الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
1. INTRODUCTION
Rheumatic heart disease (RHD) remains a significant cause of cardiovascular morbidity and mortality. It represents a medical and public health burden which requires a solution.(1) RHD prevalence is of at least 15.6 million cases, the estimated new cases are 282,000 and 233,000 deaths each year in 2005.(2)
RHD remains an important cause of morbidity and mortality in young adults in developing countries due to the restricted access to health. Also, RHD imposes an important burden on health care systems in poor nations.(3)
RHD is mostly preceded by rheumatic fever (RF) episodes. Despite that RF is not considered as a communicable disease, it results from streptococcal pharyngitis which is communicable and often leads to RHD.(4) In addition, the high familial incidence of RF suggests that genetic factors may be involved.(5) Preventive use of Penicillins and other antibiotics was not highly successful in eradication of RF necessitating more laboratory, epidemiological and clinical researches should be undertaken.(6)
Over the past decade the role of genetic factors in the development of cardiovascular diseases attracted much attention.(7) The angiotensin-converting enzyme (ACE) gene is considered one of the top candidates in genetic epidemiological studies of cardiovascular diseases. Insertion/deletion polymorphism of the ACE gene was investigated in several cardiovascular diseases.
Earlier studies reported that the ACE-D/D genotype might be related to increased local cardiac ACE activity and a higher ACE serum level, and might be implicated in the pathogenesis of cardiovascular abnormalities.(8) Others demonstrated that ACE-I/I genotype might be associated with higher susceptibility to different cardiovascular diseases.(9) ACE activities showed extensive inter individual variability and inter-ethnic variations.(10)
As ACE has an important impact on cardiovascular structure and function, its genetic polymorphism may be correlated with the pathogenesis of RHD. However, till dates few studies investigated this relationship/10,11’12,1 ) Most of these reports showed inter-ethnic variations in the frequency of allelic forms of the ACE genes. Results of these previous studies clearly demonstrated a controversy in the association of the pathogenesis of RHD and its prognosis in regards to ACE polymorphism. In this context, the present study presents a novel attempt to investigate the relationship between polymorphism I/D in angiotensin converting enzyme and susceptibility to Rheumatic heart disease (RHD) in a sample of Egyptian adults chronic patients through a case -control study.