Reduction in the intensity of follow-up during adulthood is reasonable. 1), with recent investigations suggesting even greater prevalence . The implantation of a pacemaker, a procedure that has a 30% success rate Regular clinical evaluation with specific investigations enables initiation of targeted therapies to reduce morbidity and mortality. All rights reserved. There is a small subset (up to 5%) who may progress to the so-called burnt out phase of hypertrophic cardiomyopathy with ventricular wall thinning, systolic and diastolic left ventricular failure, and heart failure requiring heart transplantation.28 Although there is considerable overlap among these phenotypes, patients generally fall predominantly into one category or another. Note: ECG = electrocardiogram, LVOT = left ventricular outflow tract. We do not capture any email address. Surgical myectomy is the primary therapy for patients who are young or fail medical management. 2019; 140(21):1706-16. https://www.alltrails.com/trail/canada/alberta/crescent-falls For example, cardiac MRI may identify noncontiguous regions of hypertrophy that are difficult to appreciate on echocardiography, and may be useful in identifying infiltrative processes, as well as scar tissue.25, Treatment depends on disease expression, which can differ greatly among individuals, even within a single family. Background — Hypertrophic cardiomyopathy (HCM) is considered a leading cause of sudden cardiac death (SCD) in younger people. These studies guide expert opinion and, in many cases, are the result of careful clinical observation of specialty care offered at select high-volume centres. However, the skew of prevalence of phenotypes is mild, making the use of this term misguided.7–9 Hypertrophic cardiomyopathy has been most extensively studied in white populations with associated genetic subtypes best appreciated in this population. Weather. We’re committed to keeping clients and staff safe during COVID-19 with NEW admittance and check-out processes. Some people with hypertrophic cardiomyopathy may not have symptoms and will have normal lifespan. Intense exertion may bring on ventricular arrhythmias and SCD. Hypertrophic Cardiomyopathy. For information about this, please see Appendix 5 (available at www.cmaj.ca/lookup/suppl/doi:10.1503/cmaj.120138/-/DC1). Men and women have the condition at the same frequency. Sudden deaths with a prior clinical diagnosis of HCM but no autopsy were considered probable HCM-related SCDs. Appendix. Cardiomyopathy can lead to heart failure.The main types of cardiomyopathy include dilated, hypertrophic and restrictive cardiomyopathy. Learn more. Our mission: To reduce the burden of cardiovascular disease. Hypertrophic cardiomyopathy (HCM) is a condition of heart muscle disease in which the muscle is thickened (hypertrophic). The selection of patients for placement of an implantable defibrillator, the method of septal reduction therapy, and the yield and utility of genetic testing remain areas of debate. An electrocardiogram (ECG), echocardiogram and cardiac magnetic resonance imaging (MRI) from a patient with hypertrophic cardiomyopathy are shown in Appendix 1 (available at www.cmaj.ca/lookup/suppl/doi:10.1503/cmaj.120138/-/DC1). It is occasionally restricted to other myocardial regions, such as the apex, the midportion, and the posterior wall of the left ventricle… We considered articles to be relevant if they addressed clinical aspects of diagnosis, assessment or treatment. Prospective randomized controlled trials are largely absent from the literature on hypertrophic cardiomyopathy. This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems.. People who have HCM may have a range of symptoms. This leads to stiffening of the walls of the heart and abnormal aortic and mitral heart valve function, both of … Diagnosis and management of valve disease in patients with hypertrophic cardiomyopathy Aortic valve disease; Mitral valve disease; Endocarditis prophylaxis; Living with cardiomyopathy: advice to patients. Simple, astute, clinical observation of the relation between genotype and phenotype within families is of great importance. In HCM, septal or wall measurements may be in the range of 1.3cm to 6.0+cm anywhere in the left ventricle. Background — Hypertrophic cardiomyopathy (HCM) is considered a leading cause of sudden cardiac death (SCD) in younger people. Confirmation of HCM was based on typical macroscopic and microscopic features (definite HCM-related SCD). International guidelines recommend that patients with HCM avoid competitive sports and strenuous physical effort. Hypertrophic cardiomyopathy (HCM) is a condition in which your heart muscle, or myocardium, becomes thicker than normal. Distribution of hypertrophy can be variable. Most SCDs occurred during rest (64.8%) or light activity (18.5%). Although the presence of such diverse phenotypes in the general population can make the identification of classic hypertrophic cardiomyopathy difficult, genetic testing can help to differentiate this disease from other subtypes of pathologic ventricular hypertrophy. Echocardiographic and ultrasono-cardiotomographic study, The prevalence, distribution, and clinical outcomes of electrocardiographic repolarization patterns in male athletes of african/afro-caribbean origin, Compound and double mutations in patients with hypertrophic cardiomyopathy: implications for genetic testing and counselling, Still a kid at heart: hypertrophic cardiomyopathy in the elderly, American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy, Phenotypic spectrum and patterns of left ventricular hypertrophy in hypertrophic cardiomyopathy: morphologic observations and significance as assessed by two-dimensional echocardiography in 600 patients, Prevalence, clinical significance, and genetic basis of hypertrophic cardiomyopathy with restrictive phenotype, Clinical challenges of genotype positive (+)–phenotype negative (−) family members in hypertrophic cardiomyopathy, Recommendations for competitive sports participation in athletes with cardiovascular disease: a consensus document from the Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of The European Society of Cardiology, The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes, Ethnic differences in left ventricular remodeling in highly-trained athletes relevance to differentiating physiologic left ventricular hypertrophy from hypertrophic cardiomyopathy, Cardiovascular manifestations of Fabry disease: relationships between left ventricular hypertrophy, disease severity, and alpha-galactosidase A activity, Cardiac involvement in Friedreich’s ataxia: a clinical study of 75 patients, Noonan syndrome: clinical features, diagnosis, and management guidelines, Constitutively active amp kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy, Enzyme replacement therapy with agalsidase alfa in patients with Fabry’s disease: an analysis of registry data, The emerging role of cardiovascular magnetic resonance in refining the diagnosis of hypertrophic cardiomyopathy, Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy, Hypertrophic cardiomyopathy is predominantly a disease of left ventricular out-Tow tract obstruction, Pharmacological treatment options for hypertrophic cardiomyopathy: high time for evidence, ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy, Long-term survival in patients with resting obstructive hypertrophic cardiomyopathy, Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects, Amelioration of angina pectoris in idiopathic hypertrophic subaortic stenosis with beta-adrenergic blockade, Long-term follow-up of patients undergoing myotomy/myectomy for obstructive hypertrophic cardiomyopathy, Surgery insight: septal myectomy for obstructive hypertrophic cardiomyopathy — the Mayo Clinic experience, Relation between severity of left-ventricular hypertrophy and prognosis in patients with hypertrophic cardiomyopathy, Sudden death in hypertrophic cardiomyopathy: identification of high risk patients, Verapamil: its potential for causing serious complications in patients with hypertrophic cardiomyopathy, Follow-up of alcohol septal ablation for symptomatic hypertrophic obstructive cardiomyopathy the Baylor and Medical University of South Carolina experience 1996 to 2007, Sudden cardiac death prediction and prevention: report from a national heart, lung, and blood institute and heart rhythm society workshop, Effects of beta adrenergic blockade on the circulation with particular reference to observations in patients with hypertrophic subaortic stenosis, Sustained improvement in left ventricular diastolic function after alcohol septal ablation for hypertrophic obstructive cardiomyopathy, Pacing in hypertrophic obstructive cardiomyopathy, Survival after transcoronary ablation of septal hypertrophy in hypertrophic obstructive cardiomyopathy (TASH): a 10 year experience, Long-term outcomes in high-risk symptomatic patients with hypertrophic cardiomyopathy undergoing alcohol septal ablation, Long term results of septal myectomy in the treatment of obstructive hypertrophic cardiomyopathy, Long-term follow-up of the first patients to undergo transcatheter alcohol septal ablation, Epidemiology of hypertrophic cardiomyopathy-related death: revisited in a large non-referral-based patient population, Assessment of permanent dual-chamber pacing as a treatment for drug-refractory symptomatic patients with obstructive hypertrophic cardiomyopathy. Development of new therapies to address these goals based on knowledge of the genetic basis of hypertrophic cardiomyopathy has been disappointing. When the ventricles are thick or stiff, your heart cannot fill with enough blood. Given the frequency of hypertrophic cardiomyopathy and the development of additional diagnostic and prognostic strategies, practitioners require a reasonable evidence-based approach to diagnose, assess and treat this disease. HCM is a disease state characterised by unexplained, marked and asymmetric left ventricular (LV) hypertrophy associated with non dilated ventricular chambers in the absence of another cardiac or systemic disease capable of producing the magnitude of hypertrophy evident in a given patient (2). About the ESC. However, when the regurgitant jet is closely related to systolic anterior motion of the mitral valve (posteriorly directed in association with normal valve structure and major left ventricular outflow tract gradient), either method of septal reduction should alleviate the mitral regurgitation.80. The heart muscle in abnormally thickened or hypertrophied. Guidelines for diagnostic evaluation take into account the above issues when recommending yearly follow-up for at-risk individuals during adolescence. For clinical practitioners, the major factors to be considered are operator and centre experience. Epub 2019 Oct 21. Thank you for your interest in spreading the word on CMAJ. Some patients with hypertrophic cardiomyopathy and atrial fibrillation will tolerate permanent atrial fibrillation with rate control; however, some have reduced exertional capacity with atrial arrhythmias. The figure in Appendix 4 provides a list of potential determinants that may lead to favouring one type of procedure over another.37 The overall focus should be to present the best option to the individual patient. While a combination of ECG and echocardiography is more readily available and serves as adequate testing for the diagnosis of hypertrophic cardiomyopathy in most cases, cardiac MRI can provide additional information that can be quite useful. The same diagnostic advances are poised to contribute meaningfully to risk stratification (e.g., likelihood of sudden cardiac death). Brackets indicate third-line therapy with, at best, borderline evidence to support their use. Incomplete disease expression is common (> 30% of mutation carriers) and lesser degrees of left ventricular hypertrophy are often seen, sometimes in association with other echocardiographic features of the disease, including reduced left ventricular cavity dimensions, hyperdynamic indices of systolic function, abnormalities of papillary muscles and mitral valve anatomy, and abnormal indices of diastolic function with atrial enlargement.14,15. Cases with typical features but no myofiber disarray were considered possible HCM. Evidence in this area comes from highly varied sources, including relatively large populations in retrospective cohort and population studies, as well as family-focused observational analyses (Box 1). Hypertrophic cardiomyopathy is a common inherited cardiomyopathy, occurring in about 1 in 500 individuals.1 The first gene mutation for this condition was identified in a large French Canadian family cohort in 1989.2 Clinical presentation typically includes left ventricular hypertrophy in the absence of abnormal loading conditions, such as hypertension or aortic stenosis. Sudden cardiac death remains the most visible outcome of hypertrophic cardiomyopathy, occurring in young, otherwise healthy individuals.48 Reasonably well-defined clinical risk factors for sudden cardiac death allow clinicians to target implantable cardioverter defibrillator therapy to those who are at the highest risk.37 Not all risk factors predict this outcome equally, and placement of this type of device in young patients is associated with an important lifetime risk of complications.52 As is the case for other forms of heart disease, a personal history of cardiac arrest or sustained ventricular arrhythmia is the most powerful risk factor; massive (> 3 cm) septal hypertrophy is one of the weakest predictors.36 Family history of sudden cardiac death is an important risk factor, particularly if there are multiple affected individuals in the same family.82,83 The presence of multiple risk factors in an individual strengthens the case for an implantable defibrillator.82,83, Discussion of the risk of sudden cardiac death versus potential adverse effects of implanting a defibrillator is complex, particularly for adolescents and young adults. The parts of the heart most commonly affected are the interventricular septum and the ventricles. Echocardiographic analysis of 4111 subjects in the cardia study. Hypertrophic cardiomyopathy (HCM) is associated with thickening of the heart muscle, most commonly at the septum between the ventricles, below the aortic valve. HCM is a common genetic cardiovascular disease with the overall prevalence estimated between 0.05-0.2% of the population (1). When cardiomyopathy develops as a way to compensate for some other underlying disease, like hypertension or valve diseases, it’s called secondary cardiomyopathy; when it develops all by itself, it’s called primary cardiomyopathy. All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association or its subsidiaries. In some cases, the condition may develop into dilated cardiomyopathy. However, in a small number of people wi… Clinical screening of first-degree relatives and other family members should be encouraged if a DNA diagnosis cannot be established or is not feasible, including: Annual clinical screening is recommended in these individuals from 12 to 18 years of age. Genetic diagnoses may be obtained for most affected patients, allowing cascade screening of family members and subsequent release of those with a negative genotype from clinical follow-up. While the media often highlight these tragic deaths, sudden death is rare. A randomized, double-blind, crossover study (M-PATHY), Dual-chamber pacing for hypertrophic cardiomyopathy: a randomized, double-blind, crossover trial, Ventricular arrhythmia following alcohol septal ablation for obstructive hypertrophic cardiomyopathy, The long-term survival and the risks and benefits of implantable cardioverter defibrillators in patients with hypertrophic cardiomyopathy, Impact of atrial fibrillation on the clinical course of hypertrophic cardiomyopathy. The latter group can be further divided into those who develop outflow tract obstruction and exertional limitations (25% of all affected);26 an additional 25% with provokable outflow tract obstruction;27 those with restrictive physiology and minimal hypertrophy (1%–2%);15 those who have a tendency for ventricular arrhythmias and sudden cardiac death; and the remainder who have hypertrophy without obstruction, but who remain at risk for atrial and ventricular arrhythmias and who may experience exertional limitation because of diastolic dysfunction. Characteristic changes may include left ventricular hypertrophy with repolarization changes, T-wave inversions and abnormal Q waves. Initial treatment is with medication. All of the authors approved the final version submitted for publication. Hypertrophic cardiomyopathy (say "hy-per-TROH-fik kar-dee-oh-my-AWP-uh-thee") happens when the heart muscle grows too thick, so the heart gets bigger and its chambers get smaller. But in some people with this condition: The heart doesn't get enough blood and oxygen, which can cause chest pain. The main feature of hypertrophic cardiomyopathy is an excessive thickening of the heart muscle (hypertrophy literally means to thicken). With current testing, pathogenic mutations will be identified in 60%–70% of patients in 1 of 9 genes encoding the components of the cardiac sarcomere.3 Although identification of a pathogenic sarcomere mutation is helpful, an inability to identify a pathogenic sarcomere gene mutation in a patient who meets the clinical criteria for diagnosis does not negate the diagnosis. The incidence of HCM-related SCD and its relationship to exercise have not been well studied in large comprehensive studies outside of tertiary care settings. The phenotype of hypertrophic cardiomyopathy overlaps with that of normal individuals who are elite athletes18,19 and with that of some black individuals with mild hypertension.10 Additionally, phenocopies of hypertrophic cardiomyopathy (e.g., Fabry disease,20 Friedrich ataxia,21 Noonan syndrome,22 cardiac specific glycogen storage disease23) can closely mimic the classic phenotypes of this disease. Data supporting the use of either a single risk-factor trigger or a multiple risk-factor trigger exist.94,95 Both approaches are subject to risk tolerance, which itself is variable across individuals and cultures. Management of hypertrophic cardiomyopathy. Retrospective cohort data support the use of disopyramide to reduce left ventricular outflow tract gradients and symptoms, with good effect and reasonable safety profile in combination with β-blockers in patients with refractory symptoms (Appendix 3). Diagnosis can be challenging given phenotypic heterogeneity. 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