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DOI:10.2214/AJR.07.2980
AJR 2008; 190:W169
© American Roentgen Ray Society


Letters

A More Detailed View Calls for More Detailed Definition: Description of Cardiac Morphology with High-Resolution CT and MRI

Tjeerd Germans, Robin Nijveldt and Albert C. van Rossum

VU University Medical Center Amsterdam, The Netherlands Interuniversity Cardiology Institute of The Netherlands Utrecht, The Netherlands

WEB—This is a Web exclusive article. T. Germans was supported by grant 2006B213 and R. Nijveldt was supported by grant 2003B126 from The Netherlands Heart Foundation.

High-resolution imaging techniques such as CT and MRI have significantly improved the noninvasive diagnostic accuracy in coronary artery disease and provide more detailed tissue characterization in ischemic and nonischemic cardiomyopathies. These techniques facilitate research focused on a more accurate description of cardiac morphologic abnormalities that are difficult to observe with echocardiography, as recently reported by Srichai and coworkers [1]. In that study, contrast-enhanced gated cardiac CT was used to describe the prevalence and morphology of cardiac diverticula. The authors found that cardiac diverticula were prevalent in 2.2% of a referral-based population and were related to various cardiomyopathies. In addition, they observed that cardiac diverticula were predominantly located in the inferior and inferoseptal segments of the left ventricle.

The muscular form of cardiac diverticula shown in Figure 4 of the Srichai et al. [1] article, strongly resembles the morphology of the crypts that we [2] recently described to be present in the majority (81%) of hypertrophic cardiomyopathy mutation carriers and that probably precede the development of left ventricular hypertrophy. We think that "crypts" was a more accurate term to describe this structural abnormality because the term diverticula suggests bulging out of a hollow organ rather than penetration into the muscular wall. We hypothesize that this penetration of compact myocardium may represent either myocyte disarray, which is in line with the exceptionally high prevalence of crypts in hypertrophic cardiomyopathy mutation carriers and the preferential location at the insertion points of the right ventricle into the left ventricle, or cleavage of the laminar myocardial sheets due to locally altered loading conditions or myocardial contractility.


Figure 1
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Fig. 1A Distinguishing crypts from noncompaction cardiomyopathy. LA = left atrium, LV = left ventricle, RV = right ventricle. Cardiac MR steady-state free precession cine images of 22-year-old woman who is hypertrophic cardiomyopathy mutation carrier (A) and 36-year-old man with noncompaction cardiomyopathy (B). Note that crypts, located in basal inferoseptum (arrowheads, A) penetrate compact myocardium whereas in noncompaction cardiomyopathy, broad noncompacted layer of myocardium (asterisk, B) aligns with compact layer of myocardium and is predominantly located in apex or lateral segments of left ventricular wall.

 


Figure 2
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Fig. 1B Distinguishing crypts from noncompaction cardiomyopathy. LA = left atrium, LV = left ventricle, RV = right ventricle. Cardiac MR steady-state free precession cine images of 22-year-old woman who is hypertrophic cardiomyopathy mutation carrier (A) and 36-year-old man with noncompaction cardiomyopathy (B). Note that crypts, located in basal inferoseptum (arrowheads, A) penetrate compact myocardium whereas in noncompaction cardiomyopathy, broad noncompacted layer of myocardium (asterisk, B) aligns with compact layer of myocardium and is predominantly located in apex or lateral segments of left ventricular wall.

 
Although this entity has been previously described as a form of noncompaction cardiomyopathy, a cardiomyopathy suggested by the authors [1] to be considered in the differential diagnosis of the crypts, we would like to emphasize that it is important to discriminate crypts from noncompaction cardiomyopathy because the clinical course of patients in whom the crypts are observed (i.e., hypertrophic cardiomyopathy mutation carriers) may significantly differ from patients with noncompaction cardiomyopathy [35]. Indeed, discrimination between these two cardiomyopathies remains challenging with echocardiography but can readily be made with cardiac MRI or CT using the following criteria: crypts penetrate compact myocardium whereas in noncompaction cardiomyopathy, a broad noncompacted layer aligns with a compact layer of myocardium; crypts are mainly located in the mid and basal inferoseptal segments of the left ventricle whereas noncompaction mainly occurs in the apical and lateral segments (Fig. 1A, 1B); and, in contrast to noncompaction cardiomyopathy, crypts are not associated with a reduced left ventricular ejection fraction [4].

State-of-the-art imaging techniques allow better description and understanding of cardiac morphology but consequently require a strict definition of the newly acquired observations. As a result, our improved knowledge of cardiomyopathies may lead to further refinement of the diagnosis and to subsequent optimization of therapy.

References

  1. Srichai MB, Hecht EM, Kim DC, Jacobs JE. Ventricular diverticula on cardiac CT: more common than previously thought. AJR2007; 189:204 –208[Abstract/Free Full Text]
  2. Germans T, Wilde AA, Dijkmans PA, et al. Structural abnormalities of the inferoseptal left ventricular wall detected by cardiac MRI in carriers of hypertrophic cardiomyopathy mutations. J Am Coll Cardiol 2006; 48:2518 –2523[Abstract/Free Full Text]
  3. McCrohon JA, Richmond DR, Pennell DJ, Mohiaddin RH. Images in cardiovascular medicine: isolated noncompaction of the myocardium—a rarity or missed diagnosis? Circulation2002; 106:e22 –e23[Medline]
  4. Germans T, Dijkmans PA, Wilde AA, Kamp O, van Rossum AC. Images in cardiovascular medicine: prominent crypt formation in the inferoseptum of a hypertrophic cardiomyopathy mutation carrier mimics noncompaction cardiomyopathy. Circulation 2007;115 :e610 –e611[Free Full Text]
  5. Stollberger C, Finsterer J. Left ventricular hyper-trabeculation/noncompaction and stroke or embolism. Cardiology 2005;103 : 68–72[CrossRef][Medline]

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