Key result
Acute HF worsening is linked to ~63% higher urinary 8-iso-PGF2α versus the chronic phase.
Why the study?
Myocardial remodeling is crucial for heart failure progression, and free radical generation by the failing myocardium is proposed to be linked to remodeling, but its relationship with oxidant stress and collagen turnover during acute worsening of congestive heart failure was unclear.
Does conventional treatment for acute worsening of congestive heart failure improve markers of oxidant stress and collagen turnover?
Observational (n=43)
No
Does conventional treatment for acute worsening of congestive heart failure improve markers of oxidant stress and collagen turnover?
Acute worsening of congestive heart failure is associated with transient increases in oxidant stress and collagen synthesis, which improve after conventional treatment.
Answers are grounded in this paper and cite their sources.
Acute HF decompensation linked to transient rises in oxidant stress and collagen markers; hypothesis-generating, needs prospective trials before clinical adoption.
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.
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Kunishige et al. (2007) conducted an observational in Acute worsening of congestive heart failure (n=43). Acute worsening of congestive heart failure (acute phase) vs. Chronic phase (after approximately 2 weeks of conventional treatment) was evaluated on Urinary excretion of 8-iso-prostaglandin F2α (pg/mg creatinine) (p=<0.0001). Acute worsening of congestive heart failure was associated with significantly higher urinary 8-iso-PGF2α (335.1 vs 205.3 pg/mg creatinine) and procollagen type I carboxyterminal peptide (171.4 vs 93.7 ng/ml) compared to the chronic phase.
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