ANGIOTENSIN-CONVERTING ENZYME GENE POLYMORPHISM AND REVERSIBILITY OF UREMIC LEFT-VENTRICULAR HYPERTROPHY FOLLOWING LONG-TERM ANTIHYPERTENSIVE THERAPY

Background. Prolonged antihypertensive therapy might be less effective in reversing the left ventricular hypertrophy (LVH) in uremics bearin g the deleted (DD) allele of the angiotensin converting enzyme (ACE) g ene than in patients with the inserted (II) allele or in those heteroz ygous (ID) for the gene. Methods. Thirteen DD and 17 II+ID hemodialyze d uremics were followed-up with yearly echocardiography and 24-hour bl ood pressure (BP) monitoring over five years while on an antihypertens ive therapy that included ACE inhibitors as first line drugs. Results. In the II+ID group there were significant decreases of the left ventr icular mass index (LVMi) and of both systolic and diastolic BPs. These changes were less pronounced in the DD group, but the difference was not statistically significant given the wide overlap between the two g roups. Further analysis of the data revealed that the only factor asso ciated to a decreased LVMi was the decrease of the systolic BP irrespe ctive of the ACE gene genotype of each individual patient. Conclusions . The ACE-gene genotype does not necessarily predict the extent to whi ch LVMi will be lowered by ACE-inhibitors therapy. The LVH of hyperten sive uremics is amenable by long-term antihypertensive therapy provide d that it results in significantly decreased systolic blood pressure.