CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 32 AFRICA Approximately half of the patients with CAD suffer from depressive symptoms and 20% of patients with CAD meet the criteria for MDD.1 Among patients undergoing CABG surgery, approximately 30–40% of patients meet the criteria for minor or major depression, with roughly 15% of patients meeting full MDD criteria.2 Inflammatory cytokines [C-reactive protein (CRP) and interleukin-6 (IL-6)] have been strongly associated with atherosclerotic plaque-related adverse events. Depression also has been linked to increased levels of cytokines (CRP, IL-1, IL-6), and also depression can predict cardiovascular mortality.13 Two possible mechanisms have been proposed to clarify the association between inflammation, depression and cardiovascular disease. First, reduced serotonin action in the medial prefrontal cortex might be associated with increased inflammatory cytokines. Second, increased levels of interferongamma is associated with elevated activity of an enzyme that degrades tryptophan (a serotonin precursor) to kynurenine in patients with CAD.14 Lower levels of serotonin may be another mechanism of the connection between inflammation and depression in patients with cardiac disease.15 Endothelial dysfunction has been associated with the development of ischaemic CAD in patients with atherosclerosis. While a normal endothelium typically releases nitric oxide (NO) in response to serotonin to ensure adequate blood flow through the coronary arteries, in atherosclerotic segments it fails. This results in vasoconstriction in the atherosclerotic segments and may lead to myocardial ischaemia and coronary thrombosis.16 Inflammation is associated with CAD, and it also impairs endothelial NO release. Depression has also been associated with impaired endothelial function in patients with or without CAD.17 Selective serotonin re-uptake inhibitor (SSRI) treatment has led to improved endothelial function in patients with depression and CAD.18 Platelet activation, adhesion and aggregation are important components of cardiovascular disease, and increased platelet activity is strongly associated with adverse cardiovascular events. Serotonin plays a key role in platelet biology through its binding with 5-hydroxytryptamine (5-HT) receptors on the platelets. In atherosclerotic arteries, serotonin leads to platelet aggregation.16 Furthermore, elevated levels of blood serotonin predict CAD and future ischaemic cardiac events in patients with suspected CAD. SSRIs consume platelet serotonin stores by inhibiting platelet uptake of serotonin, and are also associated with decreasing platelet aggregation in patients with CAD.19 Table 1. Patient characteristics Patient characteristics SS ≥ 23 (n = 124) SS < 23 (n = 85) p-value Age (years), mean ± SD 67.4 ± 9.5 64.9 ± 11.5 0.687 Female gender, % 36.9 34.6 0.672 Marital status, % Single 21.9 22.7 0.861 Married 54.6 55.3 0.637 Divorced 23.5 22.0 0.539 Body mass index (kg/m2) 26.1 24.9 0.738 Hypertension, % 73.9 71.4 0.867 Diabetes mellitus, % 60.3 31.7 < 0.001 Hyperlipidaemia, % 66.4 29.1 < 0.001 Smoking, % 57.3 34.7 < 0.001 Educational level, % Primary school 27.6 28.3 0.659 Secondary school 58.3 57.4 0.851 Tertiary education 14.1 14.3 0.962 ACEI/ARB therapy, % 56.7 54.9 0.736 Beta-blocker therapy, % 49.5 50.7 0.761 Statin therapy, % 58.3 59.1 0.738 Aspirin therapy, % 81.3 80.8 0.783 HADS, mean ± SD 24.8 ± 10.7 11.3 ± 6.4 < 0.001 ACEI: angiotensin converting enzyme inhibitor; ARB: angiotensin receptor blocker; HADS: hospital anxiety and depression scale. Table 2. Laboratory and echocardiographic parameters of the study population Laboratory parameters SS ≥ 23 (n = 124), mean ± SD SS < 23 (n = 85), mean ± SD p-value Haemoglobin (g/dl) 13.9 ± 3.1 (14.3) 14.3 ± 2.9 (14.5) 0.621 Platelets (× 103 cells/µl) 314.7 ± 74.3 (346.5) 309.6 ± 69.4 (339.1) 0.534 White blood cells (× 103 cells/µl) 8.3 ± 4.7 (9.3) 7.8 ± 3.7 (9.1) 0.639 Creatinine (mg/dl) 0.79 ± 0.27 (0.83) 0.67 ± 0.31 (0.78) 0.427 Fasting plasma glucose (mg/dl) [mmol/l] 87.1 ± 23.8 (96.3) [4.83 ± 1.32 (5.34)] 83.4 ± 26.7 (92.8) [4.63 ± 1.48 (5.15)] 0.382 C-reactive protein (mg/dl) 1.39 ± 0.73 (1.57) 1.27 ± 0.83 (1.49) 0.561 Total cholesterol (mg/dl) [mmol/l] 204.7 ± 64.9 (237.3) [5.30 ± 1.68 (6.15)] 194.6 ± 54.3 (231.4) [5.04 ± 1.41 (5.99)] 0.493 High-density lipoprotein cholesterol (mg/dl) [mmol/l] 31.6 ± 11.8 (36.7) [0.82 ± 0.31 (0.95)] 34.3 ± 10.9 (38.5) [0.89 ± 0.28 (1.00)] 0.637 Low-density lipoprotein cholesterol (mg/dl) [mmol/l] 176.3 ± 46.7 (194.8) [4.57 ± 1.21 (5.05)] 169.7 ± 51.9 (188.7) [4.40 ± 1.34 (4.89)] 0.472 Trigylicerides (mg/dl) [mmol/l] 183.6 ± 49.7 (196.5) [2.07 ± 0.56 (2.22)] 178.5 ± 51.7 (188.3) [2.02 ± 0.58 (2.13)] 0.381 TSH (mIU/ml) 3.4 ± 1.3 (3.8) 3.2 ± 1.1 (3.7) 0.847 Uric acid (mg/dl) 7.1 ± 3.4 (9.4) 7.0 ± 3.2 (9.6) 0.861 Left ventricular ejection fraction (%) 64.3 ± 6.1 (65.4) 64.7 ± 5.9 (65.9) 0.739 TSH: thyroid-stimulating hormone. Table 3. Multivariate analysis of predictors for higher SS Predictor variables OR (95% CI) p-value Diabetes mellitus 3.164 (1.937–6.934) < 0.001 Hyperlipidaemia 3.429 (1.861–7.657) < 0.001 HADS 2.736 (1.934–4.092) < 0.001 1 – Specificity (%) 0.0 0.2 0.4 0.6 0.8 1.0 Sensitivity (%) 1.0 0.8 0.6 0.4 0.2 0.0 AUC = 0.668; Confidence interval: 0.583–0.753 Sensitivity: 80.9%; Specificity: 69.9%; Cut-off: 21.4 Fig. 1. ROC curve analysis to evaluate the diagnostic performance of the HADS for differentiating low and high SS patients.
RkJQdWJsaXNoZXIy NDIzNzc=