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Letter by Andò et al Regarding Article, “Prevalence, Clinical Significance, and Natural History of Left Ventricular Apical Aneurysms in Hypertrophic Cardiomyopathy”

2009; Lippincott Williams & Wilkins; Volume: 119; Issue: 22 Linguagem: Inglês

10.1161/circulationaha.108.828293

1524-4539

Giuseppe Andò, Francesco Saporito, F Arrigo,

Coronary Artery Anomalies

HomeCirculationVol. 119, No. 22Letter by Andò et al Regarding Article, "Prevalence, Clinical Significance, and Natural History of Left Ventricular Apical Aneurysms in Hypertrophic Cardiomyopathy" Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Andò et al Regarding Article, "Prevalence, Clinical Significance, and Natural History of Left Ventricular Apical Aneurysms in Hypertrophic Cardiomyopathy" Giuseppe Andò, MD, PhD, Francesco Saporito, MD and Francesco Arrigo, MD Giuseppe AndòGiuseppe Andò Department of Medicine and Pharmacology, Section of Cardiology, University of Messina, Messina, Italy , Francesco SaporitoFrancesco Saporito Department of Medicine and Pharmacology, Section of Cardiology, University of Messina, Messina, Italy and Francesco ArrigoFrancesco Arrigo Department of Medicine and Pharmacology, Section of Cardiology, University of Messina, Messina, Italy Originally published9 Jun 2009https://doi.org/10.1161/CIRCULATIONAHA.108.828293Circulation. 2009;119:e557To the Editor:We read with great interest the article by Maron et al1 about the cohort of patients with hypertrophic cardiomyopathy (HCM) and left ventricular apical aneurysms. In the mid-1990s, the same authors drew our attention to a small group of patients with HCM and uncommon apical bulges regarded as diverticula.2 Cardiac magnetic resonance now sheds light on the structure of these apical bulges and the surrounding myocardium and demonstrates transmural myocardial fibrosis of the aneurysmal rim, largely extending in the contiguous ventricular walls.1Apical aneurysm has been classically considered a complication of acute myocardial infarction. This comprehensive series1 demonstrates that apical aneurysms can form in patients in whom obstructive coronary artery disease is ruled out. Therefore, the occurrence of myocyte loss somehow related to microvascular dysfunction is likely to play a crucial pathophysiological role.In light of the previous article,2 we recently used the term pseudodiverticulum3 to identify an apical bulge associated with HCM that now seems indistinguishable from those outlined in the current series.1 The use of such a term to describe a relatively common feature in HCM is likely to be abolished or, rather, to be limited to those congenital outpouchings typically known as diverticula.4 Indeed, Maron et al did not include in their series1 those young patients in whom the walls of the apical protrusion consisted of muscular tissue.2 Catastrophic complications are likely to occur more frequently in this subset of patients with HCM. Besides the established role of a prophylactic implantable cardioverter-defibrillator, the recent advances in catheter-based structural cardiac interventions will likely allow us to propose percutaneous aneurysm occlusion, as an alternative to oral anticoagulation, in forthcoming years to selected patients.5The mechanisms contributing to the formation of apical aneurysms in HCM are multiple and still to be clarified. In the case we observed,3 gadolinium enhancement was confined to the ventricular walls adjacent to the neck of the aneurysm. The peculiarity was the intriguing discontinuation of a normally contracting myocardium, because the walls of the apical ancillary chamber consisted of only pericardium and did not show gadolinium enhancement. The left ventricular apex has to be considered a locus minoris resistentiae due to the thinner helical architecture of myocardium in the apical loop. A critical mechanism may consist of the attempt to counterbalance the pressure exerted by the hypertrophied hypercontractile ventricle on the apex. The abnormal intracavitary stress may force a herniation of the endocardium toward the pericardium. Independently from midcavitary obstruction and according to the Laplace law, Nature in such a case would aim to normalize the wall stress of the apex, which could get less hypertrophied than the rest of the ventricle, by creating an ancillary chamber with a small radius and a thin wall thickness. This speculation might explain why ventricular rupture of apical aneurysms in HCM is uncommon.1 Simply put, wall stress inside the apical aneurysm would be unexpectedly low.DisclosuresNone. References 1 Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ. Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy. Circulation. 2008; 118: 1541–1549.LinkGoogle Scholar2 Maron BJ, Hauser RG, Roberts WC. Hypertrophic cardiomyopathy with left ventricular apical diverticulum. Am J Cardiol. 1996; 77: 1263–1265.CrossrefMedlineGoogle Scholar3 Andò G, Saporito F, Di Bella G, Trio O, Anfuso C, Zito C, Cerrito M, Oreto G, Arrigo F. Left ventricular pseudodiverticulum. J Cardiovasc Med (Hagerstown). 2008; 9: 1080–1082.CrossrefMedlineGoogle Scholar4 Marijon E, Ou P, Fermont L, Concordet S, Le Bidois J, Sidi D, Bonnet D. Diagnosis and outcome in congenital ventricular diverticulum and aneurysm. J Thorac Cardiovasc Surg. 2006; 131: 433–437.CrossrefMedlineGoogle Scholar5 Clift P, Thorne S, de Giovanni J. Percutaneous device closure of a pseudoaneurysm of the left ventricular wall. Heart. 2004; 90: e62.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails June 9, 2009Vol 119, Issue 22 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.108.828293PMID: 19506120 Originally publishedJune 9, 2009 PDF download Advertisement SubjectsCardiomyopathy