transmural infarction that appears as an ST elevation on surface ECG.[9] Myocardial damage occurs as soon as the blood flow is interrupted which makes timely management a necessity. Sudden onset acute ischmemia can result in severe microvascualr dysfunction

History and Physical

Prior to performing an ECG and collecting troponins the history and physical provide the only clues that lead to a diagnosis of myocardial infarction. Initial evaluation should include a focused physical examination and a brief history. Patients should be asked about the characteristics of the pain and associated symptoms, risk factors or history of cardiovascular disease, and recent drug use.[10] Risk factors for an ST-elevation myocardial infarction include age, gender, family history of premature coronary artery disease, tobacco use, dyslipidemia, diabetes mellitus, hypertension, abdominal obesity, sedentary lifestyle, a diet low in fruits and vegetables, psychosocial stressors.[11] Cocaine use can cause an ST-elevation myocardial infarction regardless of risk factors.[12] History of known congential abnormalities can be helpful. [13]

Evaluation

Evaluation of patients with acute onset of chest pain should begin with an electrocardiogram (ECG) and troponin level. The American College of Cardiology, American Heart Association, European Society of Cardiology, and the World Heart Federation committee established the following ECG criteria for ST-elevation myocardial infarction (STEMI)[14]:

• New ST-segment elevation at the J point in 2 contiguous leads with the cutoff point as greater than 0.1 mV in all leads other than V2 or V3
• In leads V2-V3 the cutoff point is greater than 0.2 mV in men older than 40 years old and greater than 0.25 in men younger than 40 years old, or greater than 0.15 mV in women

Patients with a pre-existing left bundle branch block can be further evaluated using Sgarbossa's criteria[15][16]:

• ST-segment elevation of 1 mm or more that is concordant with (in the same direction as) the QRS complex
• ST-segment depression of 1 mm or more in lead V1, V2, or V3
• ST-segment elevation of 5 mm or more that is discordant with (in the opposite direction) the QRS complex

Treatment / Management

After making the diagnosis of acute ST-elevation myocardial infarction, intravenous access should be obtained, and cardiac monitoring started.  Patients that are hypoxemic or at risk for hypoxemia benefit from oxygen therapy; however, recent studies show possible deleterious effects in normoxic patients.[17][18] Patients should undergo percutaneous coronary intervention (PCI) within 90 minutes of presentation at a PCI capable hospital or within 120 minutes if transfer to a PCI capable hospital is required.[19] If PCI is not possible within the first 120 minutes of first medical contact, fibrinolytic therapy should be initiated within 30 minutes of patient arrival at the hospital.[19] It is important to rule out conditions that can mimic an acute coronary syndrome like acute aortic dissection or acute pulmonary embolism.

All patients with an acute myocardial infarction should be started on a beta blocker, high intensity statin, aspirin, and a P2Y12 inhibitor as soon as possible, with certain exceptions.  Nitroglycerin administration can reduce anginal pain however it should be avoided in patients who have used phosphodiesterase inhibiting medication within the last 24 hours and in cases of right ventricular infarction. Further pain relief with morphine can be given for patients that continue report discomfort after nitroglycerin administration however judicious use is not recommended as it may adversely affect outcomes.[20] P2Y inhibiting antiplatelet medication choice depends on whether the patient underwent PCI or fibrinolytic therapy. Ticagrelor and prasugrel are preferred to clopidogrel in patients who undergo PCI due to recent trials showing superiority.[21][22] Patients undergoing fibrinolytic therapy should be started on clopidogrel.[23] It is important to be careful about relative contraindications of P2Y12 inhibitors . Prasugrel is contraindicated in pateints with h/o Transient Ischemic attack and stroke.

Anticoagulation should also be started aongside with unfractionated heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux[24]

Differential Diagnosis

Other pathologies that can cause ST-segment elevations include: myocarditis, pericarditis, stress cardiomyopathy (Takotsubo), benign early repolarization, Acute vasospasm, spontaneous coronary artery dissection, left bundle branch block, various channelopathies, and electrolyte abnormalities.

Prognosis

Mortality rates at 30 days for patients presenting with ST-elevation myocardial infarction are between 2.5% to 10%.[25][26][27][25] The most commonly used scoring system for 30-day mortality is the TIMI risk score.[28] The TIMI scoring system considers:

• Age older than 75 years (3 points); Age 64 to 74 (2 points)
• Diabetes, hypertension, or history of angina (1 point)
• Systolic blood pressure less than 100 mm Hg (3 points)
• Heart rate greater than 100 beats per minute (2 points)
• Killip class II to IV (2 points)
• Body weight less than 150 lbs (1 point)

Complications

There are 3 life-threatening mechanical complications of myocardial infarction: ventricular free wall rupture, interventricular septum rupture, and acute mitral regurgitation. Ventricular free wall rupture occurs within 5 days in half the cases and within 2 weeks in 90% of cases with an overall mortality rate of greater than 80%.[29][30] Rupture of the interventricular septum is reported about half as often as free wall rupture and typically occurs 3 to 5 days with an overall mortality rate greater than 70%.[31][32] Prompt surgery reduces the mortality rate in both conditions. Acute mitral regurgitation following a myocardial infarction is most commonly due to ischemic papillary muscle displacement, left ventricular dilatation, or rupture of the papillary muscle of chordae.[33] In ST-elevation myocardial infarction, the degree of mitral regurgitation is usually severe and associated with a 30-day survival of 24%.[33]

Enhancing Healthcare Team Outcomes

A door-to-balloon time of fewer than 90 minutes is the goal of a PCI capable facility and is one of the core measures of the Joint Commission on Accreditation of Healthcare Organizations.[34][35] This is the time between the patient's arrival in the emergency department and the crossing of the culprit lesion by a guide wire in the cardiac cath lab. Teamwork between EMS, emergency department physician, and interventional cardiologist sets the groundwork for optimal door-to-balloon times (Level 1). As of 2010, the median door-to-balloon time was 64 minutes with 91% of patients receiving PCI in under 90 minutes and 70% in under 75 minutes.[34]

Review Questions

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Disclosure: Hina Akbar declares no relevant financial relationships with ineligible companies.

Disclosure: Christopher Foth declares no relevant financial relationships with ineligible companies.

Disclosure: Rehan Kahloon declares no relevant financial relationships with ineligible companies.

Disclosure: Steven Mountfort declares no relevant financial relationships with ineligible companies.