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BACKGROUND: Reduced left ventricular ejection fraction (LVEF) ≤30% is the most powerful prognostic indicator for sudden cardiac death (SCD) in patients after myocardial infarction (MI), but there are little data about long-term changes of LVEF after revascularization and the following implantation of a cardioverter defibrillator (ICD).
METHODS: We performed a retrospective analysis of 277 patients with reduced LVEF at least 1month after MI and complete revascularization. Patients (median time post-MI 23.4months; 74.3% after PCI, 25.7% after CABG were assigned either to group 1 (LVEF<30%) or group 2 (LVEF 30-40%). Biplane echocardiography was redone after a mean follow-up of 441±220days.
RESULTS: LVEF increased significantly in both two groups (group 1: 26.2±4.8% to 32.4±8.5%; p<0.001; group 2: 38.2±2.5% to 44.4±9.6%; p<0.001). However, statistical analysis of first and second LVEF measurement by means of a LOWESS regression and with an appropriate correction of the regression towards the mean effect revealed only a moderate increase of the mean LVEF from 35 to 37% (p<0.001) with a large interindividual variation.
CONCLUSIONS: The impact of early revascularization on LVEF appears to be low in the majority of post-MI heart failure patients. Owing to the high variability, a single measurement may not be reliable enough to justify a decision on ICD indication.
Objective:
Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF).
Methods:
The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment.
Results:
Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS.
Conclusion:
Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.