CASE REPORT
Sudden Cardiac Death in 2 Young Siblings Reetu Kundu, MD,* Rajpal Singh Punia, MD,* Uma Handa, MD,* Amandeep Singh, MD,† and Harsh Mohan, MD* Abstract: Hypertrophic cardiomyopathy is a disease known for exhibiting phenotypic and genetic heterogeneity. At times, sudden cardiac death may be the first and foremost manifestation of the disease. We report 2 cases of hypertrophic cardiomyopathy causing sudden death, which were diagnosed on autopsy with special emphasis on histopathological findings of this entity. The role of a pathologist cannot be undermined as the disease is a diagnostic challenge often overlooked by the neophytes in the field due to unawareness. Key Words: hypertrophy, cardiomyopathy, autopsy, sudden death, inherited (Am J Forensic Med Pathol 2014;35: 246–248)
S
udden cardiac death (SCD) is a catastrophe complicating hypertrophic cardiomyopathy (HCM) and may be the first manifestation of the disease.1 The HCM is an inherited autosomal dominant disease characterized by left ventricular hypertrophy without cavity dilatation and in the absence of either a systemic or other cardiac illness.2 It typically affects teenagers or young adults. It is known for caveat of morphologic, physiologic, and clinical manifestations. The HCM is a disease exhibiting phenotypic and genetic heterogeneity with incomplete age-related penetrance and a prevalence of 1:500 in a general population of healthy young adults.3 It can present at any age or may be clinically silent or cause sudden death being detected on autopsy. We report 2 cases of HCM causing sudden death and diagnosed on autopsy with special emphasis on histopathological findings of this entity.
CASE REPORTS The first case is of an 11-year-old boy who had an alleged history of fall on playground during the games period in school. The boy had sudden death, and a postmortem was conducted. The heart measured 11 8 5.5 cm and weighed 340 g. The right and left ventricular wall thicknesses were 0.8 and 1.5 cm, respectively. The interventricular septum was hypertrophied with a maximum thickness of 1.8 cm and showed patchy areas of fibrosis. Left ventricular outflow tract was narrowed. The aortic, pulmonary, mitral, and tricuspid valves had a circumference of 4.8, 5, 6.5, and 7.5 cm, respectively. Both the coronaries were unremarkable. Other viscera examined were unremarkable. The second case is of a 13-year-old girl who was the sister of the deceased described previously. She had an alleged history of sudden death in the school after taking food. An autopsy
Manuscript received March 3, 2014; accepted July 19, 2014. From the *Department of Pathology, and †Forensic Medicine & Toxicology, Government Medical College and Hospital, Chandigarh, India. The authors report no conflict of interest. Reprints: Reetu Kundu, MD, Department of Pathology, Government Medical College and Hospital, Sector 32-A, Chandigarh-160030, India. E-mail: [email protected]. Copyright © 2014 by Lippincott Williams & Wilkins ISSN: 0195-7910/14/3504–0246 DOI: 10.1097/PAF.0000000000000120
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was carried out, and viscera were sent for histopathology. The organ of interest was the heart measuring 14 10.5 7.9 cm and weighing 450 g. The epicardial fat was focally increased. Cut section showed right and left ventricular wall thicknesses of 0.6 and 2.1 cm, respectively. The ventricular chamber on the left side was reduced in size (Fig. 1). The circumferences of the aortic, pulmonary (only a portion seen), mitral, and tricuspid valves were 4.2, 2, 6.6, and 8.5 cm, respectively. Both the coronaries were unremarkable. The other viscera did not show any abnormality. Representative microsections were examined from both the hearts. Sections from the left ventricle and the interventricular septum showed hypertrophied myocardium with myofiber disarray and a whorling pattern around areas of fibrosis (Fig. 2). The myofibers were short, with anisonucleosis and perinuclear vacuolation in some. The intramyocardial blood vessels showed thickened walls. Focal areas with replacement fibrosis of the endocardium were seen.
DISCUSSION Sudden death is caused by arrhythmias and pulmonary vascular disease in 30% and 13% of the cases, respectively. Simple aortic valve disease and HCM are rare (4%) causes of sudden death in childhood. In approximately 10% of cases, the cause of death remains obscured.4 In HCM, there is definitely an increased risk for SCD with an annual mortality of 2%.5 It is a frequent cause of sudden death in young athletes because the complication is favored by strenuous exercise.3 The cause of sudden death in HCM is arrhythmias, ventricular fibrillation, or sustained ventricular tachycardia.5 The underlying mechanisms for the same are yet to be fully established.
FIGURE 1. Gross photograph showing transverse sliced surface of the heart with increased left ventricular wall thickness and compressed ventricular cavity. Am J Forensic Med Pathol • Volume 35, Number 4, December 2014
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Am J Forensic Med Pathol • Volume 35, Number 4, December 2014
FIGURE 2. Histologic section showing haphazard disarray of short and hypertrophic myofibers along with interstitial fibrosis (hematoxylin and eosin staining, original magnification 10). The inset shows myofibers exhibiting anisonucleosis and perinuclear vacuolization (hematoxylin and eosin staining, original magnification 60).
The HCM exhibits clinical heterogeneity. The individual may be asymptomatic, have mild symptoms, or present with sudden death as the first manifestation of the disease.1,6 The most common clinical manifestations are exertional dyspnea, chest pain, syncopal attacks, palpitations, congestive cardiac failure, and sudden death.7 The HCM has a spectrum of variable phenotypic and genotypic expressions. Mutations in the genes encoding protein components of cardiac muscle sarcomere are implicated. Different genes or different mutations in the same gene, most being single point missense mutations or small deletions or insertions, are known to occur. These may be responsible for different cardiac morphologies, variable disease severity, and prognostic differences. Two of the frequently involved genes are MYBPC3 and MYH.8,9 The HCM is almost exclusively transmitted as an autosomal dominant trait. The 2 cases in the current study affected by the disease and being genetically linked as these were siblings also highlight this well-established fact. However, genetic studies for various mutations could not be done in our setup because of nonavailability of these. The disease may also occur sporadically although less often. The HCM phenotype may be seen in Noonan syndrome, with mitochondrial disease, Friedreich ataxia, and myotonic dystrophy.10–12 The gross findings in HCM were originally described by Teare as left ventricular hypertrophy, asymmetrical or symmetrical with thickening of the basal anterior septum causing narrowing of the outflow tract.5 The symmetrical HCM is seen in approximately 42% of cases and has concentric left ventricular hypertrophy with a shrunken cavity. Asymmetric septal hypertrophy is seen when the ratio of septum to posterior wall thickness is 1.3 or more.5,13 Septal hypertrophy may involve the whole of the septum or be restricted to the subaortic, midventricular region or the apex. The heart is oversized and overweight as seen in our cases, range extending from the upper limit of normal to more than 100% of increase in total heart weight.11 The left ventricular wall thickness generally exceeds 2 cm. The right ventricular wall is thickened in 17.6% of cases. Wall thickness is measured in millimeters with exclusion of trabeculae and papillary muscles, thus preventing overestimation of wall thickness. Small punctate gray white scars or areas showing whorling may be observed in the ventricle/septum corresponding to the replacement fibrosis. The © 2014 Lippincott Williams & Wilkins
Sudden Cardiac Death in 2 Young Siblings
anterior cusp of the mitral valve undergoes considerable distortion and thickening because of mechanical trauma. In a few cases, a subaortic mitral impact lesion or imprint lesion with mirror image of the anterior leaflet of the mitral valve is seen.5,11 This occurs because of repeated impact on the septum because of systolic anterior motion of the valve leaflet resulting in endocardial fibrosis. The HCM is peculiar in having some morphologic variants. Some cases show midventricular obstruction with or without a left ventricular apical diverticulum, associated with marked muscular midcavity narrowing with “dumb-bell” configuration of the left ventricle.5 Another variant involving ventricular hypertrophy localized to the apex has a better prognosis.14,15 In approximately 10% of patients, HCM may progress to a “burned-out” phase with left ventricular cavity dilatation probably due to loss of myocardium by replacement fibrosis.5 Microscopic examination reveals myofiber hypertrophy and disarray with interstitial fibrosis. The myofibers are bizarre, short, and thick, showing anisonucleosis and hyperchromatic nuclei along with perinuclear and cytoplasmic vacuolation. The whorled or woven appearance of myocytes around areas of fibrosis is characteristic. Our cases too showed these peculiar pointers toward the diagnosis of HCM. Myocyte disarray is absent in other conditions such as hypertensive heart disease and aortic stenosis, which grossly mimic HCM. Areas of interstitial adiposity are usually seen. The intramyocardial blood vessels show thickened wall due to intimal and medial smooth muscle cell hyperplasia, increased collagen in the media, and dense perivascular collagen deposition. Myofiber disarray is not pathognomonic of HCM. Some disarray is seen at the junction of septum with the anterior and posterior walls of the right ventricle in almost all normal hearts. Association of disarray with the irregular hypertrophy and fibrosis involving a sizeable proportion of at least 1 region of the left ventricle in at least 1 paraffin block is a diagnostic feature of HCM. To conclude, the histomorphologic confirmation of HCM at autopsy is quite sensitive and specific but is of limited clinical value for the endomyocardial biopsy is less sensitive. Many of the people who succumb to HCM have no previous functional limitations, and SCD is the first manifestation of the disease. The role of a pathologist in diagnosing HCM is unsurpassed, and the family of the deceased must undergo screening by the cardiologist as well as the genetic studies for detection of mutations affecting the myosin gene. REFERENCES 1. Michels M, Soliman OI, Phefferkorn J, et al. Disease penetrance and risk stratification for sudden cardiac death in asymptomatic hypertrophic cardiomyopathy mutation carriers. Eur Heart J. 2009; 30:2593–2598. 2. Desai MY, Ommen SR, McKenna WJ, et al. Imaging phenotype versus genotype in hypertrophic cardiomyopathy. Circ Cardiovasc Imaging. 2011;4:156–168. 3. Abdy NA, Valdes SO, Sorrell VL, et al. Apical hypertrophic cardiomyopathy in an adolescent. Congenit Heart Dis. 2010;5: 182–187. 4. Sanatani S, Wilson G, Smith CR, et al. Sudden unexpected death in children with heart disease. Congenit Heart Dis. 2006; 1:89–97. 5. Hughes SE. The pathology of hypertrophic cardiomyopathy. Histopathology. 2004;44:412–427. 6. Marian AJ, Salek L, Lutucuta S. Molecular genetics and pathogenesis of hypertrophic cardiomyopathy. Minerva Med. 2001;92:435–451. 7. Nishimura RA, Ommen SR, Tajik AJ. Hypertrophic cardiomyopathy: a patient perspective. Circulation. 2003;108:e133–e135.
www.amjforensicmedicine.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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Kundu et al
8. Richard P, Charron P, Carrier L, et al. Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations and implications for molecular diagnosis strategy. Circulation. 2003;107: 2227–2232.
12. García-Díaz L, Coserria F, Antiñolo G. Hypertrophic cardiomyopathy due to mitochondrial disease: prenatal diagnosis, management, and outcome. Case Rep Obstet Gynecol. 2013; doi:10.1155/2013/472356.
9. Page SP, Kounas S, Syrris P, et al. Cardiac myosin binding protein-C mutations in families with hypertrophic cardiomyopathy: disease expression in relation to age, gender, and long term outcome. Circ Cardiovasc Genet. 2012;5:156–166.
13. Rose AG. Evaluation of pathological criteria for diagnosis of hypertrophic cardiomyopathy. Histopathology. 1984;8: 395–406.
10. Mir A, Lemler M, Ramaciotti C, et al. Hypertrophic cardiomyopathy in a neonate associated with nemaline myopathy. Congenit Heart Dis. 2012;7:e37–e41. 11. Davies MJ, Mckenna WJ. Hypertrophic cardiomyopathy-pathology and pathogenesis. Histopathology. 1995;26:493–500.
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14. Maron BJ, Hauser RG, Roberts WC. Hypertrophic cardiomyopathy with left ventricular apical diverticulum. Am J Cardiol. 1996;77: 1263–1265. 15. Malik A. Incidental diagnosis of apical hypertrophic cardiomyopathy in an 18-year-old white man. Tex Heart Inst J. 2012;39: 756–757.
© 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Sudden Cardiac Death in 2 Young Siblings Reetu Kundu, MD,* Rajpal Singh Punia, MD,* Uma Handa, MD,* Amandeep Singh, MD,† and Harsh Mohan, MD* Abstract: Hypertrophic cardiomyopathy is a disease known for exhibiting phenotypic and genetic heterogeneity. At times, sudden cardiac death may be the first and foremost manifestation of the disease. We report 2 cases of hypertrophic cardiomyopathy causing sudden death, which were diagnosed on autopsy with special emphasis on histopathological findings of this entity. The role of a pathologist cannot be undermined as the disease is a diagnostic challenge often overlooked by the neophytes in the field due to unawareness. Key Words: hypertrophy, cardiomyopathy, autopsy, sudden death, inherited (Am J Forensic Med Pathol 2014;35: 246–248)
S
udden cardiac death (SCD) is a catastrophe complicating hypertrophic cardiomyopathy (HCM) and may be the first manifestation of the disease.1 The HCM is an inherited autosomal dominant disease characterized by left ventricular hypertrophy without cavity dilatation and in the absence of either a systemic or other cardiac illness.2 It typically affects teenagers or young adults. It is known for caveat of morphologic, physiologic, and clinical manifestations. The HCM is a disease exhibiting phenotypic and genetic heterogeneity with incomplete age-related penetrance and a prevalence of 1:500 in a general population of healthy young adults.3 It can present at any age or may be clinically silent or cause sudden death being detected on autopsy. We report 2 cases of HCM causing sudden death and diagnosed on autopsy with special emphasis on histopathological findings of this entity.
CASE REPORTS The first case is of an 11-year-old boy who had an alleged history of fall on playground during the games period in school. The boy had sudden death, and a postmortem was conducted. The heart measured 11 8 5.5 cm and weighed 340 g. The right and left ventricular wall thicknesses were 0.8 and 1.5 cm, respectively. The interventricular septum was hypertrophied with a maximum thickness of 1.8 cm and showed patchy areas of fibrosis. Left ventricular outflow tract was narrowed. The aortic, pulmonary, mitral, and tricuspid valves had a circumference of 4.8, 5, 6.5, and 7.5 cm, respectively. Both the coronaries were unremarkable. Other viscera examined were unremarkable. The second case is of a 13-year-old girl who was the sister of the deceased described previously. She had an alleged history of sudden death in the school after taking food. An autopsy
Manuscript received March 3, 2014; accepted July 19, 2014. From the *Department of Pathology, and †Forensic Medicine & Toxicology, Government Medical College and Hospital, Chandigarh, India. The authors report no conflict of interest. Reprints: Reetu Kundu, MD, Department of Pathology, Government Medical College and Hospital, Sector 32-A, Chandigarh-160030, India. E-mail: [email protected]. Copyright © 2014 by Lippincott Williams & Wilkins ISSN: 0195-7910/14/3504–0246 DOI: 10.1097/PAF.0000000000000120
246
www.amjforensicmedicine.com
was carried out, and viscera were sent for histopathology. The organ of interest was the heart measuring 14 10.5 7.9 cm and weighing 450 g. The epicardial fat was focally increased. Cut section showed right and left ventricular wall thicknesses of 0.6 and 2.1 cm, respectively. The ventricular chamber on the left side was reduced in size (Fig. 1). The circumferences of the aortic, pulmonary (only a portion seen), mitral, and tricuspid valves were 4.2, 2, 6.6, and 8.5 cm, respectively. Both the coronaries were unremarkable. The other viscera did not show any abnormality. Representative microsections were examined from both the hearts. Sections from the left ventricle and the interventricular septum showed hypertrophied myocardium with myofiber disarray and a whorling pattern around areas of fibrosis (Fig. 2). The myofibers were short, with anisonucleosis and perinuclear vacuolation in some. The intramyocardial blood vessels showed thickened walls. Focal areas with replacement fibrosis of the endocardium were seen.
DISCUSSION Sudden death is caused by arrhythmias and pulmonary vascular disease in 30% and 13% of the cases, respectively. Simple aortic valve disease and HCM are rare (4%) causes of sudden death in childhood. In approximately 10% of cases, the cause of death remains obscured.4 In HCM, there is definitely an increased risk for SCD with an annual mortality of 2%.5 It is a frequent cause of sudden death in young athletes because the complication is favored by strenuous exercise.3 The cause of sudden death in HCM is arrhythmias, ventricular fibrillation, or sustained ventricular tachycardia.5 The underlying mechanisms for the same are yet to be fully established.
FIGURE 1. Gross photograph showing transverse sliced surface of the heart with increased left ventricular wall thickness and compressed ventricular cavity. Am J Forensic Med Pathol • Volume 35, Number 4, December 2014
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Am J Forensic Med Pathol • Volume 35, Number 4, December 2014
FIGURE 2. Histologic section showing haphazard disarray of short and hypertrophic myofibers along with interstitial fibrosis (hematoxylin and eosin staining, original magnification 10). The inset shows myofibers exhibiting anisonucleosis and perinuclear vacuolization (hematoxylin and eosin staining, original magnification 60).
The HCM exhibits clinical heterogeneity. The individual may be asymptomatic, have mild symptoms, or present with sudden death as the first manifestation of the disease.1,6 The most common clinical manifestations are exertional dyspnea, chest pain, syncopal attacks, palpitations, congestive cardiac failure, and sudden death.7 The HCM has a spectrum of variable phenotypic and genotypic expressions. Mutations in the genes encoding protein components of cardiac muscle sarcomere are implicated. Different genes or different mutations in the same gene, most being single point missense mutations or small deletions or insertions, are known to occur. These may be responsible for different cardiac morphologies, variable disease severity, and prognostic differences. Two of the frequently involved genes are MYBPC3 and MYH.8,9 The HCM is almost exclusively transmitted as an autosomal dominant trait. The 2 cases in the current study affected by the disease and being genetically linked as these were siblings also highlight this well-established fact. However, genetic studies for various mutations could not be done in our setup because of nonavailability of these. The disease may also occur sporadically although less often. The HCM phenotype may be seen in Noonan syndrome, with mitochondrial disease, Friedreich ataxia, and myotonic dystrophy.10–12 The gross findings in HCM were originally described by Teare as left ventricular hypertrophy, asymmetrical or symmetrical with thickening of the basal anterior septum causing narrowing of the outflow tract.5 The symmetrical HCM is seen in approximately 42% of cases and has concentric left ventricular hypertrophy with a shrunken cavity. Asymmetric septal hypertrophy is seen when the ratio of septum to posterior wall thickness is 1.3 or more.5,13 Septal hypertrophy may involve the whole of the septum or be restricted to the subaortic, midventricular region or the apex. The heart is oversized and overweight as seen in our cases, range extending from the upper limit of normal to more than 100% of increase in total heart weight.11 The left ventricular wall thickness generally exceeds 2 cm. The right ventricular wall is thickened in 17.6% of cases. Wall thickness is measured in millimeters with exclusion of trabeculae and papillary muscles, thus preventing overestimation of wall thickness. Small punctate gray white scars or areas showing whorling may be observed in the ventricle/septum corresponding to the replacement fibrosis. The © 2014 Lippincott Williams & Wilkins
Sudden Cardiac Death in 2 Young Siblings
anterior cusp of the mitral valve undergoes considerable distortion and thickening because of mechanical trauma. In a few cases, a subaortic mitral impact lesion or imprint lesion with mirror image of the anterior leaflet of the mitral valve is seen.5,11 This occurs because of repeated impact on the septum because of systolic anterior motion of the valve leaflet resulting in endocardial fibrosis. The HCM is peculiar in having some morphologic variants. Some cases show midventricular obstruction with or without a left ventricular apical diverticulum, associated with marked muscular midcavity narrowing with “dumb-bell” configuration of the left ventricle.5 Another variant involving ventricular hypertrophy localized to the apex has a better prognosis.14,15 In approximately 10% of patients, HCM may progress to a “burned-out” phase with left ventricular cavity dilatation probably due to loss of myocardium by replacement fibrosis.5 Microscopic examination reveals myofiber hypertrophy and disarray with interstitial fibrosis. The myofibers are bizarre, short, and thick, showing anisonucleosis and hyperchromatic nuclei along with perinuclear and cytoplasmic vacuolation. The whorled or woven appearance of myocytes around areas of fibrosis is characteristic. Our cases too showed these peculiar pointers toward the diagnosis of HCM. Myocyte disarray is absent in other conditions such as hypertensive heart disease and aortic stenosis, which grossly mimic HCM. Areas of interstitial adiposity are usually seen. The intramyocardial blood vessels show thickened wall due to intimal and medial smooth muscle cell hyperplasia, increased collagen in the media, and dense perivascular collagen deposition. Myofiber disarray is not pathognomonic of HCM. Some disarray is seen at the junction of septum with the anterior and posterior walls of the right ventricle in almost all normal hearts. Association of disarray with the irregular hypertrophy and fibrosis involving a sizeable proportion of at least 1 region of the left ventricle in at least 1 paraffin block is a diagnostic feature of HCM. To conclude, the histomorphologic confirmation of HCM at autopsy is quite sensitive and specific but is of limited clinical value for the endomyocardial biopsy is less sensitive. Many of the people who succumb to HCM have no previous functional limitations, and SCD is the first manifestation of the disease. The role of a pathologist in diagnosing HCM is unsurpassed, and the family of the deceased must undergo screening by the cardiologist as well as the genetic studies for detection of mutations affecting the myosin gene. REFERENCES 1. Michels M, Soliman OI, Phefferkorn J, et al. Disease penetrance and risk stratification for sudden cardiac death in asymptomatic hypertrophic cardiomyopathy mutation carriers. Eur Heart J. 2009; 30:2593–2598. 2. Desai MY, Ommen SR, McKenna WJ, et al. Imaging phenotype versus genotype in hypertrophic cardiomyopathy. Circ Cardiovasc Imaging. 2011;4:156–168. 3. Abdy NA, Valdes SO, Sorrell VL, et al. Apical hypertrophic cardiomyopathy in an adolescent. Congenit Heart Dis. 2010;5: 182–187. 4. Sanatani S, Wilson G, Smith CR, et al. Sudden unexpected death in children with heart disease. Congenit Heart Dis. 2006; 1:89–97. 5. Hughes SE. The pathology of hypertrophic cardiomyopathy. Histopathology. 2004;44:412–427. 6. Marian AJ, Salek L, Lutucuta S. Molecular genetics and pathogenesis of hypertrophic cardiomyopathy. Minerva Med. 2001;92:435–451. 7. Nishimura RA, Ommen SR, Tajik AJ. Hypertrophic cardiomyopathy: a patient perspective. Circulation. 2003;108:e133–e135.
www.amjforensicmedicine.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
247
Am J Forensic Med Pathol • Volume 35, Number 4, December 2014
Kundu et al
8. Richard P, Charron P, Carrier L, et al. Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations and implications for molecular diagnosis strategy. Circulation. 2003;107: 2227–2232.
12. García-Díaz L, Coserria F, Antiñolo G. Hypertrophic cardiomyopathy due to mitochondrial disease: prenatal diagnosis, management, and outcome. Case Rep Obstet Gynecol. 2013; doi:10.1155/2013/472356.
9. Page SP, Kounas S, Syrris P, et al. Cardiac myosin binding protein-C mutations in families with hypertrophic cardiomyopathy: disease expression in relation to age, gender, and long term outcome. Circ Cardiovasc Genet. 2012;5:156–166.
13. Rose AG. Evaluation of pathological criteria for diagnosis of hypertrophic cardiomyopathy. Histopathology. 1984;8: 395–406.
10. Mir A, Lemler M, Ramaciotti C, et al. Hypertrophic cardiomyopathy in a neonate associated with nemaline myopathy. Congenit Heart Dis. 2012;7:e37–e41. 11. Davies MJ, Mckenna WJ. Hypertrophic cardiomyopathy-pathology and pathogenesis. Histopathology. 1995;26:493–500.
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www.amjforensicmedicine.com
14. Maron BJ, Hauser RG, Roberts WC. Hypertrophic cardiomyopathy with left ventricular apical diverticulum. Am J Cardiol. 1996;77: 1263–1265. 15. Malik A. Incidental diagnosis of apical hypertrophic cardiomyopathy in an 18-year-old white man. Tex Heart Inst J. 2012;39: 756–757.
© 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
