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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mechanical properties of arteries are altered in some rat models of hypertension, and this may influence peripheral resistance and blood pressure as well as some of the complications of hypertension. It has usually been assumed that arterial wall stiffness is increased in hypertension, although recent studies suggest that this may not necessarily be the case in large arteries. We determined whether the mechanics of human resistance arteries are altered in hypertension. Subcutaneous resistance arteries (lumen diameter<300 microm) were isolated from hypertensive and normotensive subjects of similar ages (46+/-3 and 43+/-4 years, respectively). Vessels were mounted in a pressurized myograph, deactivated, and exposed to intraluminal pressures ranging from 3 to 140 mm Hg. At each pressure, lumen and media dimensions were measured. Media-to-lumen ratio and media width were greater in hypertensive vessels, reducing wall stress (P<0.01), whereas media cross section was similar in vessels from both groups. Isobaric elastic modulus (which is influenced by vessel geometry and by wall component stiffness) was lower in hypertensive vessels (P<0. 01). Stiffness of wall components (slope of incremental elastic modulus versus stress, which is geometry-independent) was significantly lower in hypertensive vessels (8.2+/-0.7) versus normotensive vessels (11.0+/-1.0, P<0.05), whereas distensibility was unchanged. Electron microscopic analysis of the media of the small arteries showed a greater collagen to elastin ratio (P<0.05) in the media of vessels from hypertensive patients. In conclusion, the stiffness of wall components (slope of elastic modulus versus stress) is not increased but is in fact decreased in subcutaneous resistance arteries from patients with mild essential hypertension. Reduced stiffness of resistance arteries from hypertensive patients does not appear to relate to changes in volume density of extracellular matrix components but may be the result of changes in extracellular matrix architecture or cell-matrix attachment, which remains to be established.
Hypertension 1999 Jan
PMID:Mechanics and composition of human subcutaneous resistance arteries in essential hypertension. 993 Nov 67

Large and small arteries are remodelled in hypertension - their structure, function and mechanics are altered. These changes contribute to elevated blood pressure and to the complications of hypertension. The present paper concentrates on small (resistance) artery changes in hypertension. In hypertension, these vessels exhibit a form of remodelling known as 'eutrophic' remodelling, in which smooth muscle cells are restructured around a smaller lumen, without true hypertrophy, particularly in milder forms of hypertension. Changes in these small arteries are the first manifestation of target organ damage in patients with hypertension. In more severe forms of hypertension and in secondary hypertension, hypertrophic remodelling has been reported. Stiffness of the vessel wall may be decreased initially; later, as hypertension becomes more severe, the wall of resistance vessels may become stiffer. Endothelial dysfunction occurs in a percentage of patients, similar to the prevalence of left ventricular hypertrophy. Interruption of the renin-angiotensin system may correct many of these abnormalities. The present report investigated the effects of angiotensin type 1 (AT1) receptor antagonists on small arteries of hypertensive patients compared with the beta-blocker atenolol in different studies. Beta-blocker treatment did not modify either the structure or the function of small arteries in contrast to the AT1 antagonist losartan in a double-blind, randomized, one-year study. Patients previously treated with atenolol to lower blood pressure, but whose small artery structure and function did not improve, were examined. These hypertensive patients were switched to the AT1 antagonist irbesartan for one year. Gluteal subcutaneous biopsies showed that the structure and endothelial function of small arteries that had remained altered by atenolol treatment were corrected by irbesartan treatment, although blood pressure control with irbesartan was identical to that previously achieved with atenolol. Improved outcomes in clinical trials using angiotensin-converting enzyme inhibitors and AT1 receptor antagonists may be a result of the vascular protective effects offered by these agents.
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PMID:Vascular changes in hypertension in response to drug treatment: Effects of angiotensin receptor blockers. 1204 89

Epidemiological studies have demonstrated that pulse pressure and arterial stiffness are strong independent risk factors for all-cause and cardiovascular mortality, primary coronary heart disease (CHD) and stroke. Thus, treatment of hypertension and congestive heart failure (CHF) should aim to reduce arterial stiffness in order to lower afterload and pulse pressure, promote regression of left ventricular and arterial wall hypertrophy and, in CHF, increase cardiac output. Elevation of diastolic blood pressure appears to be beneficial to coronary perfusion and this may be particularly relevant in the setting of CHD. In patients with essential hypertension, numerous studies have shown a decrease in arterial stiffness with various pharmacological classes of antihypertensive agents (including beta-blockers, diuretics, ACE inhibitors, angiotensin II receptor antagonists and calcium antagonists), either acutely or during long-term studies. Their efficacy is not surprising, since blood pressure reduction unloads the stiff components of the arterial wall, such as collagen. However, it seems likely that pharmacological treatment has the capacity to decrease arterial stiffness beyond blood pressure reduction, because long-term drug administration can modify the wall components, including a reduction in collagen density or changes in the spatial arrangement of the wall materials. Whether classes of antihypertensive agents vary in their efficacy to affect arterial structure and thus influence arterial stiffness via a pressure-independent mechanism is more controversial and has yet to be evaluated in large-scale trials. A Consensus Conference on the 'Clinical Applications of Arterial Stiffness', held in Paris, June 17, 2000, recommended guidelines for further pharmacological and therapeutic studies on arterial stiffness. Among them were the following: 'To reach full normalisation of arterial stiffness, pharmacological and therapeutic trials should aim at lowering systolic and diastolic blood pressure to a larger extent than in previous studies and giving treatments for a longer duration than in most previous studies;Mainly, studies designed to demonstrate the prognostic value of the reduction of arterial stiffness are urgently needed. They should be performed in patients at high cardiovascular risk, on a large scale and a long-term basis, and include all-cause and cardiovascular mortality and cardiovascular morbidity'.
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PMID:[Drugs and arterial stiffness in hypertensive patients]. 1270 78

Major randomized clinical trials have demonstrated unquestionable clinical benefits of lowering blood pressure without establishing superiority of any specific antihypertensive medication. Most notably, these trials have indicated that a majority of patients with hypertension will require more than one drug to control blood pressure. The recognition that many patients with hypertension should receive a combination of two agents as initial therapy is reflected in current hypertension guidelines, including the recently published consensus statement by the Hypertension in African Americans Working Group (HAAWG) and the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). In addition, there are some data that suggest that combination therapy may afford greater cardioprotection compared to monotherapy. For example, findings from A Lotrel Evaluation of Hypertensive Patients with Arterial Stiffness and Left Ventricular Hypertrophy (ALERT) indicated that low-dose combined angiotensin-converting enzyme inhibitor and calcium channel blocker antihypertensive treatment improved measures of cardiovascular structure and function compared with high-dose monotherapy with either component. Intuitive clinical wisdom suggests that some combinations of antihypertensive agents may provide enhanced clinical benefits; however, clinical trial data have not established optimal combination regimens. Thus, a challenging task for investigators is to determine which combination therapy regimens will provide the greatest cardiovascular benefits for patients with hypertension. A trial that is now in progress, Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension (ACCOMPLISH), directly compares cardiovascular mortality and morbidity rates for two preselected, fixed-dose combination therapies.
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PMID:Creating a combination antihypertensive regimen: what does the research show? 1294 93

The ill effects of hypertension are usually attributed to a reduction in the caliber or the number of arterioles, resulting in an increase in total peripheral resistance (TPR). This definition does not take into account the fact that BP is a cyclic phenomenon with systolic and diastolic BP being the limits of these oscillations. The appropriate term to define the arterial factor(s) opposing LV ejection is aortic input impedance which depends on TPR, arterial distensibility (D), and wave reflections (WR). D defines the capacitive properties of arterial stiffness, whose role is to dampen pressure and flow oscillations and to transform pulsatile flow and pressure in arteries into a steady flow and pressure in peripheral tissues. Stiffness is the reciprocal value of D. These parameters are BP dependent, and arteries become stiffer at high pressure. In to D which provides information about the <<elasticity>> of artery as a hollow structure, the elastic incremental modulus (Einc) characterizes the properties of the arterial wall biomaterials, independently of vessel geometry. As an alternative, arterial D can be evaluated by measuring the pulse wave velocity (PWV) which increases with the stiffening of arteries. Arterial stiffening increases left ventricular (LV) afterload and alters the coronary perfusion. With increased PWV, the WR impacts on the aorta during systole, increasing systolic pressures and myocardial oxygen consumption, and decreasing diastolic BP and coronary flow. The arterial stiffness is altered primarily in association with increased collagen content and alterations of extracellular matrix (arteriosclerosis) as classically observed during aging or in arterial hypertension. The arterial stiffening estimated by changes in aortic PWV and intensity of WR are independent predictors of survival in end stage renal disease (ESRD) and general population. Improvement of arterial stiffening could be obtained by antihypertensive treatmen as observed with the calcium-channel blocker and ACE inhibitors. ACE inhibitors increased AC and reduced WR, and it has been shown that reversibility of aortic stiffening and use of ACE inhbitors had favorable independent effect on survival in hypertensive patients with advanced renal disease.
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PMID:Arterial stiffness: pathophysiology and clinical impact. 1570 23

Cross-sectional studies have shown a positive association between increased pulse pressure (PP) and an increased likelihood of a C-reactive protein (CRP) level >3 mg/L. In a retrospective subgroup analysis of the hypertensive subjects of the multicenter double-blind study, REASON (PREterax in Regression of Arterial Stiffness in a ContrOlled Double-BliNd), in which fixed first-line antihypertensive combination therapy with an angiotensin converting enzyme (ACE) inhibitor, perindopril (2 mg), and a diuretic, indapamide (0.625 mg), proved significantly more effective than atenolol in normalizing PP, we sought to determine whether perindopril plus indapamide was also more effective than atenolol in lowering CRP levels and, if so, whether this effect correlated with a preferential reduction in PP. At the final visit (12 months) in the 269 patients studied, the decrease in PP was greater, and the proportion of patients with CRP >3 mg/L lower (17.9% versus 28. 9%, P=0.03; adjusted odds ratio, 1.02 to 4.08, P=0.01), in the perindopril plus indapamide group than in the atenolol group. After adjustment for confounders, patients with a baseline CRP >3 mg/L displaying the greatest decrease in PP were more likely (P=0.04) to have a CRP < or =3 mg/L at 12 months. No such relationship was found with systolic or diastolic blood pressure. Perindopril-indapamide combination therapy is more effective than beta-blockade in lowering elevated CRP in hypertensive subjects. This effect is significantly associated with a more effective PP reduction in patients with baseline CRP >3 mg/L.
Hypertension 2005 Jul
PMID:C-reactive protein elevation predicts pulse pressure reduction in hypertensive subjects. 1595 15

We investigated the relation of arterial stiffness, considered an independent predictor of cardiovascular events, to cardiovascular risk factors in a population-based study of 1023 subjects. An Arterial Stiffness Index (ASI) was developed to evaluate arterial stiffness based on an analysis of the pulse wave amplitude pattern acquired from measurements of brachial blood pressure. In control subjects (n = 266) without any major risk factors, the ASI was 46 +/- 11, and increased with age (r = 0.346). The ASI was significantly higher in women ranging from 50 to 54 years of age than in age-matched men. The ASI rose in correlation with the number of risk factors. Subjects with two risk factors showed a significantly higher ASI than those without any risk factors (54 +/- 26 vs. 46 +/- 11). The ASI was significantly increased in diabetic subjects with hypertension in comparison to those without hypertension. Furthermore, hyperlipidemic subjects with hypertension showed significantly higher values than those without hypertension. ASI could be a useful predictor of cardiovascular events in hypertensive subjects with multiple risk factors.
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PMID:A population-based study of arterial stiffness index in relation to cardiovascular risk factors. 1602 Sep 19

Left ventricular hypertrophy (LVH) is a powerful independent risk predictor for cardiovascular disease and reversal of LVH has become a primary goal of antihypertensive management. Recent evidence has confirmed that most hypertensive patients will benefit from a low-dose combination strategy to manage their hypertension, and two trials have recently examined the effect of this strategy on left ventricular mass. The REASON study (pREterax in regression of Arterial Stiffness in a contrOlled double-bliNd study) compared the low-dose combination of an angiotensin-converting enzyme (ACE) inhibitor and a diuretic with beta-blocker monotherapy in hypertensive patients with LVH, and the PICXEL study (Preterax In a double-blind Controlled study versus Enalapril in LVH) compared the same low-dose combination with ACE inhibitor monotherapy in hypertensive patients with echocardiographic LVH. The REASON study demonstrated that the low-dose combination produced a significantly greater change in left ventricular mass after 1 year than the beta-blocker, despite inducing a similar change in mean blood pressure. Additionally, perindopril/indapamide reduced central (carotid) and peripheral (brachial) systolic blood pressure (SBP) and pulse pressure (PP) to a significantly greater extent than beta-blocker, and these benefits were more pronounced for the central values; LVH is affected more by central rather than peripheral haemodynamic changes. Results of the analysis of the PICXEL study showed a significantly greater decrease in LVH parameters and blood pressure over 1 year in favour of the low-dose combination. This reduction cannot be entirely explained by the better efficacy of the low-dose combination on blood pressure reduction.
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PMID:Further evidence for low-dose combinations in patients with left ventricular hypertrophy. 1607 32

Stiffness of large elastic arteries is elevated in subjects with hypertension, an effect that could potentially be explained by increased distending pressure. We examined effects of an acute change in blood pressure on carotid-femoral pulse wave velocity and carotid artery distensibility (inversely related to stiffness) in normotensive control subjects (n=20, mean age 42) with mean arterial pressure (MAP) 84+/-1.7 mm Hg (mean+/-SE) and subjects with essential hypertension (n=20, mean age 45, MAP 104+/-2.0 mm Hg). Normotensive subjects received intravenous nitroglycerin (NTG) and angiotensin II to lower/increase blood pressure. Hypertensive subjects received NTG to lower blood pressure. Pulse wave velocity was 24% (95% CI: 12% to 35%) higher and carotid distensibility 47% (95% CI: 32% to 63%) lower in hypertensive subjects compared with controls. In normotensive subjects, acute changes in blood pressure produced expected changes in stiffness. However, in hypertensive subjects, despite reducing MAP by 22 mm Hg to the same level as in normotensive subjects, there was no detectable reduction in arterial stiffness: pulse wave velocity remained 24% (95% CI: 10% to 38%) higher and carotid distensibility 48% (95% CI: 31% to 63%) lower in hypertensive compared with normotensive subjects. Because blood pressure-independent effects of NTG are, if anything, to reduce stiffness, these results indicate that elevated carotid and aortic stiffness in hypertensive subjects is not explained by elevated blood pressure but relates to structural change in the arterial wall.
Hypertension 2006 Sep
PMID:Acute reduction of blood pressure by nitroglycerin does not normalize large artery stiffness in essential hypertension. 1690 59

Cardiovascular disease is the leading cause of death worldwide and premature arterial stiffening is a key contributor to this risk. A large body of evidence now points to arterial stiffness as an independent predictor of cardiovascular events. Stiffness can be assessed by a number of indices and is itself affected by factors including mean arterial pressure, vascular smooth muscle tone and structural elements in the vessel wall, such as elastin and collagen. In addition, aging, hypertension, diabetes and hypercholesterolaemia all exacerbate the stiffening process. Stiffness is highly heritable but, despite a clear genetic basis, the precise molecular pathways regulating stiffness are poorly understood. The present review provides an overview of the current literature and examines the evidence that links genetic factors to arterial wall properties. Although the findings support stiffness as a complex genetic trait, the precise nature of the genes contributing to this are still largely unknown. There are a number of candidate genes and many of these could potentially affect the structure and function of the arterial wall. Indeed, it is likely that genes involving signalling pathways and control of the vessel wall matrix will be as important as those involved in the renin-angiotensin system, adrenergic and other vasoactive systems. Identifying the genes involved is important, since it may suggest new biomarkers as well as provide novel drug targets to reduce arterial stiffness. Current pharmacological intervention is simply to reduce blood pressure, but there are emerging therapies; for example, targeted at breaking collagen cross-links or preventing their formation, which are promising new strategies to reduce arterial stiffness and its associated cardiovascular risk.
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PMID:Genetics of arterial structure and function: towards new biomarkers for aortic stiffness? 1844 60


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