Effects of a lack of aortic "windkessel" properties on the left ventricle.

Maeta, Hajime; Hori, Motokazu

doi:10.1253/jcj.49.232

Cited by 40 publications

(24 citation statements)

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“…Therefore, the LV must generate excessive energy to maintain the cardiac output through an unchanged peripheral resistance. This results in an increase in LV work, consequently leading to hypertrophy [9]. As previously reported [9, 10], the use of woven Dacron grafts for extra-anatomic aortic bypass procedures may result in LV hypertrophy due to the significant systolic pressure increase from the loss of the natural aortic Windkessel property.…”

Section: Discussionmentioning

confidence: 90%

“…Previous studies [2, 9, 12, 16, 19, 20] have consistently shown that reducing compliance leads to an increase in systolic and pulse pressure, but their findings have varied with regard to the other variables measured. Our study differs from the previous studies in 2 aspects: first, it reports long-term data after nonstenotic banding of the aorta and, second, the reduction in aortic compliance was done in a manner preserving the native aortic flow and geometry.…”

Section: Discussionmentioning

confidence: 99%

“…Clinical observations have documented LV hypertrophy after an ascending-abdominal aorta bypass for thoracoabdominal aneurysm, most likely a result of increased aortic input impedance [9]. Later reports correlated LV hypertrophy seen after proximal or long bypass procedures with noncompliant grafts, with increased characteristic impedance, decreased Windkessel effect of the proximal aorta and increased systolic wall stress [4, 5, 10, 11].…”

Section: Introductionmentioning

confidence: 99%

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Left Ventricular Hypertrophy Induced by Reduced Aortic Compliance

et al. 2009

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Aim: It was the aim of this study to investigate the long- term effects of reduced aortic compliance on cardiovascular hemodynamics and cardiac remodeling. Method: Sixteen swine, divided into 2 groups, a control and a banding group, were instrumented for pressure and flow measurement in the ascending aorta. Teflon prosthesis was wrapped around the aortic arch in order to limit wall compliance in the banding group. Hemodynamic parameters were recorded throughout a 60-day period. After sacrifice, the mean cell surface of the left ventricle was documented. Results: Banding decreased aortic compliance by 49 ± 9, 44 ± 16 and 42 ± 7% on the 2nd, 30th and 60th postoperative day, respectively (p < 0.05), while systolic pressure increased by 41 ± 11, 30 ± 11 and 35 ± 12% (p < 0.05), and pulse pressure by 86 ± 27, 76 ± 21 and 88 ± 23%, respectively (p < 0.01). Aortic characteristic impedance increased significantly in the banding group. Diastolic pressure, cardiac output and peripheral resistance remained unaltered. The mean left ventricular cell surface area increased significantly in the banding group. Conclusions: Acute reduction in aortic compliance results in a significant increase in characteristic and input impedance, a significant decrease in systemic arterial compliance and a subsequent increase in systolic and pulse pressures leading to left ventricular hypertrophy.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Left Ventricular Hypertrophy Induced by Reduced Aortic Compliance

et al. 2009

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“…ISH can be considered a model of predominant aortic stiffening, contributing to early reflected waves that arrive in early systole, superimpose on the forward wave, and boost the systolic BP further, whereas mean and DBP are marginally modified. Indeed, animal experiments 37 showed that the replacement of the normal aorta by a stiff Dacron graft in dogs, increased to a large extent SBP and PP, minimally lowered DBP and did not change mean BP, as predicted by the mechanical properties of the arterial system. This observation implies that lowering BP with vasodilators should theoretically lower DBP to a much lesser extent than SBP.…”

Section: To What Level May Dbp Be Safely Lowered In Elderly Patients mentioning

confidence: 98%

Large and Small Artery Cross-Talk and Recent Morbidity-Mortality Trials in Hypertension

2009

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T he results of recent large clinical trials in hypertension invite re-evaluation of the mechanisms of action of antihypertensive drugs on large and small arteries in the context of their effects on cardiovascular outcomes. By increasing our understanding of the relationship between large and small artery damage, target organ damage, and clinical end points, the trials provide us with new insights into the management of hypertension. This short review aims at analyzing the following: (1) whether ␤-blockers may exert deleterious effects on cardiovascular CV prevention through the reduction in heart rate (HR) or the lack of arterial remodeling; (2) whether long-term arterial remodeling can explain the "legacy" effect of multifactorial treatment in patients with hypertension and type 2 diabetes mellitus (T2D); and (3) to which level diastolic BP (DBP) can be safely lowered in elderly patients with isolated systolic hypertension (ISH). Because these issues have the concept of large/small artery cross-talk in common, we analyzed it first. Large and Small Artery Cross-Talk in HypertensionThe damaging effect of local pulse pressure (PP) has been well demonstrated on large arteries and, to a lesser extent, on small arteries. Elevated PP can stimulate hypertrophy, remodeling (increased media:lumen ratio), or rarefaction in the microcirculation, leading to increased resistance to mean flow. Recent studies showed a close relationship between microvascular damage in the heart, brain, retina, and kidney and either PP or arterial stiffness. Indeed, significant relationships have been demonstrated between brachial PP and glomerular filtration rate, 1,2 microalbuminuria, 2 or white matter lesions 3 ; between arterial stiffness and glomerular filtration rate, 4,5 urinary albumin, 5 retinal arteriolar narrowing, 6,7 white matter lesions, 3 or cognitive function 8 ; and between carotid stiffness and glomerular filtration rate. 4,5 Although not all of these relationships are independent of confounding factors, 3 there is a large amount of evidence for linking the pulsatility of BP to target organ damage. A cross-talk between the small and large artery can be exemplified by the following sequence (Figure 1): (1) increased wall:lumen ratio and rarefaction of small arteries 9,10 are major factors for an increase in mean BP; (2) the higher mean BP, in turn, increases large artery stiffness through the loading of stiff components of the arterial wall at high BP levels; and (3) the increased large artery stiffness is a major determinant of the increased PP, which, in turn, damages small arteries 11 in the heart, brain, retina, and the kidney, 12 as seen above, and favors the development of left ventricular hypertrophy, carotid intima-media thickening, and plaque rupture. These various types of target organ damage have been shown to be related to CV events. Thus, the cross-talk between the small and large artery exaggerates arterial damage, following a vicious circle. Antihypertensive treatment, by acting on both small and large arteries,...

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“…In fact, their study was stimulated by reports of left ventricular hypertrophy occurring in patients after bypass between the ascending aorta and the abdominal aorta for thoracoabdominal aortic aneurysm [12]. They reasoned that the abnormal proximal arteries imposed an increased opposition to pulsatile flow.…”

Section: Importance Of Input Impedance On Right Ventricular Performancementioning

confidence: 99%