Wednesday, March 31, 2021

Anterior St Elevation Myocardial Infarction (STEMI) Case File

Posted By: Medical Group - 3/31/2021 Post Author : Medical Group Post Date : Wednesday, March 31, 2021 Post Time : 3/31/2021
Anterior St Elevation Myocardial Infarction (STEMI) Case File
Eugene C. Toy, Md, Michael d . Faulx, Md

Case 1
a 62-year-old man arrives to tile emergency department complaining of acute. severe precordial chest pain radiating to his arm and neck. He reports feeling like “an elephant is standing on my chest” and states that his symptoms are accompanied by nausea. His chest pain began approximately 30 minutes ago while lie was watching television and it has not completely resolved since onset. His medical history includes hypertension. hyperlipidemia. and a 50-pack/year history of cigarette smoking.

On examination the patient is diaphoretic and in moderate distress vit1i the fol lowing vital signs: blood pressure 15697 mmHg. puke 113 bpm. respiratolyrate 24 breaths min. and oxygen saturation 98% on room air. He is tachycardic with a normal Si and 52 and without murmurs, nibs, or gallops. His jugular venous pressure is not elevated: lie lias a left carotid bruit. Chest auscultation reveals faint crackles at the left base but is otherwise clear. His abdomen is protuberant but soft and without masses. His lower extremities are without edema. He has 2+ pulses in his upper and lower extremities. an electrocardiogram (ECG) is per formed and shown (Figure 1-1). Stat labs are drawn and the nurse lias just sent them to the laboratory.

c ‘What is the most likely diagnosis?
c What is the most important feature of his presenting history?
c What is the most important initial therapeutic maneuver

Case ECG

Figure 1-1. Case ECG Make note of the ST segments in leads V1—V4


Answer to Case 1:
Anterior St Elevation Myocardial Infarction (STEMI)

Summary: This is a 62-year-old man who presents with a chest pain story that is classic for acute myocardial ischemia, including precordial discomfort radiating to the arm and neck. He has risk factors for coronary artery disease, including elevated cholesterol, high blood pressure, and an extensive smoking history. He has a carotid bruit on exam that suggests significant underlying atherosclerosis. An acute surge of catecholamines is responsible for the patient’s tachycardia, elevated blood pressure, and diaphoresis. His ECG is diagnostic.

  • Most likely diagnosis: Anterior ST segment elevation myocardial in farction.
  • Most important feature of presenting history: The time since symptom onset.
  • Most important initial therapeutic maneuver: Prompt coronary revascularization..

ANALYSIS

Objectives
1. Instant recognition of patients presenting with STEMI.
2. Understanding the importance of immediate reperfusion therapy for patients with STEMI.
3. Awareness of other diagnoses that should be considered in this patient group.
4. Knowledge of the potential electrical and mechanical complications of STEMI.
5. Knowledge of the evidence-based therapies that should be employed on discharge for this patient group.


Considerations
ST elevation myocardial infarction is a true medical emergency that requires immediate recognition and prompt treatment. Time is the most important factor to consider at presentation because survival of myocardial tissue (as well as the patient) depends on prompt and early coronary revascularization. “Time is muscle” is a commonly used expression in emergency departments and catheterization laboratories around the world for good reason; the faster we recognize and treat STEMI, the more lives we save.

The first priority in this patient is to establish the diagnosis so that definitive therapy can be rendered. His ECG and clinical scenario is classic for STEMI; however, it is important to consider other potential causes of ST segment elevation and chest pain such as acute aortic dissection and pericarditis as these conditions will certainly not improve and in fact may be exacerbated by the usual treatment for STEMI [eg, anticoagulation, percutaneous coronary intervention (PCI), or thrombolysis]. These diagnoses can often be excluded by clinical history alone, but if aortic dissection is strongly suspected, it may be necessary to arrange for a stat contrast-enhanced

CT of the chest or transesophageal echocardiogram prior to definitive therapy. It is also important to carefully document this patient’s presenting physical exam so that potential complications of myocardial infarction can be readily identified should he decompensate during his hospitalization. Once the diagnosis of STEMI is secure, the patient should receive aspirin 325 mg, an ADP inhibitor, and parenteral anticoagulation while in the emergency department a decision is made regarding reperfusion strategies.

Approach To:
ST Elevation Myocardial Infarction

DEFINITIONS

Acute coronary syndrome: A term that encompasses a range of ischemic heart diseases, including unstable angina (pain from myocardial ischemia at rest), non-ST-segment elevation myocardial infarction (myocardial ischemia with ST depression and/or T wave inversion and positive biomarkers), STEMI (myocardial ischemia due to complete occlusion of affected coronary artery resulting in positive biomarkers and ST elevation of > 0.1 mV in two or more adjacent leads).

Adenosine diphosphate (Adp) receptor inhibitor: Any of the antiplatelet medications used to inhibit platelet activation and aggregation by blocking the ADP receptor on platelet cell membranes. The most widely used ADP inhibitors include clopidogrel, prasugrel, and ticagrelor.

Cardiac biomarkers: Any serum marker that is specific for necrosis of myocardial tissue such as troponin T, troponin I, and CK-MB (creatine kinase myocardial band). When these markers are positive in the appropriate clinical setting, a patient has “ruled in” for myocardial infarction.

Reperfusion therapy: The ultimate treatment goal in the management of acute myocardial infarction is to return adequate blood flow to the affected myocardium by establishing patency of the infarct-related coronary artery. reperfusion therapy refers to either direct mechanical disruption of the thrombus with percutaneous coronary intervention or through pharmacologic therapy with potent fibrinolytic medications that lyse thrombus such as streptokinase, alteplase, reteplase, and tenecteplase.


CLINICAL APPROACH

Pathophysiology
An ST segment elevation myocardial infarction (STEMI) is most commonly the result of atherosclerotic plaque rupture with subsequent acute thrombus formation and completion occlusion of the arterial lumen. Rupture of the fibrous cap reveals the highly thrombogenic extracellular lipid core, initiating platelet activation and aggregation as well as thrombin activation (Figure 1-2). Less frequently, an erosion

Pathophysiology of STEMI

Figure 1-2. Pathophysiology of STEMI. a cute coronary syndromes typic y begin with the rupture of
a vulnerable atherosclerotic plaque (a). Interaction between the bloodstream and plaque contents
(particularly oxidized l Dl cholesterol ) results in platelet activation and aggregation (b). Fibrinogen is
cleaved by thrombin to fibrin. which then complexes with activated platelets to form a thrombus
(c) that may ultimately propagate and occlude the vessel lumen, causing in farction (d). (Reprinted
with permission, Cleveland Clinic Center for Medical Art &Photography © 2013. All rights reserved.)

of a coronary plaque can occur without plaque rupture but still resulting in thrombus generation. Other rare causes of STEMI include coronary artery spasm, coronary artery dissection, arteritis, cocaine abuse, and embolism to a coronary artery. All of these pathologic mechanisms have a common final pathway to inducing myocardial ischemia and ultimately infarction if artery patency is not established within approximately 30 minutes of occlusion. In other words, the lack of blood flow results in myocyte ATP depletion and subsequent coagulation necrosis of the myocardium.

Clinical Presentation
The majority of patients presenting with STEMI will describe a crushing, heavy, pressure, or squeezing sensation. Radiation to the left arm or into the jaw is classic, although radiation to the back, right arm, shoulder, and epigastric region are also seen. The character can be similar to stable angina; however, the pain associated with STEMI is of longer duration (typically > 20–30 minutes), not relieved by nitroglycerin, and more intense. Associated symptoms include dyspnea, diaphoresis, palpitations, nausea, vomiting, extreme fatigue, or an impending sense of doom. Importantly, patients with diabetes, women, or the elderly may present without chest pain, only describing a nonspecific discomfort in combination with one of the aforementioned associated symptoms such as dyspnea or diaphoresis. One must maintain a high index of suspicion in these patient populations.

The physical exam rarely contributes to the diagnosis of STEMI; however, it is very important to perform in order to exclude other diagnoses that may present in a similar fashion. In addition, the initial exam is important to monitor for complications that may occur as a result of STEMI such as pulmonary edema with pump failure or a new apical systolic murmur in patients with papillary muscle rupture.

The most important action to take in any patient presenting with possible STEMI is to obtain an ECG. This should be performed and interpreted immediately on presentation so that emergent reperfusion therapy can be initiated if indicated. ECG criteria diagnostic of STEMI include ST elevation of 1 mm or greater in two or more contiguous leads. In leads V2–V3, at least 1.5 mm of ST elevation in women and 2 mm or greater in men are needed to make the diagnosis. The infarct-related artery can be identified according to which leads are involved (Table 1-1). In addition, any patient with symptoms suggesting ACS in the setting of a new left bundle branch block (LBBB) should be treated as diagnostic for STEMI. In patients with old LBBB, the criteria in Table 1-2 can be helpful in diagnosing STEMI. If the diagnosis remains unclear in patients with LBBB, emergent echocardiography is indicated to explore for regional wall motion abnormalities that may suggest underlying active myocardial injury. Wall motion assessment by echocardiography is also helpful in cases where ECG findings are not characteristic for STEMI although there is a high index of suspicion based on clinical presentation such as ongoing typical chest pain unrelieved with nitroglycerin administration. Complete occlusion of the left circumflex artery (LCx), for example, will occasionally present with minimal to no ECG changes. Echocardiography can reveal akinesis of the lateral wall, suggestive of STEMI and the need for emergent reperfusion therapy.

Ecg Changes and Correlation with Infarct Related Artery

Ecg Criteria for Diagnosing Stemi

Note: ≥ 3 points = 90% specific city and a 88% positive predictive value.

Laboratory investigation is also important for the diagnosis of STEMI; however, there may be a significant delay between the time of vessel occlusion and the return of the first positive biomarker assay. Thus, one should not wait for laboratory data before making a decision regarding reperfusion therapy in patients with symptoms and ECG findings diagnostic for STEMI. Contemporary cardiac biomarkers include creatine kinase (CK), creatine kinase myocardial band (CK-MB), troponin I (TnI), and troponin T (TnT). CK is present throughout skeletal tissue, whereas CK-MB is more specific to cardiac muscle. Both are released during STEMI and are measureable within 4–6 hours, peak within the first 24 hours, and normalize by 48–72 hours. TnI and TnT are both specific and sensitive for acute myocardial infarction. They are released within 4–8 hours after symptom onset and generally peak by 12–36 hours. Troponins can remain elevated for up to a week after an acute event.

Differential Diagnosis
The differential diagnosis for STEMI is extensive and includes other cardiovascular disorders, pulmonary pathology, and gastrointestinal (GI) disease. Perhaps the most important diagnosis to rule out is the presence of an aortic dissection. This is critical as fibrinolytics and anticoagulants are contraindicated in aortic dissection. One should suspect dissection in a patient with risk factors for dissection, including a history of uncontrolled blood pressure or Marfan’s disease. Classically, the patient will report sudden onset of tearing chest pain that radiates to the back. A chest x-ray can reveal a widened mediastinum, and the patient may have unequal blood pressure readings in each arm. Careful auscultation may reveal the presence of a new diastolic murmur consistent with aortic insufficiency. All of these findings, however, are nonspecific, and thus if there is any suspicion of aortic dissection, a gated CT is required for the diagnosis. Alternatively, if the patient has renal insufficiency that would be exacerbated by contrast administration, an emergent transesophageal echocardiogram (TEE) can be obtained. Occasionally, a dissection can be identified by transthoracic echocardiography (TTE) alone; however, if this is unrevealing, further imaging with CT or TEE is required. It is important to note that a patient can present with both aortic dissection and myocardial infarction should the dissection flap involve a coronary ostium. Emergent cardiothoracic surgery is required for definitive treatment in any dissection involving the ascending aorta.

Patients with pericarditis classically present with chest pain that is improved with sitting forward or upright and exacerbated when supine. ECG findings usually show diffuse concave ST elevations with PR depression. Auscultation may reveal a friction rub. If the inflammation also involves myocardium, the patient will often have positive cardiac biomarkers. It can be associated with a viral infection and generally has a more subacute presentation compared to ACS.

Another important diagnosis on the differential for sudden-onset chest pain is pulmonary embolism. This typically presents with acute onset of dyspnea and pleuritic chest pain. ECG will most often show sinus tachycardia, although it may reveal acute cor pulmonale with a S1Q3T3 pattern (prominent S wave in lead I along with a Q wave and inverted T wave in lead III). Echocardiography may reveal evidence of right ventricular strain and is helpful in ruling out regional wall motion abnormalities of the left ventricle.

Gastrointestinal (GI) disorders, including nutcracker esophagus, diffuse esophageal spasm, GI reflux disease, and acute cholecystitis, can also mimic ACS. A careful history and physical exam (H&P) helps to exclude these potential diagnoses. Chest pain that is affected by food intake, is relieved by antacids, or does not radiate is more suggestive of noncardiac chest pain. Acute cholecystitis is generally associated with right upper quadrant tenderness, leukocytosis (which can also be seen in ACS), and fever. Diagnosis can usually be established with abdominal ultrasound. Given the life-threatening nature of ACS, one should fully rule out cardiac chest pain prior to attributing symptoms to a GI source.

TREATMENT OF STEMI
After diagnosis of STEMI based on the above, all patients should be administered aspirin 325 mg unless a true aspirin allergy exists. Each patient should also receive an oral loading dose of an ADP inhibitor such as clopidogrel 600 mg, prasugrel 60 mg, or ticagrelor 180 mg. If the patient is selected for fibrinolytic therapy, then administration of clopidogrel 300 mg is recommended. All patients should also receive a parenteral anticoagulant. Traditionally, unfractionated heparin has been used. For
those undergoing fibrinolytic therapy, enoxaparin has been shown to be superior to unfractionated heparin. Glycoprotein IIb/IIIa inhibitors should not be administered at first presentation in patients who have received dual antiplatelet therapy but generally are reserved for use by an interventional cardiologist if the patient is experiencing thrombotic complications.

While the aforementioned therapies are important in the treatment of STEMI, the most important clinical decision in STEMI management pertains to the patient’s candidacy for reperfusion therapy. Time is of the essence to prevent irreversible myocardial damage as there is an inverse relationship between time to reperfusion and survival benefit. There are no absolute contraindications to PCI, and it is the recommended method of reperfusion when it can be performed in a timely manner. Specifically, the goal is to limit the “door to balloon” time at a PCI-capable facility to under 90 minutes; that is, angioplasty should be performed less than 90 minutes from the time the patient first presents for treatment. If the patient arrives to a non- PCI capable facility, an extra 30 minutes is permitted (for a total of 120 minutes) to allow time for transfer.

If facilities for PCI are not available in a timely manner, then reperfusion with a fibrinolytic, unless contraindicated, should be employed within 30 minutes of

cardiopulmonary resuscitation

Abbreviations: CPR, cardiopulmonary resuscitation; DBP, diastolic blood pressure; ICH, intracranial hemorrhage: SBP. systolic blood pressure.

hospital arrival. Absolute contraindications to fibrinolysis include suspected aortic dissection, active bleeding or diathesis (not including menses), history of hemorrhagic stroke, intracranial neoplasm or cerebral vascular lesion, or a history of ischemic stroke, closed head, or facial trauma within the last 3 months (Table 1-3). After administration of a fibrinolytic agent, all patients, especially those who are at high risk (extensive ST segment elevation, history of myocardial infarction, recentonset LBBB, tachycardia, or hypotension), should be transferred to a PCI-capable facility as soon as possible so that PCI can be performed as needed. After these initial therapies, the patient should be monitored in a coronary intensive care unit so that any potential complications can be quickly identified and treated.

COMPLICATIONS OF STEMI
Acute complications of STEMI include arrhythmias, pump failure, papillary muscle rupture or dysfunction, ventricular septal rupture, ventricular free wall rupture, or embolic complications. Late complications include postinfarct pericarditis (Dressler syndrome) and ventricular aneurysm formation. Within the first 24–48 hours of STEMI, patients are at increased risk of ventricular tachycardia (VT) or ventricular fibrillation (VF), particularly for those who are not revascularized in a timely manner or are incompletely revascularized. Patients with sustained VT or VF should be treated immediately with electrical defibrillation or cardioversion as well as intravenous amiodarone. Although premature ventricular complexes (PVCs) are frequently seen in these patients, prior studies have shown increased mortality when antiarrhythmics are used for PVC suppression; therefore, these agents should be avoided. Any electrolyte derangement such as hypokalemia or hypomagnesemia should be treated. One should not confuse VT with an accelerated idioventricular rhythm, which is a wide complex rhythm at a heart rate of 60–120 bpm that frequently accompanies myocardial reperfusion (Figure 1-3). Accelerated idioventricular rhythm is benign and almost always asymptomatic. Supraventricular tachycardias (SVTs) are less common, although they should be treated to prevent increased myocardial oxygen demand. If the SVT causes hemodynamic compromise, immediate

accelerated idioventricular rhythm

Figure 1-3. accelerated idioventricular rhythm Commonly referred to as reperfusion arrhythmia this
transient wide complex rhythm is typically asymptomatic and does not cause hemodynamic instability.

cardioversion is indicated followed by amiodarone administration. Sinus bradycardia may be seen in patients who suffer an inferior STEMI as the RCA typically gives rise to the sinoatrial nodal artery that supplies the sinoatrial node. If this rhythm is not well tolerated, a temporary transvenous pacemaker may need to be inserted. Likewise, in patients who develop high-degree AV block, a temporary pacemaker may be required. Ideally, both atrial and ventricular leads are inserted to maintain synchrony between the atria and ventricles.

Pump failure and cardiogenic shock occur in 5–8% of patients hospitalized with STEMI. cardiogenic shock is defined as a systolic blood pressure (SBP) <90 mmHg for at least 30 minutes or need for vasoactive medications or mechanical support to maintain SBP > 90 mmHg, cardiac index < 2.2 L/min/m2, and a pulmonary capillary wedge pressure (PCWP) of >15 mmHg. In patients with extensive myocardial involvement, systolic function may be profoundly compromised with decreased cardiac output. Diastolic function can also be impaired, resulting in increased filling pressures, pulmonary congestion, and hypoxemia. The mainstay of treatment for cardiogenic shock is early revascularization. After this has been performed, care is mainly supportive and focuses on maintaining adequate ventilation, oxygenation, and perfusion. Therapy may include an intraaortic balloon pump, temporary pacing if bradycardic, as well as vasoactive agents. Hemodynamic monitoring with a pulmonary artery catheter is frequently employed. In particularly dire cases in the appropriate patient, a percutaneous ventricular assist device (eg, TandemHeart or Impella) or extracorporeal membrane oxygenation (ECMO) may be employed as a bridge to recovery, cardiac transplant, or left ventricular assist device (LVAD) implantation.

Patients with inferior STEMI may experience right ventricular (RV) infarction and failure. These patients will typically present with hypotension and elevated jugular venous pressures, but with no pulmonary congestion. They are extremely volume sensitive and may require liters of fluid to maintain cardiac output and maintain a PCWP of 15 mmHg. Given their dependence on preload, nitrates and diuretics must be avoided. This cannot be overstated. Should IV fluids alone not maintain cardiac output, an inotrope such as dobutamine is indicated. In the majority of cases, RV function will improve with time and supportive care.

Patients suffering from an inferior STEMI are also at increased risk for papillary muscle dysfunction or rupture. This is due to the fact that the posteromedial papillary muscle generally is supplied by a single artery, namely, the posterior descending artery (PDA), which typically arises from the RCA. Severe papillary muscle dysfunction or, in particular, papillary muscle rupture, is an indication for emergent surgery. In the case of rupture, rapid initiation of after load reduction with vasoactive medications as well as intraaortic balloon pump (IABP) is virtually always required as a bridge to surgery.

Ventricular septal rupture (VSR) is more common in patients who are older, are female, and have no history of prior infarct. Frequently, it manifests as a sudden deterioration in clinical status with hypotension, biventricular failure, and a new pansystolic murmur at the left lower sternal border. Importantly, in patients with a large defect or those that are in cardiogenic shock, the murmur may be subtle or even inaudible. The patient should be stabilized with expeditious initiation of nitroprusside and IABP to reduce afterload. Emergent consultation with cardiothoracic surgery is indicated. Even with surgery, prognosis is still grim. In patients who are at particularly high risk, percutaneous closure may be performed by an interventional cardiologist using a ventricular septal defect closure device.

Rupture of the ventricular free wall is also more common in females, the elderly, and those who have no prior history of myocardial infarction. It generally presents with sudden onset of chest pain and is rapidly fatal unless emergent surgery is performed. As blood enters the pericardial space, the patient will develop signs of tamponade, including jugular venous distension, muffled heart sounds, and pulsus paradoxus. In dire cases, pericardiocentesis can be considered while arrangements are being made for the operating room. This is a stopgap measure only as blood will continue to fill the pericardial space; definitive surgical therapy is uniformly required for survival.

In addition to the above, one must be watchful for potential embolic complications. Shortly after the patient develops an acute occlusive coronary lesion, the patient’s ventricular function is impaired along the artery’s territory. Blood flow becomes sluggish, and the risk of a mural thrombus increases. This is particularly true in patients who suffer an anterior wall myocardial infarction or in those with large infarcts. Should this thrombus embolize, the patient may suffer stroke, acute limb ischemia, intestinal ischemia, or renal infarction. In the acute setting, the appropriate consultant should be contacted immediately to prevent permanent tissue damage. Intravenous anticoagulants followed by oral anticoagulants on an outpatient basis should also be employed.

Dressler’s syndrome or late pericarditis is a late complication of STEMI that can present up to 2 months postinfarct. Patients typically describe progressively worsening chest pain that can last for hours. The discomfort is exacerbated with the patient lying flat and alleviated when the patient leans forward. A friction rub may be heard on exam. Treatment is with aspirin 650 mg every 4–6 hours along with colchicine. Nonsteroidal anti-inflammatory medications (NSAIDs) should be avoided in the postinfarct patient given their increased cardiovascular risk.

Ventricular aneurysms are another potential late complication of STEMI. They are more commonly seen in patients who do not receive reperfusion therapy. Symptoms vary widely, and patients may be asymptomatic or present with arrhythmias and acute decompensate heart failure. If a mural thrombus is present, patients should be anticoagulated for 3–6 months. Anticoagulation should also be considered in patients with an aneurysm in combination with a low ejection fraction, as these patients have higher rates of stroke. Surgical resection should be considered in patients who develop refractory heart failure or arrhythmias.

SECONDARY PREVENTION
Because of the extensive toxic cardiovascular effects of smoking, any patient who smokes should stop immediately. For many patients, experiencing a STEMI is a profoundly life-altering experience that renders them particularly amenable to smoking cessation efforts. This is, in fact, the single most important action a patient can take to prevent subsequent morbidity and mortality and should be pursued aggressively. Other risk factors, including hypertension and diabetes, should be optimized. Prior to discharge, all patients should leave the hospital on an evidence-based medical regimen to help prevent recurrent events and death. High-dose statins, such as atorvastatin 80 mg daily, have been shown to be more effective than low-dose statins, even if their LDL (low-density lipoprotein) cholesterol is already low as statins have beneficial pleiotropic effects aside from lowering cholesterol. All patients with a history of ACS should have a lifelong LDL goal of <70 mg/dL (milligrams per deciliter). Patients should also be prescribed antiplatelet agents such as aspirin 81 mg daily for life and an ADP inhibitor for at least a year. Beta-blockers and angiotensinconverting enzyme inhibitors (ACEIs) should be employed to minimize ventricular remodeling and development of heart failure. Angiotensin receptor blockers (ARBs) can be used in those intolerant to ACEIs. These medications are particularly important in patients with an impaired ejection fraction. Eplerenone, an aldosterone antagonist, also reduces morbidity and mortality in post-infarct patients with an EF < 40%, even when added in combination with a ACEI (or ARB) and beta-blocker. After STEMI, all patients are at an increased risk of sudden cardiac death. This is particularly true for patients with a depressed ejection fraction (EF), and thus an implantable cardioverter defibrillator (ICD) should be offered to patients whose EF remains depressed (EF < 35%) 40 days after the infarct event.


COMPREHENSION QUESTIONS

1.1 A 68-year-old man with a medical history of hypertension and diabetes presents to the emergency department with 40 minutes of chest burning that began while mowing his lawn. His discomfort is precordial and does not radiate. He appears to be in moderate distress. Pertinent findings on exam include blood pressure of 153/86, heart rate of 112 bpm, and oxygen saturation of 98%. Jugular venous distension (JVD) of 9 cm is present. Lungs have bibasilar rales, and cardiac exam reveals a regular tachycardia, a S3 gallop, and a soft systolic murmur at the right upper sternal border. He is administered 325 mg aspirin and oxygen by nasal cannula. A sublingual nitroglycerin is also given which does not seem to affect his burning sensation. An ECG is immediately performed as shown in
Figure 1-4. What is the next best step?
A. Obtain stat cardiac biomarkers
B. Administer a “GI cocktail” consisting of an antacid and viscous lidocaine
C. Initiate reperfusion therapy
D. Obtain an echocardiogram
E. Administer IV metoprolol

ECG for question

Figure 1-4. ECG for question 1.1.

1.2 A 74-year-old woman with no previous medical history is recovering in the intensive care unit after presenting with STEMI and undergoing uneventful PCI 2 days ago. During morning rounds, the patient develops acute shortness of breath. Prior to this new development, she had been slowly improving. The patient’s blood pressure is 84/49 mmHg with a heart rate of 62 bpm and oxygen saturation of 92%. She is in acute distress. JVD is at 10 cm. Auscultation of the lungs reveals diffuse rales of bilateral lung fields. Cardiac exam shows regular rate and rhythm with a soft pansystolic murmur at the apex. Extremities are cool and clammy. The patient’s pulmonary artery (PA) tracing shows elevated PA pressures with a PCWP of 22 and prominent V waves. ECG shows Q waves in leads II, III, and aVF and nonspecific T wave changes. A stat bedside echocardiogram confirms the diagnosis. What is the next best step?
A. Administration of IV fluids
B. Administration of vasodilator therapy
C. Emergent pericardiocentesis
D. Emergent catheterization laboratory activation
E. Insertion of an intraortic balloon pump

1.3 A 57-year-old woman with a medical history of uncontrolled diabetes, hyperlipidemia, and smoking is being seen at 2-month follow-up after recent hospitalization for anterior STEMI. She reports feeling well and is back to her normal routine without symptoms. Physical exam reveals a blood pressure of
137/75 mmHg and a heart rate of 73 bpm. The remainder of her exam is unremarkable. Blood work shows total cholesterol of 273 mg/dL, LDL 162 mg/dL, HDL 39 mg/dL, and triglycerides of 358 mg/dL. Her HgA1c is 9.8%. Echocardiogram reveals an EF of 35%. Her medications include aspirin 81 mg daily, clopidogrel 75 mg daily, carvedilol 6.25 mg twice daily, lisinopril 20 mg daily, metformin 500 mg twice daily, and pravastatin 40 mg daily. Which of the following interventions would be the most impactful with regard to her long-term cardiovascular morbidity and mortality?
A. Smoking cessation
B. High-dose atorvastatin for optimal lipid control
C. Implantation of an ICD
D. Optimizing diabetic medical regimen for improved glycemic control
E. Titrating carvedilol and lisinopril higher as tolerated

1.4 A 39-year-old man with a medical history of hypertension and smoking presents to the emergency department with worsening chest pain. He reports that he suddenly developed the discomfort after a coughing spell this morning. It has worsened over the past 4 hours so that he now presents to the emergency room. He says it is like a “knife going through my chest to my spine.” There are no exacerbating or alleviating factors that he can identify. Physical exam reveals a blood pressure of 189/92, heart rate of 96 bpm, and oxygen saturation of 96%. He is in moderate discomfort. There is no significant JVD. His lungs are clear, and cardiac exam reveals regular rate and rhythm with a very soft diastolic murmur at the right upper sternal border. He has a trace radial pulse on his left side; the other extremities have 2+ pulses. A basic metabolic profile is remarkable for a creatinine of 1.7. His CK-MB is 22 (units here) and his TnT is 0.8 (units here). An ECG shows nonspecific ST-T changes in leads II, III, and aVF. A chest x-ray is unremarkable. What is the next best step?
A. Gated CT of the chest with contrast
B. Transesophageal echocardiogram
C. Administration of aspirin, clopidogrel, and IV heparin and trend cardiac markers with serial ECGs
D. Administration of NSAIDs and colchicine
E. Check a D-dimer


ANSWERS

1.1 C . This diabetic patient is presenting with atypical chest pain and evidence of a posterior circulation infarct on ECG. In addition to aspirin, the patient should receive an ADP inhibitor and an intravenous anticoagulant. However, “time is myocardium,” and thus the most important next step is to reperfuse the myocardium by either emergently activating the cardiac catheterization laboratory for PCI or by administering a thrombolytic agent. While beta-blockers should certainly be prescribed prior to discharge in ACS patients, they should be used judiciously within the first 24 hours of presentation. In this patient with signs of early heart failure including elevated JVD, an S3 gallop, tachycardia, and rales, beta-blockers should be avoided so as not to precipitate acute decompensated heart failure. An echocardiogram is unnecessary as the diagnosis is provided by the ECG and would only delay the patient from receiving definitive therapy. Cardiac biomarkers are likely to be normal given he presented soon after symptoms began and would not affect your treatment plan at this point. It is important to remember that the elderly, females, and diabetics may present with atypical symptoms such as a burning pain that may be confused with dyspepsia. One must maintain a high index of suspicion for ACS in these patient populations.

1.2 E . The patient’s clinical presentation is most consistent with cardiogenic shock from acute papillary muscle rupture. She has risk factors for papillary muscle rupture, including no prior history of myocardial infarction as well as an inferior STEMI as demonstrated by Q waves on ECG. It is important to note that the intensity of the murmur does not predict the severity of mitral regurgitation. The patient is in need of emergent surgical repair; however, she must first be stabilized. Given that she is hypotensive and would not tolerate afterload reduction with vasodilators, an intraaortic balloon pump should be inserted promptly. Occasionally, vasodilator therapy can be initiated after IABP insertion with hemodynamic improvement. It is also important to note that this patient’s heart rate is abnormally low in this clinical setting. She has what is termed “chronotropic incompetence,” which can be seen in patients with an inferior STEMI since the RCA supplies the sinus node. It is likely that she would need a temporary transvenous pacemaker, in addition to the IABP, to increase cardiac output. Although the patient is hypotensive, IV fluids would not be helpful as she is not hypovolemic. Her presentation is not consistent with tamponade, which might occur with free wall rupture, and thus a pericardiocentesis is not indicated. The catheterization lab should not be activated as the ECG does not show evidence of a new infarct.

1.3 A. While all of the answer choices are important interventions that should be pursued for this patient, the most impactful intervention is smoking cessation. Continuing to smoke after a myocardial infarction doubles the rate of reinfarction and death; therefore, aggressive efforts are needed to help the patient stop smoking, including use of nicotine replacements as well as medicinal therapy with bupropion or varenicline. Referral to a smoking cessation program is also appropriate. If the patient lives with another smoker, it is important to try and engage the other party to stop smoking as well since it is extremely difficult for people to cease smoking when others around them continue to smoke.

1.4 B. This patient is likely experiencing an acute aortic dissection and needs urgent, unequivocal diagnosis so that definitive surgical therapy can be administered. He has a history of hypertension, which is a risk factor for aortic dissection. His exam suggests that he may have compromised blood flow to his left upper extremity as evidenced by a diminished left radial pulse. In addition, a diastolic murmur is apparent, which can be seen in aortic dissections complicated by aortic insufficiency. It appears that there is involvement of the ostium of the right coronary artery given his elevated cardiac biomarkers and ECG changes. However, this is not due to thrombus, and anticoagulants and antiplatelets in this setting are not indicated. The patient’s creatinine is elevated, perhaps because of involvement of a renal artery by a dissection flap, and thus a CT scan with contrast should be avoided if possible. The patient’s presentation is not consistent with pericarditis, and thus NSAIDs and colchicine should not be administered. A D-dimer is frequently markedly elevated in patients with aortic dissection; however, the test is not specific and thus does not render a definitive diagnosis and thus would not be helpful in this setting. A negative D-dimer might be helpful in ruling out aortic dissection in a patient with a low pretest probability of this diagnosis. It is important to note that if one suspects a dissection, a definitive imaging test must be ordered given the potentially catastrophic outcome of missing this diagnosis. An unremarkable chest x-ray with a normal mediastinum and equal blood pressures in each arm is not sufficient to exclude a dissection.

CLINICAL PEARLS
C ST segment elevation myocardial infarction (STEMI) is due to complete occlusion of a coronary artery and is characterized by ST elevation of 1 mm or greater in two or more contiguous leads (or a new 1 BBB) in the setting of positive biomarkers.

C The location of ST elevation can help delineate the coronary anatomy that is most likely to be affected (see Table 1-1).

C The elderly. females. or patients with diabetes may present with atypical or vague symptoms of chest discomfort: one must maintain a high index of suspicion in these patient populations.

C Reperfusion therapy is of the essence and should be initiated as soon as possible. Ideal "door-to-balloon" time is < 90 minutes. or fibrinolytics should be administered within 30 minutes of presentation if PCI is not available in a timely fashion.

C Postinfarct care includes diligent monitoring for potential complications of STEMI. including electrical and mechanical complications, any sudden deterioration in clinical status should be evaluated with a stat ECG and echocardiogram.

C after STEMI, virtually all patients should receive an evidence-based car dioprotective medical regimen consisting of aspirin, a DP inhibitor. high dose statin. BB. and a CEI.

C Risk factors. including the presence of hypertension. diabetes. or hyper lipidemia. should be agressively modified. Smoking cessation is essential.

References

Antman EM. ST-segment elevation myocardial infarction: Pathology, pathophysiology, and clinical features. In Bonow RO, Mann DL, Zipes DP, Libby P, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia, PA: Saunders/Elsevier; 2012:1087–1170. 

Antman EM, Morrow DA. ST-segment elevation myocardial infarction: management. In Bonow RO, Mann DL, Zipes DP, Libby P, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia, PA: Saunders/Elsevier; 2012:1171–1177. 

Brunner MP, Menon V. Complications of acute myocardial infarction. In Griffin BP, ed. Manual of Cardiovascular Medicine, 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012:60–76. 

May CH, Lincoff AM. Antiplatelet agents in ischemic heart disease. In Gresele P, Born GVR, Patrono C, Page CP, eds. Antiplatelet Agents. London: Springer; 2012:495–518. 

O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol 2013;61(4)-e78–e140. 

Smith SC Jr, Benjamin EJ, Bonow RO, et al. AHA/ACCF Secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update. J Am Coll Cardiol 2011;58(23):2432–2446.

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