How will the human genome project change cardiovascular medicine?

Heart

Volumn 86, Issue 2, 2001, Pages 123-124

  Komajda, M ^a   Charron, P ^a  

^a PITIÉ SALPÊTRIÈRE HOSPITAL   (France)

Author keywords

[No Author keywords available]

Indexed keywords

ALTEPLASE; ETANERCEPT; ORAL CONTRACEPTIVE AGENT; SODIUM CHANNEL BLOCKING AGENT;

CARDIOVASCULAR DISEASE; DNA SEQUENCE; EDITORIAL; GENE THERAPY; GENETIC RISK; GENETIC VARIABILITY; GENOTYPE; HUMAN; HYPERTROPHIC CARDIOMYOPATHY; MEDICAL GENETICS; PHARMACOGENETICS; PHENOTYPE; PHYSIOLOGY; PREDICTION; PRIORITY JOURNAL;

EID: 0034776348     PISSN: 13556037     EISSN: None     Source Type: Journal    
DOI: 10.1136/heart.86.2.123     Document Type: Editorial

References (12)

1. Initial sequencing and analysis of the human genome
2. Myocardial diseases
3. A map of the human genome sequence variation containing 1.42 million single nucleotide polymorphisms
4. Clinical features and prognostic implications of familial hypertrophic cardiomyopathy related to the cardiac myosin binding protein C gene
5. Diagnostic value of electrocardiography and echocardiography for familial hypertrophic cardiomyopathy in a genotyped adult population
6. Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate: Implications for gene-specific therapy
7. High risk of cerebral-vein thrombosis in carriers of a prothrombin-gene mutation and in users of oral contraceptives
8. ACE gene polymorphism: Ischaemic heart disease and longevity in 10150 individuals. A case referent and retrospective cohort study based on the Copenhagen city heart study
9. The influence of the angiotensin-I converting enzyme genotype in familial hypertrophic cardiomyopathy varies with the disease gene mutation
10. Mutations in the gene encoding lamin A/C cause autosomic dominant Emery Dreyfuss muscular dystrophy
11. LMNA, encoding lamin A/C, is mutated in partial lipodystrophy
12. Familial hypertrophic cardiomyopathy: From mutations to functional defects