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

Ambulatory blood pressure monitoring can determine the average blood pressure level and the short- and long-term blood pressure variability (circadian rhythm). The circadian blood pressure rhythm appears to be mediated mainly by the circadian rhythm of the sympathetic tone which is linked to changes in physical and mental activity, e.g. the waking-sleeping cycle. A statistically significant circadian blood pressure rhythm was observed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, in patients with Cushing's syndrome, under glucocorticoid treatment, or with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, spinal cord injury, brainstem lesions, diabetic neuropathy, uremic neuropathy, etc), chronic renal failure, eclampsia, malignant hypertension, sleep apnea syndrome or systemic atherosclerosis, the normal circadian blood pressure rhythm appears to be eliminated or reversed, while in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, diabetes insipidus, acromegaly, hyperparathyroidism or hyperprolactinemia, the nocturnal blood pressure fall has been observed as in normal subjects. The alteration in the circadian blood pressure rhythm was observed with different pathophysiological conditions, although no specific pattern was observed for any condition. A disturbance in any part of the hierarchy of factors that regulate the circadian rhythm of sympathetic neural tone seems to disturb the circadian blood pressure rhythm. We conclude that ambulatory blood pressure monitoring is not critically important in the diagnosis of secondary hypertension although it does help in screening for secondary hypertension.
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PMID:Does ambulatory blood pressure monitoring improve the diagnosis of secondary hypertension? 208 1

The daily variation in blood pressure (circadian blood pressure rhythm) is characterized by a nocturnal fall and a diurnal rise. The circadian blood pressure rhythm seems to be mediated mainly by the circadian rhythm of sympathetic tone, linked to changes in physical and mental activities, e.g. the waking-sleeping cycle. Statistically significant circadian blood pressure rhythms have been confirmed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, the normal pattern of circadian blood pressure rhythm is reversed in elderly people and in those with Cushing's syndrome, those undergoing glucocorticoid treatment, and those with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, tetraplegia, diabetic or uremic neuropathy, etc), chronic renal failure, renal or cardiac transplantation, congestive heart failure, eclampsia, sleep apnea syndrome, malignant hypertension, systemic atherosclerosis and accelerated hypertensive organ damage. However, in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, or those with cardiac pacing, a nocturnal blood pressure fall is ordinarily observed. It may be that a fall in cardiac output rather than in peripheral resistance may be mainly responsible for the nocturnal fall in blood pressure. It also seems that a nocturnal heart rate fall is not responsible for it, since the nocturnal blood pressure fall remained unchanged in patients undergoing cardiac pacing and was disturbed in patients with Cushing's syndrome or hyperthyroidism in whom the circadian heart rate rhythm remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian blood pressure variations under different pathophysiological conditions. 209 80

The effect of chronic renal failure on the lipid and apolipoprotein concentrations of plasma, very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low density lipoproteins (LDL) and high density lipoproteins (HDL) was studied in an experimental uremic rat model. Control rats were sham-operated and were divided into adlibitum-fed and pair-fed groups. The rats were studied (after an overnight fast) 32 days after the onset of uremia. The uremic rats had a 4-fold increase in plasma urea nitrogen and creatinine. The pair-fed and ad-lib-fed controls had similar levels of plasma urea nitrogen and lipid profiles. In the uremic rats, plasma triglyceride (TG) levels were increased 3.8-fold due to increased TG in the VLDL, IDL and HDL fractions. Their 2-3-fold increase in plasma free cholesterol (FC), esterified cholesterol (EC) and phospholipids (PL) were due to FC, EC and PL increases in VLDL, IDL, LDL and HDL. Their increase in plasma apo B (x 2.4) and apo E (x 1.5) were due to increases in VLDL, IDL and LDL. Their plasma apo A-I increased 2.4 fold due to increases in the LDL and HDL fractions. Uremic rats also had increases in the FC/PL molar ratio in VLDL, IDL and LDL. In their LDL, the apo B/total cholesterol (TC), apo B/PL and apo B/apo E molar ratios were decreased. In their HDL, the apo E/TC and apo E/PL molar ratios were decreased and the apo A-I/apo E molar ratio was increased. In conclusion, chronic uremia causes both quantitative changes in the levels and qualitative changes in the composition of the plasma lipoprotein particles. These results are compatible with the decreased hepatic lipase activities and impairment of remnant clearance observed in human chronic renal failure.
Atherosclerosis 1990 Dec
PMID:Changes in the composition of plasma lipoproteins in the chronic uremic rat. 210 77

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called uremic heart diseases]. 210 35

Between January 1981 and April 1988, histologically proven renal cholesterol embolism was diagnosed in 13 men over 60 years of age with a previous history of hypertension and atherosclerosis. Six patients developed acute renal failure, usually induced by a triggering factor such as angiographic procedure or anticoagulation, and associated with peripheral and visceral cholesterol embolism, eosinophilia and a high sedimentation rate. In this group of patients, whose protean clinical manifestations and laboratory data mimicked necrotizing angiitis despite the absence of antineutrophil cytoplasmic antibodies, skin lesion biopsy established the diagnosis and made renal biopsy unnecessary. Six patients had chronic renal failure and elevated sedimentation rate, and the last patient had isolated microhematuria. In these 7 patients, percutaneous renal biopsy was an adequate procedure for the diagnosis of cholesterol embolism. As medical management of cholesterol embolism is essentially preventive, these unusual presentations must be emphasized.
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PMID:[Renal cholesterol embolism. Apropos of 13 cases]. 214 Nov 58

Lipoprotein [a] (Lp[a]) is known to show high values in patients with ischemic heart disease (IHD). In the present study attempts were made to determine Lp[a] levels and to investigate the association of Lp[a] and other atherosclerotic risk factors in patients with chronic renal failure treated by hemodialysis. Lp[a] concentrations were measured in 30 hemodialysis patients in the age range 34 to 77 years. Mean (+/- SD) levels of serum Lp[a] were not elevated in the hemodialysis patients compared to controls (19.3 +/- 18.0 mg/dl vs. 18.3 +/- 10.4 mg/dl, respectively). We found no statistically significant correlation of Lp[a] with either cholesterol, triglycerides, HDL-C or apoproteins. However, compared with controls, more than fivefold as many of those hemodialysis patients had high risk (greater than 30 mg/dl) concentrations of Lp[a]. Lp[a] tended to increase in hemodialysis patients with diabetes mellitus and/or ischemic heart disease. In patients with high levels of Lp[a] (greater than 30 mg/dl), Lp[a] tended to correlate positively with cholesterol, LDL-, HDL-C, apo B or apo B/AI. Incidence of IHD was also elevated in these patients. Along with other known risk factors such as hyperlipidemia and hypertension, an increased concentration of Lp[a] may play an important role in accelerating development of atherosclerosis in this condition.
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PMID:[A study of clinical significance of Lp[a] lipoprotein in patients with chronic renal failure treated by hemodialysis]. 214 55

Accelerated atherosclerosis occurs in chronic renal failure. The role of percutaneous transluminal coronary angioplasty (PTCA) in chronic renal failure patients requiring dialysis has not been characterized. We studied 17 chronic dialysis patients requiring PTCA over a 6-year period. Their mean age was 60 years, four were diabetic, eight had severe hypertension, and seven had unstable angina. Angiographic success was achieved in 47 of 49 (96%) stenoses attempted, including multivessel PTCA in 12 patients. There was one procedural death, two non-Q wave myocardial infarctions following PTCA, and one additional in-hospital noncardiac death. The 15 survivors were asymptomatic on discharge (mean stay 11 days), but recurrent angina developed within 6 months in 12 patients. Angiography in 11 of these 12 patients demonstrated restenosis of 26 of 32 (81%) dilated sites. Repeat PTCA in six patients was followed by return of angina in four patients with restenosis in 11 of 12 sites. Bypass surgery was ultimately performed in four patients with long-term angina relief. During follow-up (mean 20 months), seven patients died (five from chronic renal failure, two cardiac deaths). Thus although PTCA in chronic dialysis patients is technically feasible and provides relief of angina, aggressive restenosis limits the long-term benefit. Coronary bypass surgery may be the preferred therapy for this unique patient group.
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PMID:Short- and long-term outcome of percutaneous transluminal coronary angioplasty in chronic dialysis patients. 230 93

Patients with chronic renal failure who undergo hemodialysis experience accelerated atherosclerosis and premature death. Since the end-metabolite, oxalic acid, accumulates in plasma in proportion to the severity of renal failure, we studied whether sodium oxalate (0 to 300 microM) is an endothelial toxin and, therefore, might enhance atherogenesis. Exposure to uremic levels of oxalate (greater than 30 microM) for 9 to 28 days depressed endothelial cell replication by 33% to 84% (mean +/- SD, 54% +/- 15.7%, n = 17 experiments, p = 0.002). In contrast, replication of fibroblasts exposed to 200 microM oxalate for 45 days was not inhibited. The inhibitory effect of oxalate on endothelial cell replication was both dose- and time-dependent (both p less than 0.0001) and was first detected 3 to 7 days after the initial exposure to oxalate. Further, the inhibitory effect was fully reversible upon removal of oxalate, but only if exposure was limited to 5 days or less. Sodium salts of other carboxylic acids (citric, succinic, glyoxylic, and malonic; 200 microM) as well as HCl (200 microM) did not suppress endothelial cell replication. Oxalate also inhibited endothelial cell migration but had no effect on basal, thrombin-induced, or arachidonate-induced prostacyclin production by endothelial cells. Exposure of endothelial cells to sodium oxalate (200 microM) for as little as 24 hours-a time period sufficient to induce delayed, transient inhibition of replication not detectable until approximately 1 week after exposure-inhibited incorporation of 3H-leucine into protein by 40% (p = 0.009). We conclude that sodium oxalate acts as a uremic toxin, inhibiting endothelial cell replication and migration, functions which may be important for constitutive inhibition of atherosclerosis.
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PMID:Uremic levels of oxalic acid suppress replication and migration of human endothelial cells. 231 57

Two patients with severe hyperlipidemia receiving long-term hemodialysis were classified as type III hyperlipoproteinemic subjects. They are homozygous for apolipoprotein E2 and have an elevated VLDL-cholesterol/plasma-triglyceride ratio. The dyslipoproteinemia was severely aggravated by the renal failure, but careful treatment with bezafibrate was able to effectively lower elevated serum lipids. Accurate diagnosis of lipid abnormalities in patients with chronic renal failure seems to be necessary to plan appropriate therapeutic interventions and to lower the risk for accelerated atherosclerosis.
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PMID:Severe type III hyperlipoproteinemia in two patients maintained on chronic hemodialysis. 231 34

Lipid abnormalities have been postulated to contribute to renal insufficiency by a mechanism that is analogous to atherogenesis. The majority of patients treated for chronic renal failure die of cardiovascular complications. Lipid abnormalities in this group are thought to contribute to this high mortality. Proving a causal association between dyslipidemia and accelerated atherosclerosis in the end-stage renal disease population has been confounded by the presence of other pro-atherogenic conditions in this population. The current study compiles the lipid data we have accumulated from our renal population for the years 1987 to 1989. The report is divided into three main parts: The first is a survey of lipid levels and atherogenicity indicators in groups with different types of renal disease or modalities of treatment. The second is a multivariate analysis of the relationship of clinical and biochemical variables (and their interactions) to the serum lipid and apolipoprotein levels and their ratios and their change over time in a large dialysis population. In the third study, we quantitate the peritoneal clearances of apolipoproteins A-I and B in patients undergoing continuous ambulatory peritoneal dialysis and assess the relationship of these clearances to serum lipid and lipoprotein levels and risk ratios.
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PMID:Cholesterol and lipid disturbances in renal disease: the natural history of uremic dyslipidemia and the impact of hemodialysis and continuous ambulatory peritoneal dialysis. 248 49


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