Acute Coronary Syndrome Case File

Acute Coronary Syndrome Case File

Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 14

A 55-year-old woman presented 2 hours previously with the sudden onset of chest pain, and shortness of breath (SOB) out of proportion to the severity of her chest  pain. The ECG shows a heart rate of 55 beats/minute and ST segment elevations of 3 mm on leads II, Ill, and aVF. She has no contraindications for anticoagulation  therapy. Troponin levels are elevated and blood pressure is 130/70 mm Hg. She  has required a nitroglycerin drip at 5 μg/kg/min keeping her free of chest pain, but  ECG changes persist though now only a 1-mm elevation of the ST segment is seen. Mild JVD is diagnosed on physical examination. The lungs have minimal  rales at both lung bases. The patient is breathing at 25 breaths/minute without labor. She smokes 1 pack per day (PPD) and admits to having had a diagnosis of  COPD by her physician. The S1 and S2 heart sounds are normal without murmurs,  and there are no S3 and S4 sounds heard. There is no lower extremity edema. The  patient was given 325 mg of aspirin (ASA) on arrival in the ED. 

⯈What is the most likely diagnosis?

⯈What immediate therapeutic steps are indicated?

⯈What are the different treatment options for her condition?

ANSWER TO CASE 14:

Acute Coronary Syndrome

Summary: The patient presents with an acute ST elevation myocardial infarction (STEMI). She has no contraindications to anticoagulation. She has already received 325 mg of ASA.

• Most likely diagnosis: Inferior wall ST segment elevation MI (STEMI).
• Immediate steps in treatment: Administer ASA, anticoagulation, pain control, β-blockade, prepare patient for percutaneous coronary intervention (PCI) and notify the cardiology and catheterization team.
• Treatment options: Individualized depending upon whether the MI is an STEMI or a non-STEMI, with PCI being the preferred treatment and thrombolytic therapy (TPA) being an option when PCI is not possible. In rare cases, bypass surgery may be indicated.

ANALYSIS

Objectives

1. To understand the difference in acute coronary syndromes (ACS).
2. To understand the difference in treatment of STEMI and non-STEMI.
3. To understand the different treatment options for ACS.

Considerations

This is a 55 -year-old woman with ACS, STEMI as evidenced by the EKG changes, and elevated cardiac troponin levels. The EKG ST segment elevation in the inferior leads and the bradycardia speak for an inferior wall MI. Because the SA node as well as the inferior portion of the heart is usually supplied by the right coronary artery, inferior wall cardiac injury and sinus bradycardia are often seen together. The saying is, "Time is myocardium," and within several hours of diagnosis of ACS, the patient should have intervention, which can include TPA or PCA. PCI, placement of a stent in the affected coronary artery, is associated with a lower 30-day mortality rate compared with TPA.

Approach To:

Acute Coronary Syndrome

Introduction

ACS refers to acute myocardial ischemia. It encompasses unstable angina, non STEMI, and STEMI. Troponin elevations are common in ICU patients although not always due to myocardial ischemia or MI, elevations are associated with poor patient outcome. Loss of a viable myocardium is diagnosed when the troponins exceed the 99th percentile with at least one of the following:

• Ischemic ST- and T-wave changes
• New left bundle branch block (LBBB)
• New Q waves
• Percutaneous coronary intervention

Cardiac enzymes may be elevated due mechanical injury, which may occur in the setting of CABG or from sepsis, chest trauma, or cardioversion. STEMI has a clinical presentation consistent with acute MI and ECG changes with evidence of ST-segment elevation. Unstable angina and non-STEMI are related and differ only in the severity of the ischemia. Non-STEMI is associated with elevated biomarkers of myocardial injury while unstable angina is not. The therapy is identical for both unstable angina and non-STEMI. ACS is characterized by atherosclerotic plaque rupture, formation of a platelet and fibrin thrombi, and local release of vasoactive substances. Unstable angina and non-STEMI are caused by thrombi that are not entirely occlusive. A form of unstable angina and non-STEMI can include vasospasm of an epicardial coronary artery (Prinzmetal angina) and secondary angina (eg, hypoxemia, anemia, tachycardia, or thyrotoxicosis). Vasospastic angina can also be seen in Raynaud disease and scleroderma. The most common cause of STEMI is a totally occlusive thrombus.

PREVENTION

Asymptomatic adults >30 years old should be periodically screened for dyslipidemia, hypertension, and diabetes. Patients who smoke should stop, since this is the most significant modifiable cardiovascular risk factor. ASA reduces the risk of cardiovascular events by inhibiting platelet activation. Moderate strenuous exercise is indicated and raises protective HDL levels as well as low alcohol intake. A high-fiber diet rich in fresh fruits and vegetables, low in cholesterol, saturated fats, and refined sugars should be instituted. Hormone replacement therapy in postmenopausal women may increase the incidence of nonfatal MI.

Screening of Asymptomatic Individuals

Routine screening for CAD in asymptomatic persons without cardiovascular risk factors is not recommended. Exercise testing is limited by the low prevalence of CAD in asymptomatic adults. The presence of calcification in coronary arteries, detected by electron-beam CT scanning, is predictive of nonfatal MI. In 2007, the use of electron-beam CT-identified patients with an estimated 10% to 20% risk of a coronary event over the following 10 years.

DIAGNOSIS

Analysis of an ECG is essential for patients with suspected cardiac ischemia or infarction. ECG findings such as the evolution of ST-segment abnormalities and Q waves can provide essential information regarding the duration, size, and location of injury. When inferior MI is suspected, a right-sided ECG should be recorded to evaluate right ventricular infarction. Typical angina, characterized by substernal discomfort, exertional onset, and prompt relief with nitroglycerin or rest, is associated with a 94% probability of CAD. The failure to diagnose acute MI may be because the patient has either "noncardiac" or "atypical" symptoms of dyspnea, fatigue, nausea, abdominal discomfort, or syncope. Any of these symptoms should prompt a consideration of ACS.

Up to 25% of women, diabetics, and the elderly with ACS have atypical symptoms. Chest pain that is pleuritic, sharp, stabbing, or positional significantly increases the chance of pulmonary disease and not ACS. Physical findings alone cannot exclude the diagnosis of ACS. A new murmur may suggest valvular incompetence caused by papillary muscle dysfunction or rupture which requires immediate attention and possibly an intra-aortic balloon pump (IABP) and/or open heart surgery. A new S4 gallop can represent decreased diastolic compliance. Heart failure may be present if ischemia results in left ventricular diastolic, systolic dysfunction or valvular incompetence and is a high-risk feature for death. Physical examination features most predictive of MI are: (1) elevated central venous pressure, (2) hypotension, (3) bibasilar crackles, and (4) an S3 heart sound.

An electrocardiogram (ECG) should be performed immediately in patients suspected of ACS. New ST-segment elevation and Q waves are the most powerful predictors for MI. Half of the time, the initial ECG may be nondiagnostic, and serial ECGs are essential. The diagnostic yield of the ECG is improved if a tracing can be recorded during an episode of chest discomfort. STEMI is characterized by chest pain and ST elevations > 1 mm in 2 or more contiguous leads, new left bundlebranch block, or evidence of true posterior infarction on electrocardiography. NonSTEM! is defined by elevated cardiac biomarkers and an absence of ST-segment elevation. A persistently normal ECG decreases the probability of MI.

Transthoracic Echocardiogram

Transthoracic echocardiography (TE) in patients with myocardial ischemia provides valuable diagnostic and prognostic information and detects complications. TE is recommended when acute ischemia is not detected despite a high suspicion. The presence of left ventricular (LV) dysfunction or mitral regurgitation after MI is an adverse prognostic finding. After MI, TE can detect complications such as residual ischemia, ventricular septal defects, papillary muscle rupture or dysfunction, free wall rupture, regurgitant lesions, LV thrombus, or tamponade. Radionuclide ventriculography, myocardial perfusion scintography (MPS) , and magnetic resonance imaging (MRI ) are techniques that assess the viability of myocardial tissue and characterize the extent of tissue injury.

During MI, the cardiac myocytes lose membrane integrity and leak proteins ( eg, creatine kinase, myoglobin, cardiac troponin ), see Figure 14-1. By serially measuring the presence and concentration of these cardiac marker proteins, evidence of myocardial damage that has occurred within the past 24 hours can be detected. Repetition of these determinations is advised 6 and 12 hours after the onset of symptoms. In patients with acute ST elevations, further management should not be delayed awaiting biomarker data. An echocardiogram detecting abnormality in regional wall

Figure 14-1. Serum markers after acute myocardial infarction. CK-MB, MB fraction of creatine kinase;  cTnl, cardiac troponin I; cTnT, cardiac troponin T; LD1,  lactate dehydrogenase isoenzyme 1; MLC,  myosin light chain. (Reproduced, with permission, from Tintinalli JE, Stapczynski S, Cline DM, et al.  Tintinalli's Emergency Medicine. 7th ed. New Yo rk, NY: McG raw-Hill Education; 2011. Figure  52-1.)

motion may be helpful, especially in cases of nondiagnostic electrocardiogram when non-STEMI or unstable angina is suspected. Echocardiography can show the progressive course from hypokinesis to akinesis during ischemia, and identify impaired myocardial relaxation during diastole.

An echocardiogram that demonstrates normal wall motion excludes the possibility of extensive myocardial damage but does not rule out non-STEMI. The differential diagnosis of acute chest pain is broad. Echocardiography can be used to identify nonischemic conditions that cause chest pain, such as myocarditis, aortic stenosis, aortic dissection, pulmonary embolism, and mechanical complications of acute infarction, such as papillary muscle dysfunction or rupture and ventricular septal defect. PCA provides detailed information about the coronary anatomy and facilitates invasive management of occluded coronary arteries. It is most often considered in the setting of ACS in patients with STEMI or new LBBB in whom immediate angioplasty is an option. Other such settings include, unstable angina, non-STEMI. and high-risk features as hypotension, CHF, mitral regurgitation, and repeated episodes of ACS despite optimal therapy.

Mechanical complications occur in 0.1% of post-MI patients between days 2 and 7. These complications include ventricular septal defect, papillary muscle rupture leading to acute mitral valve regurgitation, and left ventricular free wall rupture, which will lead to cardiac tamponade. Ventricular septal defect and rupture of papillary muscle usually lead to a new, loud systolic murmur and acute pulmonary edema or hypotension. Diagnosis is critical because the 24-hour survival rate is approximately 25 % with medical therapy alone but increases to 50% with emergency surgical intervention. Pericardia! tamponade from free wall rupture usually leads to sudden hypotension, pulse-less electrical activity on electrocardiography, and death.

THERAPY

The management for STEMI includes

1 . Anticoagulation (ASA, clopidogrel, heparin, glycoprotein IIb/IIIGa inhibitor) and LMWH

2. β-Blockade

3 . ACE inhibitors

4. Statins

5. Notification of the cardiologist and activation of the interventional lab

6. Enlisting a surgical backup

7. Considering TPA only in patients where PCI is not available, cannot be done on time, or upon patient refusal

Effective analgesia early in the course of ACS is an important therapeutic intervention. Morphine sulfate reduces sympathetic tone through a centrally mediated anxiolytic affect, and also reduces myocardial oxygen demand by reducing preload and by a reduction in vagally mediated heart rate. The vasodilating action of nitroglycerin results in combined preload and afterload reduction, decreased cardiac work, and lowered myocardial oxygen requirements. Nitrates may reduce infarct size, improve regional myocardial function, prevent left ventricular remodeling, and provide a small reduction in mortality rates. In the ICU nitrates are administered IV. Endpoints are the control of symptoms or a decrease in mean arterial blood pressure (MAP) by 10%, and an MAP goal of >60 mm Hg.

Mean arterial blood pressure (MAP) = [(2 x diastolic) + systolic]/3)

Antithrombotic Therapy

ASA should be given as soon as possible to any patient with ACS. Heparin therapy is indicated in patients with likely or definite ACS. The combination of heparin and ASA reduces the incidence of MI during the in-hospital period and reduces the need for CABG. Low-molecular-weight heparin (LMWH) is superior to unfractionated heparin (UFH) in this setting.

LMWH has greater bioavailability and a more predictable dose response as compared to UFH, but LMWH should be used carefully in the morbidly obese patients, and dosage adjustment is required in renal insufficiency. Clopidogrel should be considered in patients with ACS who are unable to take ASA and in high-risk patients in whom PCI is planned. Clopidogrel, a more potent antiplatelet agent than ASA, provides additional antiplatelet activity when added to ASA. It should be withheld if CABG is a possibility due to the increased risk of perioperative bleeding. Glycoprotein lib/Ilia receptor antagonists (eg, abciximab, tirofiban) inhibit the cross-bridging of platelets secondary to fibrinogen binding to the activated glycoprotein IIb/IIIa receptor. Glycoprotein IIb/IIIa antagonists should be considered in addition to ASA and heparin in patients with non-STEMI and as adjunctive therapy in patients with STEMI undergoing angioplasty.

β-Blockers

Early intravenous β-blocker therapy (ie, atenolol, metoprolol, carvedilol) reduces infarct size, decreases the frequency of recurrent myocardial ischemia, and improves short-term and long-term survival. β-Blockers diminish myocardial oxygen demand by reducing the heart rate, lowering BP, and myocardial contractility. β-Blocker prolongs diastole, which augments perfusion to injured myocardium, and can be used in left ventricular dysfunction if CHF status is stable.

ACE Inhibitors

An angiotensin-converting enzyme ( ACE) inhibitor should be administered early in the course of ACS in most patients. ACE inhibitor therapy can attenuate ventricular remodeling, resulting in a reduction in the development of heart failure and death. ACE inhibitor therapy reduces the risk of recurrent MI and other vascular events. In patients who cannot tolerate an ACE inhibitor due to coughing, an angiotensin-receptor blocker (ARB) is an alternative. Stat in therapy improves endothelial function and reduces the risk of future coronary events. A single study showed a reduction in recurrent ischemia when a high-dose statin was administered within 24 to 96 hours of hospital admission. The concept of statin therapy suggests that there is an emerging benefit to statins in ACS beyond a reduction in LDL cholesterol.

Aldosterone Blockers

Eplerenone is a selective aldosterone blocker that limits collagen formation and ventricular remodeling after acute MI. It also has a favorable effect on the neurohormonal profile. Eplerenone reduces mortality when started 3 to 14 days after MI in patients with ejection fractions (EFs) <40% and clinical heart failure or diabetes. Aldosterone antagonists should be used with great caution or avoided in patients with renal insufficiency (creatinine >2.5 mg/dL) or preexisting hyperkalemia ( >5.0 mEq/L).

Percutaneous Angioplasty and Stent Placement

Percutaneous angioplasty (PCA) and stent placement is the preferred therapy in specific subsets of ACS patients (STEMI, new LBBB, or true posterior MI). PCI is associated with a lower 30-day mortality rate compared with TPA. The incorporation of drug-eluting stents has further increased the clinical advantage of PCI over TPA. Angioplasty is indicated in patients with a contraindication to TPA or in patients with coronary spasm (CS) . Angioplasty is most effective within 12 hours of the onset of chest pain; but the earlier the intervention, the better the outcome. Prompt transfer of the patient to angiography lab for primary PCI may be beneficial but is contingent upon the transfer occurring within 2 to 3 hours of initial hospital arrival. TPA is an alternative to PCI in suitable candidates with STEMI. By lysing the clot, TPA restores perfusion to the ischemic area, reduces infarct size, and improves survival.

Bypass Surgery

The role of CABO in the treatment of ACS is evolving. Bypass surgery is preferred in patients who have a large amount of myocardium at ischemic risk due to proximal left main disease, or multi,vessel disease, especially with decreased left ventricular EF. CABG may be preferred in patients with diabetes mellitus because of better long-term vessel patency and improved clinical outcomes. There is increasing evidence that drug-eluting stents may produce outcomes comparable to CABG. An IABP is indicated for treatment of ACS with cardiogenic shock, unresponsive to medical therapy, for acute mitral regurgitation secondary to papillary muscle dysfunction, ventricular septal rupture, or refractory angina. The IABP reduces afterload during ventricular systole and increases coronary perfusion during diastole. Patients with refractory CS who are treated with an IABP have a lower in-hospital mortality rate than patients who are not treated with this device.

Follow-Up

Following an acute MI, early cardiac catheterization during hospitalization should be considered for patients with recurrent ischemic symptoms, serious complications, or other intermediate- to high-risk features (eg, CHF, left ventricular dysfunction, ventricular arrhythmias). These complications of ACS are associated with more severe CAD and subsequent cardiac events. Exercise testing in post-MI patients without high-risk features is performed as a prognostic assessment. Early stress testing following an MI allows the clinician to assess functional capacity, evaluate efficacy of the patient's current medical regimen, and risk-stratify the patient according to the likelihood of future cardiac events. Patients with depressed left-ventricular systolic function are at increased risk for subsequent ventricular tachyarrhythmias. The finding of unsustained ventricular tachycardia more than 48 hours after MI, particularly in patients with EF of <35%, usually prompts electrophysiological testing or implantation of a cardioverter-defibrillator. High-risk patients typically do better with an implantable cardioverter-defibrillator than with antiarrhythmic therapy.

Management of hypertension, diabetes, lipid levels, cessation of smoking, and inauguration of an exercise program are essential. Patients should continue therapy ASA, β-blockers, ACE- inhibitors, statins, and nitrates as prescribed. Approximately 20% of patients experience depression after acute infarction which is associated with an increased risk for recurrent hospitalization and death. Thus, post-infarction patients should be screened for depression. In patients with acute ischemia with hemodynamic instability, intra-aortic balloon pump (IABP) counterpulsation can be used for circulatory support during revascularization. The decision to proceed with invasive interventions aimed at revascularization in addition to medical management is best accomplished with the assistance of cardiology consultation. Patients with unstable angina and non-STEMI with refractory angina despite optimal medical therapy or hemodynamic instability benefit from early invasive strategies. Both survival and QOL improved with early invasive therapy. Invasive intervention should be avoided in patients with significant comorbidities in whom the risks outweigh the potential benefits. In the perioperative setting, the risk of bleeding often precludes the institution of aggressive anticoagulation needed for revascularization.

CLINICAL CASE CORRELATION

• See also Case 4 (Hemodynamic Monitoring), Case 15 (Cardiac Arrhythmias), Case 16 (Acute Cardiac Failure).

COMPREHENSION QUESTIONS

14.1  A 73-year-old woman is evaluated in the ED and transferred to the ICU because of chest pain of 4 hours' duration. Her medical history includes a 20-year history of hypertension and Type 2 diabetes mellitus. Her medications include metformin, atenolol, and ASA. On physical examination, her blood pressure is 130/84 mm Hg and her heart rate is 87 beats/minute and regular. Her jugular vein is distended to 5 cm while the patient is upright. She has a faint left carotid bruit, bibasilar crackles to one quarter up from the lung bases. A normal S1 and S2 is heard, with a grade 2/6 holosystolic murmur heard best at the apex to the axilla. An electrocardiogram from 6 months ago was normal. The ECG in Figure 14-2 was seen during the chest pain. The initial serum troponin measurement is elevated. She is now admitted to the ICU for an MI. She is free of chest pain while on IV nitroglycerin and her vital signs are stable. Which of the following is the most likely ECG diagnosis.

A. Left bundle branch block with normal sinus rhythm

B. ldioventricular tachycardia

C. Right bundle branch block

D. Third-degree atrioventricular block (complete heart block)

E. Mobitz type II second-degree atrioventricular block

Figure 14-2. 12 lead ECG.

14.2  A 55-year-old man presents with ACS, with 2 mm of ST elevation on the leads II, III, and a VF to the ICU. The troponins are positive. The blood pressure is 130/70 mm Hg on a nitroglycerin drip at 5 μg/kg/min keeping the patient chest pain free, but ECG changes persist and only a 1 mm of ST elevation is seen. There is no lower extremity edema. The patient was given ASA upon entry into the ED. What is/are the best next steps in the management of this patient?

A. Anticoagulation, IV β-blocker, ACE inhibitor, nitroglycerin, and alert catheterization lab

B. Give tissue plasminogen activator (TPA)

C. Increase nitroglycerin to 10 μg/kg/min

D. Get β-natriuretic peptide ( BNP) level

E. Call cardiac surgeon for stat CABG post-PCI

ANSWERS TO QUESTIONS

14.1  A. LBBB is associated with absent Q waves in leads I, aVL, and V6; a large, wide, and positive R wave in leads I, aVL, and V6 ("tombstone" R waves ); and prolongation of the QRS complex to >0.12 seconds. The chest pain, elevated cardiac biomarkers, and new-onset left bundle branch block are considered equivalent to having an ST-elevation myocardial infarction (STEMI) . Repolarization abnormalities are present consisting of ST segment and T wave vectors directed opposite to the QRS complex. The presentation of ACS with new left bundle branch block should be considered equivalent to an STEMI and true posterior wall MI, with management including early coronary intervention. The maximum benefit is provided by reperfusion within 12 hours of the onset of symptoms. The QRS complex is >0.12 seconds in BBB.

14.2  A. The patient is having an STEMI. Antithrombotic (heparin) therapy is indicated. The combination of heparin and ASA reduces the incidence of MI. When administered immediately, ASA reduces mortality in patients with unstable angina or acute infarction by diminishing platelet aggregation. Clopidogrel should be considered in patients with ACS who are unable to take ASA and in high-risk patients in whom Percutaneous transluminal coronary angioplasty (PTCA) is planned. Clopidogrel provides additional antiplatelet activity when added to ASA. It should be withheld if CABG is a possibility due to the increased risk of perioperative bleeding. Glycoprotein IIb/lIIa receptor antagonists inhibit the cross-bridging of platelets secondary to binding fibrinogen. Early intravenous β-blocker therapy reduces infarct size, decreases the frequency of recurrent myocardial ischemia, and improves survival. β-Blockers diminish myocardial oxygen demand by reducing heart rate, systemic arterial pressure, and myocardial contractility. An ACE inhibitor should be administered early in the course of ACS in most patients. ACE inhibitor therapy may also reduce the risk of recurrent infarction. In patients who cannot tolerate an ACE inhibitor, an ARB is an alternative. Statin therapy appears to improve endothelial function and reduce the risk of future ACS.

CLINICAL PEARLS

⯈ ACS include STEMI, unstable angina, and non-ST elevation MI (non-STEMI). 

⯈ Atypical symptoms are found in 25% of ACS patients, especially women, diabetics, and the elderly. 

⯈ Non-STEMI is associated with elevated cardiac biomarkers while unstable angina is not. 

⯈ ICU patients, comorbidities, and instability usually preclude acute CABG or PCI. 

⯈ Therapy of MI includes β-blockade, statins, ASA, and ACE inhibitors. 

⯈ Troponin elevations are common in  ICU patients. Although not always due to myocardial ischemia or infarction, such elevations are associated with poor outcomes.

References

Grech ED, Ramsdale DR. Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarction. BM]. 2003 ;326: 1 259- 1 2 6 1. 

Loscalzo J . Harrison's Pulmonary and Critical Care Medicine. 2nd ed. New York, NY: McGraw-Hill; 2010. 

Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. Is this patient having a myocardial infarction ? lAMA. 1 998;280: 1 25 6 - 1 263 . 

Toy EC, Simon B, Takenaka K, Liu T, Rosh A. Case Files Emergency Medicine . 2nd ed. New York: McGraw-Hill, Lange, 2009.

HomeCritical Care Case FileAcute Coronary Syndrome Case File