Hypertrophic cardiomyopathy interventions

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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]Cafer Zorkun, M.D. [3]; Caitlin J. Harrigan [4]; Martin S. Maron, M.D.; Barry J. Maron, M.D.; Lakshmi Gopalakrishnan, M.B.B.S. [5]

Overview

Alcohol septal ablation, ventricular pacing, automatic implantable cardiac defibrillator placement are among interventions used to manage patients with hypertrophic cardiomyopathy.

Alcohol Septal Ablation

Alcohol septal ablation is a percutaneous technique that involves injection of alcohol into the first septal perferator of the left anterior descending artery. This is a technique with results similar to the surgical septal myectomy procedure but is less invasive, since it does not involve general anaesthesia and opening of the chest wall and pericardium (which are done in a septal myomectomy). In a select population with symptoms secondary to a high outflow tract gradient, alcohol septal ablation can reduce the symptoms of HCM.[1][2][3] When performed properly, an alcohol septal ablation induces a controlled heart attack, in which the portion of the interventricular septum that involves the left ventricular outflow tract is infarcted and will contract into a scar.

History

Alcohol septal ablation was first performed in Britain at the Royal Brompton Hospital by Ulrich Sigwart in 1994. Since that time, it has quickly gained favor among physicians and patients alike due to its minimally-invasive nature, avoiding general anesthesia, lengthy recuperation and other complications associated with open-heart surgery (septal myectomy).

Technique

Alcohol septal ablation is performed in the cardiac catheterization laboratory, and should only be performed by interventional cardiologists with specific training in the procedure. As such, it is only available in a few institutions. The technique is similar to coronary angioplasty and utilizes similar equipment. Using wires and balloons to localize the septal artery feeding the diseased muscle, a small amount of absolute alcohol is infused into the artery to produce a small heart attack. Patients typically experience mild chest discomfort during the procedure, which takes approximately 30 minutes to complete. Analgesics and mild sedatives are administered as needed. Patients typically are maintained in the hospital for three to four days to monitor for any complications, including the need for a permanent pacemaker in 5-10%.

Efficacy and Procedural Success

Relief of obstruction is noted immediately in the majority of appropriately selected patients. Clinical success is defined as a 50% or more reduction in peak gradient across the outflow tract, predicting continued improvement in gradient and cardiac remodeling over the ensuing 1 to 2 years. Over 90% of patients experience a successful procedure, with improvement in the outflow tract gradient and mitral regurgitation. Patients typically report a progressive reduction in symptoms, including improved shortness of breath, lightheadedness and chest pain.

Follow-Up

Serial echocardiograms are routinely obtained to follow the cardiac remodeling over time and document reduction in the outflow tract gradient.

Procedural complications

1. Atrioventricular block

2. Complete heart block

  • Observed in 50% of patients during the procedure.[4][5][6]

3. Ventricular tachyarrhythmias

  • The risk of arrhythmias in patients with HOCM significantly increases secondary to the ventricular arrhythmogenic potential of the scar that is formed post-ablation.
Supportive trial data
  • In a single-center study that enrolled ninety-one consecutive patients (aged 54+/-15 years) with obstructive hypertrophic cardiomyopathy underwent either alcohol septal ablation or septal myectomy to evaluate the long-term outcomes of the procedure. During a follow-up period of 5.4+/-2.5 years, the study demonstrated 21% of patients experienced sudden or other cardiac death and aborted sudden cardiac death including appropriate cardioverter-defibrillator discharges for fast ventricular tachycardia or ventricular fibrillation. The 1-, 5-, and 8-year survival-free from the primary end point was: 96%, 86%, and 67%, respectively in patients treated with septal ablation versus 100%, 96%, and 96%, respectively in patients treated with septal myectomy during 6.6+/-2.7 years (log-rank, P=0.01). The annualized event rate after ablation was reported to be 4.4% per year with an approximate 5-fold increase in the estimated annual primary end point rate (4.4% versus 0.9%) when compared with myectomy patients.[17]
  • Meta-analyses of septal reduction therapies that included 19 septal ablation studies (2207 patients) and 8 surgical myectomy studies (1887 patients) was performed to compare the rates of overall mortality and sudden cardiac death after treatment. The median follow-up was shorter for ablation than for myectomy studies (51 versus 1266 patient-years; P<0.001). No significant difference was observed in the incidence of sudden cardiac death and all-cause mortality between the two groups.[24]
  • Another recent meta-analysis of 12 studies that compared the two septal reduction therapies reported similar results with no significant difference observed in the short-term and the long-term mortality between two groups. However, septal ablation was found to increase the risk of right bundle branch block (pooled odds ratio: 56.3; 95% CI: 11.6 to 273.9) along with the need for permanent pacemaker implantation post-procedure (pooled OR: 2.6; 95% CI: 1.7 to 3.9).[25]

4. Intragenic ventricular septal defect

  • Alcohol septal ablation is contraindicated in patients with a septal thickness of greater than 15mm because of the potential for creating a ventricular septal defect.

Comparison to Myectomy

  • Non-randomized data from the Netherlands suggests caution in the utilization of alcohol septal ablation, which may be inferior to surgical myectomy [17]. The outcomes (the risk of cardiac death and aborted sudden cardiac death including appropriate cardioverter-defibrillator discharges for fast ventricular tachycardia/ventricular fibrillation) in 91 consecutive alcohol septal ablation patients were compared with 40 patients who underwent septal myectomy. The 1-, 5-, and 8-year event free survival was 96%, 86%, and 67%, respectively in the alcohol septal ablation patients which was poorer than the 100%, 96%, and 96%, event free rates in the myectomy patients over 6.6±2.7 years (P=0.01). Stated differently, the alcohol septal ablation patients faced a 5-fold increase in the risk of the primary endpoint on an annual basis (4.4% versus 0.9%) even when adjustments were made in a propensity adjusted multivariable model (p=0.02). Based upon non-randomized data, myectomy may be prefferable to alcohol septal ablation.
  • The hypertrophied muscle is directly visible and resected; however, with success rate of septal ablation is dependent on the anatomy of the septal artery which is variable in approximately 20% to 25% of patients.[18][26]

It is important to note that patients who fail to respond to alcohol septal ablation may still be candidates for surgical myectomy. Likewise, patients who fail surgical myectomy may still respond to alcohol septal ablation.

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy (DO NOT EDIT)[27]

Alcohol Septal Ablation (DO NOT EDIT)[27]

Class IIa
"1. Consultation with centers experienced in performing both surgical septal myectomy and alcohol septal ablation is reasonable when discussing treatment options for eligible patients with HCM with severe drug-refractory symptoms and LVOT obstruction. (Level of Evidence: C)"
"2. When surgery is contraindicated or the risk is considered unacceptable because of serious comorbidities or advanced age, alcohol septal ablation, when performed in experienced centers, can be beneficial in eligible adult patients with HCM with LVOT obstruction and severe drug-refractory symptoms (usually NYHA functional classes III or IV)[18][19][28][29][20][30][31]. (Level of Evidence: B)"
Class IIb
"1. Alcohol septal ablation, when performed in experienced centers, may be considered as an alternative to surgical myectomy for eligible adult patients with HCM with severe drug-refractory symptoms and LVOT obstruction when, after a balanced and thorough discussion, the patient expresses a preference for septal ablation[19][32][29][29][30][31]. (Level of Evidence: B)"
"2. The effectiveness of alcohol septal ablation is uncertain in patients with HCM with marked (i.e., >30 mm) septal hypertrophy, and therefore the procedure is generally discouraged in such patients. (Level of Evidence: C)"
Class III (Harm)
"1. Alcohol septal ablation should not be done in patients with HCM with concomitant disease that independently warrants surgical correction (e.g., coronary artery bypass grafting for CAD, mitral valve repair for ruptured chordae) in whom surgical myectomy can be performed as part of the operation. (Level of Evidence: C)"
"2. Alcohol septal ablation should not be done in patients with HCM who are less than 21 years of age and is discouraged in adults less than 40 years of age if myectomy is a viable option. (Level of Evidence: C)"

Sources


Hypertrophic cardiomyopathy ventricular pacing

The use of a pacemaker has been advocated in a subset of individuals, in order to cause asynchronous contraction of the left ventricle. Since the pacemaker activates the interventricular septum before the left ventricular free wall, the gradient across the left ventricular outflow tract may decrease. The AV interval must be shortened to do this, but not at the expense of diastolic filling. This form of treatment has been shown to provide less relief of symptoms and less of a reduction in the left ventricular outflow tract gradient when compared to surgical myectomy.[36] Dual chamber pacing does not decrease the risk of sudden cardiac death in these patients.

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy[27] and 2012 ACC/AHA/HRS Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities (DO NOT EDIT)[37][38]

Pacing (DO NOT EDIT)[27][38]

Class I
"1. Permanent pacing is indicated for SND or AV block in patients with hypertrophic cardiomyopathy as described in permanent pacing in sinus node dysfunction and acquired atrioventricular block in adults. (Level of Evidence: C)"
Class IIa
"1. In patients with HCM who have had a dual-chamber device implanted for non-HCM indications, it is reasonable to consider a trial of dual-chamber atrial-ventricular pacing (from the right ventricular apex) for the relief of symptoms attributable to LVOT obstruction.[39][40][41][42] (Level of Evidence: B)"
"2. Permanent pacing may be considered in medically refractory symptomatic patients with hypertrophic cardiomyopathy and significant resting or provoked LV outflow tract obstruction. (Level of Evidence: A)"
Class IIb
"1. Permanent pacing may be considered in medically refractory symptomatic patients with obstructive HCM who are suboptimal candidates for septal reduction therapy.[39][40][41][42][43] (Level of Evidence: B)"
Class III (No Benefit)
"1. Permanent pacemaker implantation is not indicated for patients who are asymptomatic or whose symptoms are medically controlled.[43][44][45] (Level of Evidence: C)"
"2. Permanent pacemaker implantation should not be performed as a first-line therapy to relieve symptoms in medically refractory symptomatic patients with HCM and LVOT obstruction who are candidates for septal reduction.[43][44][45] (Level of Evidence: B)"
"3. Permanent pacemaker implantation is not indicated for symptomatic patients without evidence of LV outflow tract obstruction. (Level of Evidence: C)"

2007 ESC Guidelines for Cardiac Pacing and Cardiac Resynchronization Therapy (DO NOT EDIT)[34]

Cardiac Pacing in HCM[34]

Class III
"1. Asymptomatic patients. (Level of Evidence: C)"
"2. Symptomatic patients who do not have LVOT obstruction. (Level of Evidence: C)"
Class IIa
"1. Symptomatic bradycardia due to beta-blockade when alternative therapies are unacceptable. (Level of Evidence: C)"
Class IIb
"1. Patients with drug-refractory hypertrophic cardiomyopathy with significant resting or provoked LVOT gradient and contraindications for septal ablation or myectomy. (Level of Evidence: A)"[46][47][45]

Sources

Automatic Implantable Cardiac Defibrillator (AICD) placement

The role of AICD (automatic implantable cardiac defibrillator) placement in HCM is controversial. It offers the best potential benefit for survival and should probably be implanted in survivors of SCD and those deemed at high risk by clinical parameters. Nonetheless, the impact on prognosis is unclear because tachyarrhythmias may not always be the mechanism for syncope and sudden death. In addition, older patients may be self-selected “survivors” that stand to gain less from ICD placement. One recent retrospective study showed that at an average follow-up of 128 patients at 3.1 years, 23 percent had shocks for VT (ventricular tachycardia) and 25% had inappropriate shocks. Of those receiving the ICD prophylactically, 5% were shocked per year. This study did not evaluate the role of clinical predictors, evaluate total mortality and was a non-randomized retrospective design that does not establish the need for ICD placement in all patients with HCM or superiority to amiodarone therapy.

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy (DO NOT EDIT)[48]

Selection of Patients for ICDs (DO NOT EDIT)[48]

Class I
"1. The decision to place an ICD in patients with HCM should include the application of individual clinical judgment, as well as a thorough discussion of the strength of evidence, benefits, and risks to allow the informed patient's active participation in decision making.[49][50][51][52] (Level of Evidence: C) "
"2. ICD placement is recommended for patients with HCM with prior documented cardiac arrest, ventricular fibrillation, or hemodynamically significant VT[53][54][55][50]. (Level of Evidence: B) "
Class IIa
"1. It is reasonable to recommend an ICD for patients with HCM with:
a. Sudden death presumably caused by HCM in 1 or more first-degree relatives.[56] (Level of Evidence: C)

b. A maximum LV wall thickness greater than or equal to 30 mm.[57][58][59][60] (Level of Evidence: C)
c. One or more recent, unexplained syncopal episodes.[61] (Level of Evidence: C) ''

"2. An ICD can be useful in select patients with NSVT (particularly those <30 years of age) in the presence of other SCD risk factors or modifiers.[62][49] (Level of Evidence: C) "
"3. An ICD can be useful in select patients with HCM with an abnormal blood pressure response with exercise in the presence of other SCD risk factors or modifiers.[63][64][65] (Level of Evidence: C) "
"4. It is reasonable to recommend an ICD for high-risk children with HCM, based on unexplained syncope, massive LV hypertrophy, or family history of SCD, after taking into account the relatively high complication rate of long-term ICD implantation. (Level of Evidence: C) "
Class IIb
"1. The usefulness of an ICD is uncertain in patients with HCM with isolated bursts of NSVT when in the absence of any other SCD risk factors or modifiers[49]. (Level of Evidence: C) "
"2. The usefulness of an ICD is uncertain in patients with HCM with an abnormal blood pressure response with exercise when in the absence of any other SCD risk factors or modifiers, particularly in the presence of significant outflow obstruction.[63][64][65] (Level of Evidence: C) "
Class III (Harm)
"1. ICD placement as a routine strategy in patients with HCM without an indication of increased risk is potentially harmful. (Level of Evidence: C)"
"2. ICD placement as a strategy to permit patients with HCM to participate in competitive athletics is potentially harmful. (Level of Evidence: C)"
"3. ICD placement in patients who have an identified HCM genotype in the absence of clinical manifestations of HCM is potentially harmful. (Level of Evidence: C)"

Selection of ICD Device Type (DO NOT EDIT)[48]

Class IIa
"1. In patients with HCM who meet indications for ICD implantation, single-chamber devices are reasonable in younger patients without a need for atrial or ventricular pacing.[66][67][68][69] (Level of Evidence: B)"
"2. In patients with HCM who meet indications for ICD implantation, dual-chamber ICDs are reasonable for patients with sinus bradycardia and/or paroxysmal AF.[66] (Level of Evidence: C)"
"3. In patients with HCM who meet indications for ICD implantation, dual-chamber ICDs are reasonable for patients with elevated resting outflow gradients greater than 50 mm Hg and significant heart failure symptoms who may benefit from right ventricular pacing (most commonly, but not limited to, patients >65 years of age).[43][44][45][66] (Level of Evidence: B) "

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death - Hypertrophic Cardiomyopathy (DO NOT EDIT)[70]

Class I
"1. ICD therapy should be used for treatment in patients with hypertrophic cardiomyopathy (HCM) who have sustained VT and/or VF and who are receiving chronic optimal medical therapy and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: B) "
Class IIa
"1. ICD implantation can be effective for primary prophylaxis against SCD in patients with HCM who have one or more major risk factor for SCD and who are receiving chronic optimal medical therapy and in patients who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)"
"2. Amiodarone therapy can be effective for treatment in patients with HCM with a history of sustained VT and/or VF when ICD is not feasible. (Level of Evidence: C)"
Class IIb
"1. EP testing may be considered for risk assessment for SCD in patients with HCM. (Level of Evidence: C) "
"2. Amiodarone may be considered for primary prophylaxis against SCD in patients with HCM who have one or more major risk factor for SCD, if ICD implantation is not feasible. (Level of Evidence: C) "

Sources

References

  1. ↑ Maron BJ (2002). "Hypertrophic cardiomyopathy: a systematic review". JAMA. 287 (10): 1308–20. PMID 11886323.
  2. ↑ Wigle ED, Rakowski H, Kimball BP, Williams WG (1995). "Hypertrophic cardiomyopathy. Clinical spectrum and treatment". Circulation. 92 (7): 1680–92. PMID 7671349.
  3. ↑ Brilakis ES, Nishimura RA. Severe pulmonary hypertension in a patient with hypertrophic cardiomyopathy: response to alcohol septal ablation. Heart. 2003 Jul; 89(7):790. (Medline abstract)
  4. ↑ Chen AA, Palacios IF, Mela T, Yoerger DM, Picard MH, Vlahakes G, Lowry PA, Fifer MA (2006). "Acute predictors of subacute complete heart block after alcohol septal ablation for obstructive hypertrophic cardiomyopathy". The American Journal of Cardiology. 97 (2): 264–9. doi:10.1016/j.amjcard.2005.08.032. PMID 16442376. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  5. ↑ Faber L, Welge D, Fassbender D, Schmidt HK, Horstkotte D, Seggewiss H (2007). "Percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: managing the risk of procedure-related AV conduction disturbances". International Journal of Cardiology. 119 (2): 163–7. doi:10.1016/j.ijcard.2006.07.179. PMID 17067708. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  6. ↑ Reinhard W, Ten Cate FJ, Scholten M, De Laat LE, Vos J (2004). "Permanent pacing for complete atrioventricular block after nonsurgical (alcohol) septal reduction in patients with obstructive hypertrophic cardiomyopathy". The American Journal of Cardiology. 93 (8): 1064–6. doi:10.1016/j.amjcard.2003.12.065. PMID 15081461. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  7. ↑ Montalvo AL, Bembi B, Donnarumma M, Filocamo M, Parenti G, Rossi M, Merlini L, Buratti E, De Filippi P, Dardis A, Stroppiano M, Ciana G, Pittis MG (2006). "Mutation profile of the GAA gene in 40 Italian patients with late onset glycogen storage disease type II". Human Mutation. 27 (10): 999–1006. doi:10.1002/humu.20374. PMID 16917947. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  8. ↑ Lakkis NM, Nagueh SF, Kleiman NS, Killip D, He ZX, Verani MS, Roberts R, Spencer WH (1998). "Echocardiography-guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy". Circulation. 98 (17): 1750–5. PMID 9788829. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  9. ↑ Gietzen FH, Leuner CJ, Raute-Kreinsen U, Dellmann A, Hegselmann J, Strunk-Mueller C, Kuhn HJ (1999). "Acute and long-term results after transcoronary ablation of septal hypertrophy (TASH). Catheter interventional treatment for hypertrophic obstructive cardiomyopathy". European Heart Journal. 20 (18): 1342–54. doi:10.1053/euhj.1999.1520. PMID 10462469. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  10. ↑ Boltwood CM, Chien W, Ports T (2004). "Ventricular tachycardia complicating alcohol septal ablation". The New England Journal of Medicine. 351 (18): 1914–5. doi:10.1056/NEJM200410283511824. PMID 15509832. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  11. ↑ Hori Y, Ueda M, Nakayama T, Saegusa N, Uehara M, Lee K, Sekine T, Daimon M, Kobayashi Y, Funabashi N, Komuro I (2007). "Occurrence of de novo sustained monomorphic ventricular tachycardia induced after percutaneous transluminal alcohol septal myocardial ablation for hypertrophic obstructive cardiomyopathy". International Journal of Cardiology. 119 (3): 403–7. doi:10.1016/j.ijcard.2006.07.182. PMID 17069908. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  12. ↑ Kazmierczak J, Kornacewicz-Jach Z, Kisly M, Gil R, Wojtarowicz A (1998). "Electrocardiographic changes after alcohol septal ablation in hypertrophic obstructive cardiomyopathy". Heart (British Cardiac Society). 80 (3): 257–62. PMC 1761105. PMID 9875085. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  13. ↑ Lawrenz T, Obergassel L, Lieder F, Leuner C, Strunk-Mueller C, Meyer Zu Vilsendorf D, Beer G, Kuhn H (2005). "Transcoronary ablation of septal hypertrophy does not alter ICD intervention rates in high risk patients with hypertrophic obstructive cardiomyopathy". Pacing and Clinical Electrophysiology : PACE. 28 (4): 295–300. doi:10.1111/j.1540-8159.2005.09327.x. PMID 15826262. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  14. ↑ McGregor JB, Rahman A, Rosanio S, Ware D, Birnbaum Y, Saeed M (2004). "Monomorphic ventricular tachycardia: a late complication of percutaneous alcohol septal ablation for hypertrophic cardiomyopathy". The American Journal of the Medical Sciences. 328 (3): 185–8. PMID 15367880. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  15. ↑ 15.0 15.1 Noseworthy PA, Rosenberg MA, Fifer MA, Palacios IF, Lowry PA, Ruskin JN, Sanborn DM, Picard MH, Vlahakes GJ, Mela T, Das S (2009). "Ventricular arrhythmia following alcohol septal ablation for obstructive hypertrophic cardiomyopathy". The American Journal of Cardiology. 104 (1): 128–32. doi:10.1016/j.amjcard.2009.02.056. PMID 19576333. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  16. ↑ Simon RD, Crawford FA, Spencer WH, Gold MR (2005). "Sustained ventricular tachycardia following alcohol septal ablation for hypertrophic obstructive cardiomyopathy". Pacing and Clinical Electrophysiology : PACE. 28 (12): 1354–6. doi:10.1111/j.1540-8159.2005.00278.x. PMID 16403169. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  17. ↑ 17.0 17.1 17.2 17.3 ten Cate FJ, Soliman OI, Michels M, Theuns DA, de Jong PL, Geleijnse ML, Serruys PW (2010). "Long-term outcome of alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy: a word of caution". Circulation. Heart Failure. 3 (3): 362–9. doi:10.1161/CIRCHEARTFAILURE.109.862359. PMID 20332420. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  18. ↑ 18.0 18.1 18.2 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 2012-02-11. Unknown parameter |month= ignored (help)
  19. ↑ 19.0 19.1 19.2 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 2012-02-11. Unknown parameter |month= ignored (help)
  20. ↑ 20.0 20.1 Kwon DH, Kapadia SR, Tuzcu EM, Halley CM, Gorodeski EZ, Curtin RJ, Thamilarasan M, Smedira NG, Lytle BW, Lever HM, Desai MY (2008). "Long-term outcomes in high-risk symptomatic patients with hypertrophic cardiomyopathy undergoing alcohol septal ablation". JACC. Cardiovascular Interventions. 1 (4): 432–8. doi:10.1016/j.jcin.2008.05.009. PMID 19463341. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  21. ↑ Alam M, Dokainish H, Lakkis NM (2009). "Hypertrophic obstructive cardiomyopathy-alcohol septal ablation vs. myectomy: a meta-analysis". European Heart Journal. 30 (9): 1080–7. doi:10.1093/eurheartj/ehp016. PMID 19233857. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  22. ↑ 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 2012-02-11. Unknown parameter |month= ignored (help)
  23. ↑ McLeod CJ, Ommen SR, Ackerman MJ, Weivoda PL, Shen WK, Dearani JA, Schaff HV, Tajik AJ, Gersh BJ (2007). "Surgical septal myectomy decreases the risk for appropriate implantable cardioverter defibrillator discharge in obstructive hypertrophic cardiomyopathy". European Heart Journal. 28 (21): 2583–8. doi:10.1093/eurheartj/ehm117. PMID 17483110. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  24. ↑ Leonardi RA, Kransdorf EP, Simel DL, Wang A (2010). "Meta-analyses of septal reduction therapies for obstructive hypertrophic cardiomyopathy: comparative rates of overall mortality and sudden cardiac death after treatment". Circulation. Cardiovascular Interventions. 3 (2): 97–104. doi:10.1161/CIRCINTERVENTIONS.109.916676. PMID 20197511. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  25. ↑ Agarwal S, Tuzcu EM, Desai MY, Smedira N, Lever HM, Lytle BW, Kapadia SR (2010). "Updated meta-analysis of septal alcohol ablation versus myectomy for hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 55 (8): 823–34. doi:10.1016/j.jacc.2009.09.047. PMID 20170823. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  26. ↑ Valeti US, Nishimura RA, Holmes DR, Araoz PA, Glockner JF, Breen JF, Ommen SR, Gersh BJ, Tajik AJ, Rihal CS, Schaff HV, Maron BJ (2007). "Comparison of surgical septal myectomy and alcohol septal ablation with cardiac magnetic resonance imaging in patients with hypertrophic obstructive cardiomyopathy". Journal of the American College of Cardiology. 49 (3): 350–7. doi:10.1016/j.jacc.2006.08.055. PMID 17239717. Retrieved 2012-02-11. Unknown parameter |month= ignored (help)
  27. ↑ 27.0 27.1 27.2 27.3 27.4 27.5 27.6 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)
  28. ↑ Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C, Kuhn H (2004). "Transcoronary ablation of septal hypertrophy for hypertrophic obstructive cardiomyopathy: feasibility, clinical benefit, and short term results in elderly patients". Heart. 90 (6): 638–44. PMC 1768263. PMID 15145866. Unknown parameter |month= ignored (help)
  29. ↑ 29.0 29.1 29.2 Kuhn H, Lawrenz T, Lieder F; et al. (2008). "Survival after transcoronary ablation of septal hypertrophy in hypertrophic obstructive cardiomyopathy (TASH): a 10 year experience". Clin Res Cardiol. 97 (4): 234–43. doi:10.1007/s00392-007-0616-7. PMID 18071624. Unknown parameter |month= ignored (help)
  30. ↑ 30.0 30.1 Nagueh SF, Ommen SR, Lakkis NM; et al. (2001). "Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy". J. Am. Coll. Cardiol. 38 (6): 1701–6. PMID 11704383. Unknown parameter |month= ignored (help)
  31. ↑ 31.0 31.1 Qin JX, Shiota T, Lever HM; et al. (2001). "Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery". J. Am. Coll. Cardiol. 38 (7): 1994–2000. PMID 11738306. Unknown parameter |month= ignored (help)
  32. ↑ Firoozi S, Elliott PM, Sharma S; et al. (2002). "Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathy. A comparison of clinical, haemodynamic and exercise outcomes". Eur. Heart J. 23 (20): 1617–24. PMID 12323162. Unknown parameter |month= ignored (help)
  33. ↑ 33.0 33.1 Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207
  34. ↑ 34.0 34.1 34.2 34.3 34.4 Vardas PE, Auricchio A, Blanc JJ, Daubert JC, Drexler H, Ector H; et al. (2007). "Guidelines for cardiac pacing and cardiac resynchronization therapy. The Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association". Europace. 9 (10): 959–98. doi:10.1093/europace/eum189. PMID 17726043.
  35. ↑ 35.0 35.1 35.2 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: 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 2011-12-19. Unknown parameter |month= ignored (help)
  36. ↑ Ommen SR, Nishimura RA, Squires RW, Schaff HV, Danielson GK, Tajik AJ. Comparison of dual-chamber pacing versus septal myectomy for the treatment of patients with hypertropic obstructive cardiomyopathy: a comparison of objective hemodynamic and exercise end points. J Am Coll Cardiol. 1999 Jul; 34(1):191–6. (Medline abstract)
  37. ↑ Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD (2013). "2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society". J. Am. Coll. Cardiol. 61 (3): e6–75. doi:10.1016/j.jacc.2012.11.007. PMID 23265327.
  38. ↑ 38.0 38.1 38.2 Epstein AE, Dimarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS; et al. (2008). "ACC/AHA/HRS 2008 guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: executive summary". Heart Rhythm. 5 (6): 934–55. doi:10.1016/j.hrthm.2008.04.015. PMID 18534377.
  39. ↑ 39.0 39.1 Erwin JP, Nishimura RA, Lloyd MA, Tajik AJ (2000). "Dual chamber pacing for patients with hypertrophic obstructive cardiomyopathy: a clinical perspective in 2000". Mayo Clin. Proc. 75 (2): 173–80. doi:10.4065/75.2.173. PMID 10683657. Unknown parameter |month= ignored (help)
  40. ↑ 40.0 40.1 Gadler F, Linde C, Daubert C; et al. (1999). "Significant improvement of quality of life following atrioventricular synchronous pacing in patients with hypertrophic obstructive cardiomyopathy. Data from 1 year of follow-up. PIC study group. Pacing In Cardiomyopathy". Eur. Heart J. 20 (14): 1044–50. doi:10.1053/euhj.1998.1331. PMID 10381856. Unknown parameter |month= ignored (help)
  41. ↑ 41.0 41.1 Slade AK, Sadoul N, Shapiro L; et al. (1996). "DDD pacing in hypertrophic cardiomyopathy: a multicentre clinical experience". Heart. 75 (1): 44–9. PMC 484221. PMID 8624871. Unknown parameter |month= ignored (help)
  42. ↑ 42.0 42.1 Ommen SR, Nishimura RA, Squires RW, Schaff HV, Danielson GK, Tajik AJ (1999). "Comparison of dual-chamber pacing versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy: a comparison of objective hemodynamic and exercise end points". J. Am. Coll. Cardiol. 34 (1): 191–6. PMID 10400010. Unknown parameter |month= ignored (help)
  43. ↑ 43.0 43.1 43.2 43.3 Maron BJ, Nishimura RA, McKenna WJ, Rakowski H, Josephson ME, Kieval RS (1999). "Assessment of permanent dual-chamber pacing as a treatment for drug-refractory symptomatic patients with obstructive hypertrophic cardiomyopathy. A randomized, double-blind, crossover study (M-PATHY)". Circulation. 99 (22): 2927–33. PMID 10359738. Unknown parameter |month= ignored (help)
  44. ↑ 44.0 44.1 44.2 Nishimura RA, Trusty JM, Hayes DL; et al. (1997). "Dual-chamber pacing for hypertrophic cardiomyopathy: a randomized, double-blind, crossover trial". J. Am. Coll. Cardiol. 29 (2): 435–41. PMID 9015001. Unknown parameter |month= ignored (help)
  45. ↑ 45.0 45.1 45.2 45.3 Kappenberger L, Linde C, Daubert C; et al. (1997). "Pacing in hypertrophic obstructive cardiomyopathy. A randomized crossover study. PIC Study Group". Eur. Heart J. 18 (8): 1249–56. PMID 9458416. Unknown parameter |month= ignored (help)
  46. ↑ Fananapazir L, Cannon RO, Tripodi D, Panza JA (1992). "Impact of dual-chamber permanent pacing in patients with obstructive hypertrophic cardiomyopathy with symptoms refractory to verapamil and beta-adrenergic blocker therapy". Circulation. 85 (6): 2149–61. PMID 1350522.
  47. ↑ Fananapazir L, Epstein ND, Curiel RV, Panza JA, Tripodi D, McAreavey D (1994). "Long-term results of dual-chamber (DDD) pacing in obstructive hypertrophic cardiomyopathy. Evidence for progressive symptomatic and hemodynamic improvement and reduction of left ventricular hypertrophy". Circulation. 90 (6): 2731–42. PMID 7994815.
  48. ↑ 48.0 48.1 48.2 Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS; et al. (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". Circulation. 124 (24): 2761–96. doi:10.1161/CIR.0b013e318223e230. PMID 22068435.
  49. ↑ 49.0 49.1 49.2 Maron BJ (2010). "Contemporary insights and strategies for risk stratification and prevention of sudden death in hypertrophic cardiomyopathy". Circulation. 121 (3): 445–56. doi:10.1161/CIRCULATIONAHA.109.878579. PMID 20100987. Unknown parameter |month= ignored (help)
  50. ↑ 50.0 50.1 Maron BJ, Spirito P, Shen WK; et al. (2007). "Implantable cardioverter-defibrillators and prevention of sudden cardiac death in hypertrophic cardiomyopathy". JAMA. 298 (4): 405–12. doi:10.1001/jama.298.4.405. PMID 17652294. Unknown parameter |month= ignored (help)
  51. ↑ Maron BJ, Shen WK, Link MS; et al. (2000). "Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy". N. Engl. J. Med. 342 (6): 365–73. doi:10.1056/NEJM200002103420601. PMID 10666426. Unknown parameter |month= ignored (help)
  52. ↑ Maron BJ, Spirito P (2008). "Implantable defibrillators and prevention of sudden death in hypertrophic cardiomyopathy". J. Cardiovasc. Electrophysiol. 19 (10): 1118–26. doi:10.1111/j.1540-8167.2008.01147.x. PMID 18384577. Unknown parameter |month= ignored (help)
  53. ↑ Cecchi F, Maron BJ, Epstein SE (1989). "Long-term outcome of patients with hypertrophic cardiomyopathy successfully resuscitated after cardiac arrest". J. Am. Coll. Cardiol. 13 (6): 1283–8. PMID 2703610. Unknown parameter |month= ignored (help)
  54. ↑ Elliott PM, Sharma S, Varnava A, Poloniecki J, Rowland E, McKenna WJ (1999). "Survival after cardiac arrest or sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy". J. Am. Coll. Cardiol. 33 (6): 1596–601. PMID 10334430. Unknown parameter |month= ignored (help)
  55. ↑ Fananapazir L, Chang AC, Epstein SE, McAreavey D (1992). "Prognostic determinants in hypertrophic cardiomyopathy. Prospective evaluation of a therapeutic strategy based on clinical, Holter, hemodynamic, and electrophysiological findings". Circulation. 86 (3): 730–40. PMID 1516184. Unknown parameter |month= ignored (help)
  56. ↑ Bos JM, Maron BJ, Ackerman MJ; et al. (2010). "Role of family history of sudden death in risk stratification and prevention of sudden death with implantable defibrillators in hypertrophic cardiomyopathy". Am. J. Cardiol. 106 (10): 1481–6. doi:10.1016/j.amjcard.2010.06.077. PMID 21059440. Unknown parameter |month= ignored (help)
  57. ↑ Elliott PM, Poloniecki J, Dickie S; et al. (2000). "Sudden death in hypertrophic cardiomyopathy: identification of high risk patients". J. Am. Coll. Cardiol. 36 (7): 2212–8. PMID 11127463. Unknown parameter |month= ignored (help)
  58. ↑ Elliott PM, Gimeno Blanes JR, Mahon NG, Poloniecki JD, McKenna WJ (2001). "Relation between severity of left-ventricular hypertrophy and prognosis in patients with hypertrophic cardiomyopathy". Lancet. 357 (9254): 420–4. doi:10.1016/S0140-6736(00)04005-8. PMID 11273061. Unknown parameter |month= ignored (help)
  59. ↑ Sorajja P, Nishimura RA, Ommen SR, Ackerman MJ, Tajik AJ, Gersh BJ (2006). "Use of echocardiography in patients with hypertrophic cardiomyopathy: clinical implications of massive hypertrophy". J Am Soc Echocardiogr. 19 (6): 788–95. doi:10.1016/j.echo.2006.01.005. PMID 16762758. Unknown parameter |month= ignored (help)
  60. ↑ Spirito P, Bellone P, Harris KM, Bernabo P, Bruzzi P, Maron BJ (2000). "Magnitude of left ventricular hypertrophy and risk of sudden death in hypertrophic cardiomyopathy". N. Engl. J. Med. 342 (24): 1778–85. doi:10.1056/NEJM200006153422403. PMID 10853000. Unknown parameter |month= ignored (help)
  61. ↑ Spirito P, Autore C, Rapezzi C; et al. (2009). "Syncope and risk of sudden death in hypertrophic cardiomyopathy". Circulation. 119 (13): 1703–10. doi:10.1161/CIRCULATIONAHA.108.798314. PMID 19307481. Unknown parameter |month= ignored (help)
  62. ↑ Monserrat L, Elliott PM, Gimeno JR, Sharma S, Penas-Lado M, McKenna WJ (2003). "Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients". J. Am. Coll. Cardiol. 42 (5): 873–9. PMID 12957435. Unknown parameter |month= ignored (help)
  63. ↑ 63.0 63.1 Olivotto I, Maron BJ, Montereggi A, Mazzuoli F, Dolara A, Cecchi F (1999). "Prognostic value of systemic blood pressure response during exercise in a community-based patient population with hypertrophic cardiomyopathy". J. Am. Coll. Cardiol. 33 (7): 2044–51. PMID 10362212. Unknown parameter |month= ignored (help)
  64. ↑ 64.0 64.1 Sadoul N, Prasad K, Elliott PM, Bannerjee S, Frenneaux MP, McKenna WJ (1997). "Prospective prognostic assessment of blood pressure response during exercise in patients with hypertrophic cardiomyopathy". Circulation. 96 (9): 2987–91. PMID 9386166. Unknown parameter |month= ignored (help)
  65. ↑ 65.0 65.1 Maki S, Ikeda H, Muro A; et al. (1998). "Predictors of sudden cardiac death in hypertrophic cardiomyopathy". Am. J. Cardiol. 82 (6): 774–8. PMID 9761089. Unknown parameter |month= ignored (help)
  66. ↑ 66.0 66.1 66.2 Boriani G, Maron BJ, Shen WK, Spirito P (2004). "Prevention of sudden death in hypertrophic cardiomyopathy: but which defibrillator for which patient?". Circulation. 110 (15): e438–42. doi:10.1161/01.CIR.0000144463.65977.C9. PMID 15477422. Unknown parameter |month= ignored (help)
  67. ↑ Hauser RG, Maron BJ, Marine JE; et al. (2008). "Safety and efficacy of transvenous high-voltage implantable cardioverter-defibrillator leads in high-risk hypertrophic cardiomyopathy patients". Heart Rhythm. 5 (11): 1517–22. doi:10.1016/j.hrthm.2008.08.021. PMID 18984525. Unknown parameter |month= ignored (help)
  68. ↑ Kleemann T, Becker T, Doenges K; et al. (2007). "Annual rate of transvenous defibrillation lead defects in implantable cardioverter-defibrillators over a period of >10 years". Circulation. 115 (19): 2474–80. doi:10.1161/CIRCULATIONAHA.106.663807. PMID 17470696. Unknown parameter |month= ignored (help)
  69. ↑ Maisel WH, Sweeney MO, Stevenson WG, Ellison KE, Epstein LM (2001). "Recalls and safety alerts involving pacemakers and implantable cardioverter-defibrillator generators". JAMA. 286 (7): 793–9. PMID 11497532. Unknown parameter |month= ignored (help)
  70. ↑ Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M; et al. (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (10): e385–484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995.


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