UMLS:C0020473 - FACTA Search

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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed retrospectively the clinical course and prognosis of 565 consecutive patients with acute myocardial infarction (AMI), 117 of them with a previous history of diabetes mellitus. Male/female ration was 7.9/2.1 in non diabetics and 7.0/3.0 in diabetics (p < 0.03). Incidence of hypertension and hyperlipidemia was higher in diabetic patients as well as history of congestive heart failure (13.7% vs 6.5 in non diabetics p < 0.01). The type and location of AMI did not differ among groups, however the incidence of congestive heart failure Killip class III-IV was higher in diabetic patients (31.6 vs 21.2%). Peak CPK values were lower in diabetics (1.270 +/- 1.179 vs 1.648 +/- 1.377 U/l p < 0.01). Cardiac mortality was higher one month and one year after AMI in diabetics (17.1 vs 13.6% and 21.4 vs 17.8% respectively, p < 0.01). Univeriate and multivariate analysis identified new bundle branch block, heart failure and advanced age as independent predictors of mortality in both groups of patients. It is concluded that the worst prognosis of diabetic patients with AMI may be related to a previously depressed ventricular function and that appropriate metabolic control and treatment of associated risk factors, could improve the prognosis of diabetics patients with AMI.
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PMID:[Characteristics of acute myocardial infarction in patients with diabetes mellitus]. 827

The author presented data obtained in Bangladesh, to elucidate the role of hypertension as a risk factor along with others such as smoking, cholesterol and diabetes mellitus as cofactors in ischaemic heart disease (IHD). There was a series of 100 cases with IHD admitted within 12 hours after the onset of chest pain observed in this study. They all were diagnosed as IHD for the first time. Of them, 94 were male and 6 female, with an age range of 25-77 years (mean 50.16 +/- 14 years). On grouping of IHD, 21 had angina pectoris and 79 acute myocardial infarction. 31% cases of IHD had hypertension. The blood pressure ranged between 168.54 +/- 24.85 and 106.29 +/- 16-80 mmHg. 74 out of the 100 cases with IHD were smokers. The mean value of serum cholesterol in this series was 6.48 +/- 1.66 mmol/L and that among 50 normal controls was 4.76 +/- 1.28 mmol/L (P < 0.01). The serum triglyceride determinations between the 94 cases of IHD and 50 normal controls showed values with statistically significant difference. The author concluded in this study that, hypertension, smoking and hyperlipidemia are the most important risk factor of IHD in Bangladesh.
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PMID:Evaluation of hypertension and other risk factors in ischemic heart disease. 840 84

To define the risk factors and clinical presentation of patients under age 40 who present to the emergency department (ED) of a community hospital with an acute myocardial infarction (MI), a retrospective cross-sectional study was conducted over a 7-year period. Two hundred and nine consecutive cases of initial MI who met World Health Organization criteria (chest pain, ECG changes, and serum enzyme rises) and were admitted to one of five participating hospitals were reviewed. The mean age of patients was 34.8 years (range, 17-39); 81% were male. The major risk factor was tobacco use (81%), followed by family history (40%), hypertension (26%), and hyperlipidemia (20%). One hundred and eighty-three patients (87.6%) had ECG evidence of cardiac ischemia, injury, or infarction in the ED. Approximately 24% of patients had multi-vessel coronary atherosclerosis as documented by angiography; 62% had single vessel disease; and 14% had normal coronary arteries. The most common anatomical location for the MI was the inferior wall. This study characterized the epidemiology of acute MI in young adults: 1) smoking emerged as the main coronary risk factor; 2) atherosclerosis continues to be the major etiology; 3) a common finding on angiography was single-vessel disease causing infarction of the inferior wall; and 4) the complication rate was comparable to older populations, but the in-hospital mortality was only 1.9%.
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PMID:Myocardial infarction in young adults: risk factors and clinical features. 874 Jul 43

Ten patients, eight males and two females with a mean age of 51.20 +/- 8.23 (SD) were seen in ABU Teaching Hospital, Zaria from 1985 to 1994 with either myocardial infarction or angina. Three patients were Asians and Lebanese. Seven had myocardial infarction and two had angina and one patient had ischaemic cardiomyopathy. There were four patients with anterior-lateral, two with inferior lateral and one anterior septal myocardial infarction. The diagnosis of acute myocardial infarction was based on symptoms and electrocardiograph. Five patients had angiogram with evidence of severe coronary disease. The risk factors identified were hypertension, hyperlipidaemia, smoking, Diabetes mellitus and male sex. Laboratory evidence was minimal because CK-MB is not a routine investigation in our centre, this might compromise the diagnosis.
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PMID:Ischaemic heart disease and myocardial infarction in ABU Teaching Hospital, Zaria: a 10 year review (1985 to 1994); a short report. 893 88

Women appear to be protected, until the menopause, from the development of coronary artery disease. The incidence of acute myocardial infarction in young women is very low, so there is little information on the etiology, clinical features, and prognosis for such patients. We studied 24 young female patients with acute myocardial infarction (< 50 years) among 2,457 consecutive patients with acute myocardial infarction admitted to the coronary care unit of the National Cardiovascular Center from December 1977 through August 1994. Their clinical features and in-hospital mortality were compared with 100 consecutive young male patients (< 50 years) with acute myocardial infarction. The fraction of patients of age younger than 50 years among all age groups was lower in female than in male acute myocardial infarction patients (5% vs 13%, p < 0.01). The increase of the coronary risk factors, hypercholesterolemia (25% vs 55%, p < 0.05) and cigarette smoking (17% vs 96%, p < 0.05) were less common in women. In female patients, the serum total cholesterol level was lower (195 +/- 50 vs 216 +/- 48 mg/dl, p = 0.06), and the serum high-density lipoprotein cholesterol level was higher (50 +/- 12 vs 39 +/- 12 mg/dl, p < 0.05) than in male patients. Other risk factors did not differ significantly between the two groups. Angiography 1 month after myocardial infarction showed fewer diseased coronary arteries (> 75% stenosis) in female than male patients (0.8 +/- 0.9 vs 1.8 +/- 1.0, p < 0.01), and normal coronary arteries were seen in 35% of female patients (male 6%, p < 0.05). Ten female patients (42%) had obviously non-atherosclerotic causes of acute myocardial infarction: Takayasu aortitis in three patients, coronary embolism in two, acute dissection of the aorta in two, and idiopathic coronary artery dissection, Kawasaki disease, and systemic lupus erythematosus in one each. In contrast, among male patients, only one had coronary embolism (1%). In-hospital mortality was higher in women (17%) than in men (2%, p < 0.05). Young female patients (< 50 years) with acute myocardial infarction have a low incidence of hyperlipidemia and normal coronary arteries or involvement of the left main trunk are more common compared with male patients (< 50 years). Although 42% of female patients had obvious non-atherosclerotic etiology of acute myocardial infarction, the causes varied widely.
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PMID:[Acute myocardial infarction in young Japanese women]. 898 54

Measurement of creatine kinase MB (CK-MB) and its isoforms CK-MB2 and CK-MB1 are now applied in the diagnosis of acute myocardial infarction (AMI). The most common approach for analysis includes RIA, IRMA, and electrophoresis, all of which may be time-consuming. This study examines determination of CK-MB and CK-MB2 by a rapid immunochemical extraction method followed by an automated measurement for both analytes. The automated method was sensitive to 2 U/L, linear to 180 U/L, and gave excellent interassay precision (< 10% CV). Interference studies indicated that bilirubin, hemolysis, and lipemia caused analytical problems as did the presence of high activities of other CK isoenzymes, notably CK-MM and CK-BB, requiring dilution of samples prior to analysis. Application of immunochemical extraction gave a reference interval of CK-MB (0-2.5 U/L) and CK-MB2 (0.1-1.4 U/L) for blood donors (20-60 years), peak levels for ruled-out AMI patients of CK-MB (0.5-7.3 U/L) and CK-MB2 (0.3-4.9), peak levels for ruled-in AMI patients of CK-MB (80-174 U/L) and CK-MB2 (80-155 U/L). Coronary artery bypass patients (n = 24) and all trauma patients (n = 14) also demonstrated elevations in CK-MB and CK-MB2, whereas only five of the trauma patients demonstrated increased CK-MB by IRMA. In patients (n = 7) having increased total CK and normal CK-MB by IRMA, the extraction assay for CK-MB and CK-MB2 yielded increased values in all patients. This new approach to CK-MB and CK-MB2 analysis can be performed within 30 minutes of sample receipt.
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PMID:Immunochemical extraction and automated measurement of plasma creatine kinase MB isoenzyme and creatine kinase MB2 isoform. 913 6

There are indications that beta-carotene, but not pre-formed vitamin A, is protective on the risk of acute myocardial infarction (AMI). The relationship between nonfatal AMI and the intake of beta-carotene and retinol was investigated in a case-control study conducted between 1983 and 1992 in northern Italy on 433 women with nonfatal AMI and 869 controls in hospital for acute, non-cardiovascular, non-neoplastic, non-digestive, non-hormone related conditions. Odds ratios (OR), with their 95% confidence intervals (CI), were computed by unconditional multiple logistic regression analysis, including terms for age, education, body mass index, smoking, alcohol and coffee drinking, menopausal status, hormone replacement therapy and history of diabetes, hypertension and hyperlipidemia. The risk of AMI was inversely related to beta-carotene intake, with an OR of 0.5 (95% CI: 0.3 to 0.8) for the highest quintile of intake compared to the lowest (chi2 trend = 10.53, p < 0.01). Retinol intake was not associated with AMI, with an OR of 0.9 (95% CI: 0.6 to 1.3) for the highest quintile of intake compared to the lowest. Analysis in separate strata of covariates indicated that the inverse association of beta-carotene intake with risk of AMI was appreciably stronger in younger, lean women with no history of diabetes or hypertension, and in current smokers. The results of this study indicate that the risk of nonfatal AMI in women is inversely related to intake of beta-carotene containing foods, but not foods containing retinol.
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PMID:Beta-carotene intake and risk of nonfatal acute myocardial infarction in women. 932 8

The aim of this study was to investigate the association of the Bcl I beta-chain fibrinogen polymorphism with the risk of acute myocardial infarction (AMI) and its relationship with fibrinogen levels in the Italian population. We studied 102 AMI patients, selected within the framework of the GISSI-2 trial, who had a familial history of arterial thrombosis (at least one first-degree relative suffering from AMI or stroke before 65 years) and 173 control subjects (with neither AMI nor personal or familial history of arterial thrombosis). All subjects were Italian. Patients showed fibrinogen levels higher than control subjects. There was a highly significant difference in allele frequency in cases versus control subjects, the B2 allele frequencies being respectively 0.28 versus 0.17 (P = .002). In multivariate analysis, adjusted for sex, age, smoking habits, and history of hyperlipidemia, hypertension, or diabetes, the (B1B2 + B2B2) genotype was associated with a higher risk of AMI (odds ratio 2.4, 95% confidence interval, 1.2 to 4.6). The Bcl I genotype was also associated with fibrinogen levels, independently of gender and smoking habits, the (B1B2 + B2B2) subjects showing the highest levels in both cases and control subjects. The difference in fibrinogen levels between cases and control subjects was significantly influenced by the genotype (significant interaction, P = .042). The B2 allele of the Bcl I polymorphism in the beta-chain of the fibrinogen gene is a new factor associated with the risk of familial AMI through its association with fibrinogen levels. These data provide evidence for a causal role of fibrinogen in familial AMI.
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PMID:Bcl I polymorphism in the fibrinogen beta-chain gene is associated with the risk of familial myocardial infarction by increasing plasma fibrinogen levels. A case-control study in a sample of GISSI-2 patients. 943 97

As many as 20% of the survivors of acute myocardial infarction present with the heritable form of hyperlipidemia, termed familial combined hyperlipidemia (FCHL). Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. If, as we hypothesized, the availability of retinoic acid or its precursor retinol (vitamin A) could be altered in FCHL, this could help explain some aspects of the phenotypic expression of the disease. We therefore measured plasma retinol concentrations in 30 FCHL subjects and 56 controls. Plasma retinol concentrations in FCHL subjects were significantly lower than that of control subjects (1.96 +/- 0.83 mumol/L vs 2.91 +/- 1.23 mumol/L, respectively; P < 0.0001). This novel finding of significantly decreased concentrations of plasma retinol in FCHL relative to control subjects gives support to the hypothesis that vitamin A might be involved in the expression of this disorder.
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PMID:Low plasma vitamin A concentrations in familial combined hyperlipidemia. 943 57

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

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