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Percutaneous Septal Ablation in Hypertrophic Obstructive Cardiomyopathy: From Experiment to Standard of Care.

Faber L - Adv Med (2014)

Bottom Line: Symptoms include exercise limitation due to dyspnea, angina pectoris, palpitations, or dizziness; occasionally syncope or sudden cardiac death occurs.Correct diagnosis and risk stratification with respect to prophylactic ICD implantation are essential in HCM patient management.Literature data and the own series of about 600 cases are discussed, suggesting a largely comparable outcome with respect to procedural mortality, clinical efficacy, and long-term outcome.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Heart and Diabetes Center North Rhine-Westphalia, University Hospital of the Ruhr University Bochum, Georgstraße 11, 32545 Bad Oeynhausen, Germany.

ABSTRACT
Hypertrophic cardiomyopathy (HCM) is one of the more common hereditary cardiac conditions. According to presence or absence of outflow obstruction at rest or with provocation, a more common (about 60-70%) obstructive type of the disease (HOCM) has to be distinguished from the less common (30-40%) nonobstructive phenotype (HNCM). Symptoms include exercise limitation due to dyspnea, angina pectoris, palpitations, or dizziness; occasionally syncope or sudden cardiac death occurs. Correct diagnosis and risk stratification with respect to prophylactic ICD implantation are essential in HCM patient management. Drug therapy in symptomatic patients can be characterized as treatment of heart failure with preserved ejection fraction (HFpEF) in HNCM, while symptoms and the obstructive gradient in HOCM can be addressed with beta-blockers, disopyramide, or verapamil. After a short overview on etiology, natural history, and diagnostics in hypertrophic cardiomyopathy, this paper reviews the current treatment options for HOCM with a special focus on percutaneous septal ablation. Literature data and the own series of about 600 cases are discussed, suggesting a largely comparable outcome with respect to procedural mortality, clinical efficacy, and long-term outcome.

No MeSH data available.


Related in: MedlinePlus

2D-echocardiographic findings in hypertrophic nonobstructed cardiomyopathy (HNCM, (a)) with predominant thickening of the apical segments and a wide open, unobstructed outflow tract (LVOT) and in hypertrophic obstructive cardiomyopathy (HOCM, (b)) with a protruding subaortic septum making systolic contact with the mitral valve (SAM-phenomenon, arrow). (c) shows simultaneous pressure tracing from the LV and the aorta demonstrating the outflow gradient and the Brockenbrough sign. The corresponding Doppler profiles are shown in (d). The gradient increases from 40 to 140 mm Hg. The typical CW-Doppler flow profile of left ventricular outflow obstruction in HOCM has a late-peaking signal indicating dynamic obstruction involving contracting muscle as opposed to the more symmetrical signal of fixed valvular stenosis. The peak pressure gradient equals 4  × (peak velocity)2. LA: left atrium; RA: right atrium; LV: left ventricle; Ao: aorta; and IVS: interventricular septum.
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fig1: 2D-echocardiographic findings in hypertrophic nonobstructed cardiomyopathy (HNCM, (a)) with predominant thickening of the apical segments and a wide open, unobstructed outflow tract (LVOT) and in hypertrophic obstructive cardiomyopathy (HOCM, (b)) with a protruding subaortic septum making systolic contact with the mitral valve (SAM-phenomenon, arrow). (c) shows simultaneous pressure tracing from the LV and the aorta demonstrating the outflow gradient and the Brockenbrough sign. The corresponding Doppler profiles are shown in (d). The gradient increases from 40 to 140 mm Hg. The typical CW-Doppler flow profile of left ventricular outflow obstruction in HOCM has a late-peaking signal indicating dynamic obstruction involving contracting muscle as opposed to the more symmetrical signal of fixed valvular stenosis. The peak pressure gradient equals 4  × (peak velocity)2. LA: left atrium; RA: right atrium; LV: left ventricle; Ao: aorta; and IVS: interventricular septum.

Mentions: An important distinction in HCM is between the nonobstructive (hypertrophic nonobstructive cardiomyopathy: HNCM) and the obstructive (HOCM) phenotype of the disease (Figure 1). Dependent on the distribution of hypertrophy within the left ventricle, the septal curvature, the size and configuration of the mitral valve, and left ventricular loading conditions, about 60–70% of HCM patients develop a dynamic obstruction between a “high-pressure” and a “low-pressure” compartment of the left ventricle [2–6, 8, 9, 19, 33–35]. Typically this obstruction is located between the subaortic septum and parts of the mitral valve (“SAM” phenomenon: systolic anterior movement) and is associated with mitral regurgitation. SAM-associated mitral regurgitation shows a typical posterolateral jet direction that can be used for differentiation towards primary mitral regurgitation (Figure 2). In a minority of cases outflow obstruction may be located in the midcavity region, in the apex, or occasionally in the right ventricular outflow tract. The hemodynamic significance of obstruction seems to depend on the size of the LV compartment that is working against increased afterload; apical gradients are considered to be less significant. A substantial degree of variability has been described regarding gradient severity, and provocation (by physical exercise, preload reduction, inotropic agents, or postextrasystolic augmentation) is essential to distinguish between HNCM and HOCM both during echocardiographic and invasive hemodynamic studies [6, 8, 19].


Percutaneous Septal Ablation in Hypertrophic Obstructive Cardiomyopathy: From Experiment to Standard of Care.

Faber L - Adv Med (2014)

2D-echocardiographic findings in hypertrophic nonobstructed cardiomyopathy (HNCM, (a)) with predominant thickening of the apical segments and a wide open, unobstructed outflow tract (LVOT) and in hypertrophic obstructive cardiomyopathy (HOCM, (b)) with a protruding subaortic septum making systolic contact with the mitral valve (SAM-phenomenon, arrow). (c) shows simultaneous pressure tracing from the LV and the aorta demonstrating the outflow gradient and the Brockenbrough sign. The corresponding Doppler profiles are shown in (d). The gradient increases from 40 to 140 mm Hg. The typical CW-Doppler flow profile of left ventricular outflow obstruction in HOCM has a late-peaking signal indicating dynamic obstruction involving contracting muscle as opposed to the more symmetrical signal of fixed valvular stenosis. The peak pressure gradient equals 4  × (peak velocity)2. LA: left atrium; RA: right atrium; LV: left ventricle; Ao: aorta; and IVS: interventricular septum.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4590958&req=5

fig1: 2D-echocardiographic findings in hypertrophic nonobstructed cardiomyopathy (HNCM, (a)) with predominant thickening of the apical segments and a wide open, unobstructed outflow tract (LVOT) and in hypertrophic obstructive cardiomyopathy (HOCM, (b)) with a protruding subaortic septum making systolic contact with the mitral valve (SAM-phenomenon, arrow). (c) shows simultaneous pressure tracing from the LV and the aorta demonstrating the outflow gradient and the Brockenbrough sign. The corresponding Doppler profiles are shown in (d). The gradient increases from 40 to 140 mm Hg. The typical CW-Doppler flow profile of left ventricular outflow obstruction in HOCM has a late-peaking signal indicating dynamic obstruction involving contracting muscle as opposed to the more symmetrical signal of fixed valvular stenosis. The peak pressure gradient equals 4  × (peak velocity)2. LA: left atrium; RA: right atrium; LV: left ventricle; Ao: aorta; and IVS: interventricular septum.
Mentions: An important distinction in HCM is between the nonobstructive (hypertrophic nonobstructive cardiomyopathy: HNCM) and the obstructive (HOCM) phenotype of the disease (Figure 1). Dependent on the distribution of hypertrophy within the left ventricle, the septal curvature, the size and configuration of the mitral valve, and left ventricular loading conditions, about 60–70% of HCM patients develop a dynamic obstruction between a “high-pressure” and a “low-pressure” compartment of the left ventricle [2–6, 8, 9, 19, 33–35]. Typically this obstruction is located between the subaortic septum and parts of the mitral valve (“SAM” phenomenon: systolic anterior movement) and is associated with mitral regurgitation. SAM-associated mitral regurgitation shows a typical posterolateral jet direction that can be used for differentiation towards primary mitral regurgitation (Figure 2). In a minority of cases outflow obstruction may be located in the midcavity region, in the apex, or occasionally in the right ventricular outflow tract. The hemodynamic significance of obstruction seems to depend on the size of the LV compartment that is working against increased afterload; apical gradients are considered to be less significant. A substantial degree of variability has been described regarding gradient severity, and provocation (by physical exercise, preload reduction, inotropic agents, or postextrasystolic augmentation) is essential to distinguish between HNCM and HOCM both during echocardiographic and invasive hemodynamic studies [6, 8, 19].

Bottom Line: Symptoms include exercise limitation due to dyspnea, angina pectoris, palpitations, or dizziness; occasionally syncope or sudden cardiac death occurs.Correct diagnosis and risk stratification with respect to prophylactic ICD implantation are essential in HCM patient management.Literature data and the own series of about 600 cases are discussed, suggesting a largely comparable outcome with respect to procedural mortality, clinical efficacy, and long-term outcome.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Heart and Diabetes Center North Rhine-Westphalia, University Hospital of the Ruhr University Bochum, Georgstraße 11, 32545 Bad Oeynhausen, Germany.

ABSTRACT
Hypertrophic cardiomyopathy (HCM) is one of the more common hereditary cardiac conditions. According to presence or absence of outflow obstruction at rest or with provocation, a more common (about 60-70%) obstructive type of the disease (HOCM) has to be distinguished from the less common (30-40%) nonobstructive phenotype (HNCM). Symptoms include exercise limitation due to dyspnea, angina pectoris, palpitations, or dizziness; occasionally syncope or sudden cardiac death occurs. Correct diagnosis and risk stratification with respect to prophylactic ICD implantation are essential in HCM patient management. Drug therapy in symptomatic patients can be characterized as treatment of heart failure with preserved ejection fraction (HFpEF) in HNCM, while symptoms and the obstructive gradient in HOCM can be addressed with beta-blockers, disopyramide, or verapamil. After a short overview on etiology, natural history, and diagnostics in hypertrophic cardiomyopathy, this paper reviews the current treatment options for HOCM with a special focus on percutaneous septal ablation. Literature data and the own series of about 600 cases are discussed, suggesting a largely comparable outcome with respect to procedural mortality, clinical efficacy, and long-term outcome.

No MeSH data available.


Related in: MedlinePlus