Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with end-stage renal disease (ESRD) are at high risk for cardiovascular disease (CVD) and therefore should be treated according to ACC/AHA Guidelines. Scant data are available concerning the actual use of cardioprotective drugs in this population. The use of angiotensin-converting enzyme inhibitors (ACE-I), beta-blockers, aspirin, and statins was assessed in 271 (72% males, 66% Caucasians) high-risk ESRD patients on hemodialysis. The study population comprised 27% smokers, 95% with hypertension, 38% with diabetes, and 44% with dyslipidemia; 44% of patients had overt CVD at baseline, including 9% with heart failure, 9% with prior myocardial infarction, and 3% with previous myocardial revascularization. One-third of all patients were not receiving any cardioprotective drugs; among those patients who were, 42% were on one drug, 21% were on two, 3.7% were on three, and 1.5% were on four. The most prescribed agent was ACE-I (35.8%), followed by aspirin (30.6%), and beta-blockers (28.0%). The use of statins was remarkably and significantly low (4.1%) (p < 0.001), even in the higher risk subgroups (patients with diabetes or macrovascular disease). ACE-I plus aspirin was the most prescribed combination (8.5%). Cardioprotective agents recommended for risk-factor modification by the ACC/AHA Guidelines for their well-established efficacy in the general population were underutilized in this cohort of high-risk hypertensive hemodialysis patients, despite an elevated prevalence of clinically evident CVD. Speculatively, this fact may be relevant to better understand the known increased cardiovascular morbidity-mortality associated with chronic renal disease.
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PMID:Underuse of American College of Cardiology/American Heart Association Guidelines in hemodialysis patients. 1765 18

The leading cause of acute myocardial infarction (AMI) in patients with coronary heart disease is plaque rupture. Between 6% and 12% of AMI patients have angiographically normal coronary arteries. However, new procedures have demonstrated the limits of coronarography and challenged the existence of this situation. Angiograms may fail to detect minimal lesions whereas, in many cases, intravascular sonography reveals small atherosclerotic plaques. With the development of intravascular sonography and multislice computed tomography, the prevalence of myocardial infarction with normal coronary arteries has fallen to about 1%. Myocardial infarction with normal coronary arteries may be due to coronary vasospasm, hypercoagulable states, intense sympathetic stimulation, non atherosclerotic coronary disease, alcohol or cocaine abuse, and systemic diseases. In a series of 1205 AMI patients, we found no significant coronary disease in 45 patients, but intravascular sonography showed minimal intracoronary plaque in 21 of these cases. The 24 patients without significant lesions were young, had no risk factors for AMI without a prodrome, low peak creatine release, a small reduction in the left ventricular ejection fraction after thrombolysis or angioplasty, and good outcome at 26 months. The mechanisms of AMI in these 24 patients were coronary spasm, myocardial bridge, a prothrombotic state, contraceptive pill usage, and drug or alcohol abuse. The diferential diagnoses of these cases of AMI are acute myocarditis and stress cardiomyopathy, and apical left ventricular ballooning. Initial management is the same as for "conventional" AMI, including pain relief nitrates, antiplatelet agents, heparin, thrombolysis or angioplasty in the acute phase, and ACE inhibitors. Patients with spasm should receive calcium antagonists rather than beta-blockers. The prognosis of these patients is better than that of patients with atherosclerotic lesions. They nonetheless need close follow-up and strict secondary prevention measures, including smoking cessation and prevention of dyslipidemia and diabetes.
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PMID:[Myocardial infarction with "angiographycally normal coronary arteries" myth or reality?]. 1822 36

After an MI, elderly persons should have their modifiable coronary artery risk factors--such as hypertension, dyslipidemia, and diabetes--intensively treated. Aspirin or clopidogrel, beta-blockers, and ACE inhibitors should be given indefinitely, unless contraindications exist. Long-acting nitrates are effective antianginal and anti-ischemic drugs. There are no Class I indications for the use of calcium channel blockers after MI. Postinfarction patients should not receive Class I antiarrhythmic drugs, sotalol, or amiodarone. Those at very high risk for sudden cardiac death should have an implantable cardioverter-defibrillator. Hormonal therapy should not be used in postmenopausal women after MI. The indications for coronary revascularization are prolongation of life and relief of unacceptable symptoms despite optimal medical management.
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PMID:Optimal medical therapy after MI in the elderly. 1825 17

The coexistence of hypertension and type 2 diabetes considerably increases the risk for cardiovascular and renal complications, not only after manifestation of the diseases, but also in the range of high-normal blood pressures and prediabetic states. According to recent guidelines, patients with type 2 diabetes should be treated if the blood pressure is in the high-normal (previously normal) range (130-139/85-90 mmHg), sometimes even with blood pressures in the normal oder low prehypertensive range (120-129/80-85 mmHg). In any case, blood pressure should be reduced < 130/80 mmHg, if tolerated < 125/75 mmHg. The target for diabetic patients with microalbuminuria or nephropathy is below 125/75 mmHg. All blood pressure goals cited refer to office or clinic blood pressure measurements. The corresponding values for home (self) or ambulatory blood pressure measurement during the day are lower by 5-10 mmHg for systolic and 5 mmHg for diastolic blood pressures. The proper management of patients with type 2 diabetes has to be multifactorial, aiming at controlling blood pressure, hyperglycemia and dyslipidemia by using both lifestyle changes (reduction of sodium and fat intake, regular physical activity, weight loss in overweight patients, smoking cessation) and drug therapy. Antihypertensive treatment should be started with a (fixed) combination, preferably containing an inhibitor of the renin-angiotensin system such as ACE inhibitors or AT(1)-receptor blockers and either a diuretic (preferably indapamide) or a calciumantagonist rather than combining thiazide diuretics and beta-blockers.
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PMID:[Treatment of hypertensive type 2 diabetics: too late, too little]. 1856 13

Hypertension is a highly prevalent disease and a strong risk factor for cardiovascular disease in industrialized countries in Europe and North America. About 40-50% of hypertensive patients have some other cardiovascular risk factors as smoking, dyslipidemia, glucose intolerance, metabolic syndrome and diabetes. The realization of optimal therapy of these patients is a difficult task, and reaching target blood pressure values is almost impossible by monotherapy. It was realized that the simultaneous normalization of blood pressure and that of abnormal lipid profile with 2-3 or more drugs have great importance for preventing atherosclerotic complications.We started an open-formed study with about 1000 hypertensive patients complicated with dyslipidemia, visceral obesity, metabolic syndrome and diabetes type 2. The base of our therapeutic strategy was a typical poly-pharmacologic treatment with ACE inhibitor (lisinopril), calcium antagonist (amlodipine), statin (atorvastatin) and antiplatelet therapy (if it was necessary).
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PMID:[Combined antihypertensive and antilipemic therapy as one of the pillars in the poly-pharmacologic preventive strategy for patients with high cardiovascular risk]. 1880 71

The metabolic syndrome, also known as the cardiometabolic syndrome (CMS), is a state of metabolic and vascular dysregulation that is associated with activation of the renin-angiotensin-aldosterone system (RAAS). Clinical components of the CMS include central or visceral obesity, hypertension (HTN), dyslipidemia, insulin resistance/hyperinsulinemia, and microalbuminuria that collectively convey increases in oxidative stress, inflammation, and subsequent endothelial dysfunction. The cardio-renal inflammation and oxidative stress enhanced in the CMS increases the risk for cardiovascular disease (CVD) and renal disease end-points such as stroke, congestive heart failure, and chronic kidney disease (CKD). The development of proteinuria is known to herald progressive kidney disease (e.g. CKD) and both are now well accepted as CVD risk factors. Evidence suggests a role for visceral obesity, insulin resistance/hyperinsulinemia, HTN, and other components of the CMS lead to an increased risk for proteinuria and progressive loss of renal function. Intervention with agents that block the RAAS (e.g. ACE inhibitors and Angiotensin type 1 receptor blockers) have been shown to reduce proteinuria, CKD progression, and CVD events. Herein, we will examine the relationship between RAAS intervention and reductions in CKD and CVD events.
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PMID:Renin-angiotensin-aldosterone system intervention in the cardiometabolic syndrome and cardio-renal protection. 1912 93

The aim of the study was to evaluate prevalence of arterial hypertension (AH), efficiency of preceding therapy, and quality of life (QL) in 50 women with type 2 diabetes mellitus (DM) and diabetic foot syndrome (DFS) and 139 DM patients without DFS. The analysis included individual outpatient medical records, results of AH verification (WHO, RSC, 2004), parameters of carbohydrate and lipid metabolism, insulin resistance (IR) index, and QL data (SF-36 questionnaire). The patients were above 55 years of age. Active detection of AH revealed it in 98% of the patients with DFS and in 97% without it (p < 0.05). Detection of AH preceded diagnosis of LM. The lack of adequate IR correction (inefficient treatment with metformin, absence of thiazolidinedione therapy), irregular use of statins (in 4 and 8% of patients with and without DFS respectively, p = 0.541), inadequate antihypertensive therapy (absence of treatment at AP 130-139/80-89 mm Hg), rare application of ACE inhibitors, modification or withdrawal of prescribed therapy) resulted in decompensation of DM, dyslipidemia, poor control of AP, social and psychological problems in women with DM. Those having DFS suffered dyslipidemia, elevated AP, further progress of DFS manifestations and vascular complications, reduced QL in the absence of strict control of glycemia.
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PMID:[Prevalence of arterial hypertension in women with type 2 diabetes mellitus and diabetic foot syndrome]. 1925 60

Diabetes mellitus and hypertension frequently coexist in patients with the insulin resistance syndrome (IRS). Patients with both diabetes and hypertension typically have widespread endothelial dysfunction, increased oxidative stress, an activated sympathoadrenal system, and an elevated systemic burden of inflammatory mediators. Patients with diabetes and hypertension also have concomitant mixed dyslipidemia and obesity with significant frequency, and are at high risk for the development of macro- and microvascular disease, congestive heart failure, and nephropathy. Current data suggest that ACE inhibitors or angiotensin receptor blockers with or without a diuretic are important, if not preferred, initial therapies for the patient with diabetes and hypertension. Other drug classes such as combined alpha-/beta-adrenoceptor antagonists, dihydropyridine calcium channel antagonists (CCAs), and peripheral alpha-adrenoceptor antagonists are also useful therapeutic options in these patients. In order to optimally reduce the risk for cardiovascular events in the patient with diabetes and hypertension, optimal BP control should be coupled with comprehensive lifestyle modification and aggressive management of dyslipidemia and hyperglycemia.
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PMID:A guide to the management of blood pressure in the diabetic hypertensive patient. 1946 21

Arterial stiffness plays a key role in the pathophysiology of the cardiovascular system. Some indices of arterial stiffness (pulse wave velocity, augmentation index, characteristics of central blood pressure waveform) may be presently calculated and evaluated in the clinical setting. Age and blood pressure are the two major clinical determinants of increased arterial stiffness, while molecular determinants of arterial stiffness are related to fibrotic components of the extracellular matrix, mainly elastin, collagen and fibronectin. Increased arterial stiffness has been consistently observed in conditions such as hypertension, dyslipidemia and diabetes. Arterial stiffness evaluated by means of carotid-femoral pulse wave velocity yielded prognostic significance beyond and above traditional risk factors. A more favorable effect of calcium channel blockers, diuretics and ACE inhibitors compared with beta-blockers on indices of arterial stiffness was observed in several studies. It is conceivable that newer beta-blockers with additional vasodilating properties, such as nebivolol, which has favorable effects on carbohydrate and lipid metabolism, as well as on endothelial function and on oxidative stress, may have favorable effects on arterial stiffness, compared with atenolol. In fact, in recent studies, nebivolol was demonstrated to improve artery stiffness to a greater extent than older beta-blockers. Because endothelial dysfunction and increased arterial stiffness play an important role in the early atherosclerotic processes and are associated with poor outcomes and increased mortality, independently of blood pressure, the ability of nebivolol to enhance release of endothelium-derived nitric oxide, and consequently improve endothelial function and arterial stiffness, may have significant clinical implications for the use of this agent in the treatment of hypertension and cardiovascular diseases.
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PMID:Arterial stiffness, hypertension, and rational use of nebivolol. 1947 71

Kidney transplantation is the treatment of choice for patients with end-stage renal disease. Despite improvements in short-term patient and graft outcomes, there has been no major improvement in long-term outcomes. The aim of this study was to determine the prevalence of cardiovascular risk factors, such as hypertension, dyslipidemia, diabetes, chronic kidney disease, and obesity, and the impact of their control among 526 stable renal transplant recipients according to the guidelines in the general population. Mean blood pressure was 133 +/- 16/81 +/- 9 mm Hg. The proportion of patients on antihypertensive therapy was 75%, and on ACE inhibitors or angiotensin II receptor blockers, 26%. The mean cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides were 195 +/- 41, 115 +/- 32, 51 +/- 17, and 137 +/- 75 mg/dL, respectively. The proportion of patients on statin treatment was 49.7%, and those with body mass indices between 25 and 30, 30 and 35, and >35 kg/m(2) were 35%, 15%, and 4%. We observed a high prevalence of chronic kidney disease, hypertension, dyslipidemia, and obesity among renal transplant patients. Suboptimal control was frequent and control of some of these complications was far below targets established for nontransplant patients despite progressive intensification of therapy with functional graft decline. The findings of this study may have an impact on the management of renal transplant recipients.
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PMID:Chronic renal disease in renal transplant patients: management of cardiovascular risk factors. 1954 97


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