Advances in Cardiology最新文献

Type 2 diabetes (DM-2) has become a major global health problem that has been fueled mainly by increasing obesity and aging of the population. Most studies show that arterial stiffening occurs across all age groups in both type 1 diabetes and DM-2, and among those with impaired fasting glucose, impaired glucose tolerance, and the metabolic syndrome. Arterial stiffening in DM-2 results, in part, from the clustering of hyperglycemia, dyslipidemia and hypertension, all of which may promote insulin resistance, oxidative stress, endothelial dysfunction, and the formation of pro-inflammatory cytokines and advanced glycosylation end-products. Likewise, aging may increase arterial stiffening by altering the proportions of elastin and collagen in the aorta. The consequences of arterial stiffening are increased pulse pressure, hypertension, and a greater risk of cardiovascular disease. Treatment strategies to reduce or prevent arterial stiffening include pharmacologic agents that block the renin-angiotensin-aldosterone system, relax vascular smooth muscle, enhance release of nitric oxide from endothelial cells, and break glycosylation end-product cross-links, and fish oil supplementation.

Epidemiological as well as clinical studies have shown that regardless of the severity of renal impairment the cardiovascular mortality in renal disease patients is very high compared to the general population. In uremia, cardiovascular disease is a combination of atherosclerosis, characterized by the presence of highly calcified plaques, and arteriosclerosis, an arterial wall alteration in response to both hemodynamic changes and humoral modifications such as inflammation or calcium-phosphate imbalance. Vascular endothelium, recognized as a large and complex endocrine organ strategically located between the wall of the blood vessel and the blood stream, could be the link between these two processes evolving during the same course.

Central pulse pressure is more likely to reflect the haemodynamic conditions to which the heart and coronary arteries are subjected than is peripheral pulse. We reviewed the data currently available on the correlations between central pulse pressure and both the presence and extent of coronary artery disease, as well as clinical outcomes. Five clinical studies have reported an association between central pulse pressure and the presence of coronary artery disease documented by coronary angiography. Four studies, including three of the previous ones, also found a correlation between central pulse pressure and the extent of coronary artery disease. In one of these studies, however, the correlation was present only in men, whereas no link was found between pulse pressure and coronary artery disease in women. After coronary angioplasty, increased central pulse pressure has been found correlated with the occurrence of restenosis after balloon angioplasty, but not after stent implantation. Finally, the ASCOT-CAFE trial found a positive correlation between pulse pressure and the occurrence of cardiovascular events, confirming the prognostic significance of this parameter.

The material composition and morphology of vulnerable atherosclerotic plaque components are considered to be more important determinants of acute coronary syndromes than the degree of stenosis. Rupture of a plaque causes thrombogenic material to contact the blood, resulting in a thrombus. Rupture-prone plaques contain an inflamed thin fibrous cap covering a large soft lipid pool. Mechanically, rupture occurs when plaques cannot withstand the internal stresses induced by the pulsating blood. These stresses concentrate within/around the cap/edge, since the lipid pool cannot bear much stress. During plaque development these stresses further increase when caps become thinner, lipid pools become larger, or the difference in stiffness (modulus) between the cap and the lipid pool increases. Intravascular ultrasound (IVUS) strain elastography/palpography and IVUS modulus elastography are imaging techniques that assess local plaque elasticity (strain and modulus) based on the principle that tissue deformation (strain) by a mechanical stress is a function of its elastic properties (modulus). Combined use of these techniques provides clinicians an all-in-one modality for detecting plaques, assessing their rupture proneness and imaging their elastic material composition. This chapter describes the terminology and pathophysiology of vulnerable plaques and discusses the techniques behind, the methods for and the validations of the elasticity imaging techniques.

The growing prevalence and associated risk of arterial stiffness provide a major challenge to better understand the underlying causes and the resultant physiological impact of this condition. Structural components within the arterial wall, mainly collagen and elastin, are considered to be major determinants of arterial stiffness. Thus, quantitative and qualitative alterations of collagen and elastin fibers are involved in arterial stiffening that is associated with the aging process and disease states such as hypertension, diabetes, atherosclerosis, and chronic renal failure. Elucidation of mechanisms leading to the above alterations will aid in more specifically targeted therapeutic interventions because currently available cardiovascular medications fall short at reducing the stiffness of the large arteries. Reduction of arterial stiffness will likely have a significant impact on morbidity and mortality of older adults, as well as subjects suffering from cardiovascular and renal diseases.

Animal models of large artery wall stiffness fall into two categories: firstly those that slowly develop multifactorial vascular dysfunction spontaneously, such as the ageing rat. The second type of model consists of those in which a specific pathology is induced by surgical, chemical, or genetic means. Such models are based on a short-term, highly traumatic insult to the arterial wall of a young animal and its acute reaction to such insult. This is very different from the human situation in which changes in wall stiffness arise from the long-term accumulation of relatively minor episodes of vascular insult in the vulnerable elderly.

Arterial elasticity is a common index of medical semiology, easier to understand than blood pressure measurement. This chapter summarizes the most classical aspects which are important to understand in vascular medicine.

Atherosclerosis and its complications represent the leading cause of morbidity and mortality in the industrialized as well as in the developing countries. Classical cardiovascular risk factors have been identified over the past decades leading to recommendations for life style modifications and to the development of efficient and well-tolerated drug regimens aimed at reducing the occurrence of cardiovascular complications. The endothelium due to its position in the circulation is the first organ being exposed to circulating noxious elements and solutes as well as to the mechanical aggressions generated by heartbeats and pulsating blood flow. This review addresses the relevance of the combined effects of the mechanical stress and cardiovascular risk factors on the early phases of atherosclerosis.

High plasma concentrations of the amino acid homocysteine have been associated with atherothrombotic disease, first in individuals with inborn errors of homocysteine metabolism, who have very high plasma homocysteine concentrations, and later also in the general population. In general, the cardiovascular risk associated with hyperhomocysteinemia is significant, but modest and probably differs between populations. High homocysteine concentrations are thought to impair endothelial function, increase oxidative stress, impair methylation reactions, and alter protein structure. Although some studies have shown improvement of vascular surrogate end points, homocysteine-lowering treatment has not yet been associated with a significant reduction of cardiovascular events. Studies that have examined the relationship between plasma homocysteine and arterial stiffness parameters have shown heterogenous results.

This chapter traces the history of nitroglycerin from the initial nitration of glycerol to its widespread clinical use. The pharmacologic differences between nitroglycerin and nitric oxide are described, as well as their similar mechanisms of action. The vasoactivity of nitroglycerin requires a biochemical transformation, the nature of which remains incompletely understood. This poorly defined mechanism probably also relates to the phenomenon of nitroglycerin tolerance. By increasing the distensibility of muscular arteries, nitroglycerin slows pulse wave velocity, reduces wave reflections and alters the shape of the aortic pulse. This alteration reduces the systolic blood pressure and left ventricular after load and helps to explain the usefulness of nitroglycerin in angina pectoris, congestive heart failure and isolated systolic hypertension.