Importance of left ventricular contraction for left atrial reservoir function.

BACKGROUND: The determinants of left atrial (LA) reservoir function have not been clarified. METHODS: To elucidate the effect of left ventricular (LV) contraction on LA reservoir volume (ΔVLA), volume change due to mitral annular downward motion and aortic root anterior motion, which are related to LV contraction during systole, was calculated in 72 consecutive subjects [42 patients without any cardiac disease (control group), 13 patients with heart failure with reduced ejection fraction (HFrEF group) and 17 with preserved ejection fraction (HFpEF group)]. LA volume was calculated using the modified Simpson's method of bi-plane 2-D echocardiograms. ΔVLA was the difference between the maximum and minimum LA volumes. LA volume change according to mitral annular motion (ΔVMA) and aortic root motion (ΔVAR) were calculated by assuming an oval frustum and dented wedge, respectively. RESULTS: In the normal control group, ΔVAR + ΔVMA was 11.7 ml on average, correlating to ΔVLA (r = 0.55, p < 0.01), and the contribution rate to LA reservoir volume ((ΔVAR + ΔVMA)/ΔVLA) was 56% on average. In both, the HFrEF and HFpEF groups, ΔVAR, ΔVMA, and the contribution rate were significantly smaller than those in normal control group. Stroke volume correlated to ΔVAR and ΔVMA. The larger the maximum LA volume was, the smaller the contribution rate was. The smaller the rate was, the higher the systolic pulmonary artery pressure was. CONCLUSIONS: Both mitral annular motion and aortic root anterior motion, which are related to ventricular contraction, are important for the LA reservoir volume recruitment.

Transient enhancement of oxidant stress and collagen turnover in patients with acute worsening of congestive heart failure.

BACKGROUND: Myocardial remodeling is a crucial step for progression of heart failure (HF). Free radical generation by the failing myocardium has been proposed as linked to myocardial remodeling. The aim of this study was to evaluate the urinary excretion of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha), a reliable marker for oxidant stress in vivo, and collagen turnover in patients with acute worsening of congestive HF. METHODS AND RESULTS: Enrolled were 43 patients with acute worsening of congestive HF of various etiologies. On admission (acute phase) and after approximately 2 weeks of conventional treatment (chronic phase), the following were measured: (1) immunoreactive urinary 8-iso-PGF2alpha, (2) serum total antioxidant status (TAS); and (3) serum levels of procollagen type I carboxyterminal peptide (PIP) and carboxyterminal collagen type I telopeptide (CITP), biochemical markers for collagen synthesis and degradation, respectively. From the acute to the chronic phase the parameters changed as follows: 335.1+/-245.4 to 205.3+/-107.4 pg/mg creatinine for urinary 8-iso-PGF2alpha (p<0.0001); 0.92+/-0.16 to 0.98+/-0.13 mmol/L for TAS (p<0.01); 171.4+/-72.5 to 93.7+/-33.9 ng/ml for PIP (p<0.0001); and 7.2+/-3.6 to 12.6+/-8.4 ng/ml for CITP (p<0.0001). CONCLUSIONS: Acute worsening of congestive HF promotes free radical generation and collagen synthesis.