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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following a 1-week placebo run-in phase, 20 patients with congestive heart failure (New York Heart Association class II) were treated orally for 7 days with 100 mg ibopamine t. i. d. Ten subjects had a normal renal function, whereas 10 patients suffered from chronic renal insufficiency (mean creatinine clearance 36 plus minus 3.9 ml min(minus sign1)). Ibopamine significantly increased stroke volume and cardiac output, but only 45 and 90 min after administration. After 7 days of ibopamine treatment, urine output rose significantly in both patient groups by about 400--500 ml per 24 h. The glomerular filtration rate (inulin clearance) and urine osmolality remained nearly unchanged, whereas renal plasma flow (PAH clearance) increased on ibopamine administration. Urinary sodium and potassium excretion were slightly but insignificantly elevated. Pharmacokinetic parameters of ibopamine were unaltered in impaired renal function, both on the first and seventh treatment day. Maximum plasma levels of the active metabolite epinine were achieved after 45 min and were higher on the first as compared with the seventh treatment day in both groups. In conclusion, ibopamine caused a relevant increase in stroke volume and cardiac output associated with a rise in renal perfusion and urine output in patients with normal and with impaired renal function. Ibopamine is an orally active derivative of dopamine and is used for treatment of patients with congestive heart failure, who frequently have an impaired renal function. Therefore, in the present study, the hemodynamic effects and kinetic behavior of ibopamine should be investigated in patients with different degrees of renal function.
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PMID:Ibopamine in Patients with Congestive Heart Failure and Different Degrees of Renal Function. 1185 Jun 93

When first introduced in 1981, angiotensin-converting enzyme (ACE) inhibitors were indicated only for treatment of refractory hypertension. Since then, they have been shown to reduce morbidity or mortality in congestive heart failure, myocardial infarction, diabetes mellitus, chronic renal insufficiency, and atherosclerotic cardiovascular disease. Pathologies underlying these conditions are, in part, attributable to the renin-angiotensin-aldosterone system. Angiotensin II contributes to endothelial dysfunction. altered renal hemodynamics, and vascular and cardiac hypertrophy. ACE inhibitors attenuate these effects. Clinical outcomes of ACE inhibition include decreases in myocardial infarction (fatal and nonfatal), reinfarction, angina, stroke, end-stage renal disease, and morbidity and mortality associated with heart failure. ACE inhibitors are generally well tolerated and have few contraindications. (Am Fam Physician 2002;66:473.)
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PMID:Using ACE inhibitors appropriately. 1248 85

Fatal and nonfatal complications (stroke, myocardial infarction, chronic heart failure, sudden coronary death, chronic renal insufficiency) were registered during long term follow-up of 529 patients with hypertensive disease and results were analyzed retrospectively. Duration of ambulatory treatment in two thirds of patients exceeded 15 years. There were 243 deaths in 1993-1999. Mean age of those who died was 75 years. Main fatal complications were strokes and myocardial infarctions. Their rates were similar. Strokes comprised one third of all deaths irrespective of age. There were no significant differences between rates of ischemic and hemorrhagic strokes. Among causes of death proportion of sudden death was the highest in patients younger than 60 years while that of chronic heart failure rose with age. There were no cases of chronic renal failure. Atherosclerotic lesions in coronary and cerebral vessels were found at autopsies irrespective of cause of death.
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PMID:[Fatal and nonfatal cardiovascular complications in patients with essential hypertension (hypertensive disease) during follow-up for many years]. 1249 62

Epidemiological and experimental data have clearly demonstrated a strong association between elevated LDL-cholesterol levels and coronary heart disease. In concordance lipid-lowering trials with statins have shown a significant reduction of cardiovascular events. Although stroke is mainly caused by atherosclerotic vascular events, epidemiolgical data have so far failed to show a significant relationship between elevated lipid levels and stroke incidence. However, recent lipid intervention trials with statins have clearly demonstrated a significant reduction in stroke incidence. Moreover, elevated cholesterol levels are thought to contribute to progression of chronic renal insufficiency. In addition, cholesterol crystal emboli are a rare but frequently serious complication of vascular catheter interventions. Significant hypertriglyceridemia carries a significant risk of acute pancreatitis and is thought to contribute to the development of fatty liver disease.
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PMID:[End-organ damage in hyperlipidemias]. 1463 79

Chronic renal insufficiency (CRI) is a predictor of stroke, cardiovascular, and all-cause mortality, but the mechanisms responsible for these associations are unclear. Whether CRI was associated with severity of coronary artery disease (CAD) as measured by exercise stress echocardiography among outpatients with stable CAD was evaluated. This study is a cross-sectional analysis of the Heart and Soul study, a prospective cohort of patients with known CAD. Renal function was assessed by 24-h urine collection, and CRI was defined as measured creatinine clearance < or =60 ml/min. Exercise stress echocardiography was used to identify inducible ischemia, defined as any wall motion abnormality seen at stress but not at rest. Logistic regression was used to evaluate the association of CRI with exercise-induced ischemia after adjustment for cardiovascular risk factors. Participants with CRI composed 97 (23%) of the 431 participants and were characterized by older age, worse CAD, lower ejection fraction, greater left ventricular mass and higher C-reactive protein values. The prevalence of exercise-induced ischemia was also substantially greater in the participants with CRI (42% versus 23%; odds ratio [OR], 2.3; 95% confidence interval [CI], 1.4 to 3.8; P < 0.001). This association was minimally changed by adjustment for traditional cardiovascular risk factors and coronary disease history (OR, 2.0; 95% CI, 1.3 to 3.3; P < 0.01) and remained strong even after adjustment for C-reactive protein (OR, 2.3; 95% CI, 1.0 to 5.1; P = 0.04). CRI is strongly associated with exercise-induced ischemia in patients with CAD. The greater severity of atherosclerotic disease observed in patients with CRI may in part explain the association of CRI with increased cardiovascular risk among individuals with CAD.
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PMID:Association between renal insufficiency and inducible ischemia in patients with coronary artery disease: the heart and soul study. 1463 21

Cardiovascular calcification is a common consequence of aging, diabetes, hypercholesterolemia, mechanically abnormal valve function, and chronic renal insufficiency. Although vascular calcification may appear to be a uniform response to vascular insult, it is a heterogenous disorder, with overlapping yet distinct mechanisms of initiation and progression. A minimum of four histoanatomic variants-atherosclerotic (fibrotic) calcification, cardiac valve calcification, medial artery calcification, and vascular calciphylaxis-arise in response to metabolic, mechanical, infectious, and inflammatory injuries. Common to the first three variants is a variable degree of vascular infiltration by T cells and macrophages. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clear; stroke, amputation, ischemic heart disease, and increased mortality are portended by the anatomy and extent of calcific vasculopathy. Along with dystrophic calcium deposition in dying cells and lipoprotein deposits, active endochondral and intramembranous (nonendochondral) ossification processes contribute to vascular calcium load. Thus vascular calcification is subject to regulation by osteotropic hormones and skeletal morphogens in addition to key inhibitors of passive tissue mineralization. In response to oxidized lipids, inflammation, and mechanical injury, the microvascular smooth muscle cell becomes activated. Orthotopically, proliferating stromal myofibroblasts provide osteoprogenitors for skeletal growth and fracture repair; however, in valves and arteries, vascular myofibroblasts contribute to cardiovascular ossification. Current data suggest that paracrine signals are provided by bone morphogenetic protein-2, Wnts, parathyroid hormone-related polypeptide, osteopontin, osteoprotegerin, and matrix Gla protein, all entrained to endocrine, metabolic, inflammatory, and mechanical cues. In end-stage renal disease, a "perfect storm" of vascular calcification often occurs, with hyperglycemia, hyperphosphatemia, hypercholesterolemia, hypertension, parathyroid hormone resistance, and iatrogenic calcitriol excess contributing to severe calcific vasculopathy. This brief review recounts emerging themes in the pathobiology of vascular calcification and highlights some fundamental deficiencies in our understanding of vascular endocrinology and metabolism that are immediately relevant to human health and health care.
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PMID:Osteogenic regulation of vascular calcification: an early perspective. 1510 15

Vascular calcifications are the consequence of several pathological conditions such as atherosclerosis, diabetes, hypercholesterolemia and chronic renal insufficiency. They are associated with risks of amputation, ischemic heart disease, stroke and increased mortality. A growing body of evidence indicates that vascular smooth muscle cells (VSMCs) undergo chondrogenic commitment eventually leading to vascular calcification, by mechanisms similar to those governing ossification in the cartilage growth plate. Our knowledge of the formation of cartilage growth plate can therefore help us to understand why and how arteries calcify and, consequently, develop new therapeutic strategies. Reciprocally, thorough consideration of the events leading to ectopic chondrocyte differentiation appears crucial to further increase our understanding of growth plate formation. In this context, we will review the effects of known or suspected factors that promote chondrogenic differentiation in growth plate and arteries.
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PMID:Cartilage formation in growth plate and arteries: from physiology to pathology. 1595 94

We examined the efficacy of candesartan in reducing cardiovascular events in hypertensive patients with coexisting chronic kidney disease and cardiovascular diseases. This open-label, prospective study was conducted from 1999 to 2002, and 141 hypertensive subjects 60 to 75 years old with non-diabetic chronic renal insufficiency were enrolled. Before randomization of the patients, we examined their past medical history and found that 69 patients had been hospitalized due to myocardial infarction (MI) or stroke. Therefore, the patients were divided into 2 groups, one with previous histories of MI or stroke and the other with no previous history of Ml or stroke. The patients were randomized to receive either the angiotensin receptor blocker candesartan or conventional treatment. The mean duration of follow-up was 3.1 +/- 0.4 years. The primary outcome was a primary cardiovascular event (MI, stroke, or heart failure) verified by hospitalization. At the end of the study, in the patients with past history of cardiovascular diseases, blood pressure was reduced from 146.4 +/- 7.2/79.2 +/- 5.1 to 34.4 +/- 6.1/72.3 +/- 4.0 mmHg in the candesartan group and from 145.3 +/- 5.1/80.1 +/- 3.8 to 133.4 +/- 5.8/73.8 +/- 4.2 mmHg in the conventional treatment group. In the patients without past history of cardiovascular diseases, blood pressure was reduced from 143.2 +/- 4.3/78.3 +/- 4.8 to 133.8 +/- 5.3/ 73.1 +/- 3.8 mmHg in the candesartan group and from 143.9 +/- 6.8/78.1 +/- 4.2 to 132.6 +/- 5.4/74.5 +/- 4.4 mmHg in the conventional treatment group at the end of the study. There were no significant differences between the candesartan group and the conventional treatment group in the reduction of blood pressures. Among patients with a past history of cardiovascular disease, the serum creatinine concentration increased from 1.49 +/- 0.38 to 1.58 +/- 0.42 by candesartan treatment and from 1.50 +/- 0.32 to 1.89 +/- 0.37 by conventional treatment. On the other hand, in patients with no past history of cardiovascular disease, the serum creatinine concentration increased from 1.44 +/- 0.42 to 1.46 +/- 0.40 by candesartan treatment and from 1.46 +/- 0.44 to 1.51 +/- 0.38 by conventional treatment. Although, there was no significant difference in the incidence of cardiovascular events between the 2 groups with the candesartan-based and conventional-based antihypertensive treatment, in patients without cardiovascular events (12/36 vs. 7/34: these figures indicate events per total participated persons per 3 years; following figures are the same as this), treatment with candesartan reduced the incidence of cardiovascular events in the patients with past history of cardiovascular diseases (20/33 vs. 32/ 38). In particular, candesartan-based treatment reduced the incidence of congestive heart failure by 66.4% in these patients. In conclusion, this prospective, open-labeled randomized study suggests that 1) previous history of cardiovascular diseases is a major risk factor for cardiovascular events; and 2) candesartan is effective for reduction of cardiovascular events in hypertensive patients with coexisting chronic kidney disease and cardiovascular diseases, especially for prevention of congestive heart failure.
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PMID:An angiotensin receptor blocker reduces the risk of congestive heart failure in elderly hypertensive patients with renal insufficiency. 1615 5

The objective of this study was to elucidate the relationship between outcomes from carotid endarterectomy (CEA) in patients with and without renal insufficiency. Carotid endarterectomy is one of the most commonly performed vascular procedures. The role of cardiac comorbidity in carotid endarterectomy has been extensively studied. The relationship between renal failure and surgical outcomes has also been studied for both coronary artery bypass grafting and lower extremity occlusive disease. However, the role of renal insufficiency in relationship to decision making regarding surgical intervention for carotid stenosis is not well defined. The authors hypothesized that the outcomes from CEA were negatively influenced by renal dysfunction. A retrospective review was made of consecutive CEAs performed at their institution from 1990 to 1995. Patients were grouped into 2 categories according to their renal function. Group A, 448 patients (90%) with creatinine level 1.8 mg/dL or less, and group B, 49 patients (10%) with creatinine levels more than 1.8 mg/dL. Data from patients on dialysis are presented but were excluded for the purpose of analysis. Included in the study were 497 patients with a mean age of 70 +/-8.9 and 74 +/-8.9 for groups A and B, respectively. Preoperative creatinine was 1.1 (+/-0.25) mg/dL for group A and 2.5 (+/-0.81) mg/dL for group B. Outcomes were as follows: perioperative cardiac events 5.4% vs 28.6%, stroke rates 2.7% vs 2.0%, and mortality rates 0.9% vs 8.2%, for groups A and B, respectively. At 60-month follow-up the stroke rates were 7.6% vs 6.1 %, and the mortality rates 22.8% vs 59.2%, for groups A and B, respectively. While patients with chronic renal insufficiency have no increased risk of perioperative or long-term neurologic events, perioperative and long-term mortality rates are significantly increased. This significant reduction in survival should prompt a more cautious application of CEA in patients with increased creatinine.
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PMID:Carotid endarterectomy in patients with renal insufficiency: Should selection criteria be different in patients with renal insufficiency? 1622 81

Erythropoietin is a hypoxia-induced hormone that is a major regulator of normal erythropoiesis. Over the last decade, the production of recombinant human erythropoietin has revolutionized the treatment of anemia associated with chronic renal failure, and has led to a greater understanding of anemia pathophysiology and to the elucidation of the interactions of erythropoietin, iron, and erythropoiesis. Anemia has been shown to be independently associated with increased mortality and disease progression. Potential survival benefits associated with correction of anemia have expanded considerably the indications of erythropoietin use in various patient populations and are leading to consideration of earlier, more aggressive treatment of mild to moderate anemia. The results of such treatment are promising in a variety of new clinical settings, including anemia associated with congestive heart failure. Furthermore, the erythropoietin receptor is widely distributed in the cardiovascular system, including endothelial cells, smooth muscle cells and cardiomyocytes and preclinical studies have established erythropoietin to be a pleiotropic cytokine with anti-apoptotic activity and tissue-protective actions in the cardiovascular system, beyond correction of hemoglobin levels. Despite some potential adverse effects, such as hypertension, and the occurrence of erythropoietin resistance, early studies in heart failure patients with anemia suggest that erythropoietin therapy is safe and effective in reducing left ventricular hypertrophy, enhancing exercise performance and increasing ejection fraction. Anemia is found in about one-third of all cases of congestive heart failure (CHF). The most likely common cause is chronic renal insufficiency, which is present in about half of all CHF cases. However, anemia can occur in CHF without renal insufficiency and is likely to be due to excessive cytokine production. The anemia itself can worsen cardiac function, both because it causes cardiac stress through tachycardia and increased stroke volume, and because it can cause a reduced renal blood flow and fluid retention, adding further stress to the heart. Long-standing anemia of any cause can cause left ventricular hypertrophy, which can lead to cardiac cell death through apoptosis and worsen CHF. Therefore, a vicious circle, cardio-renal anemia syndrome, is set up wherein CHF causes anemia, and the anemia causes more CHF and both damage the kidneys worsening the anemia and the CHF further and increasing mortality. There is now evidence that early correction of the CHF anemia with subcutaneous erythropoietin and intravenous iron improves shortness of breath and fatigue, cardiac function, renal function and exercise capacity, reducing the need for hospitalization and improving quality of life. In the present review we discuss the data on current clinical use of erythropoietin in cardiovascular disease, with the main focus on the treatment of congestive heart failure, and summarize the advances and progress made in the understanding of the hematopoietic and pleiotropic effects of erythropoietin in the cardiovascular system.
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PMID:Erythropoietin in heart failure and other cardiovascular diseases: hematopoietic and pleiotropic effects. 1624 29


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