Prognosis and Mortality of Hypertrophic Obstructive Cardiomyopathy

Harðarson, Þórður; Curiel, R; Calzada, Carlos Sáenz de la; Goodwin, J. F.

doi:10.1016/s0140-6736(73)92730-x

Cited by 185 publications

(44 citation statements)

References 22 publications

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“…AF and left atrial size AF and left atrial size may indirectly reflect the risk of SCD, as they may both relate to atrial remodeling secondary to increasing ventricular fibrosis which, in turn, makes the myocardium more susceptible to arrhythmias. 84 Hardarson et al 85 was the first to report the association with SCD. The effect of paroxysmal, persistent, or chronic AF as a predictor of SCD was examined in 5 studies using survival analysis.…”

Section: Syncopementioning

confidence: 99%

“…72,85,86 Despite these early observations, the effect of age on the risk of SCD has been investigated only in a limited number of more recent survival studies. 42,52,53,59 Only the largest study by Spirito et al 42 found a significant reduction in SCD risk with increasing age.…”

Section: Agementioning

confidence: 99%

“…56 There is conflicting data about a sex difference in the prevalence of LVOTO, 39,58,59 severity of LVH, 41,43,81 and incidence of SCD. 7,85 None of the 3 studies which used survival analysis showed a significant association between sex and SCD. 52,58,59 11.…”

Section: Sexmentioning

confidence: 99%

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Sudden Cardiac Death in Hypertrophic Cardiomyopathy

O’Mahony

Elliott

McKenna

2013

Circ: Arrhythmia and Electrophysiology

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SCD in HCM has been linked with physical exertion. 33 A vicious cycle of increasing myocardial ischemia, caused by diastolic dysfunction, LVOTO, systemic hypotension, and decreased stroke volume, has been suggested, but SCD can occur at rest or sleep, 33 when metabolic demands are low. The exact triggers of ventricular arrhythmias remain unclear. Risk Factors of SCD in HCMVarious phenotypic characteristics have been linked with SCD and are currently used to identify patients at risk. 34,35 These risk factors were first noted in small, comparative observational studies, and then re-examined in larger studies with multivariable survival analysis using the Cox proportional

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Section: Syncopementioning

confidence: 99%

Section: Agementioning

confidence: 99%

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Sudden Cardiac Death in Hypertrophic Cardiomyopathy

O’Mahony

Elliott

McKenna

2013

Circ: Arrhythmia and Electrophysiology

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“…'-3 A double blind trial of practolol, propranolel, and a placebo has suggested that beta blockade was associated with amelioration or disappearance of dyspnoea, anginal pain, and syncope in severely symptomatic patients4 but unfortunately beta adrenergic blockade cannot be guaranteed to prevent sudden death.5 6 Hypertrophic cardiomyopathy is a disease characterised by massive hypertrophy and impaired distensibility of the left ventricle which leads to abnormal Accepted for publication 25 March 1982 diastolic filling with a small systolic cavity and a very stiff ventricle. [7][8][9] We believe that this abnormal diastolic filling is the most important factor in determining symptoms and prognosis regardless of whether a gradient between the outflow tract of the left ventricle and aorta is present or not.…”

mentioning

confidence: 99%

Non-invasive assessment of diastolic function in hypertrophic cardiomyopathy on and off beta adrenergic blocking drugs.

Alvares¹,

Goodwin²

1982

Heart

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SUMMARY Beta adrenergic blocking drugs in hypertrophic cardiomyopathy provide symptomatic relief but their effect on long-term prognosis is uncertain.Thirty patients were studied non-invasively by simultaneous recordings of echocardiogram, apexcardiogram, phonocardiogram, and electrocardiogram in order to assess diastolic abnormalities on and off oral beta adrenergic blocking drugs. While on treatment these patients had a mean dose of propranolol 200 mg/day. The treatment was stopped for one week and then non-invasive assessment was repeated.The following diastolic time intervals were studied: isovolumic relaxation period (A2-mitral valve opening); rapid relaxation period (A2-O point of the apexcardiogram), and the period from mitral valve opening to the 0 point of the apexcardiogram (Mo-0) when most of the filling of the left ventricle occurs. The prolongation of the rapid relaxation period reflects a reduced rate of fall of the left ventricular pressure when the pressure differential does not change between A2 and the 0 point of the apexcardiogram, and in this study this period was prolonged in 19, shortened in eight, and remained the same in three patients after beta blockade. The Mo-O point was prolonged in 22, shortened in seven, and was unchanged in one patient after beta adrenergic blocking drugs. All these results were independent of heart rate.In conclusion the response of diastolic time intervals to beta blocking drugs in hypertrophic cardiomyopathy was variable but there was a significant number of patients in whom the time available for filling of the left ventricle was prolonged, suggesting better filling possibly because of improved distensibility of the left ventricle after beta adrenergic blocking drugs.

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“…4 The mortality rates in early studies were as high as 5-7 % per year. 5,6 With the advent of ICDs and early detection of the disease, modern cohorts have mortality rates of under 1 %. 7,8 SCD due to sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) is still the most common cause of mortality, however, accounting for 51 % of all HCM-related deaths.…”

Section: Epidemiology Of Hypertrophic Cardiomyopathy and Sudden Cardimentioning

confidence: 99%

ICD Therapy for Primary Prevention in Hypertrophic Cardiomyopathy

Trivedi

Knight

2016

Arrhythmia &Amp; Electrophysiology Review

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HCM is a heterogeneous disease that is classically transmitted in an autosomal dominant fashion. HCM often arises from mutations in genes responsible for the formation of cardiac sarcomeres.Sarcomeric mutations, initially discovered in the 1980s, are found in up to 70 % of patients with a family history of HCM.11 The most common mutations are in the myosin heavy chain (MYH7 gene) and myosin binding protein C (MYBPC3 gene). 12 There is marked heterogeneity in penetrance, however, and a poor understanding of how the different genotypes manifest as HCM phenotypes. Currently, there is minimal evidence to support the use of genetic testing to identify patients who are at high risk of SCD. Small studies have found that patients with a more malignant inheritance of their mutations (i.e. homozygous mutations) as well as the presence of a MYH7 gene mutation have AbstractHypertrophic cardiomyopathy (HCM) is a common and heterogeneous disorder that increases an individual's risk of sudden cardiac death (SCD). This review article discusses the relevant factors that are involved in the challenge of preventing SCD in patients with HCM.The epidemiology of SCD in patients is reviewed as well as the structural and genetic basis behind ventricular arrhythmias in HCM. The primary prevention of SCD with implantable cardioverter-defibrillator (ICD) therapy is the cornerstone of modern treatment for individuals at high risk of SCD. The focus here is on the current and emerging predictors of SCD as well as risk stratification recommendations from both North American and European guidelines. Issues related to ICD implantation, such as programming, complications and inappropriate therapies, are discussed. The emerging role of the fully subcutaneous ICD and the data regarding its implantation are reviewed. KeywordsHypertrophic cardiomyopathy, sudden cardiac death, implantable cardioverter defibrillator, subcutaneous implantable cardioverter-defibrillator Disclosure: Dr Trivedi has no conflicts of interest to declare. Dr Knight has been a consultant to manufacturers of implantable defibrillators and participated in clinical trials sponsored

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Prognosis and Mortality of Hypertrophic Obstructive Cardiomyopathy

Cited by 185 publications

References 22 publications

Sudden Cardiac Death in Hypertrophic Cardiomyopathy

Sudden Cardiac Death in Hypertrophic Cardiomyopathy

Non-invasive assessment of diastolic function in hypertrophic cardiomyopathy on and off beta adrenergic blocking drugs.

ICD Therapy for Primary Prevention in Hypertrophic Cardiomyopathy

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