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

To assess the effect of hypertension on diet-induced coronary artery plaques after a return to a nonatherogenic diet, 10 cynomolgus monkeys were fed an induction regimen containing 2% cholesterol and 25% peanut oil for 6 months and then were subjected to midthoracic aortic coarctation to induce hypertension. The animals were then fed a nonatherogenic "prudent" ration for 6 additional months (hypertension-regression group). Twelve additional monkeys were fed the atherogenic diet for 6 months; six were killed (lesion-induction control group) and six were changed to the prudent diet for 6 additional months without coarctation (normotension-regression control group). At the end of the induction period, cholesterol levels averaged 744 +/- 178 mg/dl for the 22 animals and were similar for the three groups throughout the induction period. For the animals restored to the nonatherogenic diet (hypertension-regression and normotension-regression groups), serum cholesterol levels fell to 486 +/- 252 mg/dl at 1 month, to 341 +/- 162 mg/dl at 2 months, and to 234 +/- 78 mg/dl at 6 months. There was no significant difference between the hypertensive and normotensive animals. Six months after coarctation, blood pressure proximal to the coarctations for the hypertension-regression group ranged from 100/60 to 220/145 mm Hg with a mean of 166/103 +/- 36/28 mm Hg. Cross-sectional area of coronary plaques was somewhat lower for the normotension-regression control group compared with the lesion-induction control group, but the difference was not significant. Plaque area was, however, markedly greater in the hypertension-regression group than in either the lesion-induction or the normotension-regression groups (p less than 0.05 for each) despite progressive reduction in hyperlipidemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Aug
PMID:Hypertension sustains plaque progression despite reduction of hypercholesterolemia. 188 20

Epidemiological surveys show the clear association of hypertension with an increased risk of developing ischaemic heart disease. One method of quantifying atherosclerosis is to measure, at necropsy, the percentage of the intimal surface of the coronary arteries or aorta which is occupied by raised plaques. When this is done in a large number of subjects the amount of intimal involvement in any particular geographical population correlates directly with the frequency of ischaemic heart disease. In all these populations, whether at a high risk or low risk of developing ischaemic heart disease, hypertensive subjects have a greater intimal involvement by plaques than normotensive subjects. Thus, the increased risk in hypertension is, in part, mediated by possession of more plaques. Plaque growth is due to the accumulation of lipid from the plasma, the ingress of monocytes with their conversion to lipid filled foam cells and the formation of collagen by smooth muscle cells. Hypertension may act by altering endothelial function to potentiate all these processes. Mechanical stress on endothelial cells will evoke the formation of growth factors for smooth muscle cells. Plaque growth in man is also episodic due to the formation of thrombi; a proportion of these episodes are symptomatic producing acute myocardial ischaemia but the majority are silent leading to sudden plaque expansion. Thrombi over plaques are either due to endothelial denudation injury or more commonly due to the tearing of the cap of a plaque leading to deep intimal injury. Necropsy surveys of control populations show that subjects with hypertension have a greater frequency of recent plaque tears compared with normotensive subjects.
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PMID:Hypertension and atherosclerotic (ischaemic) heart disease. 194 81

Spontaneously hypertensive male and female rats (SHR) were compared with Wistar/Kyoto (W/K) controls at 15 wk and 80 wk of age. Treatment of the young and old hypertensives with thymosin, fraction 5, lowered the blood pressure within 4 wk of the start of treatment. Following 10 wk of injections, the blood pressures of the hypertensive rats remained at a depressed level for about 6 wk. The thymic hormone raised the depressed spontaneous T-cell rosette formation of the aged hypertensive rat and increased the lymph node T-cell response to the mitogens, Con A and PHA. Thymosin administration over a period of 7 wk increased the size of the aged hypertensive thymus. No similar effect was observed in the W/K. Spleen cell production of prostaglandin E (PgE) was markedly higher in the young hypertensive and immune complex deposition was found in the glomeruli and tubules of the aged SHR kidneys. Thymosin lowered the high level of PgE to normal and decreased the immune complex deposition in the kidney. IgG1 levels were considerably depressed in the SHR as compared to the W/K. Following thymosin administration levels of IgG1 increased 2-fold in both rat strains. Plaque-forming cells from the spleens of the untreated SHR were about 3-fold less than those of the age-matched W/K. Following treatment with thymosin the number of plaque-forming cells of both groups demonstrated a substantial further decrease. Spontaneous hypertension in rats is similar, in certain respects to autoimmune-like diseases in humans with a depression in T-cell activity as well as immune complex deposition; both conditions being altered by exposure to a thymic extract.
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PMID:Immune response modulation in the spontaneously hypertensive rat. 634 14

The association of electrocardiographic left ventricular hypertrophy (ECG-LVH) (212 subjects) and haemodynamically significant internal carotid artery stenosis (ICAS) (27 subjects) with isolated systolic hypertension (ISH), mixed hypertension (MHT) and isolated diastolic hypertension (IDH) was studied in untreated elderly patients. Subjects were those aged 67-86 years, drawn from a community screening programme for hypertension in Wales. The prevalence of ECG-LVH with or without repolarisation abnormalities was higher in subjects with ISH (16.6%) than in subjects with mixed hypertension (11.6%, NS). Partial correlation of SBP, DBP, voltage of lead I and SV1+RV5 for each hypertensive subtype showed a consistent positive correlation of DBP with the voltage of lead I and SV1+RV5 in all the subtypes except with the voltage of lead I in IDH subjects. In MHT, the SBP was inversely related to both the voltage of R-wave in lead I and SV1+RV5 (P < 0.03). In IDH, the SBP was positively correlated with the voltage of R-wave in lead I and inversely with SV1+RV5. Atheromatous plaque was present in 40 of 54 (74.1%) internal carotid arteries investigated. The homogeneous type of plaque was predominant in ISH (67%). Heterogenous type of plaque was predominant in the MHT group (50%) and IDH group (43%). The normotensive group did not show any predilection to any morphological type. Plaque was invariably present in the case of ISH, chi 2 = 12.29, 0.1 > P > 0.05. There was more smooth plaque surface in normotensives (79%) and more rough or pitted plaque surface in hypertensives (all types), chi 2 = 6.51, 0.1 > P > 0.05. All normotensives and IDH subjects had non-haemodynamically significant stenosis. Haemodynamically significant stenosis was found in cases of ISH (25%) and MHT (7%); chi 2 = 7.66, 0.1 > P > 0.05. ECG-LVH and haemodynamically significant internal carotid artery stenosis were more commonly found in subjects with ISH than in subjects with MHT. Further studies with larger numbers of patient in each hypertensive subtype would be desirable to confirm these observations.
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PMID:Is isolated systolic hypertension in the elderly more associated with left ventricular hypertrophy and significant carotid artery stenosis than mixed hypertension and isolated diastolic hypertension? 857 96

Three consecutive periods in the natural history of atherosclerosis are amenable to medical treatment. Plaque development is the main target of prevention, which also aims at slowing the progression of already existing plaques. The control of several established risk factors (high blood cholesterol, high blood pressure, diabetes mellitus, tobacco smoking) has already yielded encouraging benefits, especially in the field of secondary prevention. More efficient prophylaxis is to be expected, either from the further improved control of these classic risk factors with earlier, stronger, and longer interventions or from the correction of newly established causal determinants of atherosclerosis. A plaque manifests itself clinically through progressive or abrupt obstruction of the arterial lumen, which can be avoided or retarded by interventions aimed at reducing thrombosis, at controlling plaque instability (the major cause of thrombosis), and at enhancing arterial remodeling (which allows compensatory enlargement of the arterial lumen). When ischemia has occurred, a third wave of palliative treatments aims at improving energy supply to the organ with compromised vascularization. Classic treatments reduce oxygen consumption or improve oxygen extraction by ischemic tissues. In addition, the design of drugs to enhance the development of collateral channels appears to be promising therapeutic approach.
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PMID:Pharmacologic approaches to the treatment of atherosclerotic arterial obstruction. 869 60

This study was done to clarify relationships between the degree of periventricular lucency (PVL), and lesions in the carotid arteries and the legs as detected with B-mode ultrasonography and the ankle pressure index, respectively. According to the distribution of PVL on computed tomography, 45 patients were divided into 2 groups: 22 patients with diffuse PVL (from the periventricular white matter to the subcortical area, DPVL group) and 23 patients with PVL localized in the frontal deep white matter (LPVL group). Plaque, defined as a thickened intima-media complex of 2.1 mm or more, was divided into two types; mural plaque and nodular plaque. Hypertension was more common in the DPVL group than in control groups, which consisted of 70 age-matched patients with cerebral thrombosis without PVL (CTH group) and 50 controls with neither PVL nor cerebrovascular lesions (NCT group). All patients in the DPVL group met the diagnostic criteria for Binswanger's disease proposed by Bennett DA. The incidence of low API indices (< 0.9) in the DPVL group (45%) was significantly higher than that in the NCT group, and it was slightly higher than that in the LPVL group. Carotid lesions, mainly nodular plaques, were seen in 82% of patients in the DPVL group and in 74% of those in the LPVL group; these percentages were significantly higher than those in the CTH (49%) and NCT (40%) groups. In particular, bilateral carotid lesions were more common in the DPVL group than in the other three groups. The degree of PVL correlated with lesions in the carotid arteries and the legs. These correlations suggest that the arterial lesions not only resulted from a risk factor (hypertension) for PVL, but also promoted PVL by causing extra- and intra-cranial arterial lesions. Furthermore, they imply that LPVL is a precusor to DPVL.
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PMID:[Correlation between periventricular lucency and extracranial arterial lesions]. 874 69

Recent experimental data suggest marked similarities between the effects of hypertension and hypercholesterolemia on the arterial intima. Both conditions also seem to exert proinflammatory effects on the artery, resulting in the recruitment of monocytes into the intima. These effects may be due to production of oxygen-free radicals, which in turn may stimulate genes involved in the recruitment of inflammatory cells into the arterial wall. Plaque rupture and acute myocardial infarction are related to local accumulation of inflammatory cells in vulnerable areas of the plaque. Recent clinical trials using cholesterol-lowering or antihypertensive therapies have shown a decrease in cardiovascular events that may have resulted from withdrawal of inflammatory effects on the arterial wall. Angiotensin-converting enzyme inhibitors decrease the rate of myocardial infarction in patients with overt congestive heart failure or left ventricular dysfunction. These drugs probably affect several mechanisms related to the inhibition of angiotensin production and the potentiation of bradykinin and resultant enhancement of nitric oxide and prostacyclin. The mechanisms could include reversing the proinflammatory effects of angiotensin and hypercholesterolemia on the arterial wall. Future therapeutic strategies of vascular protection in hypertension may include direct attacks on proinflammatory or pro-oxidant vascular mechanisms.
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PMID:Exacerbation of atherosclerosis by hypertension. Potential mechanisms and clinical implications. 918 40

We evaluated risk factors involved in regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both. Using ultrasonography, we examined the brachial, common carotid, and common femoral arteries in 65 hospitalized Japanese patients (15 controls, 18 patients with hypertension, 16 with diabetes mellitus, and 16 with both hypertension and diabetes mellitus). They ranged in age from 39 to 81 yr, mean 60.3 yr. The thickness of the intima-media complex of the far wall was measured, and the severity of atherosclerotic plaques was graded according to maximal lumen stenosis. The intima-media thickness in the carotid and femoral arteries was significantly greater in the hypertensive patients and the hypertensive patients with diabetes than in the controls. Severity of plaque was greater in the hypertensive patients with diabetes than in the controls. Plaque grades were higher in the carotid and femoral arteries than in the brachial artery. Multiple regression analysis revealed that age and mean blood pressure were strongly associated with the intima-media thickness in all three arteries. In the femoral artery, cigarette smoking and hyperglycemia also significantly correlated with the intima-media thickness. Plaque grades increased with age in the carotid and brachial arteries, while in the femoral artery the grade increased with cigarette smoking and serum cholesterol concentration. These findings suggest that the extent of atherosclerosis and its underlying risk factors differ among arterial sites. In addition, risk factors may partly differ according to the stage of atherosclerosis. To prevent or reverse atherosclerosis, the above differences should be taken into account.
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PMID:Ultrasonographic assessment of regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both. 932 98

Multiple risk factors for cardiovascular disease, particularly hypercholesterolemia, are often present in the hypertensive patient. Recent guidelines, ranging from those prepared by the World Health Organization/International Society of Hypertension to those of the three European Societies of Cardiology, Atherosclerosis, and Hypertension, stress the importance of evaluating global risk, based on the presence of all cardiovascular risk factors in an individual or in a group of subjects. It has also been suggested that treatment should aim to correct all modifiable risk factors. This is a reasonable recommendation, but although observational epidemiologic studies have shown that the effects of concomitant risk factors are additive, if not multiplicative, it is surprising that no intervention trial has been undertaken to determine whether the benefits of treating more than one risk factor are also additive. The Plaque Hypertension Lipid-Lowering Italian Study (PHYLLIS) is the first such study. Its aim is to investigate the potential benefit of lowering blood pressure and plasma cholesterol on the progression of carotid plaque in hypertensive patients with elevated plasma cholesterol. Using a factorial design, the antiatherosclerotic effect of two different antihypertensive drugs, the angiotensin-converting enzyme (ACE) inhibitor fosinopril and the diuretic hydrochlorothiazide will be compared. The study aims to confirm animal experiments demonstrating the benefit of ACE inhibitors on experimental atherosclerosis. PHYLLIS will also compare the effects of two lipid-lowering regimens, diet plus placebo and diet plus pravastatin, in the study population. This 3-year, multicenter, double-blind, randomized Italian study, using B-mode ultrasound evaluation of the carotid walls with central reading of the ultrasound scans (Bowman Gray University, Winston-Salem, NC) is now underway and should provide useful evidence about the benefits of multiple risk factor treatment in the hypertensive patient.
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PMID:The hypertensive patient with multiple risk factors: is treatment really so difficult? 936 77

Acute coronary syndromes (ACS) such as unstable angina, myocardial infarction, or sudden ischemic death evolve from coronary thrombosis consequence of atherosclerotic plaque disruption. Plaque stabilization is an important therapeutic strategy in the prevention of ACS. Coronary risk factors include age, male sex, cigarette smoking, hypertension, dislipidemia, diabetes mellitus, insulin resistance and/or hyper insulinemia, obesity, sedentary lifestyle, stress, and the morning surge of sympathetic activity. New risk factors are emerging such as high homocystein, inflammation, and some kinds of infection. Control of blood pressure and cholesterol clearly reduce the risk of coronary events and mortality although the effects of antihypertensive therapy have been less than expected. The benefits of smoking cessation, moderate alcohol consumption, low-dose aspirin prophylaxis, estrogen-replacement therapy in postmenoposal women have also been shown.
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PMID:[Risk factors and prevention of acute coronary syndrome]. 979 37


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