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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renin-angiotensin system traditionally has been conceived as a neuroendocrine system functioning in the circulation. Recent research has confirmed the existence of autocrine/paracrine tissue renin-angiotensin systems present and functioning at multiple sites, including cardiac, vascular, and renal tissues, which contain the majority of angiotensin-converting enzyme in the body. It appears that the circulating renin-angiotensin system is activated acutely to maintain homeostasis and is then turned off at cardiovascular compensation, while the tissue renin-angiotensin systems exert long-term actions that affect cardiovascular function and structure, which may play a pathophysiological role in congestive heart failure, hypertension, and vascular disease and influence the response to therapy with angiotensin-converting enzyme-inhibiting agents.
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PMID:Tissue renin-angiotensin system in myocardial hypertrophy and failure. 838 20

1. The primary aim of this study was to assess the impact of renal haemodynamics on the pharmacokinetic behaviour of ibuprofen enantiomers. Thirty-two patients and ten age-matched healthy volunteers participated in this study. These patients had at least one of the following risk factors for cardiovascular disorders: hypertension, diabetes mellitus, hyperlipidaemia and hyperuricaemia with or without consequent complications such as coronary artery disease, congestive heart failure, cerebral vascular disease, and chronic renal failure. Renal function in these patients was thus characterized by unstable renal haemodynamics that might render them susceptible to ibuprofen-incurred renal damage. 2. Each subject received a single oral dose of 800 mg of racemic ibuprofen. The pharmacokinetic parameters of (S)- and (R)-ibuprofen, t 1/2(S), t 1/2(R), AUC(S), AUC(R), V/F(R), and CL/F(R), for each individual were determined from respective plasma concentration-time curves. To assess the effect of individual clinical conditions on the disposition of ibuprofen enantiomers, the arithmetic means of these pharmacokinetic parameters for each disease group were compared with those of the healthy volunteers by a t-test. 3. All of these disease groups showed elevated AUC(S) and higher (S)/(R) AUC ratios. These disease states along with gender and age were analyzed by multiple linear regression to discern significant factors for elevating AUC(S). Of these, advanced age (P = 0.02) and hypertension (P = 0.03) were identified as independent factors contributing to AUC(S) increase in this population. Thus, patients with these two clinical conditions are at particular risk from the adverse renal effect of ibuprofen.
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PMID:Stereoselective disposition of ibuprofen in patients with compromised renal haemodynamics. 852 70

By using a computerized database, we have catalogued the presence of 29 co-morbid risk factors in 683 patients with end-stage renal disease who started dialysis from 1970 through 1989, with follow-up through 1992. The authors hypothesized that current end-stage renal disease patients have more serious co-morbid risk factors impacting upon their mortality rate. Quantitation of dialysis patient co-morbidity, as a measure of patient illness, is lacking in the general nephrology literature. Seven co-morbid risk factors have been reserved for new dialysis patients: hypertension, low albumin, cerebral vascular disease, peripheral vascular disease, pre-existing cardiac disease, abnormal EKG/old myocardial infarction, and congestive heart failure. Except for low serum albumin, the proportion of patients with the six other co-morbid risk factors has increased significantly over this 20-year period (p < 0.0001, chi-square test for hypertension, peripheral vascular disease, pre-existing cardiac disease, abnormal EKG/old myocardial infarction, and congestive heart failure, and p < 0.006 for cerebral vascular disease). In addition, the co-morbid risk factors of hypertension, low serum albumin, and pre-existing cardiac disease at the start of dialysis were strongly prognostic of survival. The Cox proportional hazards regression model identified these three risks, among other factors, that were significantly associated with a decreased survival, with risk ratios ranging from 1.40-1.66. These results support the authors' hypothesis that incoming end-stage renal disease patients, who recently start dialysis, are sicker than in the earlier years of the authors' program. If the authors' patients reflect the national end-stage renal disease population, the presence of co-morbid risk factors may, in part, explain the continuing high mortality of dialysis patients.
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PMID:The impact of co-morbid risk factors at the start of dialysis upon the survival of ESRD patients. 872 82

The normal functional state of the vasculature and the events leading to the development of significant arterial disease involve the interaction of important vasoactive substances, which play important modulating or initiating roles in the development of hypertension and arteriosclerosis. Three endothelins have now been identified, of which ET-1 is the best characterized. ET-1 is produced by epithelial, mesangial, neuronal and glial, and liver cells, and is the most potent vasoconstrictor yet found. Each endothelin is derived from a different gene on separate chromosomes, and each binds to at least 2 types of receptor. The plasma half-life of ET-1 is about 7 min, and this provides a rapid mechanism for adjusting vascular resistance or blood pressure. The actions of endothelin are mediated through several pathways of postreceptor signaling, including activation of the mitogen-activated protein kinase cascade, which give rise to its growth-stimulating properties. Secretion of ET-1 from cultured endothelial cells is stimulated by a wide range of substances, and is inhibited by some prostaglandins. Endothelin in turn stimulates secretion of nitric oxide, arginine vasopressin and atrial natriuretic peptide, and participates in the hormonal control of salt and water balance. Hypoxia and ischemia augment ET-1 secretion, as does insulin, and this could play a role in the accelerated vascular disease of diabetes. ET-1 also causes bronchoconstriction and has been implicated in the development of acute asthma, primary pulmonary hypertension and pulmonary fibrosis. Its role in hypertension is still debatable, though most of the manifestations of congestive heart failure can theoretically be explained by the actions of ET-1. Endothelin also has extensive renovascular and parenchymal effects in the kidney. It is hoped that a fuller understanding of the role of endothelins in normal or pathologic vasculature will lead to effective therapy based on antagonism or augmentation of specific functions.
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PMID:Endothelins as cardiovascular peptides. 873 84

The object of this study was to assess the outcome of laparoscopic colorectal surgery in patients >60 years of age and compare it to a younger group of patients who underwent similar procedures. All consecutive patients who underwent a laparoscopic or laparoscopic-assisted procedure were evaluated. The parameters analyzed included gender, indication for surgery, procedure, complications, conversions, length of ileus, length of hospitalization, and comorbidity. The results of patients 60 years of age or older were compared to a procedure-matched group of younger patients. Between August 1991 and August 1995, 165 patients underwent a laparoscopic or laparoscopic-assisted colorectal procedure. Thirty-six patients were 60 years of age or older [mean age, 73 (60-88) years; 17 males and 19 females] and were compared with 36 younger patients [mean age, 44 (20-58) years; 13 males and 23 females]. The indications for surgery included Crohn's disease in 14 patients, polyps in 23, diverticular disease in 15, carcinoma in 11, fecal incontinence in 4, rectal prolapse in 2, radiation proctitis in 2, and sigmoidocele in 1. Identical procedures were performed in each group including right colectomy or ileocolic resection in 17 patients, sigmoidectomy in 14, loop ileostomy in 3, loop colostomy in 1, and abdominoperineal resection in 1 patient. Fourteen patients (38%) in the elderly group had comorbid conditions including ischemic heart disease (3), chronic obstructive pulmonary disease (3), hypertension (2), chronic renal failure (2), atherosclerotic vascular disease (2), congestive heart failure (1), and diabetes (1). All patients were cleared for surgery by their respective specialists. There were no statistically significant differences between the younger and older groups relative to the incidence of complications (11 vs 14%, respectively) and conversion (8 vs 11%, respectively) or the length of ileus (2.8 vs 4.2 days, respectively) or hospitalization (5.2 vs 6.5 days, respectively) (P = NS for all). There was no mortality in either group. The outcome of laparoscopic colorectal surgery in older patients is similar to that noted in younger patients. Advanced age should not be a contraindication to laparoscopic colorectal surgery.
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PMID:Outcome of laparoscopic colorectal surgery in older patients. 895 49

The endothelium modulates vascular tone by the release of vasodilator and vasoconstrictor substances, among them nitric oxide (NO) and endothelin (ET). Abnormalities in NO generation have been demonstrated in various cardiac pathophysiological states, specifically atherosclerotic vascular disease, congestive heart failure, and essential and pulmonary hypertension. Moreover, increases in plasma ET has been reported as well in these disease states. When these observations are taken together, these states may be characterized by an attenuated release of NO, whereas the release of ET is augmented. An imbalance between NO and ET may contribute to the alteration in vascular tone characteristic of cardiovascular disease. The following review summarizes the present knowledge of the role of NO and ET in such disease processes with a major focus on coronary endothelial dysfunction.
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PMID:Coronary endothelial dysfunction in the hypertensive patient: from myocardial ischemia to heart failure. 911 Nov 57

Apart from the initially described vasoconstriction, endothelins have been shown to cause a variety of biological activities in non-vascular tissues. A rapidly growing body of data supports the concept of endothelin as a paracrine acting hormone. In this review, we will discuss the impact of this local endothelin system for various cardiovascular pathophysiological states, especially atherosclerotic vascular disease, restenosis, myocardial infarction, congestive heart failure, and arterial hypertension. In addition, the endothelin system is a modulator of renal function via its binding to abundant receptors in renal tissue and by the ability of renal endothelial and epithelial cells to synthesize and release endothelin. In the kidney, endothelin may function as a paracrine/autocrine factor in the regulation of renal blood flow, glomerular haemodynamics, and sodium and water homeostasis. The renal endothelin system is involved in kidney diseases such as impaired renal function in liver cirrhosis, cyclosporin toxicity, acute renal failure and renal glomerular and interstitial fibrosis. Therapeutic approaches with new orally active endothelin receptor antagonists are also discussed.
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PMID:The paracrine endothelin system: pathophysiology and implications in clinical medicine. 929 57

Allograft vascular disease is a significant cause of death of cardiac transplant recipients after the first year of transplantation. With few exceptions, angina pectoris does not develop and objective examinations, including coronary angiography, are necessary to diagnose coronary arteriopathy. Between 1983 and 1994, 214 heart transplantations in 211 patients were performed in our unit. All survivors had coronary angiography performed yearly. Thirty patients had significant localized arterial stenoses. Twelve patients with critical stenosis were accepted for percutaneous transluminal coronary angioplasty. Five patients underwent retransplantation due to progressive graft vascular disease with development of congestive heart failure. Conventional revascularization with transluminal coronary angioplasty can safely be performed with primary good results. In selected patients, retransplantation is an option if patients otherwise fulfil standard criteria for cardiac transplantation.
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PMID:Percutaneous transluminal angioplasty and retransplantation due to transplant coronary artery disease. 929 41

Progress in vascular biology, epidemiology, clinical trials, and cost-effectiveness analyses have allowed development of guidelines for risk reduction in patients with vascular disease and congestive heart failure. However, these advances appear necessary but not sufficient to promote implementation of these guidelines for treating coronary artery disease (CAD) and congestive heart failure (CHF). Evidence from the United Kingdom and Europe, and estimates from the United States, suggest that a large "treatment gap" exists between recommended therapies for patients with cardiovascular disease and the care that they are actually receiving. Despite known interventions with proven efficacy to reduce disease recurrence and death from CAD and CHF, only a minority of patients are receiving any intervention whatsoever. A second problem is that, among those receiving care, many are undertreated resulting in a very small number of patients reaching goals and recommended levels of therapy. Third, the levels of intervention and the proportion of patients at goal that should be attainable (i.e., community standards) are not known. A variety of barriers exist for implementation of preventive cardiology services. Although the patient has a chain of opportunities for risk reduction, it is not clear which of the links in this chain (inpatient/hospital programs, specialist/generalist communication, ambulatory care, or patient compliance) is the major reason for the treatment gap. An ongoing project, the American College of Cardiology Evaluation of Preventive Therapeutics (ACCEPT), will attempt to quantify the treatment gap in coronary disease patients in the United States and will try to identify those barriers playing the greatest role in limiting the optimal care of the coronary disease patient.
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PMID:The treatment gap in coronary artery disease and heart failure: community standards and the post-discharge patient. 937 98

In the past 2 decades, significant progress has been made in cardiovascular therapeutics. Effective drug therapies have been developed for hypertension, hypercholesterolemia, coronary artery disease, myocardial infarction, and congestive heart failure. Novel therapeutic strategies to treat cardiovascular disease consist of 3 major approaches: (1) changing the biology of vascular disease; (2) intervening in the ischemic event; or (3) modifying the post-ischemic course. The development of future therapies depends on continuing advancements in our understanding of the molecular mechanisms of vascular pathobiology. Novel therapies are aimed at the critical steps in vascular disease progression, which include reversing endothelial cell dysfunction, modulating thrombosis and inflammation, correcting dysregulated cell growth and apoptosis, modulating vascular phenotype, and modifying mechanicotransduction in vascular remodeling. Targeting these steps at the molecular level will stimulate the development of numerous therapeutic agents. Ongoing research will further define the role of the agents in the treatment of cardiovascular disease.
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PMID:Future horizons in cardiovascular molecular therapeutics. 937 40


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