Hypertrophic cardiomyopathy diagnostic testing

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Caitlin J. Harrigan [3]; Martin S. Maron, M.D.; Barry J. Maron, M.D.; Lakshmi Gopalakrishnan, M.B.B.S.

Overview

A diagnosis of hypertrophic cardiomyopathy is based upon a number of features of the disease process. While there is use of echocardiography, cardiac catheterization, or cardiac MRI in the diagnosis of the disease, other important factors include ECG findings and if there is any family history of HCM or unexplained sudden death in otherwise healthy individuals.

Stress Test

2011 ACCF/AHA Guideline Recommendations: Stress Testing [1][2]

“

Class IIa

1. Treadmill exercise testing is reasonable to determine functional capacity and response to therapy in patients with HOCM. (Level of Evidence: C)

2. Treadmill testing with monitoring of an ECG and blood pressure is reasonable for SCD risk stratification in patients with HOCM.[3][4][5] (Level of Evidence: B)

3. In patients with HOCM who do not have a resting peak instantaneous gradient of greater than or equal to 50 mm Hg, exercise echocardiography is reasonable for the detection and quantification of exercise-induced dynamic LVOT obstruction.[6][7][3][4] (Level of Evidence: B)

”

Electrocardiogram

Large septal q waves may be present reflective of the septal hypertrophy. In the Yamaguchi variant of apical hypertrophic cardiomyopathy there may be deeply inverted T waves in precordial leads V2-V6 and II, III, aVL (see example).

Shown below is an example of a variant of apical hypertrophic cardiomyopathy with deeply inverted T waves in precordial leads V2-V6 and II, III, aVL.

HCP ecg.JPG



Shown below is an example of hypertrophic cardiomyopathy with abnormal ST segments, deeply flipped T waves, tall R apical waves, deep Q waves. "Strain pattern" can be observed in the precordial leads.

Hypertrophic Cardiomyopathy.jpg



Shown below is an example of hypertrophic cardiomyopathy with ST depression in the lateral leads, deeper S waves in the right precordial leads and tall R waves in the left precordial leads with T wave inversions indicating "strain pattern"

Hypertrophic cardiomyopathy.jpg


2011 ACCF/AHA Guideline Recommendations: Electrocardiography [1][2]

“

Class I

1. 1. A 12-lead ECG is recommended in the initial evaluation of patients with HOCM. (Level of Evidence: C)

2. Twenty-four–hour ambulatory (Holter) electrocardiographic monitoring is recommended in the initial evaluation of patients with HOCM to detect ventricular tachycardia (VT) and identify patients who may be candidates for ICD therapy.[8][9][10][11] (Level of Evidence: B)

3. Twenty-four–hour ambulatory (Holter) electrocardiographic monitoring or event recording is recommended in patients with HOCM who develop palpitations or lightheadedness.[8][9][10] (Level of Evidence: B)

4. A repeat ECG is recommended for patients with HOCM when there is worsening of symptoms. (Level of Evidence: C)

5. A 12-lead ECG is recommended every 12 to 18 months as a component of the screening algorithm for adolescent first-degree relatives of patients with HOCM who have no evidence of hypertrophy on echocardiography. (Level of Evidence: C)

6. A 12-lead ECG is recommended as a component of the screening algorithm for first-degree relatives of patients with HOCM. (Level of Evidence: C)

Class IIa

1. Twenty-four–hour ambulatory (Holter) electrocardiographic monitoring, repeated every 1 to 2 years, is reasonable in patients with HOCM who have no previous evidence of VT to identify patients who may be candidates for ICD therapy.[11] (Level of Evidence: C)

2. Annual 12-lead ECGs are reasonable in patients with known HOCM who are clinically stable to evaluate for asymptomatic changes in conduction or rhythm (i.e., AF). (Level of Evidence: C)

Class IIb

1. Twenty-four–hour ambulatory (Holter) electrocardiographic monitoring might be considered in adults with HOCM to assess for asymptomatic paroxysmal AF/atrial flutter. (Level of Evidence: C)

”

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 [12]:

  • Left ventricular asymmetric hypertrophy
    • Parasternal long axis shows relationship of the septal hypertrophy and the outflow tract
  • Left ventricular diastolic dysfunction
    • LV inflow across the mitral valve
    • LA inflow in the pulmonary vein
    • Myocardial Doppler tissue velocity
    • Isovolumetric relaxation time
  • 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:

On parasternal long-axis view


On parasternal short-axis view


2011 ACCF/AHA Guideline Recommendations: Echocardiography [1][2]

“

Class I

1. A TTE is recommended in the initial evaluation of all patients with suspected HOCM.[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 HOCM 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 HOCM, 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 sudden cardiac death.[22][25] (Level of Evidence: C)

4. Repeat TTE is recommended for the evaluation of patients with HOCM 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 intra-operative 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 intra-procedural 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 HOCM.[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 HOCM 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 HOCM.[27][30][32][6][46] (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 HOCM or apical infarction or severity of hypertrophy is in doubt, particularly when other imaging modalities such as 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 HOCM 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 HOCM 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 HOCM and/or there is no suspicion of fixed obstruction or intrinsic mitral valve pathology. (Level of Evidence: C)

”

2011 ACCF/AHA Guideline Recommendations: Detection of Concomitant Coronary Disease [1][2]

“

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)

”

Cardiac MRI

Late Myocardial Enhancement

Late myocardial enhancement has been associated with myocardial fibrosis and may allow for earlier detection of hypertrophic cardiomyopathy than is currently available with echocardiography and ECG.

  • Choudhury et al studied 21 patients with previously diagnosed hypertrophic cardiomyopathy[47]. They noted:
  • Late myocardial enhancement following gadolinium administration in a patchy intramyocardial distribution.
  • Typically occurred in the hypertrophied regions, predominantly in the middle third of the ventricular wall in a patchy, multi focal distribution.
  • If enhancement occurred, it occurred at the junctions of the intraventricular septum and right ventricular free wall.
  • Moon et al looked at whether the extent of hyperenhancement on MR in patients with HCM would be associated with the risk of heart failure and sudden death [48] The study involved 53 patient were selected for presence or absence of an increased clinical risk of sudden death and/or progressive adverse left ventricular remodeling.
  • Myocardial hyperenhancement was present in 79% of patients.
  • They found no evidence of abnormal myocardium on non-contrast images.
  • There was more hyperenhancement in patients with progressive disease than without.
  • There was greater hyperenhancement in patients with ≥ 2 risk factors for sudden death.
  • Patients with diffuse hyperenhancement had ≥ 2 risk factors for sudden death vs patients with confluent hyperenhancement.

Of note, other investigators have discovered that in carriers without signs of hypertrophy on EKG or echocardiography, Cardiac MR can detect the presence of crypts in the LV wall which may progress to hypertrophy.

Left Ventricular Hypertrophy

MR is helpful in visualizing the asymmetric thickening of the interventricular septum in patients with HCM. However, it may be more helpful than other forms of imaging to differentiate the variant types of hypertrophic cardiomyopathy.[49]

Mitral Regurgitation and Systolic Anterior Motion

MR can be helpful in evaluating the extent of systolic anterior motion of the mitral valve.

Obstruction

MR can be help visualize turbulence in left ventricular outflow tract created by obstruction in patients with obstructive hypertrophic cardiomyopathy.


ACC/AHA Guidelines- ACCF/ACR/AHA/NASCI/SCMR 2010 Expert Consensus Document on Cardiovascular Magnetic Resonance[50] (DO NOT EDIT)

“

CMR may be used for assessment of patients with LV dysfunction or hypertrophy or suspected forms of cardiac injury not related to ischemic heart disease. When the diagnosis is unclear, CMR may be considered to identify the etiology of cardiac dysfunction in patients presenting with heart failure, including

  • evaluation of dilated cardiomyopathy in the setting of normal coronary arteries,
  • patients with positive cardiac enzymes without obstructive atherosclerosis on angiography,
  • patients suspected of amyloidosis or other infiltrative diseases,
  • hypertrophic cardiomyopathy,
  • arrhythmogenic right ventricular dysplasia, or
  • syncope or ventricular arrhythmia.
”

2011 ACCF/AHA Guideline Recommendations: Cardiac Magnetic Resonance [1][2]

“

Class I

1. CMR imaging is indicated in patients with suspected HOCM when echocardiography is inconclusive for diagnosis.[51][52] (Level of Evidence: B)

2. CMR imaging is indicated in patients with known HOCM when additional information that may have an impact on management or decision making regarding invasive management, such as magnitude and distribution of hypertrophy or anatomy of the mitral valve apparatus or papillary muscles, is not adequately defined with echocardiography.[51][52][53][54][55] (Level of Evidence: B)

Class IIa

1. CMR imaging is reasonable in patients with HOCM to define apical hypertrophy and/or aneurysm if echocardiography is inconclusive.[51][53] (Level of Evidence: B)

Class IIb

1. In selected patients with known HOCM, when sudden cardiac death risk stratification is inconclusive after documentation of the conventional risk factors, CMR imaging with assessment of late gadolinium enhancement (LGE) may be considered in resolving clinical decision making.[56][57][58][59][60] (Level of Evidence: C)

2. CMR imaging may be considered in patients with LV hypertrophy and the suspicion of alternative diagnoses to HOCM, including cardiac amyloidosis, Fabry disease, and genetic phenocopies such as LAMP2 cardiomyopathy.[61][62][63] (Level of Evidence: C)

”

Cardiac CT

Echocardiographic findings reflect the clinical and anatomic findings described above, e.g. LVH, diastolic dysfunction, MR, LA enlargement, elevated PAP.

Characteristic of obstructive HOCM is systolic anterior motion of the mitral valve (SAM). The anterior leaflet is pulled toward the LVOT during systole via the Venturi effect, leading to obstruction, a gradient and MR.

2011 ACCF/AHA Guideline Recommendations: Detection of Concomitant Coronary Disease [1][2]

“

Class I

1. Coronary arteriography (invasive or computed tomographic imaging) is indicated in patients with HOCM with chest discomfort who have an intermediate to high likelihood of CAD when the identification of concomitant CAD will change management strategies. (Level of Evidence: C)

Class IIa

1. Assessment of coronary anatomy with computed tomographic angiography (CTA) is reasonable for patients with HOCM with chest discomfort and a low likelihood of CAD to assess for possible concomitant CAD. (Level of Evidence: C)

”

Positron Emission Tomography

Positron Emission Tomography (PET) studies have demonstrated that coronary flow reserve is reduced in patients with HCM. Those patients who subsequently died had a greater reduction in coronary flow reserve at baseline. It has been hypothesized that this ischemia may mediate in part the higher risk in sudden cardiac death.

2011 ACCF/AHA Guideline Recommendations: Detection of Concomitant Coronary Disease [1][2]

“

Class IIa

1. Assessment of ischemia or perfusion abnormalities suggestive of CAD with single photon emission computed tomography (SPECT) or positron emission tomography (PET) myocardial perfusion imaging (MPI; because of excellent negative predictive value) is reasonable in patients with HOCM with chest discomfort and a low likelihood of CAD to rule out possible concomitant CAD. (Level of Evidence: C)

Class III (No Benefit)

1. Assessment for the presence of blunted flow reserve (microvascular ischemia) using quantitative myocardial blood flow measurements by PET is not indicated for the assessment of prognosis in patients with HOCM. (Level of Evidence: C)

”

Guideline Resources

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy [1][2]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 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 (December 2011). "2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: Executive Summary 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): 2703–38. doi:10.1016/j.jacc.2011.10.825. PMID 22075468. Retrieved on 2011-12-19.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 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 (December 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 on 2011-12-19.
  3. ↑ 3.0 3.1 Sadoul N, Prasad K, Elliott PM, Bannerjee S, Frenneaux MP, McKenna WJ (November 1997). "Prospective prognostic assessment of blood pressure response during exercise in patients with hypertrophic cardiomyopathy". Circulation 96 (9): 2987–91. PMID 9386166. Retrieved on 2011-12-22.
  4. ↑ 4.0 4.1 Olivotto I, Maron BJ, Montereggi A, Mazzuoli F, Dolara A, Cecchi F (June 1999). "Prognostic value of systemic blood pressure response during exercise in a community-based patient population with hypertrophic cardiomyopathy". Journal of the American College of Cardiology 33 (7): 2044–51. PMID 10362212. Retrieved on 2011-12-22.
  5. ↑ Ciampi Q, Betocchi S, Lombardi R, Manganelli F, Storto G, Losi MA, Pezzella E, Finizio F, Cuocolo A, Chiariello M (July 2002). "Hemodynamic determinants of exercise-induced abnormal blood pressure response in hypertrophic cardiomyopathy". Journal of the American College of Cardiology 40 (2): 278–84. PMID 12106932. Retrieved on 2011-12-22.
  6. ↑ 6.0 6.1 Maron MS, Olivotto I, Zenovich AG, Link MS, Pandian NG, Kuvin JT, Nistri S, Cecchi F, Udelson JE, Maron BJ (November 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 on 2011-12-22.
  7. ↑ Frenneaux MP, Counihan PJ, Caforio AL, Chikamori T, McKenna WJ (December 1990). "Abnormal blood pressure response during exercise in hypertrophic cardiomyopathy". Circulation 82 (6): 1995–2002. PMID 2242524. Retrieved on 2011-12-22.
  8. ↑ 8.0 8.1 Christiaans I, Birnie E, van Langen IM, van Spaendonck-Zwarts KY, van Tintelen JP, van den Berg MP, Atsma DE, Helderman-van den Enden AT, Pinto YM, Hermans-van Ast JF, Bonsel GJ, Wilde AA (April 2010). "The yield of risk stratification for sudden cardiac death in hypertrophic cardiomyopathy myosin-binding protein C gene mutation carriers: focus on predictive screening". European Heart Journal 31 (7): 842–8. doi:10.1093/eurheartj/ehp539. PMID 20019025. Retrieved on 2011-12-22.
  9. ↑ 9.0 9.1 Elliott PM, Gimeno JR, Tomé MT, Shah J, Ward D, Thaman R, Mogensen J, McKenna WJ (August 2006). "Left ventricular outflow tract obstruction and sudden death risk in patients with hypertrophic cardiomyopathy". European Heart Journal 27 (16): 1933–41. doi:10.1093/eurheartj/ehl041. PMID 16754630. Retrieved on 2011-12-22.
  10. ↑ 10.0 10.1 Maron BJ, Savage DD, Wolfson JK, Epstein SE (August 1981). "Prognostic significance of 24 hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: a prospective study". The American Journal of Cardiology 48 (2): 252–7. PMID 7196685. Retrieved on 2011-12-22.
  11. ↑ 11.0 11.1 Monserrat L, Elliott PM, Gimeno JR, Sharma S, Penas-Lado M, McKenna WJ (September 2003). "Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients". Journal of the American College of Cardiology 42 (5): 873–9. PMID 12957435. Retrieved on 2011-12-22.
  12. ↑ Otto, Catherine. Textbook of Clinical Echocardiography. 3rd Edition, 2004
  13. ↑ Maron BJ (March 2002). "Hypertrophic cardiomyopathy: a systematic review". JAMA : the Journal of the American Medical Association 287 (10): 1308–20. PMID 11886323. Retrieved on 2011-12-22.
  14. ↑ 14.0 14.1 Klues HG, Schiffers A, Maron BJ (December 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 on 2011-12-22.
  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 on 2011-12-22.
  16. ↑ 16.0 16.1 Wigle ED, Rakowski H, Kimball BP, Williams WG (October 1995). "Hypertrophic cardiomyopathy. Clinical spectrum and treatment". Circulation 92 (7): 1680–92. PMID 7671349. Retrieved on 2011-12-22.
  17. ↑ Adabag AS, Kuskowski MA, Maron BJ (December 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 on 2011-12-22.
  18. ↑ 18.0 18.1 Afonso LC, Bernal J, Bax JJ, Abraham TP (November 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 on 2011-12-22.
  19. ↑ Fifer MA, Vlahakes GJ (January 2008). "Management of symptoms in hypertrophic cardiomyopathy". Circulation 117 (3): 429–39. doi:10.1161/CIRCULATIONAHA.107.694158. PMID 18212300. Retrieved on 2011-12-22.
  20. ↑ Soor GS, Luk A, Ahn E, Abraham JR, Woo A, Ralph-Edwards A, Butany J (March 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 on 2011-12-22.
  21. ↑ 21.0 21.1 Bos JM, Towbin JA, Ackerman MJ (July 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 on 2011-12-22.
  22. ↑ 22.0 22.1 22.2 Maron BJ, Seidman JG, Seidman CE (December 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 on 2011-12-22.
  23. ↑ Binder J, Ommen SR, Gersh BJ, Van Driest SL, Tajik AJ, Nishimura RA, Ackerman MJ (April 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 on 2011-12-22.
  24. ↑ 24.0 24.1 Hershberger RE, Cowan J, Morales A, Siegfried JD (May 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. PMID 19808347. Retrieved on 2011-12-22.
  25. ↑ 25.0 25.1 Schwartz ML, Cox GF, Lin AE, Korson MS, Perez-Atayde A, Lacro RV, Lipshultz SE (October 1996). "Clinical approach to genetic cardiomyopathy in children". Circulation 94 (8): 2021–38. PMID 8873681. Retrieved on 2011-12-22.
  26. ↑ Harris KM, Spirito P, Maron MS, Zenovich AG, Formisano F, Lesser JR, Mackey-Bojack S, Manning WJ, Udelson JE, Maron BJ (July 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 on 2011-12-22.
  27. ↑ 27.0 27.1 Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser JR, Losi MA, Cecchi F, Maron BJ (January 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 on 2011-12-22.
  28. ↑ Maron BJ, Olivotto I, Spirito P, Casey SA, Bellone P, Gohman TE, Graham KJ, Burton DA, Cecchi F (August 2000). "Epidemiology of hypertrophic cardiomyopathy-related death: revisited in a large non-referral-based patient population". Circulation 102 (8): 858–64. PMID 10952953. Retrieved on 2011-12-22.
  29. ↑ Dimitrow PP, Dubiel JS (January 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. PMID 15604346. Retrieved on 2011-12-22.
  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 (September 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 on 2011-12-22.
  31. ↑ Ommen SR, Shah PM, Tajik AJ (October 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 on 2011-12-22.
  32. ↑ 32.0 32.1 Sorajja P, Nishimura RA, Gersh BJ, Dearani JA, Hodge DO, Wiste HJ, Ommen SR (July 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 on 2011-12-22.
  33. ↑ 33.0 33.1 Grigg LE, Wigle ED, Williams WG, Daniel LB, Rakowski H (July 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 on 2011-12-22.
  34. ↑ 34.0 34.1 Marwick TH, Stewart WJ, Lever HM, Lytle BW, Rosenkranz ER, Duffy CI, Salcedo EE (November 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 on 2011-12-22.
  35. ↑ 35.0 35.1 Yu EH, Omran AS, Wigle ED, Williams WG, Siu SC, Rakowski H (December 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 on 2011-12-22.
  36. ↑ 36.0 36.1 Sorajja P, Valeti U, Nishimura RA, Ommen SR, Rihal CS, Gersh BJ, Hodge DO, Schaff HV, Holmes DR (July 2008). "Outcome of alcohol septal ablation for obstructive hypertrophic cardiomyopathy". Circulation 118 (2): 131–9. doi:10.1161/CIRCULATIONAHA.107.738740. PMID 18591440. Retrieved on 2011-12-22.
  37. ↑ Faber L, Seggewiss H, Welge D, Fassbender D, Schmidt HK, Gleichmann U, Horstkotte D (October 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 on 2011-12-22.
  38. ↑ Monakier D, Woo A, Puri T, Schwartz L, Ross J, Jamorski M, Yang H, Liu Z, Vannan M, Wigle ED, Rakowski H (December 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 on 2011-12-22.
  39. ↑ Nagueh SF, Lakkis NM, He ZX, Middleton KJ, Killip D, Zoghbi WA, Quiñones MA, Roberts R, Verani MS, Kleiman NS, Spencer WH (July 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 on 2011-12-22.
  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 (August 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 on 2011-12-22.
  41. ↑ Carasso S, Woo A, Yang H, Schwartz L, Vannan MA, Jamorski M, Linghorne M, Wigle ED, Rakowski H (May 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 on 2011-12-22.
  42. ↑ Fernandes VL, Nielsen C, Nagueh SF, Herrin AE, Slifka C, Franklin J, Spencer WH (October 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 on 2011-12-22.
  43. ↑ Jassal DS, Neilan TG, Fifer MA, Palacios IF, Lowry PA, Vlahakes GJ, Picard MH, Yoerger DM (August 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 on 2011-12-22.
  44. ↑ Woo A, Williams WG, Choi R, Wigle ED, Rozenblyum E, Fedwick K, Siu S, Ralph-Edwards A, Rakowski H (April 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 on 2011-12-22.
  45. ↑ Yoerger DM, Picard MH, Palacios IF, Vlahakes GJ, Lowry PA, Fifer MA (May 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 on 2011-12-22.
  46. ↑ Sherrid MV, Barac I, McKenna WJ, Elliott PM, Dickie S, Chojnowska L, Casey S, Maron BJ (April 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 on 2011-12-22.
  47. ↑ Choudhury et al. Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy. J. Am Coll Card. 2002; 40: 2156.
  48. ↑ Moon et al., Toward Clinical Risk Assessment in Hypertrophic Cardiomyopathy with Gadolinium Cardiovascular Magnetic Resonance. J Am Coll Card. 2003; 41; 1561.
  49. ↑ Germans, T et al. Structural Abnormalities of the inferoseptal left ventricular wall detected by Cardiac Magnetic Resonance Imaging in carriers of Hypertrophic Cardiomyopathy mutations. J Am Coll Cardiol. 2006: 48; 2518.
  50. ↑ American College of Cardiology Foundation Task Force on Expert Consensus Documents. Hundley WG, Bluemke DA, Finn JP, Flamm SD, Fogel MA et al. (2010). "ACCF/ACR/AHA/NASCI/SCMR 2010 expert consensus document on cardiovascular magnetic resonance: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents.". Circulation 121 (22): 2462-508. doi:10.1161/CIR.0b013e3181d44a8f. PMID 20479157.
  51. ↑ 51.0 51.1 51.2 Moon JC, Fisher NG, McKenna WJ, Pennell DJ (June 2004). "Detection of apical hypertrophic cardiomyopathy by cardiovascular magnetic resonance in patients with non-diagnostic echocardiography". Heart (British Cardiac Society) 90 (6): 645–9. PMID 15145868. Retrieved on 2011-12-23.
  52. ↑ 52.0 52.1 Rickers C, Wilke NM, Jerosch-Herold M, Casey SA, Panse P, Panse N, Weil J, Zenovich AG, Maron BJ (August 2005). "Utility of cardiac magnetic resonance imaging in the diagnosis of hypertrophic cardiomyopathy". Circulation 112 (6): 855–61. doi:10.1161/CIRCULATIONAHA.104.507723. PMID 16087809. Retrieved on 2011-12-23.
  53. ↑ 53.0 53.1 Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ (October 2008). "Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy". Circulation 118 (15): 1541–9. doi:10.1161/CIRCULATIONAHA.108.781401. PMID 18809796. Retrieved on 2011-12-23.
  54. ↑ Maron MS, Lesser JR, Maron BJ (June 2010). "Management implications of massive left ventricular hypertrophy in hypertrophic cardiomyopathy significantly underestimated by echocardiography but identified by cardiovascular magnetic resonance". The American Journal of Cardiology 105 (12): 1842–3. doi:10.1016/j.amjcard.2010.01.367. PMID 20538141. Retrieved on 2011-12-23.
  55. ↑ Maron MS, Maron BJ, Harrigan C, Buros J, Gibson CM, Olivotto I, Biller L, Lesser JR, Udelson JE, Manning WJ, Appelbaum E (July 2009). "Hypertrophic cardiomyopathy phenotype revisited after 50 years with cardiovascular magnetic resonance". Journal of the American College of Cardiology 54 (3): 220–8. doi:10.1016/j.jacc.2009.05.006. PMID 19589434. Retrieved on 2011-12-23.
  56. ↑ Adabag AS, Maron BJ, Appelbaum E, Harrigan CJ, Buros JL, Gibson CM, Lesser JR, Hanna CA, Udelson JE, Manning WJ, Maron MS (April 2008). "Occurrence and frequency of arrhythmias in hypertrophic cardiomyopathy in relation to delayed enhancement on cardiovascular magnetic resonance". Journal of the American College of Cardiology 51 (14): 1369–74. doi:10.1016/j.jacc.2007.11.071. PMID 18387438. Retrieved on 2011-12-23.
  57. ↑ Maron MS, Appelbaum E, Harrigan CJ, Buros J, Gibson CM, Hanna C, Lesser JR, Udelson JE, Manning WJ, Maron BJ (September 2008). "Clinical profile and significance of delayed enhancement in hypertrophic cardiomyopathy". Circulation. Heart Failure 1 (3): 184–91. doi:10.1161/CIRCHEARTFAILURE.108.768119. PMID 19808288. Retrieved on 2011-12-23.
  58. ↑ Rubinshtein R, Glockner JF, Ommen SR, Araoz PA, Ackerman MJ, Sorajja P, Bos JM, Tajik AJ, Valeti US, Nishimura RA, Gersh BJ (January 2010). "Characteristics and clinical significance of late gadolinium enhancement by contrast-enhanced magnetic resonance imaging in patients with hypertrophic cardiomyopathy". Circulation. Heart Failure 3 (1): 51–8. doi:10.1161/CIRCHEARTFAILURE.109.854026. PMID 19850699. Retrieved on 2011-12-23.
  59. ↑ O'Hanlon R, Grasso A, Roughton M, Moon JC, Clark S, Wage R, Webb J, Kulkarni M, Dawson D, Sulaibeekh L, Chandrasekaran B, Bucciarelli-Ducci C, Pasquale F, Cowie MR, McKenna WJ, Sheppard MN, Elliott PM, Pennell DJ, Prasad SK (September 2010). "Prognostic significance of myocardial fibrosis in hypertrophic cardiomyopathy". Journal of the American College of Cardiology 56 (11): 867–74. doi:10.1016/j.jacc.2010.05.010. PMID 20688032. Retrieved on 2011-12-23.
  60. ↑ Moon JC, McKenna WJ, McCrohon JA, Elliott PM, Smith GC, Pennell DJ (May 2003). "Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance". Journal of the American College of Cardiology 41 (9): 1561–7. PMID 12742298. Retrieved on 2011-12-23.
  61. ↑ Gange CA, Link MS, Maron MS (September 2009). "Utility of cardiovascular magnetic resonance in the diagnosis of Anderson-Fabry disease". Circulation 120 (13): e96–7. doi:10.1161/CIRCULATIONAHA.109.849828. PMID 19786638. Retrieved on 2011-12-23.
  62. ↑ Maceira AM, Joshi J, Prasad SK, Moon JC, Perugini E, Harding I, Sheppard MN, Poole-Wilson PA, Hawkins PN, Pennell DJ (January 2005). "Cardiovascular magnetic resonance in cardiac amyloidosis". Circulation 111 (2): 186–93. doi:10.1161/01.CIR.0000152819.97857.9D. PMID 15630027. Retrieved on 2011-12-23.
  63. ↑ Moon JC, Sachdev B, Elkington AG, McKenna WJ, Mehta A, Pennell DJ, Leed PJ, Elliott PM (December 2003). "Gadolinium enhanced cardiovascular magnetic resonance in Anderson-Fabry disease. Evidence for a disease specific abnormality of the myocardial interstitium". European Heart Journal 24 (23): 2151–5. PMID 14643276. Retrieved on 2011-12-23.
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