Chest Discomfort, Abnormal Electrocardiogram, Clean Coronaries

Chest Discomfort, Abnormal Electrocardiogram, Clean Coronaries

Chest Discomfort, Abnormal Electrocardiogram, Clean Coronaries CASE PRESENTATION A 49-year-old Caucasian male presented with exertional chest discomf...

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Chest Discomfort, Abnormal Electrocardiogram, Clean Coronaries CASE PRESENTATION

A 49-year-old Caucasian male presented with exertional chest discomfort radiating to his left arm (relieved by nitroglycerin), accompanied by shortness of breath and dizziness. He denied palpitations, nausea, diaphoresis, or syncope. Past medical history was remarkable for untreated hypertension. He was on no medications. Surgical history was unremarkable. His father had his first myocardial infarction (MI) before age 60. There was no further family history of heart disease or sudden cardiac death. Social history revealed a nonsmoker, with rare alcohol and no illegal drug use.

cholesterol, and low-density lipoprotein were elevated. High-density lipoprotein was low. Electrocardiography

An electrocardiogram (ECG) was ordered to evaluate for myocardial infarction or ischemia. The ECG revealed a sinus rhythm rate of

IMAGE OF THE MONTH Stephanie Lickerman, MSN, ANP-BC

PHYSICAL ASSESSMENT

The patient’s vital signs were as follows: blood pressure 116/53 mm Hg; pulse 64 beats/min; respiration 16 breaths/min; oxygen saturation 98% on room air; temperature 36.6 C; body mass index 33.1. He was not in acute distress. Head, neck, and neurologic exams were unremarkable. Lungs were clear to auscultation bilaterally with nonlabored respirations. Cardiac exam revealed normal rate and rhythm, no murmur or rub, mild S4, and no jugular venous distention. His abdomen was nontender, without masses, bruits, or hepatosplenomegaly. His extremities revealed normal pulses and no peripheral edema or varicosities. DIAGNOSTICS Labs and Radiology

Comprehensive metabolic panel, complete blood count, thyroid-stimulating hormone, erythrocyte sedimentation rate, C-reactive protein, D-dimer, and chest X-ray were normal. Troponins were indeterminate. Brain natriuretic peptide was mildly elevated. Triglycerides, total www.npjournal.org

79 beats/min, marked anterolateral ST- and T-wave changes, possible ischemia or subendocardial injury, and left ventricular (LV) hypertrophy. Cardiac Catheterization

Cardiac catheterization was done because of acute ECG changes, indeterminate troponins, chest discomfort, and family history. The coronary arteries revealed no hemodynamically significant disease. LV end-diastolic pressure was severely elevated and the apex revealed severe hypertrophy with normal anterior and inferior wall motion. Echocardiography

A transthoracic echocardiogram was completed to evaluate cardiac anatomic structure and function. It revealed a hyperdynamic LV with an ejection fraction of 75%, normal LV diastolic function, mild basilar and midconcentric LV The Journal for Nurse Practitioners - JNP

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hypertrophy, LV apical hypertrophy with decreased apical cavity size, and no significant valvular disease. ETIOLOGY OF APICAL HYPERTROPHIC CARDIOMYOPATHY

Apical hypertrophic cardiomyopathy (AHCM) is a form of hypertrophic cardiomyopathy (HCM) primarily affecting the LV apex (pure type), but it may also affect the interventricular septum (mixed type). Unlike other variants of HCM, the LV outflow tract is unobstructed. In approximately half of HCM patients, the etiology is an autosomal protein mutation of the sarcomere. This results in myocardial fiber disarray and interstitial fibrosis leading to apical hypertrophy in the pure form, and apical and septal hypertrophy in the mixed form.1-3 Pathophysiology is thought to be due to “a mismatch of supply and demand secondary to small vessel coronary artery disease, delayed relaxation of the myocardium, decreased capillary-

to-myocardial-fiber ratio, and decreased coronary perfusion pressure.”4 It affects 18% of Japanese patients with hypertrophic cardiomyopathy and only 3%-10% in the rest of the world, and it is less common in North America.5 DIAGNOSIS Clinical Presentation

Common presentations include exertional chest discomfort, dyspnea, palpitations, atrial arrhythmias, syncope, and an audible S4. Sudden cardiac death and MI are found less often in this variant. Differential diagnoses include coronary artery disease, LV tumors or thrombus, endomyocardial fibrosis,6 and noncompaction of the LV myocardium. Family history should be reviewed for sudden cardiac death, MI, stroke, and atrial or ventricular arrhythmias. The ECG often resembles anterolateral ischemia due to giant negative T waves (>10 mm) in V3-V4, and ST-segment depression ( 1 mm) in V3-V6.7 LV hypertrophy

Figure 1. Top arrow points to very tall R wave, indicative of left ventricular hypertrophy. Bottom arrow points to giant negative T waves > 10 mm in size.

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(LVH); lack of septal Q-waves in I, II, III, aVF, aVL and V3-V6; and high R-wave voltage in the precordial leads are all characteristic.2 On the ECG, giant negative T waves are the most common finding (Figure 1). The second most common finding is LVH.6 Because these changes mimic acute MI, patients are frequently taken to the catheterization lab and found to have clean coronaries. Echocardiography

Asymmetric LV hypertrophy of the apex, apical wall thickness  15 mm, and apical-toposterior wall thickness ratio  1.5 mm are the echocardiographic hallmarks of ACHM.6 Heart failure with preserved ejection fraction is common. Transthoracic echocardiography is noninvasive, readily accessible, and costeffective, making it the initial imaging test of choice. AHCM may be misdiagnosed as an apical thrombus,2 or missed completely,4 as echocardiographic imaging of the apical myocardium is difficult. Thus, use of contrast is helpful in identifying hypokinesis, thrombus, and aneurysms of the apex. Cardiac MRI is considered the “gold

Figure 2. Left ventriculogram film from the cardiac catheterization lab showing a spadelike configuration.

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standard” as it is more accurate; detects early disease; defines the extent of myofibrosis, a prognostic indicator8; and aids in the differential diagnosis. Cardiac Catheterization

Apical hypertrophy causes the LV shape to appear as an “ace of spades” during end-diastole (Figure 2) and the apical cavity to disappear during end-systole due to contraction of the hypertrophied myocardium.4,7 Treatment

Referral to an HCM center of excellence is paramount. For symptomatic patients, betablockade and verapamil are the initial drugs of choice. Treating the arrhythmia, diastolic dysfunction, and hypertension is essential. Presence of apical aneurysm is associated with higher risk of stroke, sudden cardiac death, and heart failure.7 High-risk patients (syncope, nonsustained ventricular tachycardia, previous cardiac arrest, family history of sudden cardiac death) should be considered for an implantable cardioverter-defibrillator.6 Surgical myectomy and alcohol ablation are generally of little use in ACHM due to the lack of pronounced septal hypertrophy. Genetic testing is recommended. If the patient has no mutation, genetic testing is not indicated in first-degree relatives.9 If genotype positive, then clinical screening (exam, ECG, or echocardiogram) of firstdegree relatives is recommended starting at age 12, with follow-up every 12-18 months for children and adolescents and every 5 years for adults.9 Of the hypertrophic cardiomyopathies, AHCM is considered a more benign variant as cardiac mortality is lower (1.9%).6 However, approximately 33% of patients have increased cardiac morbidity from arrhythmias and heart failure.4 Thus, close clinical follow-up with an HCM specialist is recommended.

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References

Resource Toolbox Additional resources on hypertrophic cardiomyopathy for clinicians: http://doc2do.com/hcm/webHCM.html HCM Risk-SCD Calculator, European Society of Cardiology Additional resources on hypertrophic cardiomyopathy for patients and clinicians: http://www.mayoclinic.org/diseases-conditions/ hypertrophic-cardiomyopathy/symptoms -causes/dxc-20122103 http://www.heart.org/HEARTORG/Conditions/More/ Cardiomyopathy/Hypertrophic-Cardiomyopathy_ UCM_444317_Article.jsp#.VlCnEtirShc Hypertrophic Cardiomyopathy Association: https://www.4hcm.org/wp/ Clinical trials in hypertrophic cardiomyopathy: https://clinicaltrials.gov/ct2/results?term¼ hypertrophicþcardiomyopathy&Search¼Search Free patient literature: http://www.cardiomyopathy.org/medical -professionals/mp Centers of excellence: https://www.4hcm.org/wp/hcma-resources/hcm -centers/ Apps: http://www.imedicalapps.com/2015/10/yale -cardiologists-launch-researchkit-app-for-kids -and-adults-with-cardiomyopathy/ http://www.igetbetter.com/

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1. Afonso LC, Bernal J, Bax JJ, Abraham TP. Echocardiography in hypertrophic cardiomyopathy. J Am Coll Cardiol Imaging. 2008;1:787-800. 2. Yıldırım MN, Selçoki Y, Eryonucu B. Apical hypertrophic cardiomyopathy. Eur J Gen Med. 2010;7(2):206-209. 3. Elliott PM, Anastasakis A, Borger MA, et al. 2014 European Society of Cardiology guidelines on diagnosis and management of hypertrophic cardiomyopathy. Eur Heart J. 2014;35:2733-2779. 4. Lakshmanadoss U, Kulkarni A, Balakrishnan S, et al. All that glitters is not gold: apical hypertrophic cardiomyopathy mimicking acute coronary syndrome. Cardiol Res. 2012;3(3):137-139. 5. Arad M, Penas-Lado M, Monserrat L, et al. Gene mutations in apical hypertrophic cardiomyopathy. Circulation. 2005;112: 2805-2811. 6. Yusuf SW, Bathina JD, Banchs J, Mouhayar EN, Daher IN. Apical hypertrophic cardiomyopathy. World J Cardiol. 2011;3(7): 256-259. 7. Kasirye Y, Manne JR, Epperla N, et al. Apical hypertrophic cardiomyopathy presenting as recurrent unexplained syncope. J Clin Med Res. 2012;10(1):26-31. 8. Chen X, Zhao T, Lu M, et al. The relationship between electrocardiographic changes and CMR features in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy. Int J Cardiovasc Imaging. 2014;30:55-63. 9. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/AHA Guideline for the diagnosis and treatment of hypertrophic cardiomyopathy. Circulation. 2011;124:e783-e831.

Stephanie Lickerman, MSN, ANP-BC, CVNP, CHFN, is a cardiac nurse practitioner at Heart Health Specialists, LLC, and St. Luke’s Hospital in Chesterfield, MO. She can be reached at [email protected]. Department Editor Joanne Thanavaro, DNP, FAANP, would like to hear your ideas for future columns, can be reached at [email protected].

1555-4155/16/$ see front matter © 2016 Elsevier, Inc. All rights reserved. http://dx.doi.org/10.1016/j.nurpra.2015.12.002

Volume 12, Issue 3, March 2016