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Biomedical subjects

Christopher J Boos

Publications and source records attributed to Christopher J Boos.

At least 19 recordsLinked to original sources
PubMed2006

Circulating endothelial cells in cardiovascular disease.

Quantification of circulating endothelial cells (CECs) in peripheral blood is developing as a novel and reproducible method of assessing endothelial damage/dysfunction. The CECs are thought to be mature cells that have detached from the intimal monolayer in response to endothelial injury and are a different cell population to endothelial progenitor cells (EPCs). The EPCs are nonleukocytes derived from the bone marrow that are believed to have proliferative potential and may be important in vascular regeneration. Currently accepted methods of CEC quantification include the use of immunomagnetic bead separation (with cell counting under fluorescence microscopy) and flow cytometry. Several recent studies have shown increased numbers of CECs in cardiovascular disease and its risk factors, such as unstable angina, acute myocardial infarction, stroke, diabetes mellitus, and critical limb ischemia, but no change in stable intermittent claudication, essential hypertension, or atrial fibrillation. Furthermore, CEC quantification at 48 h after acute myocardial infarction has been shown to be an accurate predictor of major adverse coronary events and death at both 1 month and 1 year. This article presents an overview of the pathophysiology of CECs in the setting of cardiovascular disease and a brief comparison with EPCs.

Cardiovascular Diseases↗
PubMed2006

Blood clotting, inflammation, and thrombosis in cardiovascular events: perspectives.

Worldwide, cardiovascular disease (CVD) is a leading cause of death. Endothelial dysfunction is now recognized to be a key platform for the pathophysiological effects of atherosclerosis. It is now well accepted that atherosclerosis is not merely a benign and passive process, but is in fact a dynamic and progressive disease arising from a combination of endothelial damage/dysfunction, inflammation, thrombosis and coagulation leading to potential clot-related vessel occlusion. The between inflammation, thrombosis and coagulation in the pathogenesis of CVD is more than simply association, as it clear that these processes are critically influenced by one another. In this preface we present a basic overview of the evidence in support of this relationship, which will be expanded upon in sequential chapters. In addition we briefly discuss a number of novel anticoagulants which not only reduce coagulation, but have ancillary antiinflammatory properties, thus further supporting the triad of inflammation, thrombosis and coagulation in the development of CVD.

Animals↗
PubMed2006

Temporal and venepuncture-related decline in circulating endothelial cell capture from mixed venous blood.

BACKGROUND: The quantification of circulating endothelial cells (CECs) in whole blood has evolved as a novel method for the assessment of endothelial function, although major methodological issues remain. We hypothesized that there is a temporal decline in CEC counts in static venesected blood and that venepuncture itself may lead to increased CEC detachment. METHODS: CEC isolation was performed using the immunobead method. For the temporal decline experiment, we included 52 patients presenting with acute coronary syndrome (ACS). We performed CEC counts immediately and at 4 and 24 h later. For the venepuncture decline experiment, we studied 40 patients with stable cardiovascular disease (CVD). CEC counts were determined from the first 4 mL of aspirated venous blood and compared with counts obtained from a subsequent 4 mL sample of blood after at least 7.5 mL of blood had been collected. RESULTS: Among the ACS patients there was a significant temporal decline in CEC counts in static venous blood over a 24 h period (p = 0.013). Among the patients with stable CVD, the median CEC counts obtained from the initial 4 mL of aspirated venous blood were significantly higher (by 32%) than that obtained from the later 4 mL of aspirated venous blood (p = 0.041). CONCLUSIONS: We demonstrated a significant temporal fall in CEC numbers in static venous blood over 24 h following venesection. Furthermore, we have shown that CEC counts are higher in the initial aspirated blood compared with that aspirated from the same needle subsequently. These data would have implications for how CEC determination is undertaken by researchers in studies related to ACS or CVD.

Adult↗
PubMed2006

Detection and quantification of mature circulating endothelial cells using flow cytometry and immunomagnetic beads: a methodological comparison.

Mature circulating endothelial cells (CECs) are novel cellular markers of endothelial damage/dysfunction. The two main techniques of CEC enumeration are flow cytometry (FC) and immunomagnetic bead (IB) isolation. Both quantify CECs accurately, but a direct comparison of both methods has not been reported. We sought to assess the agreement between the two methods in two patient populations, and a group of healthy subjects, with emphasis given to methodological issues. We included 34 patients with acute coronary syndrome (ACS), 60 patients with primary breast cancer (PBC) and 30 healthy controls (HC). We quantified CECs using the IB method [CD146 and FITCUlex europaeus lectin-1] and FC [CD45, CD34 and CD146]. Bland-Altman plots suggested reasonable agreement (<5% of events >2 standard deviations from the mean) between FC and the IB methods for CEC quantification in whole blood in the two disease groups (ACS and PBC), but not among the HCs. There were no statistically significant differences in CEC levels by the two methods amongst all three patient groups. There is reasonable agreement between the FC and the IB methods for mature CEC quantification in whole blood, especially amongst disease groups. The agreement between the two methods appears to weaken in healthy controls, and at lower and higher absolute CEC counts.

Adult↗
PubMed2006

Is hypertension an inflammatory process?

The risk factors for hypertension are only partly known, and accounts for the some of the deficiencies in current primary prevention strategies and in the design of new drugs for the management of this common condition. Recently, chronic low grade low-grade inflammation has been identified as an integral part in the pathogenesis of vascular disease. Of note, inflammation may also be implicated in the development of hypertension, either as a primary or secondary event. Indeed, several clinical studies have demonstrated increased numbers of well recognised pro-inflammatory markers, such as high sensitive C-reactive protein (hsCRP), in patients with hypertension, even after adjustment for potential confounding factors. Furthermore, elevated hsCRP levels have also been shown to be predictive for the development of hypertension in prehypertensive and normotensive patients. Pathophysiologically, inflammation has been implicated in both endothelial (dys)function and arterial stiffness in hypertension, with reduced availability of nitric oxide (NO) being integral to this process. Oxidative stress also appears to be a key feature in the reduced availability of NO and is aggravated by increased circulating angiotensin II (Ang II). Importantly, there is some evidence that drugs commonly used in the management of hypertension, such as statins, angiotensin converting enzyme inhibitors and Ang II receptor blockers have anti-inflammatory properties that can positively influence outcomes in patients with hypertension. The inflammatory state in hypertension may pose a new therapeutic target for future drug design.

Angiotensin II↗
PubMed2005

Is atrial fibrillation an inflammatory disorder?

There is mounting evidence to support the influence of inflammation in the pathogenesis of atrial fibrillation (AF). Indeed, AF is associated with increased levels of known inflammatory markers, even after adjustment for confounding factors. The renin-angiotensin-aldosterone system (RAAS) appears to play a key role in this process. Atrial biopsies from patients with AF have also confirmed the presence of inflammation. Furthermore, there is preliminary evidence to support a number of drug therapies that have the potential to reduce the clinical burden of AF. In this review, we present an overview of the evidence supporting a link between inflammation and AF, and some of the drug therapies, such as the angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, steroids, fish oils, and vitamin C, that might be efficacious in the prevention of AF by modulating inflammatory pathways.

Ascorbic Acid↗