Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High renin hypertension has been associated with a higher risk of stroke than low-to-normal renin hypertension. Accordingly, we investigated prospectively the prevalence of the extracranial carotid artery lesions in a case-control study of 70 patients (38 women and 32 men, aged 16 to 77 years) without history or symptoms of cerebrovascular disease. Renovascular hypertension was diagnosed in 35 patients on the basis of the angiographic demonstration of renal artery stenosis and of the favorable outcome after revascularization. It was caused by atherosclerosis in 20 patients and by fibrodysplasia in 15. Each renovascular hypertensive patient was individually matched with a control with primary hypertension for sex, race, age, blood pressure levels, duration of hypertension, smoking, diabetes mellitus, total serum cholesterol, and triglycerides. Carotid arteries were evaluated by a High Resolution Duplex system (Biosound 2000, probe 4 cm, 8 mHz). Our results show that after the matching the two groups were similar in terms of demographic features and overall cardiovascular risk profile (all P = NS). In renovascular hypertensives the prevalence of carotid artery lesions (82.6%) was significantly (P less than .01) higher than in primary hypertensives (42.9%). The higher prevalence of lesions in renovascular hypertension was observed not only in patients with atherosclerosis (100% v 55%, P less than .001), but also in those with fibrodysplasia (57% v 27%, P less than .01). Thus, for the same demographic features and overall cardiovascular risk profile, renovascular hypertension carries a more detrimental effect on the carotid artery than primary hypertension.
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PMID:Excess prevalence of extracranial carotid artery lesions in renovascular hypertension. 129 42

The treatment of hypertension in arteritic patients must take account of several parameters: respective severity of hypertension and of arteriopathy, possibility of other sites of atherosclerosis and supposed cause of hypertension. The association of essential hypertension and of an arteriopathy does not sum up all possibilities. Hypertension may be purely systolic, due to decreased compliance. A stenosis of the renal arteries is also worth evoking in the context of an already symptomatic atherosclerotic disease. For the confirmation of the latter hypothesis, Doppler associated to echography may be an alternative to the intravenous or intra-arterial opacification of the renal arteries. In case of moderate hypertension (diastolic pressure ranging from 90 to 104 mmHg), non-medicamentous treatments should be preferred: low-sodium diet, suppression of tobacco and other risk factors, weight loss. Beta-blockers, whatever their class, reduce the walking distance in case of intermittent claudication. Though not formally contraindicated, especially when their use is justified by an associated coronary insufficiency, they are not advised in hypertensive arteritic patients. On the other hand, captopril allows both reducing blood pressure and preserving the walking distance. However, a prerequisite to the possible use of agents inhibiting the conversion enzyme is the preliminary search for a stenosis of the renal arteries. In fact, when these medications are carelessly used in case of bilateral stenosis or of stenosis on a functionally single kidney, they entail a risk of renal failure or of thrombosis of the stenosed renal artery. Calcium inhibiting agents are also anti-hypertensive substances of choice in hypertensive arteritic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of hypertension in arteritic patients]. 179 78

The authors analyze the laboratory and instrumental data obtained before and after single administration of leeches. Demonstrate that the animal's saliva corrects the coagulation properties of the circulating blood; inhibits platelet aggregation; that it may be used for blood letting; possesses hypotensive and anti-sclerotic properties; improves myocardial supply and its contractility. Based on a large clinical material the authors provide evidence for advisability of the use of hirudotherapy in patients suffering from coronary heart disease, essential hypertension, atherosclerosis, chronic cer pulmonale, and circulatory decompensation.
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PMID:[Medicinal leeches: their medical use in the therapy clinic]. 179 97

As many as 40 men suffering from essential hypertension (EH) and left ventricular hypertrophy (LVH) or hypertrophic cardiomyopathy (HCMP) were examined. All the patients exercised on a treadmill according to the Cornell protocol taking into consideration the ST/HR slope and the ST/HR index, underwent echocardiography with measurements of the left ventricular mass (LVM), and coronary ventriculography. Coronary insufficiency was revealed in all the patients. Of these, 11 patients suffered from it due to associated EH and coronary heart disease (CHD), 31 had relative coronary insufficiency in the presence of associated EH and LVH phenomena with no stenosis of coronary vessels, and 7 patients showed up relative coronary insufficiency in the presence of HCMP. The ST/HR slope and the ST/HR index correlated well with the LVM and the asymmetry index of the left ventricle but in patients with associated relative coronary insufficiency and EH. In patients with associated EH and CHD, the ST-dependent parameters correlated well neither with the degree of atherosclerosis spreading nor with the LVM. This may indicate that both factors influence the gravity of coronary insufficiency at a time. In case a patient suffering from associated EH and coronary insufficiency phenomena has the ST/HR slope greater than or equal to greater than or equal to 4.5 microV/stroke/min and/or the ST/HR index greater than or equal to greater than or equal to 2.5 microV/stroke/min, it is more likely that myocardial ischemia is provoked by concomitant atherosclerosis of coronary arteries (sensitivity 28%, specificity 71%).
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PMID:[The ST-segment-dependent indices of patients with left ventricular hypertrophy and coronary failure]. 183

Erythrocyte sodium-lithium countertransport (SLC) was measured in 17 patients with either combined hyperlipidaemia or hypercholesterolaemia before and after lipid lowering therapy. Before treatment SLC related to the serum triglyceride level and was increased in combined hyperlipidaemia. After treatment the SLC had returned to normal and the change in SLC was related to the change in serum triglyceride levels. Raised SLC is associated with essential hypertension but is not related to blood pressure. Therefore, the association of raised SLC with hyperlipidaemia and essential hypertension appears to have different underlying mechanisms.
Atherosclerosis 1991 Apr
PMID:Lipid lowering therapy leads to a reduction in sodium-lithium countertransport activity. 185 57

The smooth muscle cell invasion and macrophage stimulation within the intima during prolonged exposure to high blood levels of cholesterol esters contribute to increased production of connective tissue matrix. The thickened intima in turn immobilising more LDL derived lipid from the plasma. With damage to the internal elastic lamellae, from essential hypertension, the absorbed lipid can move down a concentration gradient into the medial tissue. This model was supported by our laboratory finding of a lipid gradient across the aorta wall. The gradient commenced shortly after completion of body growth, when the transmedial gradient became detectable. The slope of the gradient progressively increased during ageing. Association of the lipid medial gradient with the degree of atherosclerotic involvement suggested that the gradient influenced the development of intimal lesions. Accumulation of lipid within the medial tissue may then reduce the inward lipid transfer rate from the intima, promoting increased intimal retention and cause the formation of atherosclerotic plaques from the fat saturated intima.
Atherosclerosis 1991 Apr
PMID:Formation of a lipid gradient across the human aortic wall during ageing and the development of atherosclerosis. 185 67

Epidemiologic studies have shown that insulin is a risk factor for coronary heart disease (CHD). Clinical studies have also demonstrated positive correlations between insulin and blood pressure, triglycerides, total cholesterol, fibrinogen, and plasminogen activator inhibitor. Moreover, there is an inverse correlation between insulin and high-density lipoprotein (HDL). These studies have provided evidence in support of the biologic plausibility of epidemiologic observations, but they have not clearly established insulin's role in the pathogenesis of human cardiovascular diseases (CVD) such as hypertension. In fact, there is considerable evidence that insulin resistance (abnormal nonoxidative glucose disposal), not hyperinsulinemia, is the primary insulin-related abnormality in human hypertension, and that hyperinsulinemia occurs as a response to insulin resistance. Skeletal muscle appears to be the primary site of insulin resistance in essential hypertension, although other organs, such as the kidneys and liver--key sites for cell and water homeostasis and lipoprotein regulation, respectively--may respond normally to insulin. Adipocytes also appear to be a site of insulin resistance. Thus, the putative interrelationship between hyperinsulinemia and insulin resistance, on the one hand, and with blood pressure and lipoproteins, on the other, is a complex one and may involve organ-specific insulin resistance. Altered cation transport is one of several mechanisms by which insulin resistance might raise blood pressure. The Na+, K(+)-ATPase and Ca(2+)-ATPase pumps are insulin sensitive. Thus, when insulin resistance is present, the activity of these pumps in the smooth muscle of the arterial wall might be reduced. This would lead to an intracellular accumulation of sodium and calcium, thereby sensitizing the vascular wall to pressor substances. Moreover, secondary hyperinsulinemia will occur, and insulin has been shown to stimulate sympathetic nervous system activity and to increase renal tubular absorption of sodium. Insulin is also a growth factor and therefore might have a trophic effect on the vessel wall, one that could initiate and/or sustain hypertension as well as atherosclerosis. Abnormal lipoprotein metabolism is yet another possible explanation for the accelerated atherosclerosis that has been observed in persons with abnormal carbohydrate tolerance and insulin resistance. Hyperinsulinemia and insulin resistance both play a role in the expression of elevated very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) levels as well as in the depression of HDL levels. Coronary risk reduction has been disappointing when blood pressure has been lowered with treatment regimens based on thiazide diuretics and/or beta blockers. Thiazides and some beta blockers may further impair tissue insulin sensitivity and often cause blood lipoprotein abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiologic and clinical aspects of insulin resistance and hyperinsulinemia. 186 24

Fifty hypertensive untreated outpatients (34 women, 16 men), with stage I and II essential hypertension, were studied in comparison to 50 age- and sex-matched controls with similar life-styles. Total cholesterol triglycerides, LDL-cholesterol, VLDL-cholesterol, and HDL-cholesterol were measured by enzymatic methods, and apolipoproteins AI, AII, B, CII, CIII and E by RID. The results showed significant differences between hypertensives and controls respectively in triglycerides (135.2 +/- 73.9 versus 90.2 +/- 33.8, P less than 0.01) and VLDL cholesterol (26.7 +/- 14.8 versus 17.7 +/- 6.6, P less than 0.01) while no significant differences were observed in total, LDL and HDL cholesterol. Significant differences between the two groups were also observed in apolipoproteins, particularly in apo AI (130.0 +/- 28.2 versus 144.9 +/- 27.9, P less than 0.05), apo AII (32.9 +/- 10.2 versus 39.6 +/- 11.4, P less than 0.01), apo CII (4.0 +/- 2.6 versus 5.4 +/- 2.9, P less than 0.05) and apo E (5.0 +/- 1.8 versus 4.3 +/- 1.8, P less than 0.05), while no significant differences were observed in apo B and CIII values. The results suggest that in untreated hypertensive patients alterations in the apolipoproteins profile are present which, in part, may be responsible for the elevated incidence of cardiovascular disease, independently from the blood pressure values.
Atherosclerosis 1991 Mar
PMID:Serum lipids and apolipoproteins in patients with essential hypertension. 187 22

The increased growth potential of vascular smooth muscle cells (VSMCs) represents one of the crucial anomalies responsible for the development of essential hypertension, diabetic macroangiopathy, and atherosclerosis. The exaggerated response to growth factors of VSMC from spontaneously hypertensive rats (SHRs) persists in culture when compared with normotensive Wistar-Kyoto control rats, indicating an intrinsic defect in the hypertension-producing mechanism. This greater proliferation is characterized by two intermediate phenotypes: (1) accelerated entry into the S phase of the cell cycle, which results from hyperresponsiveness to epidermal growth factor and platelet-derived growth factor, and (2) abnormal contact inhibition. The enhanced expression of transforming growth factor beta 1 (TGF-beta 1) messenger ribonucleic acid in SHRs precedes this altered contact inhibition, and only VSMCs from SHRs respond to exogenously added TGF-beta 1 at a high cell density, which suggests that abnormal TGF-beta 1 autoregulation may be implicated in the second phenotype. Platelets contain major growth factors for VSMC. Platelet extracts from hypertensive and diabetic patients present augmented growth-promoting activity on VSMCs, which is most evident when both diseases occur simultaneously. Growth-promoting activity may be further influenced by antihypertensive therapy. This growth-promoting activity is increased by hydrochlorothiazide but not by indapamide, atenolol, or captopril in diabetic hypertensive and nondiabetic hypertensive patients. In conclusion, VSMCs in hypertension manifest an intrinsic growth defect that is modulated by extrinsic platelet growth factors and antihypertensive drugs.
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PMID:Vascular smooth muscle cell proliferation and its therapeutic modulation in hypertension. 192 87

The effects of a beta-blocker, carvedilol, on peripheral hemodynamics and hemorheologic parameters were evaluated in 11 geriatric patients with essential hypertension [3 men and 8 women aged 62-79 years (mean, 68.6 years)]. Carvedilol was given orally after breakfast at a dose of 10 or 20 mg daily for 8 weeks. Peripheral hemodynamics, the common carotid arterial flow, and hemorheologic parameters were determined twice prior to administration and after 4 and 8 weeks of carvedilol treatment. The common carotid arterial flow was determined using the pulsed Doppler method. Peripheral hemodynamics were assessed by venous occlusion plethysmography. The hemorheologic parameters assessed include erythrocyte aggregation, erythrocyte deformability, plasma viscosity, whole-blood hematocrit, and platelet function tests. Erythrocyte aggregation was measured using an Erythrocyte Aggregometer MA-1 (Myrenne, USA), taking a high shear rate of 600 s-1 and a low shear rate of 3 s-1 as the indices. Statistical comparisons of values before and after carvedilol administration were made using the paired Student's t-test. Systolic and diastolic blood pressure were decreased by carvedilol. The common carotid arterial flow was increased, and peripheral hemodynamics were improved by carvedilol. Erythrocyte aggregation (measured at both a high and a low shear rate) and plasma viscosity were decreased, erythrocyte deformability was increased, and levels of circulating platelet aggregates were also improved by carvedilol. This improvement of hemorheologic variables may contribute to prevention of the initiation and progression of thrombosis and atherosclerosis in geriatric patients with essential hypertension.
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PMID:Effects of carvedilol on common carotid arterial flow, peripheral hemodynamics, and hemorheologic variables in hypertension. 197


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