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BACKGROUND: We investigated whether depressive disorder and Type D personality refer to different forms of distress in the Myocardial INfarction and Depression - Intervention Trial (MIND-IT).MethodA total of 1205 myocardial infarction (MI) patients were screened at 3, 6, 9 and 12 months post-MI; those with a Beck Depression Inventory (BDI) score 10 underwent the World Health Organization (WHO) Composite International Diagnostic Interview (CIDI). Patients completed the DS14 measure of Type D personality at 12 months and were stratified to one of four subgroups: depressed/Type D, depressed/non-Type D, non-depressed/Type D, or non-distressed. RESULTS: Two hundred and six (17%) patients were diagnosed with depression and 224 (19%) with Type D. Only 7% (n=90) had both forms of distress, and 60% of Type D patients were free of depression in the first year post-MI. Type D moderated the relationship between depressive and cardiac disorder. Depressed patients without Type D had the worst clinical status (left ventricular dysfunction, heart failure, Killip class 2) as compared to other patients, whereas depressed patients with a Type D personality did not differ in clinical status from non-distressed patients. Contrasting 'pure' Type D and depression subgroups showed that Type D patients without depression were less likely to have left ventricular dysfunction [odds ratio (OR) 0.47, 95% confidence interval (CI) 0.35-0.65, p<0.0001] than depressed patients without Type D. CONCLUSIONS: Depression and Type D refer to different forms of distress in post-MI patients; most Type D patients display non-psychiatric levels of distress and Type D moderates the relationship between depressive and cardiac disorder. Different depression/Type D subgroups may be involved in the prediction of cardiac prognosis. [ABSTRACT FROM AUTHOR]

Purpose: Systemic-to-pulmonary collateral flow is a well-recognised phenomenon in patients with single ventricle physiology, but remains difficult to quantify. The aim was to compare the reported formula's that have been used for calculation of systemic-to-pulmonary-collateral flow to assess their consistency and to quantify systemic-to-pulmonary collateral flow in patients with a Glenn and/or Fontan circulation using four-dimensional flow MRI (4D flow MR)., Methods: Retrospective case-control study of Glenn and Fontan patients who had a 4D flow MR study. Flows were measured at the ascending aorta, left and right pulmonary arteries, left and right pulmonary veins, and both caval veins. Systemic-to-pulmonary collateral flow was calculated using two formulas: 1) pulmonary veins - pulmonary arteries and 2) ascending aorta - caval veins. Anatomical identification of collaterals was performed using the 4D MR image set., Results: Fourteen patients (n = 11 Fontan, n = 3 Glenn) were included (age 26 [22-30] years). Systemic-to-pulmonary collateral flow was significantly higher in the patients than the controls (n = 10, age 31.2 [15.1-38.4] years) with both formulas: 0.28 [0.09-0.5] versus 0.04 [-0.66-0.21] l/min/m 2 (p = 0.036, formula 1) and 0.67 [0.24-0.88] versus -0.07 [-0.16-0.08] l/min/m 2 (p < 0.001, formula 2). In patients, systemic-to-pulmonary collateral flow differed significantly between formulas 1 and 2 (13% versus 26% of aortic flow, p = 0.038). In seven patients, veno-venous collaterals were detected and no aortopulmonary collaterals were visualised., Conclusion: 4D flow MR is able to detect increased systemic-to-pulmonary collateral flow and visualise collaterals vessels in Glenn and Fontan patients. However, the amount of systemic-to-pulmonary collateral flow varies with the formula employed. Therefore, further research is necessary before it could be applied in clinical care.

Objective: N-terminal pro-brain natriuretic peptide has an established role in the diagnosis and prognosis of heart failure. In Fontan patients, this peptide is often increased, but its diagnostic value in this particular non-physiologic, univentricular circulation is unclear. We investigated whether N-terminal pro-brain natriuretic peptide represents ventricular function or other key variables in Fontan patients., Methods and Results: Ninety-five consecutive Fontan patients ≥10 years old who attended the outpatient clinic of the Center for Congenital Heart Diseases in 2012-2013 were included. Time since Fontan completion was 16 ± 9 years. Median N-terminal pro-brain natriuretic peptide was 114 (61-264) ng/l and was higher than gender-and age-dependent normal values in 54% of the patients. Peptide Z-scores were higher in patients in NYHA class III/IV compared to those in class I/II, but did not correlate with ventricular function assessed by MRI and echocardiography, nor with peak exercise capacity. Instead, peptide Z-scores significantly correlated with follow-up duration after Fontan completion (p < 0.001), right ventricular morphology (p = 0.004), indexed ventricular mass (p = 0.001), and inferior caval vein diameter (p < 0.001) (adjusted R2 = 0.615)., Conclusions: N-terminal pro-brain natriuretic peptide levels in Fontan patients correlate with functional class, but do not necessarily indicate ventricular dysfunction. Increased peptide levels were associated with a longer existence of the Fontan circulation, morphologic ventricular characteristics, and signs of increased systemic venous congestion. Since the latter are known to be key determinants of the performance of the Fontan circulation, these findings suggest increase in N-terminal pro-brain natriuretic peptide levels to indicate attrition of the Fontan circulation, independent of ventricular function.

Background: Depression following myocardial infarction is associated with poor cardiac prognosis. It is unclear whether antidepressant treatment improves long-term depression status and cardiac prognosis., Aims: To evaluate the effects of antidepressant treatment compared with usual care in an effectiveness study., Method: In a multicentre randomised controlled trial, 2177 myocardial infarction patients were evaluated for ICD-10 depression and randomised to intervention (n=209) or care as usual (n=122). Both arms were evaluated at 18 months post-myocardial infarction for long-term depression status and new cardiac events., Results: No differences were observed between intervention and control groups in mean scores on the Beck Depression Inventory (11.0, s.d.=7.5 v.10.2, s.d.=5.1, P=0.45) or presence of ICD-10 depression (30.5 v. 32.1%, P=0.68). The cardiac event rate was 14% among the intervention group and 13% among controls (OR=1.07, 95% CI 0.57-2.00)., Conclusions: Antidepressant treatment did not alter long-term depression post-myocardial infarction status or improve cardiac prognosis.