Abstract 4890: Myocardial Fibrosis and Diastolic Dysfunction Following Calcium-Channel Blockers or Angiotensin II Receptor Blockers in Hypertensive Patients
Objectives: Myocardial fibrosis develops in the hypertensive heart, and brings about LV diastolic dysfunction. Myocardial fibrosis is regulated by collagen production and degradation. Collagen degradation is regulated by matrix metalloproteinases (MMPs), a family of zinc-dependent interstitial enzymes, and their tissue inhibitors (TIMPs). We investigated how long-term administration of calcium-channel blockers (CCB) or Angiotensin II receptor blockers (ARB) affects collagen production/degradation and LV diastolic dysfunction.
Methods: Study population consisted of 44 untreated hypertensive patients (31 females, 13 males, mean age:57±11 years). They were randomly assigned to one of the 2 groups: CCB group in which Amlodipine of 5–10mg was given daily (n=22) and ARB group in which Losartan of 50–100mg was given daily (n=22). LV mass index (LVMI) and tissue Doppler early diastolic mitral annular velocity (E′) were echocardiographically assessed before and 6 and 12 months after treatment. Procollagen type I C-terminal propeptide (PICP) was determined with enzyme immunoassay as a serum marker of collagen production, while MMP-2 and TIMP-1 were determined with ELISA as makers of collagen degradation.
Results (table⇓): E′ increased in the ARB group but not in the CCB group while reductions in blood pressure (BP) and LVMI were comparable between the group. PICP did not change after treatment in either group, but MMP-2 increased only in the ARB group. TIMP-1 did not change in either group.
Conclusions: In spite of similar reduction of SBP and LVMI, ARB provided larger benefits on LV diastolic function than CCB. Collagen production was constant in both groups, but ARB facilitated more collagen degradation than CCB, and the difference should have contributed to the impact on LV diastolic function.