These data indicate that in habitual smokers, smoking one cigarette causes short-term increases in arterial wall stiffness that might be harmful to the artery and increase the risk for plaque rupture. Except for a higher heart rate, no obvious long-term effect of smoking was observed on hemodynamic variables and arterial stiffness. Because acute cardiovascular events are mainly due to plaque rupture, the short-term effects of smoking might be a more important risk than long-term effects for these acute ischemic events.
Abstract-Epidemiological studies in the past decade have stressed the importance of pulse pressure as an independent risk factor for cardiovascular morbidity and mortality. We briefly review the epidemiological evidence and discuss in more detail the pathophysiological basis for this observation and the therapeutic consequences. We focus on the vascular determinants of increased pulse pressure. Both longitudinal and cross-sectional components of the vascular system contribute to the shape of the arterial pressure wave and, thereby, to pulse pressure. The primary longitudinal component is the architecture of the arterial tree, which determines the major reflection sites for the pressure wave. The cross-sectional architecture of the vascular system consists of a geometric (diameter) and a structural (composition vessel wall) component. Both diameter and composition of the vessel wall vary greatly when going from central to more peripheral arteries. We review the implications for the functional properties of various arterial segments. Finally, we discuss the therapeutic consequences of targeting pulse pressure rather than mean blood pressure with various drug classes. Among the antihypertensive agents, nitrates, NO donors, and drugs that interfere with the renin-angiotensinaldosterone system may offer useful tools to lower pulse pressure, in addition to mean blood pressure. Future developments may include non-antihypertensive agents that target collagen or other components of the arterial wall matrix. However, large-scale clinical trials will have to confirm the therapeutic value of these agents in the treatment of increased pulse pressure and arterial stiffness. Key Words: antihypertensive agents Ⅲ arterial stiffness Ⅲ epidemiology Ⅲ pulse pressure Ⅲ blood pressure H ypertension is a cardiovascular (CV) risk factor, the mechanisms of which are generally attributed to the reduction in the caliber or number of small arteries or arterioles with a resulting increase in total peripheral resistance and mean blood pressure (MBP). MBP, the product of cardiac output and total peripheral resistance, refers to steady phenomena, considering pressure and flow as constant over time. This definition does not take into account that blood pressure and flow fluctuate during the cardiac cycle. In clinical practice, pressure is defined in terms of systolic (SBP) and diastolic (DBP) blood pressure, which refer to a pulsatile phenomenon, with SBP and DBP representing the extremes of the blood pressure oscillation around a mean value, the MBP. In fact, the blood pressure curve may be considered as the summation of a steady component, MBP, and a pulsatile component, the pulse pressure (PP). 1 Besides the pattern of left ventricular ejection, the determinants of PP (and SBP) are the cushioning capacity (compliance) of arteries and the timing and intensity of arterial wave reflections. 1 Compliance of arteries depends on arterial volume and the elastic properties (distensibility) of arterial walls. Compliance and distensibility are quantit...
In conclusion, the vessel wall movement detector system has a good technical reproducibility. Intraobserver intrasession and intersession variability are comparable, and are larger in muscular arteries. This might be due to a larger variation in tone of these arteries, which are under permanent neurohumoral control. Interobserver intrasession variability was larger than intraobserver variability and might be influenced by differences in observers' skill and spontaneous variation in vessel wall properties.
A reduced venous compliance (VC) and inadequate venoconstriction may impair hemodynamics during hemodialysis, the first by impairing plasma volume preservation and by inducing a steep fall in central venous pressure (CVP) during minor plasma volume loss, the second by inadequate mobilization of hemodynamically inactive blood volume. For the protocol A, the relation between VC, the fall in plasma volume and the decline in central venous pressure (CVP) was assessed in 12 hemodialysis (HD) patients, aged 40 to 74 years, during isolated ultrafiltration (UF). The patients were ultrafiltrated for one hour at an UF rate of 1 to 1.5 liter/hr. VC was measured by strain gauge plethysmography with direct i.v. pressure measurements. CVP was assessed directly via a subclavian catheter. PVP was measured using the serial hematocrit method. VC correlated inversely with the fall in plasma volume (r = -0.66; P less than 0.025) and with the fall in CVP (corrected for UF volume) (r = -0.62; P less than 0.025). In the protocol B, the constriction of veins and resistance vessels was assessed sequentially during isolated UF and during UF combined with bicarbonate HD (UF + HD) by measuring the change in venous tone (VT) and vascular resistance (FVR) of the forearm. Twelve HD patients were studied (age 30 to 64 years). VT and FVR were measured using strain gauge plethysmography. The UF rate was equal during isolated UF and UF + HD (1 liter/hr). In six patients, the measurements were started with isolated UF and in six patients with UF + HD.(ABSTRACT TRUNCATED AT 250 WORDS)
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