Hypertrophic cardiomyopathy echocardiography and ultrasound

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

Overview

Echocardiography is the imaging modality of choice in the diagnosis of hypertrophic cardiomyopathy. Classically there is a small left ventricular cavity with hypertrophy out of proportion to any underlying condition that would cause LVH. The hypertrophy is often asymmetric.

Echocardiography

Echo with doppler is the primary procedure used to diagnose hypertrophic cardiomyopathy. There is a prolonged isovolumic relaxation time, reduced peak E velocity, prolonged deceleration time, increased peak A velocity and decreased E/A ratio as compared to normal controls.

Proper examination should evaluate: [1]

  • Dynamic outflow tract obstruction
    • SAM (systolic anterior motion) of the mitral leaflet
    • Mid-systolic closure of the aortic valve
    • Late peaking, high-velocity flow in the outflow tract
    • Variability of obstruction with maneuvers (exercise, amyl nitrate inhalation, and post-PVC beats)
  • Doppler Techniques
    • Use continuous wave doppler to measure the systolic flow velocity in the LV outflow tract and mid-cavity (both at rest and during maneuvers such as the Valsalva maneuver or during dobutamine administration.

Because of the turbulent, high-velocity jet in the left ventricular outflow tract (LVOT), the anterior mitral leaflet moves anteriorly in systole, exacerbating the outflow tract obstruction, and promoting mitral regurgitation. The following images show classic systolic anterior motion (SAM) of the mitral valve leaflets:

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Frequency of Hypertrophy

While LVH is usually present, not all carriers with HCM demonstrate left ventricular hypertrophy. Left ventricular hypertrophy may be absent in childhood. It may then appear following the rapid growth of adolescence and may first appear at age 17 to 18.[2][3][4] LVH may be time-dependent and may appear late, particularly in patients with a mutation in the myosin-binding protein C gene. Patients generally present later in life and in general, have a better prognosis than beta myosin heavy chain or cardiac troponin T mutations. Up to 60% of patients at age 50 years have no evidence of LVH. LVH may appear later in life in these patients. Because of this, a normal EKG and a normal ECHO at maturity does not exclude the presence of an HCM mutation. [5]

Diagnostic Features of Hypertrophy

  • Left ventricular hypertrophy (LVH) most often in an asymmetric distribution,
  • Thickening of the left ventricular wall in the absence of cavitary dilation and the presence of hyperdynamic activity (in fact there may be systolic cavity obliteration or near obliteration)
  • Absence of any other cause of left ventricular hypertrophy such as aortic stenosis or hypertension

Left Ventricular Wall Thickness

  • The traditional definition requires a wall thickness > 15 mm.
  • Borderline wall thicknesses of 13-14 mm must be distinguished from extreme variants of athletes heart
  • There are some genetic variants that yield a normal wall thickness. [6][7][8][9][10]
  • Among children < 13 years of age, LVH is often absent.

2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy A Report of the American College of Cardiology/American Heart  Association Joint Committee on Clinical Practice Guidelines[11]

Recommendations for Echocardiography Referenced studies that support the recommendations are summarized in The Online Data Supplement

Class I
1. In patients with suspected HCM, a TTE is recommended in the initial evaluation(Level of Evidence: B-NR)

2. In patients with HCM with no change in clinical status or events, repeat TTE is recommended every 1 to 2 years to assess the degree of myocardial hypertrophy, dynamic LVOTO, MR, and myocardial function(children:Level of Evidence: B-NR adults:Level of Evidence: C-LD ) 3. For patients with HCM who experience a change in clinical status or a new clinical event, repeat TTE is recommended.(Level of Evidence: B-NR) 4. For patients with HCM and resting LVOT gradient <50 mm Hg, a TTE with provocative maneuvers is recommended(Level of Evidence: B-NR) 5. For symptomatic patients with HCM who do not have a resting or provocable outflow tract gradient ≥50 mm Hg on TTE, exercise TTE is recommended for the detection and quantification of dynamic LVOTO(Level of Evidence: B-NR) 6. For patients with HCM undergoing surgical septal myectomy, intraoperative transesophageal echocardiogram (TEE) is recommended to assess mitral valve anatomy and function and adequacy of septal myectomy(Level of Evidence: B-NR) 7. For patients with HCM undergoing alcohol septal ablation, TTE or intraoperative TEE with intracoronary ultrasound-enhancing contrast injection of the candidate’s septal perforator(s) is recommended.(Level of Evidence: B-NR) 8. For patients with HCM who have undergone SRT, TTE within 3 to 6 months after the procedure is recommended to evaluate the procedural results(Level of Evidence: B-NR) 9. Screening: In first-degree relatives of patients with HCM, a TTE is recommended as part of initial family screening and periodic follow-up(Level of Evidence: B-NR) 10.    Screening: In individuals who are genotype-positive or phenotype-negative, serial echo-cardiography is recommended at periodic intervals depending on age (1 to 2 years in children and adolescents, 3 to 5 years in adults) and change in clinical status(Level of Evidence: B-NR)

Class IIa
11.    For patients with HCM, TEE can be useful if TTE is inconclusive in clinical decision-making regarding medical therapy, and in situations such as planning for myectomy, exclusion of subaortic membrane or MR secondary to structural abnormalities of the mitral valve apparatus, or in the assessment of the feasibility of alcohol septal ablation.(Level of Evidence: C-LD)

12.    For patients with HCM in whom the diagnoses of apical HCM, apical aneurysm, or atypical patterns of hypertrophy is inconclusive on TTE, the use of an intravenous ultrasound-enhancing agent is reasonable, particularly if other imaging modalities such as CMR are not readily available or contraindicated.(Level of Evidence: B-NR) 13.    For asymptomatic patients with HCM who do not have a resting or provocable outflow tract gradient ≥50 mm Hg on standard TTE, exercise TTE is reasonable for the detection and quantification of dynamic LVOTO(Level of Evidence: C-LD)

Recommendations for Exercise Stress Testing Referenced studies that support the recommendations are summarized in the Online Data Supplement

Class I
1. For symptomatic patients with HCM who do not have resting or provocable outflow tract gradient ≥50 mm Hg on TTE, exercise TTE is recommended for the detection and quantification of dynamic LVOTO (Level of Evidence: B-NR)
Class IIa
4. For asymptomatic patients with HCM who do not have a resting or provocable outflow tract gradient ≥50 mm Hg on standard TTE, exercise TTE is reasonable for the detection and quantification of dynamic LVOTO(Level of Evidence: C-LD)


2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy (DO NOT EDIT)[12]

Echocardiography (DO NOT EDIT)[12]

Class I
"1. A TTE is recommended in the initial evaluation of all patients with suspected HCM.[13][14][15][16][17][18][19][20] (Level of Evidence: B) "
"2. A TTE is recommended as a component of the screening algorithm for family members of patients with HCM unless the family member is genotype negative in a family with known definitive mutations.[21][22][23][24] (Level of Evidence: B) "
"3. Periodic (12 to 18 months) TTE screening is recommended for children of patients with HCM, starting by age 12 years or earlier if a growth spurt or signs of puberty are evident and/or when there are plans for engaging in intense competitive sports or there is a family history of SCD.[22][25] (Level of Evidence: C) "
"4. Repeat TTE is recommended for the evaluation of patients with HCM with a change in clinical status or new cardiovascular event.[26][27][28][29][30][31][32] (Level of Evidence: B) "
"5. A transesophageal echocardiogram (TEE) is recommended for the intraoperative guidance of surgical myectomy.[33][34][35] (Level of Evidence: B) "
"6. TTE or TEE with intracoronary contrast injection of the candidate’s septal perforator(s) is recommended for the intraprocedural guidance of alcohol septal ablation.[36][37][38][39] (Level of Evidence: B) "
"7. TTE should be used to evaluate the effects of surgical myectomy or alcohol septal ablation for obstructive HCM.[36][40][41][42][43][44][45] (Level of Evidence: C) "
Class IIa
"1. TTE studies performed every 1 to 2 years can be useful in the serial evaluation of symptomatically stable patients with HCM to assess the degree of myocardial hypertrophy, dynamic obstruction, and myocardial function.[14][16][18] (Level of Evidence: C) "
"2. Exercise TTE can be useful in the detection and quantification of dynamic LVOT obstruction in the absence of resting outflow tract obstruction in patients with HCM.[27][30][32][46][47] (Level of Evidence: B) "
"3. TEE can be useful if TTE is inconclusive for clinical decision making about medical therapy and in situations such as planning for myectomy, exclusion of sub-aortic membrane or mitral regurgitation secondary to structural abnormalities of the mitral valve apparatus, or in assessment for the feasibility of alcohol septal ablation.[33][34][35] (Level of Evidence: C) "
"4. TTE combined with the injection of an intravenous contrast agent is reasonable if the diagnosis of apical HCM or apical infarction or severity of hypertrophy is in doubt, particularly when other imaging modalities such as cardiovascular magnetic resonance (CMR) are not readily available, not diagnostic, or are contraindicated. (Level of Evidence: C)"
"5. Serial TTE studies are reasonable for clinically unaffected patients who have a first-degree relative with HCM when genetic status is unknown. Such follow-up may be considered every 12 to 18 months for children or adolescents from high-risk families and every 5 years for adult family members.[21][22][24][25] (Level of Evidence: C)"
Class III (No Benefit)
"1. TTE studies should not be performed more frequently than every 12 months in patients with HCM when it is unlikely that any changes have occurred that would have an impact on clinical decision making. (Level of Evidence: C) "
"2. Routine TEE and/or contrast echocardiography is not recommended when TTE images are diagnostic of HCM and/or there is no suspicion of fixed obstruction or intrinsic mitral valve pathology.(Level of Evidence: C) "

Detection of Concomitant Coronary Disease [12]

Class III (No Benefit)
"1. Routine SPECT MPI or stress echocardiography is not indicated for detection of silent CAD-related ischemia in patients with HOCM who are asymptomatic. (Level of Evidence: C) "

References

  1. ↑ Otto, Catherine. Textbook of Clinical Echocardiography. 3rd Edition, 2004
  2. ↑ Hagege AA, Dubourg O, Desnos M et al. Familial hypertrophic cardiomyopathy. Cardiac ultrasonic abnormalities in genetically affected subjects without echocardiographic evidence of left ventricular hypertrophy. Eur Heart J 1998;19:490–9.
  3. ↑ Maron BJ, Spirito P, Wesley Y, Arce J. Development and progression of left ventricular hypertrophy in children with hypertrophic cardiomyopathy. N Engl J Med 1986;315:610–4.
  4. ↑ Spirito P, Maron BJ. Absence of progression of left ventricular hypertrophy in adult patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1987;9:1013–7.
  5. ↑ Erdmann J, Raible J, Maki-Abadi J et al. Spectrum of clinical phenotypes and gene variants in cardiac myosin-binding protein C mutation carriers with hypertrophic cardiomyopathy. J Am Coll Cardiol 2001;38:322–30.
  6. ↑ Niimura H, Bachinski LL, Sangwatanaroj S et al. Mutations in the gene for cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy. N Engl J Med 1998;338:1248–57.
  7. ↑ Maron BJ, Niimura H, Casey SA et al. Development of left ventricular hypertrophy in adults in hypertrophic cardiomyopathy caused by cardiac myosin-binding protein C gene mutations. J Am Coll Cardiol 2001;38:315–21.
  8. ↑ Charron P, Dubourg O, Desnos M et al. Diagnostic value of electrocardiography and echocardiography for familial hypertrophic cardiomyopathy in a genotyped adult population. Circulation 1997; 96:214–9.
  9. ↑ Charron P, Dubourg O, Desnos M et al. Diagnostic value of electrocardiography and echocardiography for familial hypertrophic cardiomyopathy in genotyped children. Eur Heart J 1998;19:1377–82.
  10. ↑ Panza JA, Maron BJ. Relation of electrocardiographic abnormalities to evolving left ventricular hypertrophy in hypertrophic cardiomyopathy during childhood. Am J Cardiol 1989;63:1258–65.
  11. ↑ Ommen SR, Mital S, Burke MA, Day SM, Deswal A, Elliott P; et al. (2020). "2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Circulation. 142 (25): e558–e631. doi:10.1161/CIR.0000000000000937. PMID 33215931 Check |pmid= value (help).
  12. ↑ 12.0 12.1 12.2 Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, Naidu SS, Nishimura RA, Ommen SR, Rakowski H, Seidman CE, Towbin JA, Udelson JE, Yancy CW (2011). "2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". Journal of the American College of Cardiology. 58 (25): e212–60. doi:10.1016/j.jacc.2011.06.011. PMID 22075469. Retrieved 2011-12-19. Unknown parameter |month= ignored (help)
  13. ↑ Maron BJ (2002). "Hypertrophic cardiomyopathy: a systematic review". JAMA : the Journal of the American Medical Association. 287 (10): 1308–20. PMID 11886323. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  14. ↑ 14.0 14.1 Klues HG, Schiffers A, Maron BJ (1995). "Phenotypic spectrum and patterns of left ventricular hypertrophy in hypertrophic cardiomyopathy: morphologic observations and significance as assessed by two-dimensional echocardiography in 600 patients". Journal of the American College of Cardiology. 26 (7): 1699–708. doi:10.1016/0735-1097(95)00390-8. PMID 7594106. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  15. ↑ Wigle ED, Sasson Z, Henderson MA, Ruddy TD, Fulop J, Rakowski H, Williams WG (1985). "Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review". Progress in Cardiovascular Diseases. 28 (1): 1–83. PMID 3160067. Retrieved 2011-12-22.
  16. ↑ 16.0 16.1 Wigle ED, Rakowski H, Kimball BP, Williams WG (1995). "Hypertrophic cardiomyopathy. Clinical spectrum and treatment". Circulation. 92 (7): 1680–92. PMID 7671349. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  17. ↑ Adabag AS, Kuskowski MA, Maron BJ (2006). "Determinants for clinical diagnosis of hypertrophic cardiomyopathy". The American Journal of Cardiology. 98 (11): 1507–11. doi:10.1016/j.amjcard.2006.07.029. PMID 17126660. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  18. ↑ 18.0 18.1 Afonso LC, Bernal J, Bax JJ, Abraham TP (2008). "Echocardiography in hypertrophic cardiomyopathy: the role of conventional and emerging technologies". JACC. Cardiovascular Imaging. 1 (6): 787–800. doi:10.1016/j.jcmg.2008.09.002. PMID 19356516. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  19. ↑ Fifer MA, Vlahakes GJ (2008). "Management of symptoms in hypertrophic cardiomyopathy". Circulation. 117 (3): 429–39. doi:10.1161/CIRCULATIONAHA.107.694158. PMID 18212300. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  20. ↑ Soor GS, Luk A, Ahn E, Abraham JR, Woo A, Ralph-Edwards A, Butany J (2009). "Hypertrophic cardiomyopathy: current understanding and treatment objectives". Journal of Clinical Pathology. 62 (3): 226–35. doi:10.1136/jcp.2008.061655. PMID 18930982. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  21. ↑ 21.0 21.1 Bos JM, Towbin JA, Ackerman MJ (2009). "Diagnostic, prognostic, and therapeutic implications of genetic testing for hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 54 (3): 201–11. doi:10.1016/j.jacc.2009.02.075. PMID 19589432. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  22. ↑ 22.0 22.1 22.2 Maron BJ, Seidman JG, Seidman CE (2004). "Proposal for contemporary screening strategies in families with hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 44 (11): 2125–32. doi:10.1016/j.jacc.2004.08.052. PMID 15582308. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  23. ↑ Binder J, Ommen SR, Gersh BJ, Van Driest SL, Tajik AJ, Nishimura RA, Ackerman MJ (2006). "Echocardiography-guided genetic testing in hypertrophic cardiomyopathy: septal morphological features predict the presence of myofilament mutations". Mayo Clinic Proceedings. Mayo Clinic. 81 (4): 459–67. PMID 16610565. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  24. ↑ 24.0 24.1 Hershberger RE, Cowan J, Morales A, Siegfried JD (2009). "Progress with genetic cardiomyopathies: screening, counseling, and testing in dilated, hypertrophic, and arrhythmogenic right ventricular dysplasia/cardiomyopathy". Circulation. Heart Failure. 2 (3): 253–61. doi:10.1161/CIRCHEARTFAILURE.108.817346. PMC 2927103. PMID 19808347. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  25. ↑ 25.0 25.1 Schwartz ML, Cox GF, Lin AE, Korson MS, Perez-Atayde A, Lacro RV, Lipshultz SE (1996). "Clinical approach to genetic cardiomyopathy in children". Circulation. 94 (8): 2021–38. PMID 8873681. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  26. ↑ Harris KM, Spirito P, Maron MS, Zenovich AG, Formisano F, Lesser JR, Mackey-Bojack S, Manning WJ, Udelson JE, Maron BJ (2006). "Prevalence, clinical profile, and significance of left ventricular remodeling in the end-stage phase of hypertrophic cardiomyopathy". Circulation. 114 (3): 216–25. doi:10.1161/CIRCULATIONAHA.105.583500. PMID 16831987. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  27. ↑ 27.0 27.1 Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser JR, Losi MA, Cecchi F, Maron BJ (2003). "Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy". The New England Journal of Medicine. 348 (4): 295–303. doi:10.1056/NEJMoa021332. PMID 12540642. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  28. ↑ Maron BJ, Olivotto I, Spirito P, Casey SA, Bellone P, Gohman TE, Graham KJ, Burton DA, Cecchi F (2000). "Epidemiology of hypertrophic cardiomyopathy-related death: revisited in a large non-referral-based patient population". Circulation. 102 (8): 858–64. PMID 10952953. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  29. ↑ Dimitrow PP, Dubiel JS (2005). "Echocardiographic risk factors predisposing to sudden cardiac death in hypertrophic cardiomyopathy". Heart (British Cardiac Society). 91 (1): 93–4. doi:10.1136/hrt.2003.030353. PMC 1768636. PMID 15604346. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  30. ↑ 30.0 30.1 Efthimiadis GK, Parcharidou DG, Giannakoulas G, Pagourelias ED, Charalampidis P, Savvopoulos G, Ziakas A, Karvounis H, Styliadis IH, Parcharidis GE (2009). "Left ventricular outflow tract obstruction as a risk factor for sudden cardiac death in hypertrophic cardiomyopathy". The American Journal of Cardiology. 104 (5): 695–9. doi:10.1016/j.amjcard.2009.04.039. PMID 19699347. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  31. ↑ Ommen SR, Shah PM, Tajik AJ (2008). "Left ventricular outflow tract obstruction in hypertrophic cardiomyopathy: past, present and future". Heart (British Cardiac Society). 94 (10): 1276–81. doi:10.1136/hrt.2008.154435. PMID 18653577. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  32. ↑ 32.0 32.1 Sorajja P, Nishimura RA, Gersh BJ, Dearani JA, Hodge DO, Wiste HJ, Ommen SR (2009). "Outcome of mildly symptomatic or asymptomatic obstructive hypertrophic cardiomyopathy: a long-term follow-up study". Journal of the American College of Cardiology. 54 (3): 234–41. doi:10.1016/j.jacc.2009.01.079. PMID 19589436. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  33. ↑ 33.0 33.1 Grigg LE, Wigle ED, Williams WG, Daniel LB, Rakowski H (1992). "Transesophageal Doppler echocardiography in obstructive hypertrophic cardiomyopathy: clarification of pathophysiology and importance in intraoperative decision making". Journal of the American College of Cardiology. 20 (1): 42–52. PMID 1607537. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  34. ↑ 34.0 34.1 Marwick TH, Stewart WJ, Lever HM, Lytle BW, Rosenkranz ER, Duffy CI, Salcedo EE (1992). "Benefits of intraoperative echocardiography in the surgical management of hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 20 (5): 1066–72. PMID 1401604. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  35. ↑ 35.0 35.1 Yu EH, Omran AS, Wigle ED, Williams WG, Siu SC, Rakowski H (2000). "Mitral regurgitation in hypertrophic obstructive cardiomyopathy: relationship to obstruction and relief with myectomy". Journal of the American College of Cardiology. 36 (7): 2219–25. PMID 11127464. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  36. ↑ 36.0 36.1 Sorajja P, Valeti U, Nishimura RA, Ommen SR, Rihal CS, Gersh BJ, Hodge DO, Schaff HV, Holmes DR (2008). "Outcome of alcohol septal ablation for obstructive hypertrophic cardiomyopathy". Circulation. 118 (2): 131–9. doi:10.1161/CIRCULATIONAHA.107.738740. PMID 18591440. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  37. ↑ Faber L, Seggewiss H, Welge D, Fassbender D, Schmidt HK, Gleichmann U, Horstkotte D (2004). "Echo-guided percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: 7 years of experience". European Journal of Echocardiography : the Journal of the Working Group on Echocardiography of the European Society of Cardiology. 5 (5): 347–55. doi:10.1016/j.euje.2004.01.001. PMID 15341870. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  38. ↑ Monakier D, Woo A, Puri T, Schwartz L, Ross J, Jamorski M, Yang H, Liu Z, Vannan M, Wigle ED, Rakowski H (2004). "Usefulness of myocardial contrast echocardiographic quantification of risk area for predicting postprocedural complications in patients undergoing septal ethanol ablation for obstructive hypertrophic cardiomyopathy". The American Journal of Cardiology. 94 (12): 1515–22. doi:10.1016/j.amjcard.2004.08.030. PMID 15589007. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  39. ↑ Nagueh SF, Lakkis NM, He ZX, Middleton KJ, Killip D, Zoghbi WA, Quiñones MA, Roberts R, Verani MS, Kleiman NS, Spencer WH (1998). "Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy". Journal of the American College of Cardiology. 32 (1): 225–9. PMID 9669274. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  40. ↑ Ommen SR, Maron BJ, Olivotto I, Maron MS, Cecchi F, Betocchi S, Gersh BJ, Ackerman MJ, McCully RB, Dearani JA, Schaff HV, Danielson GK, Tajik AJ, Nishimura RA (2005). "Long-term effects of surgical septal myectomy on survival in patients with obstructive hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 46 (3): 470–6. doi:10.1016/j.jacc.2005.02.090. PMID 16053960. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  41. ↑ Carasso S, Woo A, Yang H, Schwartz L, Vannan MA, Jamorski M, Linghorne M, Wigle ED, Rakowski H (2008). "Myocardial mechanics explains the time course of benefit for septal ethanol ablation for hypertrophic cardiomyopathy". Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 21 (5): 493–9. doi:10.1016/j.echo.2007.08.020. PMID 17961980. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  42. ↑ Fernandes VL, Nielsen C, Nagueh SF, Herrin AE, Slifka C, Franklin J, Spencer WH (2008). "Follow-up of alcohol septal ablation for symptomatic hypertrophic obstructive cardiomyopathy the Baylor and Medical University of South Carolina experience 1996 to 2007". JACC. Cardiovascular Interventions. 1 (5): 561–70. doi:10.1016/j.jcin.2008.07.005. PMID 19463359. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  43. ↑ Jassal DS, Neilan TG, Fifer MA, Palacios IF, Lowry PA, Vlahakes GJ, Picard MH, Yoerger DM (2006). "Sustained improvement in left ventricular diastolic function after alcohol septal ablation for hypertrophic obstructive cardiomyopathy". European Heart Journal. 27 (15): 1805–10. doi:10.1093/eurheartj/ehl106. PMID 16774986. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  44. ↑ Woo A, Williams WG, Choi R, Wigle ED, Rozenblyum E, Fedwick K, Siu S, Ralph-Edwards A, Rakowski H (2005). "Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy". Circulation. 111 (16): 2033–41. doi:10.1161/01.CIR.0000162460.36735.71. PMID 15824202. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  45. ↑ Yoerger DM, Picard MH, Palacios IF, Vlahakes GJ, Lowry PA, Fifer MA (2006). "Time course of pressure gradient response after first alcohol septal ablation for obstructive hypertrophic cardiomyopathy". The American Journal of Cardiology. 97 (10): 1511–4. doi:10.1016/j.amjcard.2005.12.040. PMID 16679095. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  46. ↑ Maron MS, Olivotto I, Zenovich AG, Link MS, Pandian NG, Kuvin JT, Nistri S, Cecchi F, Udelson JE, Maron BJ (2006). "Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction". Circulation. 114 (21): 2232–9. doi:10.1161/CIRCULATIONAHA.106.644682. PMID 17088454. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  47. ↑ Sherrid MV, Barac I, McKenna WJ, Elliott PM, Dickie S, Chojnowska L, Casey S, Maron BJ (2005). "Multicenter study of the efficacy and safety of disopyramide in obstructive hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 45 (8): 1251–8. doi:10.1016/j.jacc.2005.01.012. PMID 15837258. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
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