Hypertrophic cardiomyopathy.

By M. Burch. 1994

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. D. Corrado
2. A. Pelliccia
3. Min Xie
4. C. Basso
5. Jana S. Burchfield
6. P. Vardas
7. G. Thiene
8. A. Selcuk Adabag

Citations in the corpus

• Pathological Ventricular Remodeling: Mechanisms: Part 1 of 2 (2013, background): “One prominent example in which personalized medicine has emerged to parse these elements is hypertrophic cardiomyopathy (HCM), in which distinct genetic variants have been identified that are informative in predicting phenotype and outcome.(15) Classically, familial HCM is caused by mutations in sar”
• Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases. (2007, background): “Left ventricular hypertrophy in the absence of hypertension and valve disease occurs in approximately 1:500 of the general population.(8,9) Many individuals have familial disease with an autosomal dominant pattern of inheritance caused by mutations in genes that encode different proteins of the card”
• Hypertrophic cardiomyopathy: a systematic review. (2002, background): “whether outflow obstruction is present (Figure 3).(2-8,10,158-162) Patients who do not experience improvement of symptoms with one drug may subsequently benefit from the other, but combined administration is not advantageous.”
• Impact of Atrial Fibrillation on the Clinical Course of Hypertrophic Cardiomyopathy (2001, methodology): “Conclusions—In a community-based HCM population, AF (1) was common, with 22% prevalence over 9 years; (2) was associated with substantial risk for heart failure–related mortality, stroke, and severe functional disability, particularly in patients with outflow obstruction, those 50 years of age, or t”
• Recommendations for interpretation of 12-lead electrocardiogram in the athlete. (2009, background): “On the basis of published series from the USA and Italy, these conditions account for approximately two-thirds of SCD in young competitive athletes.(26,27) Electrocardiogram abnormalities associated with these cardiovascular diseases include repolarization abnormalities such as inverted T-waves and ”
• Epidemiology of hypertrophic cardiomyopathy-related death: revisited in a large non-referral-based patient population. (2000, methodology): “Three modes of death were defined (Figure 1 and Table 1): (1) sudden and unexpected (44 patients, including 11 with aborted cardiac arrest and 3 with appropriate ICD interventions for ventricular tachycardia or fibrillation); (2) resulting from progressive, refractory heart failure (31 patients, inc”
• Occurrence and frequency of arrhythmias in hypertrophic cardiomyopathy in relation to delayed enhancement on cardiovascular magnetic resonance. (2008, background): “hese findings may have implications for the risk stratifiation of HCM patients, because NSVT is generally rearded to be an independent determinant of increased risk f sudden death in this disease (2,3,23,24,30,31).”
• Mutation of junctophilin type 2 associated with hypertrophic cardiomyopathy (2007, background): “HCM is a primary myocardial disorder that results in hypertrophy of the ventricle wall histologically characterized by cardiac myocyte disarray and fibrosis (Elliott and McKenna 2004).”
• Task Force on Sudden Cardiac Death of the European Society of Cardiology. (2001, background): “Cardiac arrest (or sustained VT) Class I B [285–287] Family history of SD Class IIa B [253,256,263,268,274] Syncope* Class IIa B [259260,261,273,274,284] Extreme LVH ( 3 cm max.”