Chief Complaint: chest pain

History of Present Illness

Past Medical History

Social History

Family History

Figure 2

Table 2 (pertinent positives/negatives)

Figure 3

Table 3

Figure 4

Table 4

Figure 5

Figure 1 ECG on Admission

Electrocardiogram (ECG) is the single most important test that aids diagnosis of STEMI, and should be performed and shown to an experienced provider within 10 minutes of a patient’s complaint of chest pain whether inpatient or arrival to the ED. The ECG is at the center of decision pathway for treating patients that present with this symptom. If initial ECG does not show STEMI but the patient’s symptoms persist with a high clinical suspicion of STEMI, serial ECGs every five to ten minutes or continuous 12-lead ECG is recommended to detect potential development of ST elevation.³ (Further discussions on ECG will under the Diagnostic Review section).

Cardiac biomarkers such as CPK, CK-MB, and troponin are proteins released from infarcted heart muscle after any damage to the myocardium as seen in STEMI and NSTEMI. These substances become detectable in serum when cardiac lymphatics become overwhelmed and unable to clear the amount being spilled into the venous circulation.² These biomarkers can be useful in the diagnosis of myocardial damage, and provide supportive non-invasive evidence for reperfusion therapy; however pending lab results should not delay therapy for patients with ST elevation on ECG and symptoms of STEMI.³ Due to their high sensitivity and specificity for myocardial damage, cardiac troponins are preferred for diagnosis of myocardial damage and infarction. Cardiac troponins typically rise within 3-6 hours of a cardiac event and therefore may not typically be elevated during initial work-up for a patient that presents with chest pain suspicious for an MI, and may persist for up to 14 days.³ This patient’s troponin level was not elevated on initial admission but significantly elevated at 0.54 ng/ml at the onset of chest pain. This finding leads to the suspicion that a previous episode of unstable angina or vague epigastric discomfort may have been a MI. CK-MB is the second option if cardiac troponin assays are not available, and has the advantage of diagnosing patients who present early with symptoms. This biomarker appears rapidly in the blood long before troponins are detected, but returns to normal within 24-48 hours. CK-MB, however, is found in the blood of healthy people with any skeletal muscle damage, and is not as specific as cardiac troponin in detecting myocardial damage.³ This biomarker can therefore be used to estimate the time of injury in patients with elevated troponins, as well as detect re-infarction during a treatment course, ¹ and is very useful in assessing reperfusion following treatment.³

Other Laboratory Examinations

Complete Blood Count

Basic Metabolic Panel

Coagulation Studies

Brain Natriuretic Peptide (BNP)

D-dimer

Electrocardiography is a fast, non-invasive, and accessible bedside screening tool that guides emergency treatment strategies for patients that present with chest pain. Because of decreased blood supply, a 12-lead ECG may show ST segment elevation for patients with acute myocardial infarction.¹¹ ACC and AHA recommend that a 12-lead ECG be performed and read by an experienced practitioner within ten minutes of presentation to the emergency department by all patients with chest pain or symptoms suggestive of a STEMI. The initial ECG can shed light on patients with important predictors of mortality such as a left bundle branch block (LBBB), and anterior injury/infarct location, and can guide choice of reperfusion therapy.³ This patient’s ECG on admission and at the time of the event 10 days later can be seen in Figures 1 and 4 below. Figure 2 is ECG on encounter 1 showing diffuse ST elevation (leads I, AVL, V₃, V₄, V₅, V₆,) indicating anterior-lateral injury, left axis deviation (negative in lead II), right bundle branch block (split R wave in lead V1). Note pathological Q waves in these anterior-lateral leads with marked repolarization abnormalities indicating injury to the myocardium. Mortality also increases with the number of ECG leads showing ST elevation.³

Figure 6

Figure 2 ECG at Encounter 10 Days Later

Figure 7

Figure 3 Chest x-ray on Admission

Kushner et al.,⁴ writing for ACC/AHA, recommend a high-quality portable chest x-ray as one imaging study that should be used to differentiate a STEMI from aortic dissection in a subset of patients whose diagnosis is unclear. Aortic dissection appears as a widened mediastinum on chest film. However, an imaging study should not delay implementation of reperfusion if a definitive diagnosis of STEMI exists.³ Chest radiography is also indicated when a relevant history or physical examination calls for further investigation of pulmonary symptoms such as cough, shortness of breath, suspicion of pneumonia, lung congestion, and mass or any other finding that may be significant in clinical patient care.⁴ The case study patient complained of chest pain associated with shortness of breath, and physical exam also supported the need to get an imaging of his cardiac silhouette and lung parenchyma (shown in Figures 3 and 4).

Figure 8

Figure 4 Chest x-ray at Encounter 10 Days Later

Impression:

The heart is upper normal in size. Moderate pleural thickening is demonstrated at the inferior part of the chest on both sides and at both apices. The appearance is similar 2 months ago. There is no significant interval change. Presence of any new air space consolidation is not suspected. The pulmonary vascularity is within range of normal

Figure 9

Figure 5 Rupture of Arterial Fibrous Cap

Impression:

Probable bilateral small pleural effusions, with associated basilar sub-segmental atelectasis. Early pneumonia in the right lower lobe is not excluded. Posterior-anterior and lateral views of the chest are recommended when feasible.

Working Diagnosis: ST segment elevated myocardial infarction

Myocardial infarction occurs when a coronary artery suddenly becomes partially or completely blocked by a blood clot, causing at least some of the heart muscle being supplied by that artery to become injured or permanently damaged due to an imbalance of oxygen supply and oxygen demand.^2,12 Signs and symptoms that suggest MI include: chest pain (pressure, squeezing, pain in the center of the chest), discomfort in one or both arms, back, neck, jaw, or stomach, shortness of breath, nausea and vomiting, weakness, fatigue, and diaphoresis.³ Elderly patient are less likely to experience chest discomfort and are more likely to present with shortness of breath, nausea, and syncope.³ In patients with diabetes, pain recognition may be altered due to autonomic neuropathy. These patients may present instead with dyspnea, nausea/vomiting, diaphoresis and/or fatigue.³ Women may also present without the chest pressure. Atypical symptoms need to be evaluated in these special populations or in individuals at high risk for coronary heart disease (CHD).

Atherosclerotic plaques have long been implicated in the pathology of heart disease. ST elevation myocardial infarction (STEMI) is not usually precipitated by slow-building high-grade stenosis of the coronary artery that may cause complete occlusion of the vessel, rather by non-obstructive plaques that are made with abundant macrophages and inflammatory cells. These plaques are lipid laden, and are referred to as vulnerable and high-risk plaques that are easily disrupted. Once disrupted or injured, exposure of substances occurs that promotes platelet aggregation, activation and adhesions, as well as thrombin generation and formation. The formed thrombus can completely occlude the coronary artery, and without sufficient collateral circulation, myocardial ischemia and subsequent infarction occurs within 15 minutes of myocardial oxygen deprivation.³ In STEMI, the coronary artery previously affected by atherosclerosis is abruptly occluded by a thrombus at the site of vascular injury and completely blocks off oxygen and blood supply to all the heart muscle being supplied by the affected artery causing death to the heart muscle.

STEMI in very rare cases may be due to coronary artery occlusion caused by coronary emboli, congenital abnormalities, coronary spasm, and other systemic inflammatory diseases, but in most cases occurs when the surface of an atherosclerotic plaque becomes disrupted, exposing the intima to an inflammatory process that favors thrombogenesis. A mural thrombus forms at the site of plaque disruption, and the involved coronary artery becomes occluded.^{1, 2} (See Figure 3) This injury process is produced or facilitated by factors such as smoking, hypertension, and lipid accumulation.

Figure 10

Table 5 Killip’s Classification of STEMI

Acute coronary syndrome (ACS) is an umbrella term which encompasses a spectrum of myocardial ischemia including: unstable angina (USA), myocardial infarction without ST segment elevation (NSTEMI), and STEMI.^1,2 USA is non-specific chest pain syndrome that may indicate ischemia with or without ischemic changes seen on ECG, but without abnormal cardiac biomarkers.¹³ STEMI shows persistent ST-segment elevation in two or more contiguous leads on ECG with elevated cardiac markers, while NSTEMI does not show elevation of the ST-segment, but also has elevated cardiac biomarkers. Non-specific ischemic changes like ST depression or T wave inversion may also occur in NSTEMI and USA. The percentage of patients with ACS who develop STEMI is 2%.¹The previously classification of Q-wave and non–Q-wave MI for ACS recently has been abandoned as not all STEMIs evolve into a Q-wave MI, and a NSTEMI may develop a Q-wave MI. Recent classification is based on the initial or subsequent ECG findings: those with ST-elevation (STEMI) and those without ST elevation (NSTEMI), but with enzyme evidence of myocardial damage. The current classification coincides with current treatment strategies because patients presenting with ST elevation can benefit from immediate reperfusion therapy.^{1, 2}

Coronary heart disease is one components of the metabolic syndrome, and a major risk factor for MI.¹⁴ Primary care providers have been charged with identifying and assisting patients with modifiable risks of CHD to reduce such risk factors. Some of the risk factors of CHD that can result in MI are smoking, family history of CHD, hyperlipidemia, hypertension, abdominal obesity, and diabetes mellitus.

Patients with two or more risk factors are at increased ten-year risk and can benefit greatly from primary prevention. Patients with established CHD also benefit from secondary prevention of the disease.³ Several health promotion and prevention strategies may help in the reduction of fatality from STEMI. These include:

Risk stratification of patients with STEMI through physical assessment can be achieved by using the Killip’s classification of STEMI (Table 5) to predict clinical outcomes and mortality based on the degree of heart failure following acute STEMI.¹ This classification stratifies STEMI patients into four groups based on the degree of heart failure (HF). Killip's Class I is STEMI patients with no evidence of heart failure who have a 6% mortality risk. Class II is those with mild HF as evidenced by rales, S₃ heart sound, and congestion evident on chest imaging. This class of patients has a 17% mortality rate. Class III is patients with STEMI who have developed subsequent pulmonary edema, and have a 38% mortality rate. STEMI patients in cardiogenic shock are classified under Killip’s class IV, with an 81% mortality risk. Early assessment and risk stratification of patients with acute STEMI enables prediction of outcomes.¹

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