Persisting Effect of Ca2+-Channel Blockers on Left Ventricular Function in Hypertrophic Cardiomyopathy After 14 Years' Treatment

Hartmann, Andreas; Schnell, Joachim; Hopf, R.; Kneissl, Georg Dieter

doi:10.1177/000331979604700803

Cited by 7 publications

(3 citation statements)

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“…These agents reduce contractility and improve lusitropy, a combination that is generally favorable for this disease. Sustained improvement in diastolic relaxation is generally noted in response to verapamil administration due to improved relaxation and secondary reduction in diastolic pressure and mean left atrial pressure [26,27]. Improved distribution of subendocardial flow and diminished inducible ischemia have been noted as well [28].…”

Section: Calcium Channel Blockersmentioning

confidence: 98%

Treatment of hypertrophic cardiomyopathy in childhood

Colan

2011

Progress in Pediatric Cardiology

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Section: Calcium Channel Blockersmentioning

confidence: 98%

Treatment of hypertrophic cardiomyopathy in childhood

Colan

2011

Progress in Pediatric Cardiology

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“…Sustained improvement in diastolic relaxation is generally noted in response to verapamil administration with secondary reduction in diastolic pressure and mean left atrial pressure 31;32, resulting in a reduction in dyspnea and increase in exercise capacity. Improved distribution of subendocardial flow and diminished inducible ischemia have been noted as well 33.…”

Section: Familial Hypertrophic Cardiomyopathymentioning

confidence: 99%

Hypertrophic Cardiomyopathy in Childhood

Colan

2010

Heart Failure Clinics

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Keywordscardiomyopathy; hypertrophic cardiomyopathy; sudden death; pediatrics; children; infants Hypertrophic cardiomyopathy (HCM) is defined as the presence of a hypertrophied, nondilated ventricle in the absence of another disease that creates a hemodynamic disturbance that is capable of producing the existent magnitude of wall thickening (eg, hypertension, aortic valve stenosis, catecholamine secreting tumors, hyperthyroidism, etc). HCM accounts for 42% of childhood cardiomyopathy and has an incidence of 0.47/100,000 children 1 and represents a heterogeneous group of disorders with a diversity that is more apparent in childhood than at any other age. It is possible to further subdivide these diseases based on a number of characteristics. A classification is presented in List 1 based on groupings of familial, syndromic, neuromuscular, and metabolic (storage disease and mitochondrial disorders). Other classification schemes are commonly used, including division into primary and secondary forms, where the primary form is a familial disorder ("familial hypertrophic cardiomyopathy", FHC) typically devoid of findings outside of the heart, and the secondary forms include diseases such as Friedreich ataxia 2 where ventricular hypertrophy is common but is not the dominant clinical manifestation and others, such as glycogenosis Type IX 3 , in which a systemic disorder has primarily or exclusively cardiac manifestations.Most of the available information for HCM derives from studies in adult populations, and the implication of these observations for pediatric populations is often uncertain. The purpose of this review is not to attempt to review the vast body of literature that has accumulated about HCM but rather to summarize key findings and to discuss their implications for diagnosis and management of children with HCM. Epidemiology and SurvivalThe Pediatric Cardiomyopathy Registry is a multicenter observational study of pediatric cardiomyopathies initiated in 1995 that in 2003 reported the sex, age, and race-specific incidence of the several forms of cardiomyopathy based on 2 geographically diverse sections of the United States 1 . Of note, the incidence of HCM was found to be 69% more common in males, occurred at 10 times the rate in subjects under age 1, and was significantly more common in blacks than in whites or Hispanics. Subsequently, the distribution of etiologies and the etiology-specific survival in 849 children, the largest series to date, was reported 4 . Overall, Corresponding author for proof and reprints: Steven D. Colan, M.D., Department of Cardiology, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, (617) 355-7893, (617) 739-6282 (fax), colan@alum.mit.edu (email). Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable fo...

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“…Hartmann et al. found that calcium channel blockers effects on diastolic filling persisted after long‐term treatment in HCM 25 . Yamagishi et al.…”

Section: Discussionmentioning

confidence: 99%