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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systematic blood coagulation analyses were conducted in 32 severely hypertensive patients treated with the angiotensin converting enzyme inhibitor captopril. Two hours after the first captopril dose, fibrin monomer complexes had already increased. This rise was even more distinct after 26 h and 1 week. Tests after 6 and 12 months of therapy showed a regression of fibrin monomer complexes to pretreatment values. In several patients with a marked increase in fibrin monomer complexes, the partial thromboplastin time (PTT) became shorter and antiplasmin activity increased. The most pronounced increase in fibrin monomer complexes was seen in patients with a rapid and excessive blood pressure reduction. The concentration of fibrin monomer complexes also rose in 15 healthy normotensive subjects, after a single oral dose of captopril (25 mg). Additionally, the PTT was shortened and antiplasmin significantly rose. An inhibition of fibrinolysis by captopril could be demonstrated by the effect on fibrin plates and thrombus weight after streptokinase. Out of 58 patients with severe hypertension and atherosclerosis treated with captopril, 7 patients suffered vascular complications during antihypertensive therapy: myocardial infarction (n = 2), coronary insufficiency (1), cerebral ischemia (1), renal insufficiency (3). These ischemic lesions may be partly explained by the alterations of coagulation and fibrinolysis under captopril therapy.
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PMID:Effects of the converting enzyme inhibitor captopril on blood coagulation and fibrinolysis in man. 675 Feb 21

Seventy-two patients, aged 6-69 years, were operated on because of presumed renovascular hypertension and subjected to follow-up studies for 4-60 months (mean 28). Unilateral renal artery stenosis was present in 47 patients. Surgery was followed by normalization of blood pressure (BP) in 28 and improvement in 7, whereas 12 showed no response. Sixteen were below the age of 40 and only one failed to respond to surgery. Peripheral venous plasma renin activity (PRA) was increased in 32 and urinary aldosterone elevated in 22 of 35 patients responding favourably to surgery. Renal vein PRA was higher from the kidney with the stenotic renal artery as compared to the contralateral side in all patients responding to surgery. Preoperative peripheral PRA difference was also found in 7 of 12 patients not responding to surgery. Preoperative peripheral PRA was increased in 26 of the patients becoming normotensive after surgery. In 20 of these patients normalization of BP was associated with a fall in peripheral PR. Twenty-five patients had bilateral renal artery stenosis. Four of them had severe hypertension, renal insufficiency and generalized atherosclerosis. They died in immediate connection with operation. Unilateral operation, performed in 11 of the remaining 21 patients, was followed by normalization of BP in 3 and no response in 8. Bilateral reconstructive surgery, performed in 10 patients, resulted in normotension in 2 and improvement in 7. Our studies indicate that determination of peripheral PRA and/or urinary aldosterone can serve as a useful prognostic indicator after surgery in hypertensive patients with renal artery stenosis.
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PMID:Pre- and postoperative studies in 72 hypertensive patients with renal artery stenosis, with special reference to renin activity and aldosterone. 703 32

Disturbances in lipid metabolism and accelerated atherosclerosis are well-known phenomena of chronic renal insufficiency. The disturbance in lipid metabolism has been repeatedly described as secondary type IV hyperlipoproteinemia according to the classification of Fredrickson. The classification of Fredrickson, however, does not take into account the role of the alpha-lipoproteins (the HDL lipoproteins and HDL cholesterol). Hence, HDL cholesterol was determined and correlated to other routine parameters of lipid metabolism in 66 patients with different degrees of renal insufficiency. Furthermore, an intravenous fat tolerance test was performed in 14 patients with terminal renal insufficiency. Beside the well-known hypertriglyceridemia with cholesterol values near the upper limits of normal, a significant reduction in HDL cholesterol was found, showing a significant inverse correlation to plasma creatinine values. Patients with advanced or terminal renal insufficiency additionally showed a significant inverse correlation between HDL cholesterol and plasma triglycerides. The disappearance rate of intravenously administered fat emulsion (which corresponds to the clearance rate of chylomicrons and VLDL) was diminished in azotaemic patients, showing a significant inverse correlation between HDL cholesterol and disappearance rate in the intravenous FTT. Beside hypertriglyceridemia, the diminished HDL cholesterol values represent an additional risk factor for the genesis of accelerated atherosclerosis. The diminished k value demonstrates a diminished activity of lipoprotein lipase as cause of hypertriglyceridemia, whereby the positive correlation between the k value and HDL cholesterol and the inverse correlation between HDL cholesterol and triglycerides suggest a causal relationship between the decreased activity of lipoprotein lipase and diminished HDL cholesterol levels.
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PMID:[High-density-lipoprotein and renal insufficiency (author's transl)]. 708 Apr 95

Renal cholesterol embolization can occur spontaneously or as a complication of aortic surgery or major vessel angiography in patients with diffuse atherosclerosis. The demonstration of characteristic cholesterol crystals in tissue biopsy specimens is a pathognomonic finding. However, renal cholesterol embolism may be clinically diagnosed when renal failure develops after known inciting factors or together with systemic manifestations of atheromatous embolization such as lower extremity livedo reticularis, focal digital ischemia or retinal embolism. Previous investigators have emphasized the progressive nature of renal insufficiency due to cholesterol embolism, its poor prognostic significance and almost uniformly fatal outcome. In this report, we describe five additional patients with renal cholesterol embolization. In three of them only moderate renal insufficiency developed, and kidney function subsequently improved in all. In two patients the condition progressed to end-stage renal disease; one died with chronic renal failure whereas the other patient required four months of hemodialysis before kidney function eventually improved. Thus, cholesterol embolization may produce a spectrum of renal functional impairment. In some patients there is only a moderate loss of renal function with subsequent improvement; in others renal failure ensues. In this latter group, eventual return of kidney function can occur even after a prolonged period of renal insufficiency.
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PMID:The clinical spectrum of renal cholesterol embolization. 724 79

The development of experimental atherosclerosis was studied in subtotally nephrectomized rats which were subjected to preimmunization with horseradish peroxidase and subsequent feeding with atherogenic diet. Both in sham-operated pair-fed control animals and in uremic animals, the atherogenic diet caused hyperlipemia which was more pronounced in uremic than in control animals (control animals: triglycerides 1.11 +/- 0.04 mmol/l; cholesterol 5.82 +/- 0.21 mmol/l; uremia: triglycerides 1.33 +/- 0.06; cholesterol 10.9 +/- 0.31). An increase of cholesterol was seen both in the VLDL and in the LDL fractions. Despite more pronounced hyperlipemia, lipid concentration in the aortic wall was not increased nor were more marked histological abnormalities encountered in the aorta of uremic animals (cholesterol-fed control: cholesterol 95.4 +/- 4.4 micrograms/mg protein; phospholipids 2.42 +/- 0.9 micrograms/ml protein; cholesterol-fed uremia: cholesterol 96.8 +/- 4.9; phospholipids 2.52 +/- 0.8). The results suggest that despite hyperlipemia short-term experimental renal insufficiency does not promote atherogenesis.
Atherosclerosis
PMID:Atherogenesis in experimental uremia. 733 7

Patients with analgesic nephropathy are reported to have a higher risk of atherosclerosis. One possible reason for this is a high incidence of hyperlipaemia in patients with analgesic nephropathy. In a retrospective study, serum cholesterol and serum triglyceride concentrations of patients with analgesic nephropathy and moderately restricted renal function were significantly higher compared to a control group with other renal diseases of similar age and degree of renal insufficiency. Hyperlipaemia in analgesic nephropathy is not explained by end-stage renal failure on one side or protein loss as in nephrotic syndrome on the other side. Some possible mechanisms for hyperlipaemia in analgesic nephropathy are discussed.
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PMID:Hypercholesterolaemia and hypertriglyceridaemia in patients with analgesic nephropathy. 741 66

Calcium antagonists block calcium entry into cells, resulting in relaxation of smooth muscle and limitation of the cytotoxic effects of ischaemia in various organ systems. They are most frequently used for clinical conditions requiring vasodilatation, i.e. hypertension and Raynaud's phenomenon, and this also suggests that the most common adverse effect of these drugs for noncardiovascular indications is an unwanted decline in blood pressure. Other uses include treatment of supraventricular arrhythmias and angina. There is some evidence that these drugs retard the development of atherosclerosis. Calcium channel blockers also improve renal reperfusion and may reduce renal insufficiency due to various nephrotoxins, and are particularly useful in renal transplantation for protection against cyclosporin toxicity and post-transplant acute tubular necrosis. These drugs are also useful in pregnancy-induced hypertension and unwanted uterine contraction. Affective disorders and malignancies may be other conditions which benefit from calcium antagonist therapy. Calcium antagonists, in particular nimodipine which is most selective for the cerebral vasculature, have been approved for treating vasospasm after subarachnoid haemorrhage. They are probably also effective for treatment of migraine. Calcium channel blockers may be effective for treating acute cerebral infarction, but results of clinical trials to date have been equivocal, largely because it has been difficult to recruit patients within the short interval after the onset of stroke when these drugs would be most effective, and because of the unwanted hypotensive effect of high doses.
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PMID:New uses for calcium channel blockers. Therapeutic implications. 751 Jun 13

Vascular endothelial cells produce various biologically active factors regulating blood pressure, coagulation, and possibly cell growth of the vascular wall. Of the factors, nitric oxide (NO) has been the object of attention because of its quite simple molecular structure and variety of biological functions. In the present review, we focused on the physiologic and pathologic aspects of NO in hypertension. In experimental animals, both acute and chronic inhibition of NO synthase (NOS) with arginine derivatives produce a significant rise in blood pressure, indicating that tonic production of NO regulates basal vascular tonus. The chronic hypertension caused by NOS inhibitor is associated with cardiac hypertrophy and renal insufficiency. Sodium retention, though transient, and the plasma and tissue renin/angiotensin system in addition to the reduced production of NO have been implicated in the development of hypertension. Hypertension and the associated target organ failure can be reversed by co-administration of L-arginine or blockades of the renin/angiotensin system. Studies in which L-arginine as the substrate of NO or NOS inhibitor was administered demonstrated an important role of NO in the regulation of tonic vascular tonus also in normal subjects. In hypertensive subjects, however, endothelium-dependent vasorelaxation and production of NO are impaired, possibly due to a deficiency of L-arginine and/or a disorder of its utilization. Recent advances in the methods of detecting NO enabled us to demonstrate its diminished production from endothelial cells of hypertensive rats in vitro, although no definite biochemical evidence has been obtained in hypertensive subjects. The endothelial dysfunction, however, is not a primary cause of hypertension but a secondary result since it is commonly observed in various types of hypertension and can be reversed by correcting the blood pressure. Other common diseases including atherosclerosis and diabetes mellitus are also associated with similar abnormalities of the endothelium. NO has anti-atherogenic actions: inhibition of platelet functions and proliferation of vascular smooth muscle cells. Therefore, potentiation of endogenous NO and/or supplement of exogenous NO donors could be novel therapeutic approaches for the treatment of hypertension and atherosclerosis, while potential adverse effects of NO including cytotoxicity, immunosuppressibility, and hypotensive shock should be taken into account.
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PMID:[Clinical significance of nitric oxide in hypertension]. 752 65

The coexistence of different clinical syndromes due to atherosclerosis in different organs is not rare and emphasizes the diffuse nature of this vascular process. Although renovascular disease may cause hypertension and/or renal insufficiency, it may also occur in the absence of the usual clinical markers that suggest renovascular hypertension. We report a patient with stable coronary anatomy who presented with crescendo angina pectoris. Diagnosis of renovascular hypertension was made by screening renal angiography at the time of the cardiac catheterization. Renal artery stenting resulted in stabilization of the coronary syndrome and obviated the need for further coronary intervention. To our knowledge, this is the first case of renovascular hypertension precipitating an unstable coronary syndrome in a patient with documented stable coronary anatomy. Review of the literature supports that patients undergoing cardiac catheterization are a high risk population for renovascular disease, particularly in the presence of other predictive factors such as documented coronary artery disease, older age, female gender, congestive heart failure, peripheral vascular disease, renal insufficiency, and smoking. Firm recommendations for routine screening renal angiography in patients undergoing peripheral or coronary angiography will need further studies.
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PMID:Renal artery stenosis presenting as crescendo angina pectoris. 755 35

Renovascular disease (RVD) in older patients can cause progressive renal insufficiency and even end-stage renal disease (ESRD). The frequency of this clinical problem is not well defined. Renal duplex sonography (RDS) correctly identifies the presence of RVD with an overall accuracy of approximately 95%. Therefore, the purpose of this study was to utilize RDS as a noninvasive tool to identify the presence of critical RVD (> or = 60% diameter-reducing stenosis or occlusion) in patients 50 years of age or older beginning renal replacement therapy. A total of 53 consecutive participating patients were prospectively interrogated. Complete interrogations occurred in 45 of the 53 patients (85%), and 92 of the 103 kidneys (89%). Critical RVD was noted in 10 of 45 patients (22%). RVD was bilateral in 5 patients, unilateral in 5 patients, and there were 4 renal artery occlusions noted. All patients with critical RVD were white (10 of 25 white patients or 40%). Total pack years of smoking as well as associated cardiovascular and cerebrovascular conditions were greater in those patients with critical RVD compared to those without. These results indicate that RDS remains technically feasible as renal blood flow and function decline. Unsuspected RVD possibly contributory to renal insufficiency exists in a significant number of primarily white patients 50 years of age or older beginning renal replacement therapy. These patients are generally smokers with a high frequency of associated extrarenal atherosclerosis The addition of RVD as a separate category of disease causing ESRD would improve U.S. Renal Data System ESRD classification. RVD should be recognized as a cause of ESRD.
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PMID:Renovascular disease in older patients beginning renal replacement therapy. 756 74


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