Secondary Logo

Share this article on:

Dynamic obstruction in hypertrophic cardiomyopathy

Popescu, Bogdan A.a,b; Rosca, Monicaa,b; Schwammenthal, Ehudc

doi: 10.1097/HCO.0000000000000199

Purpose of review The present article reviews the recent advances in the echocardiographic assessment of left ventricular outflow tract (LVOT) obstruction in hypertrophic cardiomyopathy (HCM). In particular, it highlights the role of novel imaging techniques in promoting our understanding of the pathophysiology of obstruction and discusses the prognostic value of information obtained from exercise echocardiography and the emerging role of image-guidance technologies for interventional relief of obstruction.

Recent findings The advent of novel echocardiography technologies, such as vector flow mapping, continues to expand our understanding of the exact mechanism of systolic anterior motion leading to dynamic LVOT obstruction by providing new insights into the interaction between pathologic mitral geometry and the left ventricular flow field. New studies provide evidence for the prognostic value of exercise echocardiography in the assessment of patients with HCM. Myocardial contrast perfusion imaging can delineate the anatomy of septal perforator arteries and identify the downstream septal perfusion bed, which is critical for safely guiding the procedure of alcohol septal ablation.

Summary Echocardiography represents a versatile, continuously evolving, and easily repeatable technique, allowing truly dynamic imaging studies, and is therefore most appropriate to evaluate a dynamic disease condition such as LVOT obstruction in HCM. It provides profound insights into the pathophysiology of LVOT obstruction, information on its clinical impact, and guidance for its relief by interventional strategies.

Supplemental Digital Content is available in the text

aDepartment of Cardiology, University of Medicine and Pharmacy ‘Carol Davila’, Euroecolab

bInstitute of Cardiovascular Diseases ‘Prof. Dr C. C. Iliescu’, Bucharest, Romania

cHeart Center, Chaim Sheba Medical Center, Tel Hashomer, Tel Aviv University, Israel

Correspondence to Bogdan A. Popescu, MD, PhD, Department of Cardiology, University of Medicine and Pharmacy ‘Carol Davila’, Euroecolab, Institute of Cadiovascular Diseases ‘Prof. Dr C. C. Iliescu’ Sos Fundeni 258, sector 2, 022328, Bucharest, Romania. Tel/fax: +40 213175227; e-mail:

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website (

Back to Top | Article Outline


Echocardiography is central to the diagnosis of left ventricular outflow tract (LVOT) obstruction; it delineates its mechanism and dynamic nature in real-time and precisely quantifies its severity; it identifies patient anatomies suitable for interventional therapy and provides image-guidance throughout the procedure [1]. Evidence for the clinical utility of data derived from a comprehensive assessment of LVOT obstruction is steadily growing. The present article reviews the recent advances with particular attention to new pathophysiological, prognostic and therapeutic insights.

Box 1

Box 1

Back to Top | Article Outline


Dynamic LVOT obstruction is a unique phenomenon, which typically ensues when a geometrically abnormal mitral valve is interposed into an abnormal left ventricular flow field. Increased leaflet area generates leaflet slack, and anterior papillary muscle displacement reduces the force that restrains the leaflets posteriorly. As flow is forced to circumvent the asymmetric septal hypertrophy, it impacts the mitral valve and moves it anteriorly [systolic anterior motion (SAM); Fig. 1] [2]. SAM can thus be characterized as ‘prolapse into the LVOT’ of the central leaflet segment A2 (or A2 and P2).



Although septal hypertrophy may also directly contribute to dynamic obstruction by reducing LVOT cross-sectional area, the primary role of mitral valve disorder as a cause of SAM has been clearly established clinically and experimentally [3–8]. Its central importance explains not only the occurrence of SAM in the absence of septal hypertrophy, such as following ring-annuloplasty in myxomatous disease [9–13], but also the absence of SAM in the presence of septal hypertrophy [14] (Fig. 2, Video 1, and Video 2, These data have refuted the original Venturi theory, which explained the initiation of SAM as a result of high flow velocities caused by septal hypertrophy narrowing the LVOT; in fact, flow velocities are normal at the time of SAM onset, i.e. too low to generate significant Venturi forces [15–17]. However, once flow velocities increase as SAM-septal contact develops, SAM might potentially be augmented by Venturi forces.



Although morphological abnormalities responsible for mitral valve prepositioning in the LVOT (facilitating obstruction) are widely documented, it was previously not possible to analyze the flow vectors acting on the valve in vivo because of the limitations of color Doppler flow mapping, which only provides accurate velocity information parallel to the ultrasound beam.

By using vector flow mapping, a novel method of Doppler data processing capable of calculating velocity components orthogonal to the beam direction, Ro et al. [18▪▪] provided new insights into the mechanism of SAM. The authors analyzed pre-SAM and post-SAM velocity vector flow maps and two-dimensional frames in patients with obstructive hypertrophic cardiomyopathy (HCM) and compared them with time-corresponding data in patients with nonobstructive HCM and normal volunteers. This analysis demonstrated that the push force of the left ventricular streamlines of flow impacting on the posterior aspect of the mitral valve represents the dominant hydrodynamic force initiating SAM. In 59% of patients, flow impacted the posterior aspect of the valve because ejection flow was deflected posteriorly by the bulging septum. In another 41%, this impact on the posterior aspect of the valve was the result of an initially anteriorly directed late-diastolic inflow bouncing back from the septum, thus generating a vortex during isovolumic contraction that prepositioned the mitral leaflets into the ejection stream. In fact, diastolic anterior mitral position and motion functioned as a precursor of SAM [19]. In both cases, septal reduction over a sufficient length will redirect flow away from the mitral valve and reduce drag forces on the leaflets, thereby preventing occurrence of obstruction.

Better understanding of mechanisms may lead to more effective surgical and catheter therapy, guided by visualization not only of valve structures but also of varying intraventricular flow patterns, which so far have eluded our attention in clinical practice.

Back to Top | Article Outline


The clinical course of HCM is characterized by extreme heterogeneity with unpredictable development of heart failure symptoms despite normal/supranormal left ventricular ejection fraction [20]. Multiple hemodynamic mechanisms were proposed to explain reduced exercise tolerance [21]: impaired left ventricular relaxation, increased left ventricular chamber stiffness, and compromised left ventricular function with elevated left ventricular filling pressures have all been postulated as the main mechanisms of heart failure in HCM. Myocardial ischemia, left ventricular pressure overload associated with LVOT obstruction, and the associated mitral regurgitation can further elevate left ventricular diastolic pressures and lead to more severe symptoms. However, the relationship between LVOT obstruction and heart failure symptoms is variable, possibly because of the labile nature of LVOT obstruction. Outflow gradients are highly influenced by left ventricular size and contractility, loading conditions, and peripheral vascular resistance [22]. They may increase after heavy meals [23] or alcohol intake [24], explaining postprandial symptom exacerbation [25]. Increases in LVOT gradients can be provoked using several physiological maneuvers, such as the standing position, Valsalva maneuver, or exercise [26]. Although only 25–30% of patients with HCM have significant LVOT obstruction at rest, this figure may exceed 60% with exertion, potentially contributing to the identification of patients in whom heart failure symptoms are largely explained by latent exercise-induced obstruction [27].

On the other hand, patients with significant LVOT gradients at rest (i.e., >50 mmHg) may have an unexpectedly good exercise tolerance. Starting from this observation, Lafitte et al. [28] have analyzed the response of LVOT gradients and left ventricular function to semisupine exercise in 107 patients with and without resting obstruction. Nine of the 38 patients (23%) with intraventricular gradients at rest showed a paradoxical response to exercise, defined as a decrease in gradient of ≥30 mmHg during exercise. These patients had lower New York Heart Association class, better exercise capacity, and a trend toward a reduced rate of cardiac events compared with patients with HCM in whom the LVOT gradient increased or did not change during exercise. The presence of larger left ventricular volumes (both at rest and during exercise) decreasing mitral leaflet slack and thus the preposition to SAM may explain the decrease in obstruction in these patients. Moreover, exercise echocardiography proved to be safe even in patients with significant resting obstruction, supporting its use for risk stratification in patients with HCM regardless of obstruction severity.

Microvascular dysfunction is another mechanism potentially involved in the clinical deterioration of patients with HCM. Fibrosis, myocardial disarray, vascular remodeling, reduced capillary density relative to the myocardial mass, and extravascular compression because of elevated LV pressure may all be responsible for perfusion abnormalities in these patients [21]. Coronary flow reserve (CFR), noninvasively assessed by Doppler echocardiography, provides a reasonable measure of microcirculation in the absence of epicardial stenoses that can further contribute to risk stratification in HCM [29]. Tesic et al. [30] demonstrated in a group of 61 patients with HCM (20 with obstructive HCM) that regional differences in CFR (lower CFR in the left anterior descending artery compared with the posterior descending artery) are present only in patients with significant LVOT obstruction. In fact, LVOT gradient was an independent predictor of CFR in the left anterior descending coronary artery, compatible with a greater exhaustion of vasodilatory reserve with increasing severity of LVOT obstruction, predominantly in the asymmetrically hypertrophied septum and anterior wall. The potential clinical impact of regional differences in CFR still needs to be investigated.

Back to Top | Article Outline


LVOT obstruction at rest is a well-documented strong independent predictor of heart failure progression and cardiovascular death [31]. More severe disease complications seem to be linked to the duration of LVOT obstruction rather than its severity at rest [31]. Therefore, interest arose in the possible impact of latent LVOT obstruction. Initial studies failed to show a correlation between more severe latent obstruction and outcome [32,33]; recently published data reveal a more complex picture [34,35,36▪].

Finocchiaro et al. [34] showed in a group of 283 patients with HCM that 22% of those with latent LVOT obstruction and 33% of those with resting obstruction had clinical deterioration leading to septal reduction therapy during a mean follow-up of 42 ± 31 months. Development of an LVOT gradient more than 30 mmHg during stress emerged as the strongest independent outcome predictor in this population, suggesting that even a gradient between 30 and 50 mmHg (below the 50 mmHg guideline-recommended cut-off as a prerequisite for intervention) could be clinically significant.

The comparative value of resting and exercise echocardiography parameters as outcome predictors was assessed in 115 patients with HCM by Reant et al. [35]. A gradient more than 50 mmHg at peak exercise (not in the recovery phase) was independently associated with a worse outcome. The peak exercise gradient had additive prognostic value particularly in patients with global longitudinal left ventricular strain more than −15% or resting gradient more than 30 mmHg.

In a group of 426 patients with asymptomatic or minimally symptomatic HCM followed for 8.7 ± 3.0 years, Desai et al. [36▪] reported impaired functional capacity, abnormal heart rate recovery and atrial fibrillation as independent predictors of adverse clinical outcomes. Only 17% achieved more than 100% of age-sex predicted metabolic equivalents (METs). Patients who achieved at least 100% of age-sex predicted METs had a very low event rate during follow-up regardless of the presence or severity of LVOT obstruction, showing that simple exercise testing is in itself a useful tool to assess functional status and prognosis in patients with apparently asymptomatic HCM [37].

The impact of LVOT obstruction on the risk of sudden cardiac death (SCD) is still controversial. As a result of the inconsistent association between LVOT obstruction and SCD [31,38–40], the 2011 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines on HCM [41] include marked LVOT obstruction only as a potential SCD risk modifier to be considered in borderline situations. In contrast, the 2014 European Society of Cardiology (ESC) guidelines on HCM [1] consider LVOT obstruction as a major clinical feature associated with increased risk of SCD. This is based on the results of a recent multicenter retrospective longitudinal cohort study of 3675 patients that developed and validated a new SCD risk prediction model [42▪▪]. The model provides individualized 5-year risk estimates using variables that have been associated with an increased risk of SCD in at least one published multivariable analysis. The LVOT gradient at rest or during physiological maneuvers other than exercise is one of these variables. Because the prognostic role of exercise-induced LVOT obstruction is uncertain, this is not included in the calculation of SCD risk score at present.

Back to Top | Article Outline


Echocardiography plays a key role in identifying patients who may benefit from interventional relief of obstruction, in choosing the most appropriate intervention, and in guiding the procedure. The relief of LVOT obstruction is accompanied by reduction in heart failure symptoms and improvements in myocardial metabolism, oxygen consumption, and exercise capacity [43,44]. Current guidelines recommend septal reduction therapy in patients with HCM with advanced heart failure symptoms refractory to maximum pharmacological therapy and with a peak LVOT gradient at rest or during exercise of more than 50 mmHg [1,41]. Therefore, the proper identification and quantification of LVOT obstruction is of great importance for clinical decision making.

Several meta-analyses have shown that both surgical myectomy and septal alcohol ablation (SAA) improve functional status with a similar procedural mortality [45–47]. The risk of malignant ventricular tachycardia and SCD due to septal scar induced by SAA is still not well defined [48]. Recently, Vriesendorp et al. [49▪] reported in a group of 1047 consecutive patients treated at referral centers for HCM care and followed for 7.6 ± 5.3 years that survival after both myectomy and SAA is similar to that in patients with nonobstructive HCM. This finding indicates that the survival disadvantage associated with LVOT obstruction may be effectively annulled by appropriate therapy. The annual rate of SCD was low after invasive therapy, but still higher after SAA than after myectomy, suggesting that surgical intervention should be preferred in younger and otherwise healthy patients with HCM.

The choice of the type of intervention for obstruction relief should be based on both clinical and anatomical features. Intrinsic mitral valve abnormalities, anomalous papillary muscle insertion, extensive septal scarring on cardiac magnetic resonance, or very severe hypertrophy (≥30 mm) should preclude SAA [1]. As a result of the variability of septal blood supply, clear definition of the territory perfused by each septal perforator artery using myocardial contrast echocardiography is mandatory prior to SAA [50–52]. If the contrast agent is not confined exclusively to the target septal area adjacent to the mitral–septal contact, the procedure should be abandoned [1]. Of note, the myocardium perfused by septal perforator arteries is not always limited to the interventricular septum but can also involve remote areas such as papillary muscles, the right ventricular moderator band, or even the right ventricular free wall.

Recently, Wallace et al. [53] showed in a group of 47 patients with HCM who underwent SAA that extra-septal perfusion was present in 25% of patients in whom the diameter of the first septal perforator was also found to be greater than in those without extra-septal perfusion. Therefore, in patients with large (first) septal perforators special attention should be paid to the optimal visualization of both the interventricular septum and extra-septal remote structures, which might preclude the SAA procedure.

Back to Top | Article Outline


Echocardiography is the most accessible and versatile method to evaluate the structural and functional features of HCM. It allows the assessment of dynamic LVOT obstruction, a unique feature of this disease, providing important information about the pathophysiology of obstruction and its prognostic role. Advances in technology have allowed a better understanding of the obstruction's mechanism that can lead to changes in management strategy. The evidence for the prognostic role of information derived from exercise echocardiography in this setting is steadily growing. The impact of provocable LVOT obstruction on the risk of SCD is still controversial. The use of myocardial contrast echocardiography is mandatory in all patients undergoing SAA, providing critical information regarding the feasibility and safety of this procedure. Three-dimensional echocardiography combined with velocity flow mapping at rest and during exercise could provide further insights regarding the interactions between structural and functional anomalies and their potential impact on management strategy.

Back to Top | Article Outline



Back to Top | Article Outline

Financial support and sponsorship

This work was supported by a grant of the Romanian Ministry of National Education, CNCS-UEFISCDI, project number PN-II-ID-PCE-2012-4-0560 (contract 21/2013); by the Sectorial Operational Programme Human Resources Development (SOPHRD) financed by the European Social Fund and the Romanian Government (contract number POSDRU 141531); and by Programme Projects Young Researchers 2012 financed by the University of Medicine and Pharmacy ‘Carol Davila’ (contract number 28329/2013).

Back to Top | Article Outline

Conflicts of interest

There are no conflicts of interest.

Back to Top | Article Outline


Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest
Back to Top | Article Outline


1. Elliott PM, Anastasakis A, Borger MA, et al. Authors/Task Force members. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy: the Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology (ESC). Eur Heart J 2014; 35:2733–2779.
2. Schwammenthal E, Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? J Am Coll Cardiol 1996; 28:203–206.
3. Maron BJ, Harding AM, Spirito P, et al. Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy. Circulation 1983; 68:282–293.
4. Schwammenthal E, Nakatani S, He S, et al. Mechanism of mitral regurgitation in hypertrophic cardiomyopathy: mismatch of posterior to anterior leaflet length and mobility. Circulation 1998; 98:856–865.
5. Cape EG, Simons D, Jimoh A, et al. Chordal geometry determines the shape and extent of systolic anterior mitral motion: in vitro studies. J Am Coll Cardiol 1989; 13:1438–1448.
6. Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes systolic anterior motion of the mitral valve. Experimental validation and insights into the mechanism of subaortic obstruction. Circulation 1995; 91:1189–1195.
7. Spirito P, Maron BJ. Significance of left ventricular outflow tract cross-sectional area in hypertrophic cardiomyopathy: a two-dimensional echocardiographic assessment. Circulation 1983; 67:1100–1108.
8. Klues HG, Maron BJ, Dollar AL, Roberts WC. Diversity of structural mitral valve alterations in hypertrophic cardiomyopathy. Circulation 1992; 85:1651–1660.
9. Delling FN, Sanborn DY, Levine RA, et al. Frequency and mechanism of persistent systolic anterior motion and mitral regurgitation after septal ablation in obstructive hypertrophic cardiomyopathy. Am J Cardiol 2007; 100:1691–1695.
10. Smedira NG, Lytle BW, Lever HM, et al. Current effectiveness and risks of isolated septal myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg 2008; 85:127–133.
11. Jebara VA, Mihaileanu S, Acar C, et al. Left ventricular outflow tract obstruction after mitral valve repair. Results of the sliding leaflet technique. Circulation 1993; 88 (Pt 2):II30-4.
12. Lee KS, Stewart WJ, Lever HM, et al. Mechanism of outflow tract obstruction causing failed mitral valve repair. Anterior displacement of leaflet coaptation. Circulation 1993; 88 (Pt 2):II24-9.
13. Maslow AD, Regan MM, Haering JM, et al. Echocardiographic predictors of left ventricular outflow tract obstruction and systolic anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease. J Am Coll Cardiol 1999; 34:2096–2104.
14. Ginghina C, Calin A, Ilie I Cardiomyopathies (in Romanian). In: Ginghina C, Popescu BA, Jurcut R editors. The essentials in echocardiography (in Romanian). 2nd ed. Bucuresti: Editura Medicala Antaeus; 2013. pp. 235–245.
15. Jiang L, Levine RA, King ME, et al. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. Am Heart J 1987; 113:633–644.
16. Sherrid MV, Gunsburg DZ, Moldenhauer S, et al. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2000; 36:1344–1354.
17. Shah PM, Taylor RD, Wong M. Abnormal mitral valve coaptation in hypertrophic obstructive cardiomyopathy: proposed role in systolic anterior motion of mitral valve. Am J Cardiol 1981; 48:258–262.
18▪▪. Ro R, Halpern D, Sahn DJ, et al. Vector flow mapping in obstructive hypertrophic cardiomyopathy to assess the relationship of early systolic left ventricular flow and the mitral valve. J Am Coll Cardiol 2014; 64:1984–1995.

An interesting study that provides new insights into the pathophysiology of LVOT obstruction.

19. Levine RA, Schwammenthal E, Song JK. Diastolic leading to systolic anterior motion: new technology reveals physiology. J Am Coll Cardiol 2014; 64:1996–1999.
20. Melacini P, Basso C, Angelini A, et al. Clinicopathological profiles of progressive heart failure in hypertrophic cardiomyopathy. Eur Heart J 2010; 31:2111–2123.
21. Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002; 287:1308–1320.
22. Maron BJ, Maron MS, Wigle ED, Braunwald E. The 50-year history, controversy, and clinical implications of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy from idiopathic hypertrophic subaortic stenosis to hypertrophic cardiomyopathy: from idiopathic hypertrophic subaortic stenosis to hypertrophic cardiomyopathy. J Am Coll Cardiol 2009; 54:191–200.
23. Adams JC, Ommen SR, Klarich KW, et al. Significance of postprandial symptom exacerbation in hypertrophic cardiomyopathy. Am J Cardiol 2010; 105:990–992.
24. Paz R, Jortner R, Tunick PA, et al. The effect of the ingestion of ethanol on obstruction of the left ventricular outflow tract in hypertrophic cardiomyopathy. N Engl J Med 1996; 335:938–941.
25. Gilligan DM, Chan WL, Ang EL, Oakley CM. Effects of a meal on hemodynamic function at rest and during exercise in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1991; 18:429–436.
26. Joshi S, Patel UK, Yao SS, et al. Standing and exercise Doppler echocardiography in obstructive hypertrophic cardiomyopathy: the range of gradients with upright activity. J Am Soc Echocardiogr 2011; 24:75–82.
27. Maron MS, Olivotto I, Zenovich AG, et al. Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction. Circulation 2006; 114:2232–2239.
28. Lafitte S, Reant P, Touche C, et al. Paradoxical response to exercise in asymptomatic hypertrophic cardiomyopathy: a new description of outflow tract obstruction dynamics. J Am Coll Cardiol 2013; 62:842–850.
29. Cortigiani L, Rigo F, Gherardi S, et al. Prognostic implications of coronary flow reserve on left anterior descending coronary artery in hypertrophic cardiomyopathy. Am J Cardiol 2008; 102:1718–1723.
30. Tesic M, Djordjevic-Dikic A, Beleslin B, et al. Regional difference of microcirculation in patients with asymmetric hypertrophic cardiomyopathy: transthoracic Doppler coronary flow velocity reserve analysis. J Am Soc Echocardiogr 2013; 26:775–782.
31. Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med 2003; 348:295–303.
32. Vaglio JC Jr, Ommen SR, Nishimura RA, et al. Clinical characteristics and outcomes of patients with hypertrophic cardiomyopathy with latent obstruction. Am Heart J 2008; 156:342–347.
33. Peteiro J, Bouzas-Mosquera A, Fernandez X, et al. Prognostic value of exercise echocardiography in patients with hypertrophic cardiomyopathy. J Am Soc Echocardiogr 2012; 25:182–189.
34. Finocchiaro G, Haddad F, Pavlovic A, et al. Latent obstruction and left atrial size are predictors of clinical deterioration leading to septal reduction in hypertrophic cardiomyopathy. J Card Fail 2014; 20:236–243.
35. Reant P, Reynaud A, Pillois X, et al. Comparison of resting and exercise echocardiographic parameters as indicators of outcomes in hypertrophic cardiomyopathy. J Am Soc Echocardiogr 2015; 28:194–203.
36▪. Desai MY, Bhonsale A, Patel P, et al. Exercise echocardiography in asymptomatic HCM: exercise capacity, and not LV outflow tract gradient predicts long-term outcomes. JACC Cardiovasc Imaging 2014; 7:26–36.

This study shows that exercise capacity and not left ventricular outflow tract gradient is able to predict long-term outcomes in asymptomatic HCM patients.

37. Rakowski H, Li Q. Predicting long-term outcomes in asymptomatic or minimally symptomatic patients with HCM: back to basics. JACC Cardiovasc Imaging 2014; 7:37–39.
38. Cecchi F, Olivotto I, Montereggi A, et al. Hypertrophic cardiomyopathy in Tuscany: clinical course and outcome in an unselected regional population. J Am Coll Cardiol 1995; 26:1529–1536.
39. Spirito P, Bellone P, Harris KM, et al. Magnitude of left ventricular hypertrophy and risk of sudden death in hypertrophic cardiomyopathy. N Engl J Med 2000; 342:1778–1785.
40. Elliott PM, Gimeno JR, Tome MT, et al. Left ventricular outflow tract obstruction and sudden death risk in patients with hypertrophic cardiomyopathy. Eur Heart J 2006; 27:1933–1941.
41. Gersh BJ, Maron BJ, Bonow RO, et al. 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. J Am Coll Cardiol 2011; 58:e212–e260.
42▪▪. O’Mahony C, Jichi F, Pavlou M, et al. A novel clinical risk prediction model for sudden cardiac death in hypertrophic cardiomyopathy (HCM risk-SCD). Eur Heart J 2014; 35:2010–2020.

A large multicentre, retrospective, longitudinal cohort study that developed and validated a new SCD risk prediction model.

43. Cannon RO, McIntosh CL, Schenke WH, et al. Effect of surgical reduction of left ventricular outflow obstruction on hemodynamics, coronary flow, and myocardial metabolism in hypertrophic cardiomyopathy. Circulation 1989; 79:766–775.
44. Diodati J, Schenke W, Waclawiw MA, et al. Predictors of exercise benefit after operative relief of left ventricular outflow obstruction by the myotomy-myectomy procedure in hypertrophic cardiomyopathy. Am J Cardiol 1992; 69:1617–1622.
45. Agarwal S, Tuzcu EM, Desai MY, et al. Updated meta-analysis of septal alcohol ablation versus myectomy for hypertrophic cardiomyopathy. J Am Coll Cardiol 2010; 55:823–834.
46. Alam M, Dokainish H, Lakkis NM. Hypertrophic obstructive cardiomyopathy alcohol septal ablation vs. myectomy: a meta-analysis. Eur Heart J 2009; 30:1080–1087.
47. Zeng Z, Wang F, Dou X, et al. Comparison of percutaneous transluminal septal myocardial ablation versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy: a meta-analysis. Int J Cardiol 2006; 112:80–84.
48. Maron BJ, Ommen SR, Semsarian C, et al. Hypertrophic cardiomyopathy: present and future, with translation into contemporary cardiovascular medicine. J Am Coll Cardiol 2014; 64:83–99.
49▪. Vriesendorp PA, Liebregts M, Steggerda RC, et al. Long-term outcomes after medical and invasive treatment in patients with hypertrophic cardiomyopathy. JACC Heart Fail 2014; 2:630–636.

A long-term follow-up study showing that survival after both medical and invasive treatment in obstructive HCM is similar to that in patients with nonobstructive HCM. The annual rate of SCD was higher after SAA than after myectomy.

50. Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intraprocedural myocardial contrast echocardiography. Circulation 1998; 98:2415–2421.
51. Nagueh SF, Lakkis NM, He ZX, et al. Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1998; 32:225–229.
52. Faber L, Seggewiss H, Welge D, et al. Echo-guided percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: 7 years of experience. Eur J Echocardiogr 2004; 5:347–355.
53. Wallace EL, Thompson JJ, Faulkner MW, et al. Septal perforator anatomy and variability of perfusion bed by myocardial contrast echocardiography: a study of hypertrophic cardiomyopathy patients undergoing alcohol septal ablation. J Interv Cardiol 2013; 26:604–612.

dynamic obstruction; echocardiography; hypertrophic cardiomyopathy

Supplemental Digital Content

Back to Top | Article Outline
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.