No abstract

The important role of the vascular endothelium in cardiovascular health is increasingly recognized. However, mature endothelial cells possess limited regenerative capacity. There is therefore much interest in circulating endothelial progenitor cells (EPCs) among the scientific community, especially into their purported role in maintenance of endothelial integrity and function, as well as postnatal neovascularization. It has been suggested that these cells might not only be responsible for the continuous recovery of the endothelium after injury/damage, but also might take part in angiogenesis, giving the hope of new treatment opportunities. Indeed, there is accumulating evidence showing reduced availability and impaired EPC function in the presence of both cardiovascular disease and associated comorbid risk factors. Thus, many studies into the potential for use of EPCs in the clinical setting are being undertaken. The goal of this review article is to provide an overview of data relevant to the clinical role of EPCs and perspectives for treatment of cardiovascular disorders.

Aspirin is well recognized as an effective antiplatelet drug for secondary prevention in subjects at high risk of cardiovascular events. However, most patients receiving long-term aspirin therapy still remain at substantial risk of thrombotic events due to insufficient inhibition of platelets, specifically via the thromboxane A2 pathway. Although the exact prevalence is unknown, estimates suggest that between 5.5% and 60% of patients using this drug may exhibit a degree of "aspirin resistance," depending upon the definition used and parameters measured. To date, only a limited number of clinical studies have convincingly investigated the importance of aspirin resistance. Of these, few are of a sufficient scale, well designed, and prospective, with aspirin used at standard doses. Also, most studies do not sufficiently address the issue of noncompliance to aspirin as a frequent, yet easily preventable cause of resistance to this antiplatelet drug. This review article provides a comprehensive overview of aspirin resistance, discussing its definition, prevalence, diagnosis, and therapeutic approaches. Moreover, the clinical implications of aspirin resistance are explored in various cardiovascular disease states, including diabetes mellitus, hypertension, heart failure, and other similar disorders where platelet reactivity is enhanced. (J Am Coll Cardiol 2008;51:1829-43)

The Vicorder and SphygmoCor devices provide reliable estimates of cSBP when calibrated to invasive pressure. When calibrated to brachial BP, both devices underestimated cSBP, although this was attenuated when SphygmoCor was calibrated to brachial MAP/DBP. Vicorder may be a simple alternative to tonometry-based methods for noninvasive assessment of cBP.

With a prevalence in excess of 20%, hypertension is a common finding among Western adult populations. Hypertension is directly implicated in the pathophysiology of various cardiovascular disease states and is a significant contributor to ill health, leading to an excess of both morbidity and mortality. The etiology of hypertension has been explored in depth, but the pathophysiology is multifactorial, complex, and poorly understood. Recent interest has been directed toward investigating the purported role of the endothelium, which acts as an important regulator of vascular homeostasis. Endothelial dysfunction is now recognized to occur in hypertension, regardless of whether the etiology is essential or secondary to endocrine or renal processes. Nitric oxide (NO) is a volatile gas produced by endothelial cells that acts to maintain vascular tone. Reduced bioavailability of NO appears to be the key process through which endothelial dysfunction is manifested in hypertension. The result is of an imbalance of counteracting mechanisms, normally designed to maintain vascular homeostasis, leading to vasoconstriction and impaired vascular function. It has become increasingly apparent that these changes may be effected in response to enhanced oxidative stress, possibly as a result of systemic and localized inflammatory responses. This article provides an overview of endothelial dysfunction in hypertension and focuses on the purported role of oxidative stress and inflammation as the catalysts for this process.