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Angiotensin-converting enzyme gene polymorphism and reversibility of uremic left ventricular hypertrophy following
G Cannella1, E Paoletti, S Barocci
1Divisione di Nefrologia e Dialisi, Laboratorio di Immunologia, Istituto di Statistica Medica dell'Università, Genova, Italy. gcannella@smartino.ge.it
Insights
Antihypertensive therapy effectively reduces left ventricular hypertrophy (LVH) in hemodialysis patients. Achieving lower systolic blood pressure is key, regardless of angiotensin-converting enzyme (ACE) gene type.
Area of Science:
- Nephrology
- Cardiology
- Genetics
Background:
- Left ventricular hypertrophy (LVH) is a common complication in uremic patients.
- The angiotensin-converting enzyme (ACE) gene polymorphism (DD, ID, II) may influence LVH response to antihypertensive therapy.
Purpose of the Study:
- To investigate the impact of ACE gene genotype on LVH regression in hemodialyzed uremic patients undergoing long-term antihypertensive treatment.
Main Methods:
- A five-year follow-up study involving 30 hemodialyzed uremic patients (13 DD, 17 II+ID).
- Yearly echocardiography and 24-hour blood pressure monitoring were performed.
- Antihypertensive therapy included ACE inhibitors as first-line treatment.
Main Results:
- Patients with II+ID genotypes showed significant reductions in left ventricular mass index (LVMi) and blood pressure (BP).
- While less pronounced in the DD group, differences were not statistically significant.
- Decreased systolic BP was the sole predictor of LVMi reduction, independent of ACE genotype.
Conclusions:
- ACE gene genotype does not definitively predict LVMi reduction with ACE inhibitor therapy.
- Long-term antihypertensive therapy can effectively reduce LVH in hypertensive uremic patients if significant systolic BP reduction is achieved.
Background:
Prolonged antihypertensive therapy might be less effective in reversing the left ventricular hypertrophy (LVH) in uremics bearing the deleted (DD) allele of the angiotensin converting enzyme (ACE) gene than in patients with the inserted (II) allele or in those heterozygous (ID) for the gene.
Methods:
Thirteen DD and 17 II + ID hemodialyzed uremics were followed-up with yearly echocardiography and 24-hour blood pressure (BP) monitoring over five years while on an antihypertensive therapy that included ACE inhibitors as first line drugs.
Results:
In the II + ID group there were significant decreases of the left ventricular 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 groups. Further analysis of the data revealed that the only factor associated to a decreased LVMi was the decrease of the systolic BP irrespective of the ACE gene genotype of each individual patient.
Conclusions:
The ACE-gene genotype does not necessarily predict the extent to which LVMi will be lowered by ACE-inhibitors therapy. The LVH of hypertensive uremics is amenable by long-term antihypertensive therapy provided that it results in significantly decreased systolic blood pressure.