Advances in Cardiology最新文献

Insulin resistance is associated with increased cardiovascular morbidity and mortality but the underlying mechanism(s) are incompletely understood. Epidemiological data suggest that insulin resistance and arterial stiffness are interrelated. In insulin sensitive-subjects, insulin acutely decreases the augmentation index as measured using pulse wave analysis. In insulin-resistant subjects, this effect of insulin is blunted implying that insulin resistance involves also large arteries. This may provide one mechanism linking insulin resistance and cardiovascular disease.

Assessment of intima-media thickness or of measures of large arteries compliance may identify patients at increased risk for stroke. In fact, carotid atherosclerosis and arterial stiffness are both related to risk factors associated with the occurrence of stroke. In addition, several cross-sectional studies have shown that risk factors associated with the occurrence of stroke have been correlated with carotid atherosclerosis development and progression and with increased arterial stiffness. Some studies have also shown that aortic stiffness is associated with the extent of atherosclerosis in the carotid and in other vascular beds. More importantly, longitudinal studies have demonstrated that carotid atherosclerosis and arterial stiffness are independent predictors of stroke (and other cardiovascular events). Interventional studies have demonstrated that treatment with statins, calcium antagonists, ACE inhibitors, and insulin sensitizers may be particularly effective on slowing the progression or favoring the regression of atherosclerotic changes, and may reduce large artery stiffness. It remains to be proven, in large prospective studies, whether the regression of increased arterial stiffness or of carotid intima-media thickness and plaque have a prognostic significance, i.e. are associated with a reduction of the risk of cerebrovascular events.

Unlabelled: Vascular calcification can occur in either the intimal or medial layers of the arterial wall. Intimal calcification is associated with atherosclerosis, which is characterized by lipid accumulation, inflammation, fibrosis and development of focal plaques. Medial calcification is associated with arterio sclerosis, i.e. age- and metabolic disease-related structural changes in the arterial wall which are related to increased arterial stiffness. It has been hypothesized that vascular calcification, either intimal or medial, may directly increase arterial stiffness. Alternatively, arterial stiffness may contribute to the development of calcification and focal plaque. Ample evidence (i.e. animal data and studies of diabetes and end-stage renal disease) has demonstrated that medial calcification of elastic fibers contributes to increased arterial stiffness. Evidence linking intimal calcification with arterial stiffness is less definitive, partly because it is very difficult to differentiate vascular calcification due to focal plaques (intimal) from medial calcification, and partly because the number of studies has been small.

Conclusion: Current evidence supports that medial calcification is associated with increases in arterial stiffness. The association between intimal (atherosclerotic-associated) calcification and arterial stiffness is less definitive.

Of the atherosclerotic diseases, peripheral arterial disease is the most characterized by its association with systolic hypertension, increased arterial stiffness and disturbed wave reflection. This disease raises the question to which extent sclerosis in 'atherosclerosis' is necessary per se to cause an increase in systolic blood pressure.

Increased aortic stiffness is a consequence of cardiovascular (CV) aging and may be observed in the elderly with or without hypertension. Hypertension and arterial stiffness are independent risk factors for CV events, but such events may also be complicated by atherosclerosis, especially in the older population. The purpose of this chapter is to determine whether, in the presence of atherosclerosis, systolic hypertension in the elderly requires specific drug therapy. It will be shown that, in addition to the targeted drug treatment of associated hypercholesterolemia and/or hyperglycemia, the major problem nowadays is to find specific antihypertensive drugs causing a selective reduction of systolic blood pressure (SBP).

Blood pressure is a complex phenomenon that can be divided into two components: a steady and a pulsatile component. The pulsatile component is estimated by the pulse pressure which is mainly influenced by the large artery stiffness. The purpose of this review was to describe the relation between pulse pressure, cardiovascular risk factors and atherosclerosis. Epidemiological studies have shown positive correlations between pulse pressure and smoking or glucose metabolism impairment. More controversial data have been reported on the relation between blood lipids and large artery stiffness or pulse pressure. In cross-sectional studies, carotid, aortic and coronary plaques were associated with aortic stiffness, particularly echogenic or ulcerative plaques, and in a longitudinal study, the progression of atherosclerosis is accompanied by an increase in pulse pressure. From a pathophysiological point of view, the deleterious influence of most risk factors on endothelial function and the development of atheroma are likely to contribute to these relations. Furthermore, with respect to the connections observed between C-reactive protein, most cardiovascular risk factors, atherosclerotic diseases and pulse pressure, subclinical inflammation might also underlie these relations.

Coronary heart disease is a major cause of death and morbidity. Due to the increased longevity of most developed societies, there is an increasing overlap between arteriosclerosis associated with normal vascular ageing and atherosclerosis associated with cardiovascular risk factors. There is therefore a need for improvements, both in the early identification of individuals at risk, and in cardiovascular risk stratification. Arterial stiffness is an important determinant of cardiovascular risk and can now be measured simply and noninvasively in large populations. This review will therefore focus on the current evidence as to the predictive value of arterial stiffness in relation to coronary events and also on the possible pathophysiological mechanisms linking arterial stiffness and atherosclerosis.

Recent studies have reported positive associations between pulse pressure (PP) and markers of inflammation. These studies are intriguing because they suggest that elevations in PP could induce an inflammatory state and thereby increase the risk of inflammation- related diseases such as atherosclerotic cardiovascular disease. In the present chapter, we review potential mechanisms by which an elevated PP could increase inflammation. We also review human-based studies that have investigated the association between PP and inflammatory biomarkers such as C-reactive protein. The majority of studies support a positive association between PP and inflammatory markers. However, it remains unclear whether the association is truly causal and whether it has relevance in terms of predicting cardiovascular diseases.

Brachial pulse pressure (PP) is an established risk marker for cardiovascular disease. PP is largely determined by the stroke volume in young subjects, although the progressive amplification of pulse wave from central to peripheral arteries could make brachial PP not representative of the central PP in the young. With advancing age, brachial PP better reflects the progressive stiffening of aorta and the large elastic arteries. PP correlates with vascular and cardiac hypertrophy, although the association with cardiac hypertrophy seems more closely attributable to systolic blood pressure (BP). An association has been noted in several longitudinal studies between PP and the incidence of major cardiovascular events. However, some longitudinal studies carried out in subjects with predominantly systolic and diastolic hypertension showed that PP is the dominant predictor of coronary events, while mean BP is the major predictor of cerebrovascular events. Such an assumption may not be held in subjects with isolated systolic hypertension, where a wide PP seems to predict coronary and cerebrovascular events to a similar extent. From a pathophysiological standpoint, a wide PP might reflect diffuse atherosclerotic processes potentially involving also the large coronary arteries. Some data suggest that a wide PP could also represent a direct and independent stimulus for progression of atherosclerosis.

Aging and hypertension interact and are associated with long-term changes in arterial structure and function. Systolic BP is not constant along the arterial tree due to different proportional contributions of forward and reflected pressure waves. Brachial cuff BP values are inadequate to detect these changes. Increased PP is the result of an imbalance between arterial flow and arterial impedance, which can be due to increased effective arterial wall stiffness or to a smaller proportional arterial diameter. After middle age, there is both dilation and stiffening of large arteries, along with increased effective stiffness caused by the corresponding changes in content of collagen, elastin, and VSM in the vascular wall. Intermediate conduit arteries also dilate with age but their functional characteristics remain relatively preserved. In the microcirculation, vasoconstriction, VSM hypertrophy and rarefaction accompany and may contribute to changes in organ function.