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)

A 17-year-old male was admitted with an acute myocardial infarction. A coronarography showed 90% occlusion in of the descendent anterior artery. A coronary angioplasty was done with excellent response. As coronary risk factors he had diabetes mellitus for 5 years and dyslipidemia with a phenotype IIb and hypo-alpha-lipoproteinemia. The case is discussed in regard to the possible etiopathogenic causes for his premature atherosclerosis.
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PMID:[Premature atherosclerosis in a 17-year-old male with diabetes mellitus and familial dyslipoproteinemia]. 163 17

To assess the prognostic significance of supraventricular tachyarrhythmias (SVTA) during acute myocardial infarction (AMI), we studied 388 patients with first AMI, without ventricular preexcitation or chronic atrial fibrillation. The prevalence of SVTA was 14% (56/388), including atrial fibrillation (57%), atrial flutter (22%), polyfocal atrial tachycardia (14%), monofocal atrial tachycardia (7%). The arrhythmia appeared within 72 hours from the onset of chest pain in 61% of patients (early SVTA < 72 hours), while in 39% appeared later (late SVTA > 72 hours). Patients with SVTA (Group I n = 56) and without SVTA (Group II n = 232) were similar regarding prevalence of hypertension, dyslipidemia, diabetes, site of infarction and fibrinolysis, but SVTA was associated with a significant increase in death (Group I 18% versus Group II 9%; p < 0.05) and complications as pulmonary oedema and cardiogenic shock (Group I 25% versus Group II 14%; p < 0.05). Left atrial dimensions (LAD), end-diastolic left ventricular volume (EDLVV), end-systolic left ventricular volume (ESLVV) and echo-score, evaluated at admission, were not different between Group I and II (LAD 41.3 +/- 6 mm versus 40.1 +/- 5 mm, NS; EDLVV 181 +/- 34 ml versus 173 +/- 30 ml, NS; ESLVV 80 +/- 21 ml versus 75 +/- 18 ml, NS; echo-score 6.7 +/- 3.1 versus 6 +/- 2.7, NS) while pre-discharge echo-grams in Group I showed a trend towards the increase in volumes and echo-score (EDLVV from 181 +/- 34 ml to 194 +/- 36 ml, p = 0.052; ESLVV from 80 +/- 23 ml to 88 +/- 23 ml, p = 0.051; echo-score from 6.7 +/- 3.1 to 7.8 +/- 3.3, p = 0.070).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Supraventricular hyperkinetic arrhythmias in acute myocardial infarct: their prognostic assessment and correlation with the echocardiographic evolution]. 785 30

To characterize acute myocardial infarction (AMI) in young adults and octogenarians, 475 AMI patients, in age subsets, were examined. The clinical features, risk factors and in-hospital mortality were compared among 17 young patients (< 40 years), 426 patients of common age (40-79 years), and 32 very elderly patients (> or = 80 years). The octogenarian patients were mainly female (male/female ratio, 0.9 vs. 4.7 in other subgroups, P < 0.005), and had more frequent atypical presentation and postinfarctional congestive heart failure; whereas infarct size, location and development of Q-wave, major arrhythmias and cardiac wall rupture were not different among these age subsets. The most common risk factors in the young group were dyslipidemia (67%) and cigarette smoking (65%), and in the octogenarian group were dyslipidemia (52%) and hypertension (50%). Among age subsets, however, the prevalence of risk factors was not significantly different except for a relatively lower smoking rate in the octogenarians. Compared with 40- to 79-year-old patients who had predominantly multi-vessel diseases, the young patients had milder coronary atherosclerosis and were more likely to have normal coronaries (27% vs. 5%, P < 0.01). Significantly more octogenarians than young patients succumbed to AMI in the hospital (44% vs. 18%, P < 0.005), usually because of a cardiogenic complication (93%). Also, the octogenarians were less likely than the younger patients to have received thrombolytic therapy, mostly because of delayed diagnosis and arrival at the hospital, or because of old age itself.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute myocardial infarction in young and very old Chinese adults: clinical characteristics and therapeutic implications. 802 Oct 47

The fibrinolytic system is thought to be impaired in older hypertensive adults, thus contributing to the elevated risk of atherothrombosis, stroke, and acute myocardial infarction in this population. However, studies that have examined the fibrinolytic system in hypertensive individuals have failed to control for the confounding effects of other metabolic risk factors, making it difficult for one to determine the independent effect of hypertension on the fibrinolytic system. The purpose of the present study was to test the hypothesis that the fibrinolytic system is not impaired in older sedentary hypertensive men when the confounding effects of cardiovascular disease, diabetes, and dyslipidemia are controlled. Plasma concentrations of tissue-type plasminogen activator antigen and activity as well as plasminogen activator inhibitor-1 antigen and activity were measured under resting conditions in 12 hypertensive (69.4 +/- 1.4 years) and 11 normotensive 65.2 +/- 1.3 years) older men. The hypertensive and normotensive subjects had similar anthropometric and metabolic characteristics. There were no significant differences between the hypertensive and normotensive men in tissue-type plasminogen antigen (7.3 +/- 0.5 versus 6.1 +/- 0.6 ng/mL) and activity (1.8 +/- 0.3 versus 1.7 +/- 0.2 IU/mL) or plasminogen activator inhibitor-1 antigen (14.1 +/- 2.3 versus 10.8 +/- 2.2 ng/mL) and activity (17.4 +/- 1.2 versus 17.5 +/- 1.8 arbitrary units [AU]/mL) levels. In addition, the molar concentration ratio of active tissue type plasminogen activator to active plasminogen activator inhibitor-1 did not differ between the hypertensive (1:9.7 +/- 2.3) mmol/L) and normotensive (1:10.5 +/- 2.2 mmol/L) subjects, indicative of no impairment in fibrinolytic potential in either group. These results support the hypothesis that hypertension does not directly result in impaired fibrinolytic function in older adults. Furthermore, our findings suggest that abnormalities in fibrinolytic function in older hypertensive men are likely due to the primary effects of other metabolic disorders that usually accompany hypertension, such as hyperinsulinemia and dyslipidemia.
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PMID:The fibrinolytic system is not impaired in older men with hypertension. 862 Nov 96

Cardiovascular complications account for more than 50% of death in hemodialysis patients. Strong and independent predictors of mortality or cardiovascular complications are low levels of serum albumin, high plasma C-reactive protein and lipoprotein(a), plasma proteins that are described to function as negative or positive acute phase reactants. Further prominent and known risk factors that contribute to the increased incidence of atherosclerosis in hemodialysis patients are disorders in lipoprotein metabolism and elevated plasma fibrinogen concentrations. The latter has also been described to increase following acute or chronic inflammation. The main metabolic abnormality of the lipoprotein profile is a delayed catabolism of triglyceride-rich apoB-containing lipoproteins caused by a decreased activity of lipolytic enzymes. Inhibition of lipoprotein lipase activity by cytokines or parathyroid hormone impedes conversion of very-low-density lipoprotein to low-density lipoprotein, resulting in remnant accumulation and hypertriglyceridemia. Another acute phase condition, namely, acute myocardial infarction, results in a similar pattern of dyslipidemia and coagulation disorder. In summary, the acute phase response deeply influences serum lipids and lipoproteins as well as other atherogenic acute phase proteins in hemodialysis patients. Appreciation of acute phase lipoprotein changes is essential for accurate diagnosis of dyslipidemias, proper design of future clinical studies, and correct interpretation of published data.
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PMID:Inflammation, dyslipidemia and vascular risk factors in hemodialysis patients. 935 Jun 81

Carnitine and its derivative propionyl-L-carnitine are endogenous cofactors which enhance carbohydrate metabolism and reduce the intracellular buildup of toxic metabolites in ischemic conditions. The carnitines have been, and are being used in a spectrum of diseases including multiple cardiovascular conditions. These include angina, acute myocardial infarction, postmyocardial infarction, congestive heart failure, peripheral vascular disease, dyslipidemia, and diabetes. Most published data on carnitine, propionyl-L-carnitine, and other carnitine congeners are favorable but the clinical trials have been relatively small. In currently used doses, these substances are virtually devoid of significant side effects.
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PMID:Carnitine and its derivatives in cardiovascular disease. 940 79

Although first suggested at the turn of the 20th century, there is a renewed interest in the infectious theory of atherosclerosis. Studies done in many laboratories around the world over the past several years have shown an association between markers of inflammation and coronary atherosclerosis with an exacerbation of the inflammatory process during acute myocardial ischemia, particularly in the early stages of reperfusion. It is also being recognized that the traditional risk factors, such as smoking, dyslipidemia, hypertension and diabetes mellitus, do not explain the presence of coronary atherosclerosis in a large proportion of patients. We believe that in certain genetically susceptible people, infection with very common organisms, such as Chlamydia pneumoniae or cytomegalovirus, may lead to a localized infection and a chronic inflammatory reaction. Persistence of infection may relate to the degree of inflammation and severity of atherosclerosis. Early trials with appropriate antibiotic agents in some patients with a recent history of acute myocardial infarction have led to very salutary results. If patients with an infectious basis of atherosclerosis can be identified, a therapy directed at eradication of the offending organism may be appropriate.
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PMID:Interactive role of infection, inflammation and traditional risk factors in atherosclerosis and coronary artery disease. 980 69

Percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI) achieves high patency rates. Conversely, it has been shown that after thrombolysis, early reocclusion of the infarct-related artery (IRA) is associated with substantial morbidity and mortality. The aim of this retrospective study was to study the incidence, prognostic implications, and clinical risk factors for in-hospital reocclusion of the IRA after successful emergency PTCA for AMI. We studied 399 consecutive patients (aged 59+/-14 years, 52% with anterior wall infarction) admitted <6 hours after AMI onset, of whom 374 (94%) were successfully treated with primary (n = 297) or rescue (n = 77) PTCA, with a stenting rate of 8%. Predischarge angiography was performed in 306 (82%). Early reocclusion of the IRA occurred in 28 patients (9%) and was silent in 6 (2%). The reocclusion rate was 10% for primary PTCA and 8% for rescue PTCA (p = NS). Twenty-two of 28 patients (6%) underwent repeat emergency coronary angiography because of early recurrent ischemia and most (n = 18) were treated with emergency PTCA. Early recurrent ischemia occurred mostly (86%) within 5 days of AMI onset. There was a higher prevalence of on-site hemorrhage (18% vs 5%, p = 0.007), blood transfusion (11% vs 2%, p = 0.01), pulmonary edema (21% vs 4%, p <0.01), and in-hospital death (21% vs 1%, p = 0.0001) in patients with predischarge reocclusion. On multivariate analysis, cardiogenic shock on admission and absence of dyslipidemia were strong and independent predictors (p = 0.01) of IRA reocclusion. In conclusion, early reocclusion after emergency PTCA occurred in 9% of the patients and was associated with substantial morbidity and mortality. This warrants attempts to decrease its incidence, e.g., with more frequent use of stents.
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PMID:Incidence, consequences, and risk factors of early reocclusion after primary and/or rescue percutaneous transluminal coronary angioplasty for acute myocardial infarction. 973 78

Approximately 80% of all patients with diabetes die of cardiovascular disease. The traditional management of type 2 diabetes has been ineffective in altering this dismal prognosis. Insulin resistance is the fundamental defect of type 2 diabetes. Insulin resistance often leads to hyperinsulinemia, which is associated with hypertension, atherogenic dyslipidemia, left ventricular hypertrophy, impaired fibrinolysis, visceral obesity, and sedentary lifestyle. Although all these conditions are associated with atherosclerosis and adverse cardiovascular events, the therapeutic efforts in patients with diabetes have focused predominantly on normalizing glucose levels. Improved insulin sensitivity through lifestyle modifications or pharmacologic therapy (troglitazone and metformin) will lower both insulin and glucose levels as well as diminish dyslipidemia and hypertension. In contrast, sulfonylurea agents lower glucose by increasing insulin levels and may increase the risk of cardiovascular events. Therapy including aspirin, lipid agents (for example, statins), angiotensin-converting enzyme inhibitors, beta-adrenergic blockers, postmenopausal estrogen replacement, and vitamin E should be considered for patients with type 2 diabetes. In most patients with diabetes who have multivessel coronary artery disease, coronary artery bypass grafting is superior to coronary angioplasty for improving long-term cardiovascular prognosis. This superiority is mediated in part by the use of a left internal mammary graft to the left anterior descending coronary artery. Urgent coronary angioplasty or thrombolytic therapy should be considered for all patients with diabetes who have acute myocardial infarction.
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PMID:Improving the adverse cardiovascular prognosis of type 2 diabetes. 1006 57

The management of dyslipidemia after myocardial infarction (MI) is an important aspect of post-myocardial infarction care. However, acute changes in the lipid profile immediately following myocardial infarction have resulted in uncertainty regarding the clinical utility of lipid levels assessed during hospitalization for MI. We studied the effect of the timing of plasma lipid assessment among 294 patients who presented with MI to determine whether the differences between the serum lipid values in-hospital when compared with post-discharge values (generally 2-3 months after MI) would have a substantial impact on the decision to initiate lipid-lowering therapy. We found that the mean total and LDL cholesterol levels were significantly lower in-hospital when compared with generally 2-3 months later. However, patients whose lipids were measured within 48 h of presentation did not have significantly different values compared with generally 2-3 months post-discharge. Moreover, despite slightly lower in-hospital levels, 83.7% of patients were above the National Cholesterol Education Program target LDL for secondary prevention and 57.6% met the criteria for drug therapy based on in-hospital assessment. Total and LDL cholesterol levels fall modestly after an acute MI; however, from a clinical perspective, in-hospital levels can be used to guide decisions regarding lipid-lowering therapy which can begin in the immediate post-MI setting. In-hospital levels approximate post-MI levels, particularly if drawn within 48 h of presentation. All patients with acute myocardial infarction should have complete lipid profiles measured prior to discharge.
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PMID:Clinical utility of lipid and lipoprotein levels during hospitalization for acute myocardial infarction. 1061 26


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