Chikako Yoshida

Role of plasma aldosterone concentration in regression of left-ventricular mass following antihypertensive medication

Background Aldosterone is known to bring about damage to various organs; however, it is unclear how important the changes in plasma aldosterone concentration (PAC) are as contributors to regression of left-ventricular (LV) mass in hypertensive patients following long-term treatment with calcium channel blockers (CCBs) or angiotensin II receptor blockers (ARBs). Objective To assess the importance of changes in PAC during antihypertensive treatment. Methods Forty-four untreated hypertensive patients were randomly assigned to either CCB (amlodipine) group or ARB (losartan) group. In addition to PAC measurements LV geometry was echocardiographically assessed with LV mass index (LVMI) and relative wall thickness (RWT) before and 6 and 12 months after treatment. Results Reduction of systolic blood pressure (SBP) in 12 months was greater in the CCB group than in the ARB group (−19 ± 8 vs. −11 ± 15%, P < 0.05 as percentage reduction from the values before treatment). PAC decreased in 12 months in the ARB group but not in the CCB group (−31 ± 31 vs. 17 ± 53%, P < 0.01 as percentage reduction from the values before treatment). Larger percentage drop in PAC was associated with larger percentage reduction of LVMI (r = 0.45, P < 0.01 for all). Multiple step-wise regression analysis showed that the percentage reduction of LVMI is related to the percentage changes in SBP and the percentage changes in PAC (r = 0.46, P < 0.01). Conclusion Regression of LV mass was the larger in patients with the greater decrease in PAC associated with antihypertensive medication regardless of CCB or ARB. Changes in PAC and SBP may be key determinants of regression of LV mass in hypertensive patients regardless of the medication selected.

Intraleaflet haemorrhage as a mechanism of rapid progression of stenosis in bicuspid aortic valve

BACKGROUND The mechanisms are unknown why aortic stenosis (AS) progresses faster in patients with bicuspid aortic valve (BAV) than those with tricuspid aortic valve (TAV). The objective of this study is to examine whether neoangiogenesis, haemorrhage in the aortic valve leaflet (intraleaflet haemorrhage) and macrophage infiltration are involved in the mechanisms of rapid progression of AS with BAV. METHODS We retrospectively examined specimens of aortic valve leaflets obtained from patients who had undergone aortic valve replacement for AS (AS with BAV: n=22, AS with TAV: n=86). The stenotic valve leaflets were examined by immunohistochemistry to detect vascular endothelial cells, red blood cell remnant and macrophage. We assessed the progression of AS by annualized changes in the aortic valve area (ΔAVA: cm(2)/year) which was evaluated by serial echocardiography with the continuity equation. RESULTS Neoangiogenesis, intraleaflet haemorrhage and macrophage infiltration were frequently observed in leaflets obtained from AS patients with BAV (neoangiogenesis: 82%, intraleaflet haemorrhage: 91%, macrophage infiltration 91%). These pathological changes were more severe in AS with BAV than TAV, and they were positively correlated with progression of AS in patients with BAV. Multivariated analysis revealed that bicuspid anatomy was the only factor that predicted neoangiogenesis, intraleaflet haemorrhage and macrophage infiltration when patients with BAV and those with TAV were combined. CONCLUSIONS Neoangiogenesis, intraleaflet haemorrhage and macrophage infiltration are more severe in leaflets from AS with BAV than TAV and associated with rapid progression of AS with BAV. This pathological process may account for rapid progression of AS with BAV.

Inappropriateness of ventricular hypertrophy is important as a determinant of BNP but not of diastolic filling in untreated hypertensive patients

Echocardiographically determined inappropriateness of left ventricular mass (LVM) is an independent risk factor for cardiovascular events. Although LV hypertrophy is associated with an increase in the plasma brain natriuretic peptide level and decreased LV diastolic filling, it is unknown whether the inappropriateness of LVM affects them. We studied 77 untreated hypertensive patients (49 men, 28 women, aged 59±12 years). The plasma brain natriuretic peptide level was measured, in addition to routine echo Doppler indexes of LV geometry and function. The appropriateness of LVM to cardiac workload was evaluated by the ratio of the observed LVM to the value predicted for individual sex, stroke work and height2.7 (oLVM/pLVM). Multivariate analysis showed that the plasma brain natriuretic peptide level increased with LVM index but decreased when oLVM/pLVM increased. The ratio of the peak early diastolic flow velocity of mitral flow to the peak early diastolic velocity of mitral annulus (E/E′) correlated not only with oLVM/pLVM but also with the LVM index (r=0.30, P<0.05; r=0.37, P<0.05, respectively). However, when a multiple stepwise regression analysis was carried out, only LVM index was determined to be a significant correlate of the E/E′ ratio, indicating that the inappropriateness of LVM does not affect the E/E′ ratio in hypertensive patients. Brain natriuretic peptide levels are influenced not only by the extent of LV hypertrophy but also by the inappropriateness of hypertrophy in untreated hypertensive patients. Diastolic filling is mostly affected by the extent of LV hypertrophy and not by the appropriateness of hypertrophy.