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Acute heart failure (AHF), 1 2 early development of left ventricular (LV) systolic dysfunction, 3 LV remodelling, 4 inflammatory responses during myocardial infarction (MI) 5 6 or newly developed acute kidney injury (AKI) 7 8 have been identified repeatedly to be independent and important factors influencing the long-term prognosis of patients with acute coronary syndrome (ACS).
We conducted a prospective, randomised, controlled, open-label, pilot clinical trial in 40 patients fulfilling two of the following three criteria for AHF: (1) left ventricular ejection fraction <40%, (2) acute pulmonary oedema or respiratory failure of predominantly cardiac origin requiring mechanical ventilation and (3) currently receiving vasopressor and/or inotropic support.
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Over the last decade, there have been nearly one million annual emergency department (ED) visits for acute heart failure (AHF) [1].
Table 8 demonstrates the basic characteristics of recent comparable registries based on the classifications of The European Society of Cardiology ESCC) guidelines on diagnosis and treatment of AHF 2005 [ 3].
Our literature search yielded 316 potential papers, of which 57 were included (20 papers on AHF, 15 ACS and 22 Cs).
The mortality of cardiogenic shock was 62.7%, of right AHF 16.7%, of pulmonary edema 7.1%, of high output HF 6.1%, whereas the mortality of hypertensive AHF or ADHF was < 2.5%.
The inclusion criteria for the database adhere to the European guidelines for AHF (2005) and patients were systematically classified according to the basic syndromes, type and etiology of AHF.
In a study by Metra et al., detectable serum troponin T levels were found in 48% of the patients admitted for AHF (54% of the patients with coronary artery disease and 40% of those with idiopathic dilated cardiomyopathy) [ 20].
Our results are also in agreement with van Kimmenade et al. who demonstrated that, elevated GAL3 levels in patients presenting to ED for AHF, GAL3 was the best independent predictor for 60-day mortality [ 4].
To investigate three hypotheses: (1) the use of PTX leads to improved outcome in AHF; (2) this effect is dose dependent; and (3) improved outcome is limited by temporal constraints.
This study also showed that levels of uric acid, a marker of oxidative stress, inflammation, and/or poor renal function associated with poor prognosis in AHF [ 14, 61, 62], were reduced in patients with AHF receiving serelaxin compared with placebo [ 14].
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