Motivation A close association exists between hypertension and arterial stiffness. Whether the increased arterial stiffness seen in hypertensives are due to structural or functional adaptations in the vasculature is uncertain. Hypertension is more common in blacks and they have an increased arterial stiffness and higer stroke prevalence than white populations. Arterial stiffening, or a loss of arterial distensibility, increases the risk for cardiovascular events, including stroke and heart failure, as it increases the afterload on the heart, as well as creating a higher pulsatile load on the microcirculation. The stiffness of the carotid artery is associated with cardiovascular events, like stroke, and all-cause mortality. Furthermore, carotid stiffness is independently associated with stroke, probably because stiffening of the carotid artery may lead to a higher pressure load on the brain. Inflammation, endothelial activation, dyslipidemia, hyperglycemia and health behaviours may also influence hypertension and arterial stiffness. Limited information is availiable on these associations in black South Africans. The high prevalence of hypertension and cardiovascular disease in blacks creates the need for effective prevention and intervention programs in South Africa. Aim We aimed to compare the characteristics of the carotid artery between 5-year sustained hypertensive and normotensive black participants. Furthermore, we aimed to determine whether blood pressure, conventional cardio-metabolic risk factors, markers of inflammation, endothelial activation and measures of health behaviours are related to these carotid characteristics. Methodology This sub-study forms part of the South African leg of the multi-national Prospective Urban and Rural Epidemiology (PURE) study. The participants of the PURE-SA study were from the North West Province of South Africa, and baseline data collection took place in 2005 (N=2010), while follow-up data was collected five years later, in 2010 (N=1288). HIV-free participants who were either hypertensive or normotensive (N=592) for the 5-year period, and who had complete datasets, were included in this sub-study. The study population thus consists of a group of 5-year sustained normotensive (n=241) and hypertensive (n=351) black participants. Anthropometric measurements included height, weight, waist circumference and the calculation of body mass index (BMI). We included several cardiovascular measurements, namely brachial systolic- and diastolic blood pressure, heart rate, central systolic blood pressure, central pulse pressure and the carotid dorsalis-pedis pulse wave velocity. Carotid characteristics included distensibility, intima media thickness, cross sectional wall area, maximum and minimum lumen diameter. Biochemical variables that were determined included HIV status, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglycerides, fasting glucose, glycated haemoglobin (HbA1c), creatinine clearance, interleukin-6, C-reactive protein, intracellular adhesion-molecule-1 and vascular adhesion molecule-1. Health behaviours were quantified by measuring γ-glutamyltransferase and by self-reported alcohol, tobacco and anti-hypertensive, anti-inflammatory and lipid-lowering medication use. We compared the normotensive and hypertensive groups by using independent t-tests and chi-square tests. The carotid characteristics were plotted according to quartiles of central systolic blood pressure by making use of standard analyses of variance (ANOVA) and the analyses of co-variance (ANCOVA). Pearson correlations done in the normotensive and hypertensive Africans helped to determine covariates for the multiple regression models. We used forward stepwise multiple regression analyses with the carotid characteristics as dependent variables to determine independent associations between variables. Results and Conclusion The cardiovascular measures, including pulse wave velocity, were significantly higher in the hypertensive group (all p≤0.024). The lipid profile, markers of inflammation, endothelial activation and glycaemia, as well as health behaviours, did not differ between the hypertensives and normotensives after adjustments for age, sex, waist circumference, γ-glutamyltransferase, tobacco use and anti-hypertensive medication use. After similar adjustments, all carotid characteristics, except IMT, were significantly different between the groups (all p≤0.008). However, upon additional adjustment for cSBP, significance was lost. The stiffness and functional adaptation seen in this study are not explained by the classic cardio-metabolic risk factors, markers of endothelial activation or health behaviours of the participants. The differences that exist in terms of arterial stiffness between the normotensive and hypertensive groups may be explained by the increased distending pressure in the hypertensive group. Despite their hypertensive status, it seems that there are no structural adaptations in these hypertensive Africans. / MSc (Physiology), North-West University, Potchefstroom Campus, 2015

Motivation A close association exists between hypertension and arterial stiffness. Whether the increased arterial stiffness seen in hypertensives are due to structural or functional adaptations in the vasculature is uncertain. Hypertension is more common in blacks and they have an increased arterial stiffness and higer stroke prevalence than white populations. Arterial stiffening, or a loss of arterial distensibility, increases the risk for cardiovascular events, including stroke and heart failure, as it increases the afterload on the heart, as well as creating a higher pulsatile load on the microcirculation. The stiffness of the carotid artery is associated with cardiovascular events, like stroke, and all-cause mortality. Furthermore, carotid stiffness is independently associated with stroke, probably because stiffening of the carotid artery may lead to a higher pressure load on the brain. Inflammation, endothelial activation, dyslipidemia, hyperglycemia and health behaviours may also influence hypertension and arterial stiffness. Limited information is availiable on these associations in black South Africans. The high prevalence of hypertension and cardiovascular disease in blacks creates the need for effective prevention and intervention programs in South Africa. Aim We aimed to compare the characteristics of the carotid artery between 5-year sustained hypertensive and normotensive black participants. Furthermore, we aimed to determine whether blood pressure, conventional cardio-metabolic risk factors, markers of inflammation, endothelial activation and measures of health behaviours are related to these carotid characteristics. Methodology This sub-study forms part of the South African leg of the multi-national Prospective Urban and Rural Epidemiology (PURE) study. The participants of the PURE-SA study were from the North West Province of South Africa, and baseline data collection took place in 2005 (N=2010), while follow-up data was collected five years later, in 2010 (N=1288). HIV-free participants who were either hypertensive or normotensive (N=592) for the 5-year period, and who had complete datasets, were included in this sub-study. The study population thus consists of a group of 5-year sustained normotensive (n=241) and hypertensive (n=351) black participants. Anthropometric measurements included height, weight, waist circumference and the calculation of body mass index (BMI). We included several cardiovascular measurements, namely brachial systolic- and diastolic blood pressure, heart rate, central systolic blood pressure, central pulse pressure and the carotid dorsalis-pedis pulse wave velocity. Carotid characteristics included distensibility, intima media thickness, cross sectional wall area, maximum and minimum lumen diameter. Biochemical variables that were determined included HIV status, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglycerides, fasting glucose, glycated haemoglobin (HbA1c), creatinine clearance, interleukin-6, C-reactive protein, intracellular adhesion-molecule-1 and vascular adhesion molecule-1. Health behaviours were quantified by measuring γ-glutamyltransferase and by self-reported alcohol, tobacco and anti-hypertensive, anti-inflammatory and lipid-lowering medication use. We compared the normotensive and hypertensive groups by using independent t-tests and chi-square tests. The carotid characteristics were plotted according to quartiles of central systolic blood pressure by making use of standard analyses of variance (ANOVA) and the analyses of co-variance (ANCOVA). Pearson correlations done in the normotensive and hypertensive Africans helped to determine covariates for the multiple regression models. We used forward stepwise multiple regression analyses with the carotid characteristics as dependent variables to determine independent associations between variables. Results and Conclusion The cardiovascular measures, including pulse wave velocity, were significantly higher in the hypertensive group (all p≤0.024). The lipid profile, markers of inflammation, endothelial activation and glycaemia, as well as health behaviours, did not differ between the hypertensives and normotensives after adjustments for age, sex, waist circumference, γ-glutamyltransferase, tobacco use and anti-hypertensive medication use. After similar adjustments, all carotid characteristics, except IMT, were significantly different between the groups (all p≤0.008). However, upon additional adjustment for cSBP, significance was lost. The stiffness and functional adaptation seen in this study are not explained by the classic cardio-metabolic risk factors, markers of endothelial activation or health behaviours of the participants. The differences that exist in terms of arterial stiffness between the normotensive and hypertensive groups may be explained by the increased distending pressure in the hypertensive group. Despite their hypertensive status, it seems that there are no structural adaptations in these hypertensive Africans. / MSc (Physiology), North-West University, Potchefstroom Campus, 2015

Submitted in partial fulfilment of the requirements for the Degree of Masters in Technology: Clinical Technology, Durban University of Technology, 2009. / Currently, off-pump coronary artery bypass surgery (OPCAB) is a selectively employed technique for myocardial revascularization used in the majority of heart units worldwide. This strategy obviates the documented deleterious effects of cardiopulmonary bypass. However the occurrence of neurological sequelae associated with OPCAB ranges from minor cognitive dysfunction to major stroke. Haemodynamic instability throughout the positioning, stabilization and interruption of coronary blood flow are regarded as important factors that affect the performance of off-pump surgery. Fluctuations during the perioperative period, in particular manipulation of the heart could result in temporary brain hypoperfusion and neurological sequelae. To predict those patients that are predisposed to cerebral complications, investigators have used neurological monitoring, in particular Near-infra red spectroscopy (NIRS) during cardiac surgery. Aims and Objectives of the study This prospective, observational study was carried out to assess the correlation between cerebral oxygen saturation and central venous saturation during OPCAB surgery. Central venous saturation is an important variable used to assess global tissue perfusion and could therefore be advocated as a surrogate measure of cerebral oxygen saturation. In addition variables such as mean arterial (MAP) pressure, heart rate (HR), patient oxygen saturation (SpO2), partial pressure of carbon dioxide (PcvCO2), haematocrit (Hct) and lactate were also measured to determine if they were independent predictors of cerebral desaturation. This study is one of the first done in the South African population group. iv Methodology Twenty patients undergoing OPCAB surgery from the Cardiothoracic unit at Inkosi Albert Luthuli Central Hospital, Durban, South Africa were recruited in the trial. Cerebral somasensors were placed on the patients forehead to measure left and right cerebral saturations. These sensors were linked by cables to the cerebral monitor (NIRS), INVOS model 5100C. Eight time periods throughout the surgical procedure whereby patients would be haemodynamically unstable were identified. These time periods included, post induction and pre sternotomy, pre and post placement of swabs beneath the heart, pre and post placement of the stabilizer device (Octopus), pre and post snaring of the LAD (left anterior branch of the coronary arteries), pre anastomosis and during anastomosis of the coronary arteries, second sample during anastomosis and post anastomosis, pre and post removal of swabs from beneath the heart, pre and post transfer of the patient to the ICU bed. These time periods constituted the sampling period pre and post manoeuvres. Eight paired measurements, i.e., MAP, PaCO2, HR, Hct, lactate, SpO2, central venous saturation (ScvO2) and cerebral oxygen saturation (rSo2) per patient were taken during these time periods. Recording of cerebral saturations and blood samples from the central venous line were taken during these eight time periods in order to determine the correlation between central venous and cerebral oxygen saturations. Results Strong positive correlations between central venous saturation and cerebral saturation presented in majority of the sampling time periods throughout the study (post induction and pre sternotomy, post placement of swabs beneath the heart, post snaring of the LAD (left anterior branch of the coronary arteries, pre anastomosis and during anastomosis of the coronary arteries, second sample during v anastomosis, pre and post transfer of the patient to the ICU bed). The positive correlation indicates that central venous saturation can be used as a surrogate measure of cerebral oxygen saturation during OPCAB surgery. Conclusion The absence or poor correlation of MAP, HR, PcvCO2, heamatocrit, lactate, and patient saturation to cerebral saturation in this study suggests that insertion of a central venous line (CVP) during OPCAB should be a fundamental clinical requirement.

Submitted in partial fulfilment of the requirements for the Degree of Doctor of Technology: Clinical technology, Durban University of Technology, 2011. / Surgical revascularization of the coronary arteries is a cornerstone of cardiothoracic surgery. The enduring nature of coronary artery bypass grafting (CABG) bespeaks of its history and proven efficacy. However, cerebral deoxygenation during on-pump coronary artery bypass graft surgery may be associated with adverse neurological sequelae. Advanced age and the incidence of preoperative co-morbidity in patients presenting for coronary artery bypass graft surgery increases the potential for stroke and other adverse perioperative outcomes (Murkin, Adams, Quantz, Bainbridge and Novick, 2007). It is hypothesized, that by using the brain as an index organ, interventions to improve cerebral oxygenation would have systemic benefits for cardiac surgical patients. In an attempt to predict those patients that are predisposed to cerebral complications, investigators have used neurological monitoring ie, Near infrared spectroscopy (NIRS) to enhance detection of hypoxic conditions associated with neurological injury (Hoffman, 2006). Serum S100B protein has been used as a biochemical marker of brain injury during cardiac surgery. Elevated levels serve as a potential marker of brain cell damage and adverse neurological outcomes (Einav, Itshayek, Kark, Ovadia, Weiniger and Shoshan, 2008). Aims and Objectives of the study This prospective, quantitative, interventional study was carried out to maintain cerebral tissue oxygen saturation during cardiopulmonary bypass above 75% of the baseline level by implementation of a proposed interventional protocol. The analysis of S100B which is a marker of neurological injury and optimization of regional cerebral oxygen saturation would allow for the formulation of an algorithm which could be implemented during on-pump coronary artery bypass graft surgery as a preventive clinical measure further reducing the risk of neurological injury. Central venous lines (CVP) are inserted routinely during cardiac surgery. Central venous oxygen saturation is a global marker of tissue oxygenation. A secondary aim of the study was to determine if a correlation existed between central venous and cerebral tissue oxygen saturations. If a positive correlation existed then central venous oxygen saturation could be used as a surrogate measure of cerebral tissue oxygen saturation during on-pump coronary artery bypass graft surgery. This study is one of the first done in the South African population group. Methods Forty (40) patients undergoing on-pump coronary artery bypass graft surgery were recruited at Inkosi Albert Luthuli Central Hospital. Patients were randomized into a control group (n=20) and interventional group (n=20) using a sealed envelope system. The envelope contained designation to either group. Envelopes were randomly chosen. Intraoperative regional cerebral oxygen saturation (rSO2 ) monitoring with active display and treatment intervention protocol was administered for the interventional group. In the control group regional cerebral oxygen saturation monitoring was not visible to the perfusionist operating the heart lung machine during cardiopulmonary bypass (blinded). Recording of regional cerebral saturation was conducted by an independent person (another perfusionist) who was not involved in the management of the case so as to ensure that no interventions were carried out on the control group. Arterial blood samples for the measurement of serum S100B were taken pre and postoperatively. An enzyme immunoassay (ELISA) was used for the quantitative and comparative measurement of human S100B concentrations for both groups. Central venous oxygen saturation was monitored from the CVP using the Edwards Vigileo monitor. Cerebral monitoring constituted the use of Near infrared spectroscopy monitoring using the Invos 5100c, Somonetics Corp, Troy MI monitor. Adhesive optode pads were be placed over each fronto- temporal area for cerebral oxygen measurement. During cardiopulmonary bypass, eight time period measurements of mean arterial pressure (MAP), heart rate, temperature, activated clotting time (ACT), patient oxygen saturation (SpO2), partial pressure of carbon dioxide (pCO2), haematocrit, lactate, pH, haemoglobin (Hb), base excess (BE), potassium (K+), sodium (Na+), glucose, calcium (Ca2+), central venous oxygen saturation (ScvO2), cerebral tissue oxygen saturation (rSO2), fraction inspired oxygen (FiO2 ), sweep rate, pump flow rate (cardiac index), and percentage isoflurane per patient were taken. The time periods when data was recorded included: 5 minutes after onset of cardiopulmonary bypass, aortic cross clamping, after cardioplegic arrest, during distal anastomosis, during proximal anastomosis, during rewarming, after aortic cross clamp release and before termination of cardiopulmonary bypass. Baseline measurements were also taken. Clinical data recorded for both groups included: the number of grafts performed, cardiopulmonary bypass time, cross clamp time, red blood cells administered (packed cells), amount of adrenalin infused and total cerebral desaturation time. A prioritized intraoperative management protocol to maintain rSO2 values above 75% of the baseline threshold during cardiopulmonary bypass was followed. Cerebral desaturation was defined as a decrease in saturation values below 70% of baseline for more than one minute. Interventions commenced within 15 seconds of decrease below 75% of baseline value. Results The results of the study show that there was a highly significant difference in the change in S100B concentrations pre and post surgery between the interventional and control groups. The intervention vii group showed a smaller increase in S100B concentration of 37.3 picograms per millilitre (pg/ml) while the control group showed a larger increase of 139.3 pg/ml. Therefore, the control group showed a significantly higher increase in S100B concentration over time than the intervention group (p < 0.001). Maximizing pump flow rates was the most common intervention used (45 times) followed by maintaining partial pressure of carbon dioxide to approximately 40 mmHg (28 times), increasing mean arterial pressure by administration of adrenalin (11 times) and administration of red blood cells to increase haematocrit (11 times). There was a highly statistically significant treatment effect within the intervention group for each of the above interventions compared with no intervention. The above mentioned interventions significantly affected right and left cerebral oxygen saturations. However, administration of red blood cells was not found to significantly increase right (p = 0.165) and left (p = 0.169) cerebral oxygen saturation within the intervention group. The study highlighted a significant difference between the intervention and control groups in terms of cerebral desaturation time (p <0.001). The mean desaturation time for the control group was 63.85 minutes as compared to 24.7 minutes in the interventional group. Cerebral desaturation occurred predominantly during aortic cross clamping, distal anastomosis of coronary arteries and aortic cross clamp release. Predictors of cerebral oxygen desaturation included, partial pressure of carbon dioxide (pCO2), temperature, pump flow rate (LMP), mean arterial pressure (MAP), haematocrit, heart rate (HR) and patient oxygen saturation (SpO2). Central venous oxygen saturation was not significantly related to right (p = 0.244) or left (p = 0.613) cerebral oxygen saturations. Therefore central venous oxygen saturation cannot be used as a surrogate measure of cerebral tissue oxygen saturation during on-pump coronary artery bypass graft surgery. viii Conclusion These findings demonstrate the positive effect of optimizing cerebral oxygen saturation using an interventional protocol on markers of neurological injury (S100B). Optimization of pump flow rate, partial pressure of carbon dioxide and mean arterial pressure would result in increased cerebral oxygen saturation levels and a reduction in neurological injury. Therefore, an algorithm incorporating these interventions can be formulated. Monitoring specifically for brain oxygen saturation together with an effective treatment protocol to deal with cerebral desaturation during on-pump CABG must be advocated.

No description available.

Compliant (flexible) structures play an important role in several biofluid problems including flow in the lungs, heart and arteries. Atherosclerosis is a vascular disease which causes a remodelling of the arterial wall causing a restriction (stenosis) by thickening the intima and the formation of vascular plaque by the deposit of fatty materials. This remodelling alters the compliance of the artery stiffening the arterial wall locally. A common location for this to occur is in the carotid artery which supplies blood to both the brain and the face. It can lead to complete occlusion of the artery in the extreme case and is a major cause of stroke and ischemic infarction. Stroke is the third largest cause of death in the U.S.A., but even if not fatal it can cause coma, paralysis, speech problems and dementia. Atherosclerosis causes a change in the local hemodynamics. It can produce areas of flow separation and low wall shear stress, which can lead to endothelial dysfunction and to promotion of plaque growth. In-vitro modelling with artificial flow phantoms allows the fluid mechanics of the circulatory system to be studied without the ethical and safety issues associated with animal and human experiments. Extensive work has been performed using both experimental and computational techniques to study rigid models representing the arterial system. Computational methods, in which the equations governing the flow and the elastic walls are coupled, are maturing. There is a lack of experimental data in compliant arterial systems to validate the numerical predictions. This thesis sets out to address the problems associated with the in vitro experimental analysis of compliant structures representing the human vasculature. A novel construction technique that produced idealised compliant geometries representing both a healthy and stenosed carotid artery from transparent silicone material was developed. A complete analysis was performed of the circumferential and longitudinal response of the geometry, which allowed for dynamic similarity between in vitro and in vivo conditions to be achieved. Inherent difficulties associated with thin walled phantom construction were overcome, which included the design of a novel endplate that allowed for a smooth transition from the flow system to the flow phantom and a bottom up silicone injection system that ensured the phantom was free of bubbles. The final phantom evolution had a wall thickness that could be produced to within a tolerance of 5%. The constructed flow phantom was ported to a flow system producing a physiological inlet flow waveform scaled to in vitro conditions via Reynolds and Womersley number matching. Experimental analysis was performed using a laser based optical technique, particle image velocimetry (PIV). A novel Light Emitting Diode (LED) illumination system was also implemented to obtain to obtain high speed planar PIV measurements. The combined set up of the LED light source, driver unit components and fibre optics for high speed imaging costs in the region of $US 650 which provides a far cheaper option in comparison to the pulse laser system (In the region of $US 50,000). Results obtained in the healthy geometry were compared to a rigid geometry with the same dimensions. It was found that compliance reduced the peak velocity experienced. It also caused a reduction in wall shear stress (WSS) observed and acted to ameliorate the magnitude of the WSS. This is physiologically significant as high WSS can promote atherosclerosis. The introduction of a stenosis caused an increase in the peak velocity observed over the cardiac cycle. A large increase in WSS can be seen to occur in the stenosis throat in both a symmetric and asymmetric stenosed geometry. It is also evident that stenosis eccentricity is important, with asymmetry (where the centre of the stenosis does not coincide with the centre of the artery) producing a major change in WSS and flow field. The study of the flow field downstream of a symmetric stenosis exit showed a Kelvin-Helmholtz vortex ring system to occur between the jet exiting the stenosis throat and the low velocity reverse flow region that surrounded it. The strength of these vortices varied between the acceleration and deceleration phase, demonstrating the failings of a quasi-steady assumption. It was shown that varying the external pressure applied to the flow phantom, along with stenosis eccentricity, affected the inlet flow and pressure waveform and the failings of the common assumption to idealise the physiological flow wave with a sinusoidal input was presented.

Monocrotaline is a pyrrolizidine alkaloid found in plants implicated in livestock and human poisoning. Laboratory rats given monocrotaline develop pulmonary hypertension and right heart hypertrophy in the weeks following administration of the chemical. Lung weight increases and right heart hypertrophy correlate with increased pulmonary artery pressure. Rats which consumed monocrotaline drinking water (20 mg/l) for only 4 days developed significant increases in lung and heart weights 14 days after exposure began. This exposure was equivalent to a dose of 15 mg/kg. Other treatment combinations of time (0-10 days exposure) and monocrotaline concentration (5-60 mg/l in drinking water) were tested. The accumulative dose calculated for each of the treatment combinations which produced toxicity was in the range of 15 to 20 mg/kg. Monocrotaline injury appears to be cumulative, but organ weight increases reverse once exposure is stopped. As pulmonary hypertension develops and pulmonary arteries hypertrophy, the force with which isolated pulmonary artery segments contract decreases. This is a loss of efficacy rather than potency to the contracting agents KCl, norepinephrine, and 5-hydroxytryptamine. Relaxation of arteries under conditions of potassium-return (a measure of Na⁺/K⁺ ATPase activity) was also altered by monocrotaline treatment. In vivo monocrotaline treatment had little effect on the force of K⁺-return relaxation. However, the rate at which arteries relaxed was significantly decreased following 4 days ingestion of monocrotaline drinking water (20 mg/l). In vitro ouabain treatment and endothelial injury also decreased the rate of K⁺-return relaxation. Another Na⁺/K⁺ ATPase activity, ⁸⁶Rb⁺ uptake, was decreased following monocrotaline treatment only when 5-hydroxytryptamine was present and only uptake associated with the endothelium was affected. These studies utilized a very low exposure to monocrotaline (4 days ingestion of 20 mg/l monocrotaline drinking water or 15 mg/kg) to produce toxicity in rats. Monocrotaline-induced toxicity measured 20 days after treatment included right heart and lung hypertrophy and decreased contractions of isolated pulmonary arteries. Monocrotaline treatment decreased the rate of Na⁺/K⁺ ATPase-dependent relaxation of isolated pulmonary arteries 4 days after treatment began.

Depression is highly prevalent in coronary artery disease (CAD) and confers an increased risk of morbidity and mortality, yet mechanisms are unknown. Platelet activating factor (PAF) lipids are associated not only with CAD but also with inflammation, oxidative/nitrosative stress, vascular endothelial dysfunction and platelet reactivity which are proposed etiopathological mechanisms for depression. This study investigated the relationship between PAF species and depressive symptoms in 20 CAD patients. Plasma analyses were performed using electrospray ionization mass spectrometry (precursor ion scan). Primary analysis revealed no association between the potent pro-inflammatory PAF PC(O-16:0/2:0) and depressive symptoms measured by the Hamilton Depression Rating Scale [HAM-D] (F=0.405, p=0.533) or Beck Depression Inventory [BDI]-II (F=0.120, p=0.733) in a linear regression. Exploratory analyses revealed potential associations between greater PC(O-18:1/0:0) and greater HAM-D score and greater PC(O-22:6/2:0) concentrations with a greater BDI-II score. This study suggests that specific PAFs might be biomarkers for depressive symptoms in CAD patients.

Depression is highly prevalent in coronary artery disease (CAD) and confers an increased risk of morbidity and mortality, yet mechanisms are unknown. Platelet activating factor (PAF) lipids are associated not only with CAD but also with inflammation, oxidative/nitrosative stress, vascular endothelial dysfunction and platelet reactivity which are proposed etiopathological mechanisms for depression. This study investigated the relationship between PAF species and depressive symptoms in 20 CAD patients. Plasma analyses were performed using electrospray ionization mass spectrometry (precursor ion scan). Primary analysis revealed no association between the potent pro-inflammatory PAF PC(O-16:0/2:0) and depressive symptoms measured by the Hamilton Depression Rating Scale [HAM-D] (F=0.405, p=0.533) or Beck Depression Inventory [BDI]-II (F=0.120, p=0.733) in a linear regression. Exploratory analyses revealed potential associations between greater PC(O-18:1/0:0) and greater HAM-D score and greater PC(O-22:6/2:0) concentrations with a greater BDI-II score. This study suggests that specific PAFs might be biomarkers for depressive symptoms in CAD patients.

M.Tech. (Chiropractic) / Please refer to full text to view abstract