Major Trypanosoma cruzi antigenic determinant in Chagas' heart disease shares homology with the systemic lupus erythematosus ribosomal P protein epitope.
Several recent reports have examined whether there is a correlation between the presence of some minor alleles of the highly polymorphic apolipoprotein B gene and atherosclerosis and premature heart disease.
The coexistence of these major malformations with heart disease raises the possibility of incomplete expression of the VA(C)TER (vertebral, anal, cardiac, tracheal, esophageal renal) association.
Coordinate HNF-4-mediated regulation of several blood protease genes as well as genes involved in lipid metabolism might account for the positive correlation of these factors with increased risk of occlusive heart diseases.
Cardiac MyBP-C is therefore specifically equipped with sensors for adrenergic regulation of cardiac contraction, possibly implicating cardiac MyBP-C in cardiac disease.
In contrast, the gene with the nonsense mutation would encode for a cardiac beta-MHC protein of only 53 amino acid residues, which may be too short to be incorporated into the thick filament assembly of cardiac myosin chains and showed no dominant phenotype of heart disease.
These findings may reflect a broad personality trait, i.e., generalized lack of self-control, which could underlie much CHD risk not associated with a family history of heart disease.
Initially, a prospective analysis of factor VII antigen and prothrombin activity was performed in two groups of young subjects without symptoms who differed in their risk of ischemic heart disease based on a history (or lack thereof) of premature heart disease in a first-degree relative.
Capillary electrophoresis (CE) in entangled polymer solution was applied to the analysis of polymerase chain reaction (PCR) amplified apoB VNTR locus for DNA diagnosis of heart disease.
In this study of 104 Chinese patients with end-stage heart failure due to idiopathic dilated or ischemic cardiomyopathy, the DD genotype frequency was low (12% and 11%, respectively) and was not seen more often than in a control group of 183 subjects without cardiac disease (13%).
Our data indicate that this TTR variant is present at equal frequency in African-Americans throughout the U.S., and suggest that this mutation may be a common, often unrecognized cause of cardiac disease in African-Americans.
The previously described relationship between heart disease and the ACE-gene polymorphism in diabetes could thus be founded in an increased extent of atherosclerosis among patients with the ID- and DD-ACE-gene subtypes.
By using a method based on activated partial thromboplastin time, with DNA technique derived from the polymerase chain reaction, we investigated nine children with underlying cardiac disease in whom thromboembolism had previously occurred.
We conclude that, within the limits of presently available techniques, myoglobin mutations are unlikely to contribute substantially to the genotypic background of cardiac disease in the general population.