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British Journal of Radiology (2006) 79, e200-e204
© 2006 British Institute of Radiology
doi: 10.1259/bjr/53601277
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Case report

Comprehensive multidetector CT assessment of apical hypertrophic cardiomyopathy

E Ghersin, MD1, J Lessick, MD2, D Litmanovich, MD1, A Engel, MD1 and S Reisner, MD2

Departments of 1 Diagnostic Imaging and 2 Cardiology, Rambam Medical Center, Haifa, Israel

Correspondence: Eduard Ghersin, Department of Diagnostic Radiology, Rambam Medical Center, P.O.B 9602, Haifa 31096, Israel. E-mail: e_ghersin{at}rambam.health.gov.il


   Abstract
Top
 Abstract
Introduction
 Case report
 Discussion
 References
 
16-slice multidetector CT (MDCT) cardiac findings of a middle-aged man with known apical hypertrophic cardiomyopathy (AHC) and recent atypical chest pain are presented. MDCT enabled comprehensive evaluation of the coronary arteries, diagnosing myocardial bridging of the left anterior descending (LAD) and first diagonal arteries. It also enabled dynamic evaluation of myocardial thickness and left ventricular global and regional function. This case illustrates the full capabilities of MDCT in the evaluation of AHC.


   Introduction
Top
 Abstract
 Introduction
Case report
 Discussion
 References
 
In this paper we describe a middle-aged man with severe apical hypertrophic cardiomyopathy (AHC) evaluated using electrocardiography (ECG) gated multidetector CT (MDCT) and transthoracic echocardiography (TTE). MDCT documented significant apical myocardial hypertrophy as well as myocardial bridging of the LAD and first diagonal arteries. MDCT also demonstrated normal left ventricular systolic function associated with a classic systolic spade-shaped left ventricular cavity. To the best of our knowledge, such an analysis has not been described previously with MDCT.


   Case report
Top
 Abstract
 Introduction
 Case report
Discussion
 References
 
A 44-year-old man with a 7 year history of AHC was investigated for recent atypical chest pain. His blood pressure was 108/69 mm Hg and his physical examination was normal. ECG demonstrated normal sinus rhythm and signs of left ventricular hypertrophy. Also noted were giant T waves and T wave inversion in all pre-cordial leads. TTE documented mild concentric left ventricular hypertrophy and profound left ventricular apical hypertrophy. Left ventricular end-diastolic wall thickness was 1.4 cm, 1 cm and 2.9 cm at the level of the interventricular septum, left ventricular posterior wall and apex, respectively. To investigate the cause of the patient's chest pain, cardiac MDCT was ordered. ECG gated MDCT was performed with a Brilliance TM 16-slice scanner (Philips Medical Systems, Cleveland, OH). The post-processing reformations were performed on an Extended Brilliance Workspace TM workstation (Philips Medical Systems, Cleveland, OH). The average heart rate during image acquisition was 65 beats min–1. CT coronary angiography (CTCA) disclosed small eccentric non-significant calcified plaques in the proximal left anterior descending artery (LAD), just proximal to a segment of myocardial bridging. This segment, measuring 4.2 cm in its length, also involved the origin and very proximal portion of the first diagonal artery, without evidence of any wall or luminal abnormalities both during diastole and systole as well (Figure 1Go). The rest of the coronary arterial tree was within normal limits (Figure 2Go). Global left ventricular function analysis, using end diastolic and end systolic reformats of the CT data, disclosed an ejection fraction of 75%. Regional functional analysis using cine films of vertical short axis reformations of the CT data depicted profound apical wall thickening with systolic obliteration of the apical cavity (Figure 3Go). Vertical long axis reformations of the CT data documented a classic spade-shaped ventricular cavity during systole (Figure 3Go). Systolic anterior motion of the mitral valve could clearly be ruled out. Wall thickness, measured from end-diastolic short axis reformations of the CT data, at the apex and base of the interventricular septum was 26 mm and 11 mm, respectively, giving a ratio of 2.4. These findings fulfilled the accepted diagnostic criteria of the AHC [1] and, in the absence of significant coronary artery stenosis, the patient was placed on medical therapy with beta-blockers and aspirin, and remained under close clinical follow-up.


Figure 1
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  		Figure 1. (a) Curved multiplanar reformat of the left main and left anterior descending artery (LAD) depict a small non-significant calcified plaque in the proximal LAD (white arrow), and an elongated segment of myocardial bridging affecting the proximal and mid segments of the LAD (black arrow). (b) Curved multiplanar reformat of the left main proximal LAD and first diagonal arteries shows a small non-significant calcified plaque in the proximal LAD (white arrow), an elongated segment of myocardial bridging affecting the proximal and mid segments of the LAD (black arrow) and myocardial bridging of the origin and very proximal portion of the first diagonal artery (arrowhead). (c) Cross sectional reformat of the proximal LAD calcified plaque perpendicular to the long axis of the artery clearly demonstrates a relatively wide patent lumen (+) adjacent to an eccentric small calcified plaque (*), indicating its non-significance.

 

Figure 2
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  		Figure 2. (a) Volume rendering reformat and (b) "Globe view" presentation of the left coronary tree demonstrate the left anterior descending artery (LAD) and first diagonal myocardial bridging (*) in (a) and the non-significant calcified plaque in the proximal LAD (arrowhead) in (b).

 

Figure 3
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  		Figure 3. (a,b) Vertical short axis slabs of cardiac ventricles during (a) end diastole and (b) peak systole and (c,d) vertical long axis slabs of cardiac ventricles during (c) end diastole and (d) peak systole. Note the profound apical wall thickening (white *) with systolic obliteration of the apical cavity (black *) on (a,b), and the classic spade shaped ventricular cavity during systole (black *) on (d).

 

   Discussion
Top
 Abstract
 Introduction
 Case report
 Discussion
References
 
AHC is believed to be a distinct type of hypertrophic cardiomyopathy (HCM), possessing typical clinical features. Unlike usual HCM, it shows a predilection for middle aged men, is rarely associated with sudden cardiac death, is frequently complicated by hypertension and has a relatively good prognosis [2, 3]. Nevertheless, it seems that the clinical course is less benign in western countries than in Japan, with the occurrence of atrial fibrillation and myocardial infarction in up to one third of western patients [1]. AHC may also show typical ECG abnormalities in the form of giant negative T waves. The diagnosis is primarily based on demonstrating localized apical hypertrophy, which is usually accomplished by non-contrast TTE. Nonetheless, poor visualization of the apical endocardial border, by non-contrast TTE, may lead to false negative interpretations, and reports favour the use of contrast-enhanced TTE or MRI as the optimal imaging techniques [1, 4, 5]. TTE can further document a lowered coronary flow reserve capacity of penetrating intramyocardial coronary arteries in patients with AHC using tissue Doppler [6]. During the last 5 years, evolving MDCT technology with its improved spatial, contrast and temporal resolutions enables non-invasive acquisition of high resolution 3D images depicting accurate anatomical and functional information concerning the coronary arteries, heart chambers, myocardium and pericardium [7–13]. To the best of our knowledge, this case report documents for the first time application of MDCT in the comprehensive evaluation of a patient with AHC and myocardial bridging. As demonstrated, contrast enhanced MDCT enabled accurate delineation of the apical endocardial border, as well as dynamic evaluation of heart chambers and lumen. By enabling accurate measurements of the apical myocardial thickness and demonstration of the classic spade-shaped ventricular cavity during systole, it confirmed the diagnosis of AHC. Furthermore, it enabled high quality non-invasive coronary angiography, which excluded significant coronary atherosclerotic disease, but documented myocardial bridging of the LAD and first diagonal arteries. Myocardial bridging, a congenital coronary anomaly, is a clinical condition with several possible manifestations, and its clinical relevance is debated [14]. It has been reported that the prevalence of myocardial bridging in HCM is about 22%, usually occurring in the middle and distal portions of the LAD [15]. On the other hand, an association between AHC and myocardial bridging using invasive coronary angiography has rarely been reported [15]. Although Sorajja et al [16] observed no increased risk of death, including sudden cardiac death, among adult patients with HCM who also had myocardial bridging diagnosed at coronary angiography, myocardial bridging by itself can lead to myocardial ischaemia from significant narrowing of the intramyocardial segment during peak systole or from significant atherosclerosis in the adjacent proximal epicardial myocardial segment, as demonstrated by Schunkert [17]. In our case, CTCA findings ruled out both possibilities of significant coronary compromise. These findings coupled with the atypical nature of patient's chest pain guided clinicians to start medical therapy with beta-blockers, an accepted medical treatment in cases of myocardial bridging [12].

In conclusion, we demonstrated that cardiac MDCT can offer comprehensive non-invasive evaluation of patients with AHC, providing high quality CTCA, detailed anatomical information of heart chambers and accurate evaluation of myocardial function.

Received for publication September 9, 2005. Revision received January 31, 2006. Accepted for publication February 3, 2006.


   References
Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 

  1. Moon JC, Fisher NG, McKenna WJ, Pennell DJ. Detection of apical hypertrophic cardiomyopathy by cardiovascular magnetic resonance in patients with non-diagnostic echocardiography. Heart 2004;90:645–9.[Abstract/Free Full Text]
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  6. Youn HJ, Lee JM, Park CS, et al. The impaired flow reserve capacity of penetrating intramyocardial coronary arteries in apical hypertrophic cardiomyopathy. J Am Soc Echocardiogr 2005;18:128–32.[CrossRef][Medline]
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  8. Ghersin E, Lessick J, Litmanovich D, et al. Septal bounce in constrictive pericarditis: diagnosis and dynamic evaluation with multidetector CT. J Comput Assist Tomogr 2004;28:676–8.[CrossRef][Medline]
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  12. Ropers D, Baum U, Pohle K, et al. Detection of coronary artery stenoses with thin-slice multi-detector row spiral computed tomography and multiplanar reconstruction. Circulation 2003;107:664–6.
  13. Yamamuro M, Tadamura E, Kubo S, et al. Cardiac functional analysis with multi-detector row CT and segmental reconstruction algorithm: comparison with echocardiography, SPECT, and MR imaging. Radiology 2005;234:381–90.[Abstract/Free Full Text]
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CT assessment of apical hypertrophic cardiomyopathy
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This Article
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