OBJECTIVE: To demonstrate the presence and importance of apoptotic activity in heart failure during acute exacerbations and to investigate the effects of different drugs used and co-morbidities on levels of N-Terminal pro-Brain Natriuretic Peptide and apoptotic activity on admission and during hospitalisation. METHODS: The descriptive study was conducted at the emergency department of Istanbul University Cardiology Institute between October 2010 and May 2011 and comprised patients with complaints of shortness of breath, and who were evaluated as acutely exacerbated decompensated heart failure with an aetiology of ischaemic or dilated cardiomyopathy. Apoptotic activity and N-Terminal pro-Brain Natriuretic Peptide levels were measured on admission and on the seventh day of treatment. SPSS 15 was used for statistical analysis. RESULTS: Of the 89 patients in the study, 67(75%) were males. Overall mean age of the study sample was 61 +/- 12 years. Patients who had N-Terminal pro-Brain Natriuretic Peptide levels higher than 6000 pg/ml on admission had greater in-patient mortality rate (p < 0.001). N-Terminal pro-Brain Natriuretic Peptide levels decreased significantly on the seventh day of treatment compared to the admission values (p < 0.012). Apoptotic activity levels, although not statistically significant, increased on the seventh day compared with admission values (p < 0.12). Apoptotic activity levels on the 7th day were associated with in-patient deaths (p < 0.002). Dopamine infusion in the treatment group during hospitalisation significantly increased apoptotic activity (p < 0.035), whereas there was a trend towards decreased apoptotic activity levels with spironolactone (p < 0.07). Treatment with beta-blockers did not change apoptotic activity levels (p < 0.751), whereas lack of beta-blocker therapy increased apoptotic activity (p < 0.02). CONCLUSION: N-Terminal pro-Brain Natriuretic Peptide may be an important risk predictor in decompensated heart failure exacerbations during hospatilasation but not apoptotic activity. Beta-blocker therapy seems to positively affect the process of apoptosis.
OBJECTIVE: To demonstrate the presence and importance of apoptotic activity in heart failure during acute exacerbations and to investigate the effects of different drugs used and co-morbidities on levels of N-Terminal pro-Brain Natriuretic Peptide and apoptotic activity on admission and during hospitalisation. METHODS: The descriptive study was conducted at the emergency department of Istanbul University Cardiology Institute between October 2010 and May 2011 and comprised patients with complaints of shortness of breath, and who were evaluated as acutely exacerbated decompensated heart failure with an aetiology of ischaemic or dilated cardiomyopathy. Apoptotic activity and N-Terminal pro-Brain Natriuretic Peptide levels were measured on admission and on the seventh day of treatment. SPSS 15 was used for statistical analysis. RESULTS: Of the 89 patients in the study, 67(75%) were males. Overall mean age of the study sample was 61 +/- 12 years. Patients who had N-Terminal pro-Brain Natriuretic Peptide levels higher than 6000 pg/ml on admission had greater in-patient mortality rate (p < 0.001). N-Terminal pro-Brain Natriuretic Peptide levels decreased significantly on the seventh day of treatment compared to the admission values (p < 0.012). Apoptotic activity levels, although not statistically significant, increased on the seventh day compared with admission values (p < 0.12). Apoptotic activity levels on the 7th day were associated with in-patient deaths (p < 0.002). Dopamine infusion in the treatment group during hospitalisation significantly increased apoptotic activity (p < 0.035), whereas there was a trend towards decreased apoptotic activity levels with spironolactone (p < 0.07). Treatment with beta-blockers did not change apoptotic activity levels (p < 0.751), whereas lack of beta-blocker therapy increased apoptotic activity (p < 0.02). CONCLUSION: N-Terminal pro-Brain Natriuretic Peptide may be an important risk predictor in decompensated heart failure exacerbations during hospatilasation but not apoptotic activity. Beta-blocker therapy seems to positively affect the process of apoptosis.