Supplementary Material for: The Monocyte-to-Lymphocyte Ratio Correlates with Psycho-Neuro-Inflammatory Factors in Patients with Stable Coronary Artery Disease

<b><i>Background:</i></b> Psychosocial stress and depression have been recognized as major risk factors of coronary artery disease (CAD). Although monocytes are known to be key players in atherosclerosis, monocyte-based associations with psychoneuroendocrino-immuno-inflammatory (PNI) markers have not been widely investigated in stable CAD. <b><i>Objective:</i></b> We examined associations between the monocyte-to-lymphocyte ratio (MLR) and key PNI markers in stable CAD. <b><i>Methods:</i></b> We studied 23 patients with stable CAD who completed the Beck Depression Inventory (BDI) and Rahe's Brief Stress and Coping Inventory. A white blood cell differential was performed, and levels of cortisol, chromogranin A (CgA), LL-37, interleukin-6 (IL-6) and C-reactive protein (CRP) were assayed in plasma. <b><i>Results:</i></b> Monocyte fraction, MLR and plasma CgA levels exceeded reference values, the social support score was low, and 7 patients had elevated BDI scores. In the multivariate-adjusted analysis, a higher MLR was associated with greater depressive symptom severity (r = 0.624, p < 0.01) as well as with higher concentrations of CgA (r = 0.660, p < 0.01), LL-37 (r = 0.643, p < 0.01), IL-6 (r = 0.532, p < 0.05) and CRP (r = 0.470, p < 0.05). BDI scores associated with CgA concentration (r = 0.618, p < 0.01) and CgA level correlated negatively with the social support score (r = -0.511, p < 0.05). <b><i>Conclusions:</i></b> Our findings suggest that, in patients with stable CAD, elevated MLR may be associated with depressive symptoms, with increased neuroendocrine-sympathetic activity (marked by CgA) and inflammatory markers that are pertinent to atherosclerosis initiation and progression. The increased neuroendocrine-sympathetic activity correlated with low social support and depressive symptom severity. The MLR might serve as an easy-to-obtain and inexpensive proxy measure of an activated PNI network in stable CAD

Supplementary Material for: Inflammatory Activation after Experimental Cardiac Tamponade

<b><i>Background/Purpose:</i></b> Cardiac tamponade is a medical emergency situation associated with a high rate of life-threatening complications, even after immediate interventions. Our aim was to characterize the acute inflammatory consequences of this event in a clinically relevant large animal model. <b><i>Methods:</i></b> Cardiac tamponade was induced for 60 min in anesthetized, ventilated and thoracotomized minipigs by intrapericardial fluid administration, the mean arterial pressure (MAP) being maintained in the interval of 40-45 mm Hg (n = 8). A further group (n = 7) served as sham-operated control. The global macrohemodynamics, including the right- and left-heart end-diastolic volumes (RHEDV and LHEDV), the pulmonary vascular resistance index (PVRI) and the superior mesenteric artery (SMA) flow, were monitored for 240 min, and the intestinal microcirculatory changes (pCO₂ gap) were evaluated by indirect tonometry. Blood samples were taken for the determination of cardiac troponin T and vasoactive inflammatory mediators, including histamine, nitrite/nitrate, big-endothelin, superoxide and high-mobility group box protein-1 levels in association with intestinal leukocyte and complement activation. <b><i>Results:</i></b> The cardiac tamponade induced significant decreases in MAP, cardiac output, LHEDV and SMA flow, while the PVRI and the pCO₂ gap increased significantly. After the removal of fluid from the pericardial sac, the MAP and the LHEDV were decreased, while the PVRI and the pCO₂ gap remained elevated when compared with those in the sham-operated group. In the posttamponade period, the abrupt release of inflammatory mediators was accompanied by a significant splanchnic leukocyte accumulation and complement activation. <b><i>Conclusions:</i></b> The macrocirculatory and splanchnic microcirculatory disturbances were accompanied by a significant proinflammatory reaction; endothelin and the complement system may be significant components of the inflammatory cascade that is activated in this porcine model of pericardial tamponade