2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy

Abstract

members are required to recuse themselves from voting on sections to which their specific relationships with industry and other entities may apply; see Appendix 1 for detailed information. † ACCF/AHA Representative.

Comparison of Long-Term Outcome between Apical and Asymmetric Septal Hypertrophic Cardiomyopathy

“…The diagnosis of HCM was based on an LV maximal wall thickness of ≥15 mm by two-dimensional echocardiogram in the absence of any other cardiac or systemic disease capable of producing a similar degree of cardiac hypertrophy [15]. The diagnostic criterion for ApHCM was LV hypertrophy confined predominantly to the LV apex (only the apical 4 segments and the apical cap) with a maximal apical wall thickness of ≥15 mm or a ratio of maximal apical to posterior wall thickness of ≥1.5 at the end diastole, regardless of the presence of systemic hypertension [6,15,16].…”

“…The diagnostic criterion for ApHCM was LV hypertrophy confined predominantly to the LV apex (only the apical 4 segments and the apical cap) with a maximal apical wall thickness of ≥15 mm or a ratio of maximal apical to posterior wall thickness of ≥1.5 at the end diastole, regardless of the presence of systemic hypertension [6,15,16]. The definition of ASHCM was based on the presence of a septal wall thickness of ≥15 mm and a septal to free wall thickness ratio of ≥1.3 in the absence of another disease that could justify the magnitude of hypertrophy [8,17,18].…”

“…The primary clinical end points were defined as follows [9,15,21]: (1) SCD, in which death occurred in the absence of or within 1 h from the onset of symptoms in patients who previously showed a relatively stable or uneventful clinical course; (2) heart failure (HF)-related death occurring in patients who had progressive cardiac decompensation ≥1 year before death; (3) stroke-related death that occurred as a consequence of a probable or proven embolic stroke; (4) patients who experienced aborted cardiac arrest or received appropriate discharge through implantable cardioverter defibrillator (ICD) therapy were regarded as surrogate SCD; (5) patients who underwent heart transplantation for drug-refractory HF were recorded as surrogate HF-related death. Cardiovascular morbidity included the following [15]: atrial fibrillation; nonsustained ventricular tachycardia (NSVT), which was defined as a minimum of three premature ventricular contractions lasting up to 30 s and was documented by 24-hour Holter monitoring; myocardial infarction; embolic stroke (ES) or transient ischemic attack (TIA), or progressive HF with an increase of at least one New York Heart Association (NYHA) functional class.…”

Decision-Making of Patients With Implantable Cardioverter-Defibrillators at End of Life: Family Members’ Experiences

“…Secondary prevention is for those who survived SCD. 4,5 When HF progresses to end-stage disease, the frequency of arrhythmias and number of shocks from ICD may increase. The result would be that these patients with advance HF consider not only the decision of end-of-life (EOL) treatment but also the maintaining of defibrillator function in the ''life-saving'' ICD devices.…”

Clinical Outcomes of Myocardial Bridging versus No Myocardial Bridging in Patients with Apical Hypertrophic Cardiomyopathy

“…Follow-up started at the time of admission, and was performed via subsequent clinic visits and telephone calls. The primary clinical end points were cardiovascular (CV) mortality [18]: (1) SCD (unexpected within 1 h of witnessed collapse or nocturnal in previously stable patients); (2) HF-related death occurring in patients who had progressive cardiac decompensation ≥1 year before death; (3) stroke-related death that occurred as a consequence of a probable or proven embolic stroke (ES); (4) aborted cardiac arrest or appropriate discharge of an implantable cardioverter defibrillator (ICD) for ventricular fibrillation; (5) heart transplantation for drug-refractory HF (these patients were recorded as surrogate HF-related deaths). The secondary end points were CV-related morbidity [19]: unexplained syncope; nonsustained ventricular tachycardia (VT), i.e., <30 consecutive ventricular beats; atrial fibrillation; myocardial infarction; mural thrombus; ES, transient ischemic attack, or progressive HF with an increase of at least 1 NYHA functional class.…”