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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 7  |  Issue : 2  |  Page : 172-174

Hypertrophic cardiomyopathy: Totally a ST-elevation myocardial infarction mimic


Department of Cardiology, AIIMS, Bhubaneswar, Odisha, India

Date of Submission01-May-2021
Date of Decision04-Jul-2021
Date of Acceptance06-Jul-2021
Date of Web Publication31-Aug-2021

Correspondence Address:
Debasish Das
Department of Cardiology, AIIMS, Bhubaneswar - 751 019, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpcs.jpcs_26_21

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  Abstract 


Hypertrophic cardiomyopathy (HCM) commonly presents with nonspecific ST-T changes in an electrocardiogram (EKG), and a paucity of literature description exists about index presentation of HCM totally as ST-elevation myocardial infarction (STEMI) in a very young age. The presence of convex ST elevation in surface EKG in HCM patients indicates disease progression, becomes evident in the fifth or sixth decade of life, and warrants further risk stratification for the need of automated intracardiac defibrillator therapy. We present a rare presentation of nonobstructive HCM totally mimicking acute anterior wall STEMI in a very young male in his third decade of life, which has not been described in the literature so far. Because of the presence of typical convex shaped ST elevation with biphasic terminal T wave inversion across anterior precordial leads with ongoing typical angina, the patient was subjected to right transradial coronary angiogram which revealed the presence of normal nonatherosclerotic coronaries.

Keywords: Cardiomyopathy, hypertrophic, mimic, ST-elevation myocardial infarction


How to cite this article:
Das D, Acharya D, Das T, Singh S, Gupta JD, Pramanik S. Hypertrophic cardiomyopathy: Totally a ST-elevation myocardial infarction mimic. J Pract Cardiovasc Sci 2021;7:172-4

How to cite this URL:
Das D, Acharya D, Das T, Singh S, Gupta JD, Pramanik S. Hypertrophic cardiomyopathy: Totally a ST-elevation myocardial infarction mimic. J Pract Cardiovasc Sci [serial online] 2021 [cited 2021 Dec 1];7:172-4. Available from: https://www.j-pcs.org/text.asp?2021/7/2/172/325223




  Introduction Top


Differential diagnosis of ST elevation in the electrocardiogram (EKG) other than myocardial infarction includes early repolarization syndrome in the young, left ventricular hypertrophy, hyperkalemia, hypercalcemia, and variant angina. We present a 30-year-old male with effort intolerance in New York Heart Association (NYHA) Class II for the past 6 months with rest angina for the past 7 days with hypertrophic cardiomyopathy (HCM), whose EKG resembled typical anterior wall ST-elevation myocardial infarction (STEMI). Although invasive coronary angiogram most often in HCM reveals megacoronaries without obstructive coronary artery disease, we subjected the patient for invasive right transradial coronary angiogram in view of the presence of typical ischemic ST elevation with convexity upward and biphasic, ischemic terminal T-wave inversion, which revealed the presence of normal nonatherosclerotic coronaries.


  Case Report Top


A 30-year-old young male nondiabetic, nonhypertensive, nondyslipidemic presented with effort intolerance NYHA Class II for the past 6 months with rest angina for the past 7 days, and EKG revealed anterior wall ST elevation myocardial infarction [Figure 1]. Serial EKG revealed no dynamic changes and serial troponin I was negative. Close differential diagnosis was anomalous coronary artery causing obligatory ischemia in the young, inflammatory myocarditis, pericarditis, aortic dissection, aortic stenosis, HCM, and pulmonary embolism. He had classical Herbeden angina with retrosternal heaviness radiating such as a flower base to jaw and arm persisting >15–20 min relieved with nitroglycerine. He revealed no history of febrile illness, pain radiating to trapezius, or tearing pain radiating to back. Serial troponin was negative, and echocardiography revealed the presence of nonobstructive HCM with asymmetrical septal hypertrophy with intraventricular septum (IVS) thickness of 22 mm and posterior wall thickness of 6 mm [Figure 2] and [Figure 3] without any resting or provocative left ventricular outflow tract gradient or mitral regurgitation. In view of the presence of typical ischemic ST elevation with convexity upward with biphasic, ischemic terminal T-wave inversion in such a young age with ongoing chest pain and known association of coronary artery disease with HCM, we subjected the patient to a coronary angiogram which revealed the presence of nonatherosclerotic normal coronaries. Although the EKG of the patient resembled typical anterior wall STEMI, the presence of normal coronaries suggested that typical coved or hockey stick ST-elevation across anterior precordial leads was due to the repolarization anomaly owing to myofiber disarray present in HCM. Association of HCM with coronary artery disease in Asian subset is well described. Patients with ongoing typical angina, troponin positive, dynamic EKG changes, with worsening of left ventricular ejection fraction or mitral regurgitation, with conventional risk factors, family history of coronary artery disease, or ventricular tachycardia (VT) storm should have a check coronary angiogram to rule out associated obstructive coronary artery disease although most often those do not require coronary stenting and are simple ischemic in nature.
Figure 1: Electrocardiogram of hypertrophic cardiomyopathy resembling ST elevation myocardial infarction.

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Figure 2: Parasternal long axis view (PLAX) view showing asymmetrical septal hypertrophy.

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Figure 3: Short-axis parasternal short axis view (PSAX) view showing asymmetrical septal hypertrophy.

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  Discussion Top


HCM is a primary disease of myocardium, resulting in myocardial hypertrophy without pressure or volume overload. The typical triad of symptoms includes exertional angina, syncope, and shortness of breath. Sudden cardiac death can be the first manifestation of the disease process in young patients. Elderly patients with HCM have a relatively benign course with normal life span. The classic ECG finding in HCM is large dagger-like “septal Q waves” in lateral leads due to abnormally hypertrophied IVS. Apical variant of HCM, known as the apical variant of HCM also known as Yamaguchi syndrome, does not result in septal Q-waves, as the septum is normal in thickness in this condition. The cardiac apex is abnormally thickened in Yamaguchi disease, resulting in diffuse precordial T-wave changes which is referred as “giant T wave inversion.” Apical HCM (ApHCM) has been recognized as Japanese variant of HCM since its high prevalence in the Japanese population,[1],[2] which present with classical arrowhead or “spade like” T-wave inversion pattern across anterior precordial leads. This spade-like T-wave inversion occurs due to differences in localized wall thickness, leading to disparities in the duration of repolarization. This giant T-wave inversion in HCM often resembles non-ST-elevation acute coronary syndrome (NSTEACS); only way to differentiate NSTEACS from HCM is the presence of reciprocal ST changes or “mirror changes” in NSTEACS whereas they are not observed in ApHCM.[3] The electrocardiographic features of HCM also include ST-segment elevation[4] that may simulate other ST-segment elevation syndromes, including acute myocardial infarction, variant angina, acute pericarditis, bundle branch blocks, ventricular paced rhythm, dyskinetic ventricular segment, ventricular aneurysm, left ventricular hypertrophy, Wolff-Parkinson-White syndrome, and early repolarization syndrome. Most often, due to the presence of classical sickle shape or half-moon-shaped ST-elevation across anterior precordial leads, those patients are subjected to invasive coronary angiogram which usually reveals normal coronaries which are larger in diameter as compared to the normal population otherwise known as megacoronaries. In our case, we did a Holter analysis in the patient to rule out runs of nonsustained VT (NSVT) or paroxysmal atrial fibrillation which was absent; we advised the patient to take metoprolol 50 mg twice daily with ranolazine 500 mg twice daily with follow-up after 6 months. We started the patient ranolazine as the patient presented with typical angina and this late sodium current inhibitor reverses the main electrophysiological and mechanical abnormalities of human HCM cardiomyocytes in vitro, suggesting potential clinical benefit. HCM presenting as acute anterior wall STEMI can also present as sudden cardiac death.[5] ApHCM can also present with concave ST-segment elevation across anterior precordial leads.[6] Convex type ST elevation as noted in our case can be a presenting feature in HCM also.[7] Furuki et al. classified ST-segment elevation in HCM into three types: concave type, ST-T segment rises with downward convexity; straight type, ST-T segment rises obliquely like an inclined plane; and convex type in which ST-T segment rises with an upward convexity.[7] ST elevation in our case was of Furuki Type III or with convexity upward mimicking anterior wall STEMI. They concluded that the presence of convex type ST elevation or abnormal false Q-waves indicates disease progression in HCM. In view of the presence of convex ST-segment elevation, we concluded that the disease has progressed and assessed the patient for the need of automated intracardiac defibrillator (AICD) therapy. The patient revealed no history of syncope, presyncope, or aborted sudden cardiac death in the past or family members, and Holter also did not reveal any documented VT or runs of NSVT, for which we put the patient on beta-blocker therapy. HCM can be a cause of false-positive STEMI in young patients.[8] We present a rare index presentation of HCM mimicking anterior wall STEMI in a young person in the third decade as most of the cases of HCM presenting with STEMI have been described in the fifth or sixth decade of life.


  Conclusion Top


We present a rare index presentation of HCM mimicking anterior wall STEMI in the third decade of life, whereas the presence of ST elevation in HCM indicates disease progression and commonly becomes evident in the fifth or sixth decade of life. The presence of convex-type ST elevation in HCM indicates disease progression and warrants careful evaluation with risk stratification for the need of AICD therapy. Echocardiography plays a substantial role in those cohort of patients and avoids emergency cardiac catheterization to delineate the coronary anatomy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Ethics clearance

The authors declare that Institutional Ethical Committee (IEC) clearance has been obtained.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sakamoto T, Tei C, Murayama M, Ichiyasu H, Hada Y. Giant T wave inversion as a manifestation of asymmetrical apical hypertrophy (AAH) of the left ventricle. Echocardiographic and ultrasono-cardiotomographic study. Jpn Heart J 1976;17:611-29.  Back to cited text no. 1
    
2.
Kitaoka H, Doi Y, Casey SA, Hitomi N, Furuno T, Maron BJ. Comparison of prevalence of apical hypertrophic cardiomyopathy in Japan and the United States. Am J Cardiol 2003;92:1183-6.  Back to cited text no. 2
    
3.
Vaidya GN, Antoine S, Imam SH, Kozman H, Smulyan H, Villarreal D. Reciprocal ST-segment changes in myocardial infarction: Ischemia at distance versus mirror reflection of ST-elevation. Am J Med Sci 2018;355:162-7.  Back to cited text no. 3
    
4.
Khan IA, Ajatta FO, Ansari AW. Persistent ST segment elevation: A new ECG finding in hypertrophic cardiomyopathy. Am J Emerg Med 1999;17:296-9.  Back to cited text no. 4
    
5.
Daralammouri Y, El Garhy M, Same K, Lauer B. Hypertrophic cardiomyopathy mimicking acute anterior myocardial infarction associated with sudden cardiac death. Case Rep Med 2012;2012:236154.  Back to cited text no. 5
    
6.
Parr CJ, Sharma R, Garber PJ. Apical hypertrophic cardiomyopathy treated as ST-elevation myocardial infarction. CJEM 2018;20:S51-5.  Back to cited text no. 6
    
7.
Furuki M, Kawai H, Onishi T, Hirata K. Value of convex-type ST-segment elevation and abnormal Q waves for electrocardiographic-based identification of left ventricular remodeling in hypertrophic cardiomyopathy. Kobe J Med Sci 2009;55:E16-29.  Back to cited text no. 7
    
8.
Didi G, Kalim M, Sahara E, Atmadikoesoemah CA. The role of cardiac magnetic resonance imaging in patients with hypertrophic obstructive cardiomyopathy. Eur Heart J Suppl 2017;19:E53-73.  Back to cited text no. 8
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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