Current Vascular Pharmacology

ISSN: 1570-1611

Upcoming Articles


Occurrence and Clinical Impact of Microembolic Signals (MES) in Patients with Chronic Cardiac Diseases and Atheroaortic Plaques - A Systematic Review
Ralf Dittrich and E. Bernd Ringelstein
[Abstract]


Models to Study Atherosclerosis: A Mechanistic Insight
V. Singh, R.L. Tiwari, M. Dikshit and M.K. Barthwal
[Abstract]


Postprandial Glucose - A Potential Therapeutic Target to Reduce Cardiovascular Mortality
R. Peter, O.E. Okoseime and A. Rees
[Abstract]




Abstracts


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Occurrence and Clinical Impact of Microembolic Signals (MES) in Patients with Chronic Cardiac Diseases and Atheroaortic Plaques - A Systematic Review
Ralf Dittrich and E. Bernd Ringelstein

Background: In various cardiac diseases, thrombembolism constitutes a major risk, and in these patients clinically silent microembolic signals (MES) are detectable within the transcranial Doppler frequency spectrum (TCD) of the major brain arteries. MES are already an accepted surrogate parameter of the future risk of stroke in patients with carotid artery stenosis. The aim of this review is to summarize and evaluate the data about occurence and clinical impact of MES in patients with chronic cardiac diseases and to clarify whether cardiogenic MES can serve as a surrogate parameter of the heart’s future thrombembolic risk as well.

Methods: We performed a systematic MEDLINE search and reviewed the currently available literature about chronic cardiac diseases and atheroaortic plaques leading to MES apart from cardiosurgical procedures.

Conclusion: The cardiac conditions producing MES are heterogenous and therefore the prevalence of MES is highly variable. The data in patients with acute or after myocardial infarction, endocarditis, patent foramen ovale, mitral valve prolapse, dilatative cardiomyopathy and intracardiac thrombus is promising but only small patient cohorts have been investigated by means of TCD in these categories. MES in atrial fibrillation, or derived from atheroaortic plaques, have been investigated more intensively, but again larger cohorts need to be explored to draw firm conclusions. In all cardiac diseases there is a lack of large prospective studies allowing to reliably correlating MES with clinical events. Compared to carotid artery disease, the current knowledge about the impact of cardiogenic MES on the patient’s risk is sparse. This should encourage the clinical research in this promising field.


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Models to Study Atherosclerosis: A Mechanistic Insight
V. Singh, R.L. Tiwari, M. Dikshit and M.K. Barthwal

The recent failure of candidate drugs like cholesterol ester transfer protein (CETP) and acyl-CoA:cholesterol acyltransferase (ACAT) inhibitors calls for a revised approach for screening anti-atherosclerotic drugs and development of new models of atherosclerosis. For this it is important to understand the mechanism of the disease in a particular model. Models simultaneously showing hyperlipidemia, inflammation and associated complications of diabetes and hypertension will serve the purpose better as they mimic the actual clinical condition. Besides this, analyzing candidate molecules in vivo, in vitro and at various levels of atherosclerosis progression is important. Models based on various cells and process involved in atherosclerosis should be used for screening candidate molecules. The challenge lies in bridging the gap between genetically friendly small animal and human-like bigger animal models. Sequencing of the mouse and human genome, development of a single nucleotide polymorphism (SNP) database and in silico quantitative trait loci (QTL) linkage analysis may enhance the understanding of atherosclerosis and help develop new therapeutic targets.


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Postprandial Glucose - A Potential Therapeutic Target to Reduce Cardiovascular Mortality
R. Peter, O.E. Okoseime and A. Rees

Cardiovascular disease (CVD) accounts for almost 75% of mortality in subjects with type 2 diabetes (T2DM). The relationship between hypertension, dyslipidaemia and CVD is now well established. However, the precise link between glycaemia and macrovascular complications has remained unclear. There is now emerging evidence that postprandial glucose (PPG) contributes significantly to CVD risk, although to date there are no large scale interventional studies underway which test the hypothesis that targeting PPG will reduce CVD risk. Until recently, there was no consensus about the definition of postprandial hyperglycaemia. The International Diabetes Federation (IDF) has now developed new clinical guidelines for postprandial glucose and recommend that 2-hour post meal glucose levels are kept <7.8 mmol/L. In the last few years more has become known about the cellular mechanisms triggered in response to glucose excursions which may explain this increased susceptibility to CVD. Recently, investigation into the contribution of PPG to HbA_1c in subjects with T2DM, has shown that this is maximal in relatively well controlled diabetic subjects. Hence PPG is emerging as a legitimate therapeutic target to minimise CVD risk.

This review addresses the evidence linking postprandial hyperglycaemia to cardiovascular disease, the cellular mechanisms explaining this enhanced risk and a therapeutic strategy to address postprandial glucose excursions.