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Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Jackson CE, Solomon SD, Gerstein HC, Zetterstrand S, Olofsson B, Michelson EL, Granger CB, Swedberg K, Pfeffer MA, Yusuf S, McMurray JJ; CHARM Investigators and Committees.
The authors assessed the prevalence and the prognostic value of a urinary albumin to creatine ratio in 2310 patient with chronic heart failure enrolled in the CHARM trial. Among them, 30% had microalbuminuria, and 11% had macroalbuminuria. The prevalence of these pathologies did not differ between those with reduced versus preserved left ventricular ejection fractions. The presence of both macro- and microalbuminuria was related to the higher rates of the primary combined end-point (death from cardiovascular causes and admission to hospital with worsening heart failure) and the higher all-cause mortality. Therapy with candesartan did not modify the excessive excretion of urinary albumin.
Although impaired glomerular filtration rate (GFR) and albuminuria reflect an impaired renal function, their pathophysiological backgrounds and therefore further clinical interpretations are different. Reduced GFR is related to impaired renal blood flow rate and urine renal filtration rate, whereas albuminuria reflects mainly structural renal damage. Although in general impaired GFR is accompanied by increased urine albumin secretion, in the reported study around 50% patients with heart failure with macroalbuminuria had preserved GFR. Reduced GFR and albuminuria independently of each other predicted poor outcome, suggesting the impact on prognosis through different pathomechanisms. It is suggested that albuminuria might be another index of renal dysfunction beyond reduced GFR and future interventions should be targeted to ameliorate it.
van Diepen S, Majumdar SR, Bakal JA, McAlister FA, Ezekowitz JA.
Circulation. 2008 Nov 4;118(19):1946-52.
The paper demonstrates that among patients aged 65 years and over admitted to emergency departments in Canada, these with a primary diagnosis of CHF have an increased risk of bone fracture in comparison to subjects with cardiovascular disease but not CHF (acute myocardial infarction, cardiac dysrhythmia, chest pain, stable and unstable angina) during the 12-month follow-up. Any orthopedic fracture and hip fracture occur respectively in 4.6% and 1.3% of patients with CHF as compared to 1.0% and 0.1% of patients with non-CHF cardiovascular diagnoses. CHF constitutes an independent risk factor for osteoporosis and subsequent bone fractures.
The paper provides another argument that CHF is a serious disease affecting the whole body, in this case also bone tissue. Although at the first look, the pathophysiological link between CHF and osteoporosis might seem to be remote, in fact, several factors related to CHF contribute to the accelerated bone loss. The following mechanisms may play a role: increased levels of parathyroid hormone, reduced levels of vitamin D, low-grade inflammatory state, reduced levels of anabolic hormones (testosterone, IGF-1), increased levels of catabolic hormones (cortisol), calciuretic properties of furosemide, immobilization and reduced exercise activities. Patients with CHF (both men and women) should be screened for reduced bone mineral density, and an individual risk of bone fracture should be determined. The efficacy of standard therapy decelerating bone loss needs to be verified in prospective studies in patients with CHF.
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