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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an interview with Treatment Issues, Dr. Joseph Sonnabend indicates that use of protease inhibitors may contribute to the development of heart disease. Protease inhibitors appear to abnormally increase triglycerides and cholesterol levels, without a corresponding increase in HDL. The addition of androgenic and anabolic steroids in the HIV treatment mix adds to cardiovascular risk. Preventive measures for patients on steroids include monitoring hematocrit levels, and possibly testosterone levels, to make sure they are not too high. Standard preventive measures for heart disease, such as diet, exercise, and the use of certain drugs, are recommended, although an aggressive approach may be required. Drugs such as Lipitor and Zocor can be used to help reduce lipid abnormalities.
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PMID:Heart disease in people with HIV: an interview with Joseph Sonnabend, M.D. Interview by Dave Gilden. 1136 76

The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk to develop cardiovascular disease. The metabolic syndrome is characterized by atherogenic dyslipidemia (elevated triglycerides, increased small dense low-density lipoproteins, and decreased high-density lipoproteins), hypertension, insulin resistance and obesity. To decrease the risk of cardiovascular disease events decreasing body weight by ingesting a healthy diet, increasing physical activity, cessation of smoking and managing dyslipidemia are recommended. Pharmacological treatment of dyslipidemia is based on different drug classes. For LDL-cholesterol-lowering mainly statins and for triglyceride-lowering mainly fibrates are used. In primary and secondary prevention trials of heart disease they have shown to reduce the incidence of coronary artery disease or coronary events by 25-60 percent. Statins reduce mainly LDL-cholesterol levels by competitive inhibition of HMG-CoA reductase but have also shown to reduce fasting and postprandial triglyceride levels. Fibrates effectively reduce fasting and postprandial lipemia, shift the distribution of LDL particles towards less dense particles and increase HDL-cholesterol. Thus fibrates particularly address components of the metabolic syndrome and features of diabetic dyslipidemia. However studies still are needed showing definite evidence on differential therapy in lipid lowering based on prospective controlled trials with endpoints of macro- and microangiopathy in diabetic patients.
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PMID:Treatment of dyslipoproteinemia in the metabolic syndrome. 1145 42

Progesterone receptors are present in the arterial wall and it is, therefore, likely that the arterial effects of progestins are mediated through progesterone receptors as well as through down-regulation of the estradiol receptor. Progestin therapy affects arterial function, as it can stabilize arteries in a state of vasomotor instability, but may also induce vasoconstriction of estrogenized vessels. Thus, the cardiovascular effects of progestins may influence the cardioprotective effect of estrogens. There has been some concern that a combined estrogen-progestogen therapy may attenuate some of estrogen's beneficial effects on cardiovascular health. This is a reflection of the past epidemiologic studies which have used primarily unopposed estrogen. The PEPI trial is the only large-scale, long-term study to compare directly the effects of different combined hormone replacement therapy regimens upon plasma lipids in healthy women. This study has shown that the adjunctive clinical impact of different progestogens on the beneficial effect of estrogen replacement therapy is trivial. It has never been proved that in normocholesterolemic women, e.g., those included in the PEPI trial, the increase in HDL reduces cardiovascular mortality or morbidity. Based on the results of PEPI, hormone replacement therapy has positive effects on key heart disease risk factors and endometrial tissue, and the magnitude of those effects does not differ significantly across the hormone replacement therapy regimens used. At present there are only few and inconclusive data available on the vascular effect of progestins in menopausal women. Some studies found that progestins reduced the beneficial effect of estrogens, while others did not. Our group has recently shown that different estrogen-progestin treatments have different effects upon vascular reactivity and that a careful selection of the progestin to be added to estrogen is of capital importance to preserve, or even enhance the positive vascular effects of estrogens. Few epidemiological studies have investigated the effect of adding a progestin to estrogen therapy upon cardiovascular mortality and morbidity, and all have suggested that hormone replacement therapy may be more effective than estrogen replacement alone in reducing cardiovascular events in primary prevention. The results of the recently published Heart and Estrogen/progestin Replacement Study (HERS) have added some critical data on the effect of hormone replacement therapy for secondary prevention in women with coronary artery disease. The study, however, is affected by several important methodological and statistical problems, which make its interpretation difficult and its conclusions useless for clinical practice. The results of the study should be evaluated with caution by physicians who give advice on hormone replacement therapy, and no woman should be taken off hormone replacement therapy because of HERS. Of importance, the results of HERS should not be used to suggest alternative forms of treatment, especially the selective estrogen receptor modulators (SERMs), for cardiovascular protection in postmenopausal women.
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PMID:Comparative cardiovascular effects of different progestins in menopause. 1172 Jan 97

This study was conducted to evaluate the effect of a teaching program on patients with myocardial infarction. Forty-five patients were randomly selected 22 were assigned to a teaching group and 23 to a control group. An individualized teaching program was delivered to the teaching group during the hospitalization period. It covered aspects such as: the characteristics of heart disease, the anatomy and physiology of the heart, risk factors of atherosclerosis, medication and diet and exercise therapy. When these subjects were discharged to their homes, they received regular supportive care via telephone or mail for 12 weeks. Atherosclerotic risk factors, including, smoking, exercise, blood lipid profile and BMI were measured before and after the teaching program. Post-testing revealed that the numbers of those who exercised and the number of non-smokers were significantly higher in the teaching group than in the control group. Increased HDL cholesterol (High-Density Lipoprotein cholesterol) was significantly greater in the teaching group than in the control group. The above findings suggest that this individualized teaching program might be helpful at reducing the risk factors of atherosclerosis in myocardial infarction patients.
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PMID:An individualized teaching program for atherosclerotic risk factor reduction in patients with myocardial infarction. 1185 38

We investigated the genetic determination of high-density-lipoprotein cholesterol (HDL-C) levels in the NHLBI Family Heart Study by segregation analysis. Included was a total of 3755 subjects from 560 randomly selected nuclear families and 522 families selected due to a high family risk of coronary heart disease (CHD). In the whole dataset, there was no evidence for an allele at a major gene locus responsible for HDL-C levels lower than the population mean or even for significant bimodality for low levels of HDL-C. However, we observed evidence for a recessive allele that was associated with higher HDL-C levels than average. This evidence for a recessive major gene was independent of triglyceride concentrations and was most strongly observed in families recruited for CHD. The environmental model was rejected (P=0.0027) while the codominant and recessive models were not rejected (P=0.085 and P=0.133, respectively). The dominant model was also rejected (P<0.0001). In the recessive segregation model, the means of those inferred to be homozygous for the high HDL-C allele and those without the high HDL-C allele were separated by about 25 mg/dl HDL-C (73.9+/-1.99 vs 48.2+/-0.36 mg/dl). Because these results were unexpected, segregation was tested in a separate sample of 2013 individuals in 85 large pedigrees ascertained for early heart disease deaths, early stroke deaths, and early hypertension in Utah. Similar evidence for an allele at a major gene locus for high HDL-C was found. In summary, we did not find evidence for an allele at a major gene locus associated with low HDL-C levels segregating in pedigrees recruited for the NHLBI Family Heart Study, or in pedigrees ascertained in Utah for early CHD or related phenotypes. Instead we found some evidence for the segregation of an allele associated with high HDL-C. d
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PMID:Segregation analysis of HDL cholesterol in the NHLBI Family Heart Study and in Utah pedigrees. 1208 Mar 88

In the enrollment phase of the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), a number of heart disease-free potential subjects did not qualify to participate in the study because their low-density lipoprotein cholesterol (LDL-C) levels fluctuated. This report looks at the incidence of lability of LDL-C levels and premature coronary heart disease (CHD) in the nuclear family based on data collected on a group excluded primarily based on lipid levels during the enrollment phase at the TexCAPS site. Lipid inclusion criteria were total cholesterol (TC), 180 mg/dL to 264 mg/dL; low-density lipoprotein cholesterol (LDL-C), 130 mg/dL to 190 mg/dL; high-density lipoprotein cholesterol (HDL-C), less than or equal to 45 mg/dL for men and less than or equal to 47 mg/dL for women; and triglyceride (TG) concentrations, less than or equal to 400 mg/dL. After participants had been on the American Heart Association (AHA) step 1 diet for 8 to 10 weeks, lipid parameters were again tested in a total of 4257 individuals. Both lipid screening measurements at 8 and 10 weeks were required to be within 15% of each other for inclusion in subsequent study. A total of 2868 individuals met the study criteria and were randomly assigned to groups; 1389 failed to qualify for a variety of reasons. Of these, 1070 (25.1% of those who initially qualified based on lipid levels) were excluded because of unacceptable lipid levels on the evaluations repeated at 8 and 10 weeks. This excluded subpopulation (n = 1070) was stratified into three groups based on changes of LDL-C between 8 and 10 weeks on the AHA step 1 diet. One group had a less than 15% fluctuation in LDL-C (LN group, n = 637, 15.0% of cohort, n = 4257). Of those with LDL-C variability, 177 had a greater than 15% increase in LDL-C (LI group, n = 177, 4.2% of cohort); and 256 had a greater than 15% decrease in LDL-C (LD, n = 256, 6.0% of cohort). At week 8, TC and LDL-C levels were lower and the HDL-C level was higher in the LN group compared with both groups having labile lipid levels (LI and LD groups). Changes by gender showed similar trends; however, HDL-C was 5 mg/dL lower at 8 weeks in both groups of women with labile LDL-C levels (groups LI and LD) when compared with the women in the LN group (P < .01). The frequency of TG concentrations greater than 150 mg/dL was greater in men having labile LDL-C level when compared with the control group. The trend was similar for women. In assessing the incidence of CHD in the nuclear family, parents of probands with labile LDL-C levels (LI and LD groups) had a higher frequency (P = .0044) of premature CHD than parents of probands with stable LDL-C (LN). The following conclusions can be drawn: (1) within the general population, there is a substantial number (10%, 433 of 4257) of individuals with labile LDL-C levels; (2) labile LDL-C levels in the probands were found to be associated with an increased familial frequency of premature CHD in their parents. Definition of the molecular basis for this lability of LDL-C could reveal new opportunities to regulate plasma cholesterol levels and thus have an impact on CHD-associated morbidity and mortality in a substantial portion of the general population.
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PMID:Lability of serum low-density lipoprotein cholesterol levels during screening in subgroup of Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) cohort. 1213 52

Coronary heart disease is a complex disease reflecting the interaction of multiple genes with the environment (e.g. diet, life style). Lipoprotein lipase (LPL) plays an important role in lipid metabolism and the pathogenesis of coronary atherosclerosis. Recent associations between single-nucleotide polymorphisms in the LPL gene and heart disease have been reported, but little is known in Chinese. The LPL gene spans >26 kb, with an mRNA of 3549 bp. In the present study, we screened 5155 bp (565 bp of 5' flanking region, nine exons and donor- and acceptor-splice sites, and some intronic bases) in 160 Chinese patients with confirmed coronary heart disease and 150 age- and gender-matched controls. Thirteen of the sixteen single-nucleotide polymorphisms that we found have not been previously reported. In males, significant (P<0.05) differences between the coronary heart disease patients and controls were found for five single-nucleotide polymorphisms: -421G>A (5' flanking region); +13,577C>A (intron 2); +16,052G>A, R192Q (exon 5); +16,173C>G and +16,177T>C (intron 5). In females, significant differences between the patients with coronary heart disease and controls were found for only the -421G>A and +16,052G>A (R192Q) mutations. Among the coronary heart disease males, significant (P<0.05) associations were found between the low-HDL high-triglyceride (LHDL/HTG) phenotype and the non-LHDL/HTG trait for the 5' flanking-421G, the intron 2+13,577C, and the exon 5+16,052G mutations, with odds-ratios (ORs)[confidence intervals] of 3.90[1.12-13.66], 3.38[1.22-9.40], and 3.22[1.04-10.01], respectively; no corresponding associations were found in females. There were 69, 51, 57 and 41 unphased haplotype patterns in male coronary heart disease, male control, female coronary heart disease and female control groups, respectively; the computer program PM-Plus found the heterogeneity model by far the best fit (P<0.0001 in males, >0.01 in females). These data show that some single-nucleotide polymorphisms in the LPL gene among Chinese are associated with abnormal lipid and lipoprotein profiles and predisposition to coronary heart disease, a genetically heterogeneous complex disease, and that they are gender-specific.
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PMID:Single-nucleotide polymorphisms in the lipoprotein lipase gene associated with coronary heart disease in Chinese. 1240 99

C-reactive protein (CRP), a nonspecific marker of inflammatory status, is associated with cardiovascular disease (CVD) risk factors and the late occurrence of heart disease in adults. However, few studies assess the plasma CRP levels in healthy children. The purpose of this study is to evaluate the relationship between plasma CRP levels and anthropometric and lipid characteristics among children in Taiwan. After a multi-stage sampling of 85 junior high schools in Taipei, we randomly selected 835 children (410 boys and 425 girls) aged 12 to 16 years. Anthropometric and lipid profiles, including total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), and lipoprotein (a) were measured. We also calculated low-density lipoprotein cholesterol levels and the total cholesterol-to-HDL-C ratio as shown on the atherosclerotic index. In both genders, plasma CRP levels were significantly positively correlated with anthropometrics measures and inversely correlated with HDL-C levels. After adjusting for age, cigarette smoking, alcohol consumption, heart rate, and puberty development, children in the fourth quartile CRP subgroups were heavier and had significantly higher body mass index (BMI) and lower HDL-C levels than children with nondetected CRP. In multivariate regression models, CRP was significantly negatively associated with HDL-C levels even after adjusting for BMI in both genders. In this study, anthropometrics measures, especially BMI, were positively associated with plasma CRP levels. Furthermore, elevated CRP levels were associated with adverse lipids profiles. These data suggest that elevated plasma CRP levels might be associated with CVD risk factors that may be related to the late development of CVD in some Taiwanese children.
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PMID:Plasma C-reactive protein levels and their relationship to anthropometric and lipid characteristics among children. 1258 76

The presence of Chlamydia pneumoniae infection was examined in 66 patients with unstable angina pectoris (UAP), 155 patients with acute myocardial infarction (AIM) and 112 controls without signs of a heart disease. Besides evaluation of anamnestic data, ECG and coronarographic examination, serologic examination of C. pneumoniae by the microfluorescent method anti-MOMP and ELISA of anti-LPS of globulin IgA and IgG serum classes in every patient was performed. Moreover, in patients with UAP, routine biochemical methods for the detection of total cholesterol levels and its lipoprotein fractions LDL, HDL and triacylglycerols were used. The levels of anti-MOMP C. pneumoniae antibodies and anti-LPS of the IgA class in sera of patients with UAP were statistically highly significantly increased (chi 2 = 19.54; chi 2 = 12.92; p < 0.01) and anti-LPS of the IgG class significantly increased (chi 2 = 6.15; p < 0.05) in comparison with controls. It can be assumed that the participation of C. pneumoniae is aetiologically possible. Total cholesterol levels, LDL, HDL and triacylgylcerols were increased above the normal range in 34.8%, 48.5%, 39.4% and 28.8% of patients, respectively. The anti-LPS C. pneumoniae ELISA test of globulin class IgA in patients with UAP seems to be the most suitable method for the determination of infections with C. pneumoniae.
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PMID:[Occurrence of chlamydia infection in relation to lipidemia indicators in the etiology of unstable angina pectoris]. 1293 30

Heart disease is a major cause of morbidity and mortality among patients with renal failure. Premature atherosclerotic coronary heart disease is driven by multiple risk factors, including dyslipidemia and oxidative stress. In the nondialysis population, there is overwhelming evidence that treatment of dyslipidemia can significantly improve cardiovascular outcomes. Accumulating data indicate that dialysis patients have atherogenic lipid abnormalities. Although LDL cholesterol (LDL-C) levels in patients who undergo hemodialysis are normal or near normal, increased oxidized LDL-C, triglycerides, and lipoprotein (a) [Lp(a)]; decreased HDL cholesterol (HDL-C); and triglyceride-rich VLDL have been noted. Patients who receive peritoneal dialysis have a more atherogenic lipid profile with increased LDL-C, apolipoprotein B, oxidized LDL-C, triglycerides, and Lp(a) and decreased HDL-C. Furthermore, the LDL particles of peritoneal dialysis patients are small and dense. However, there is a dearth of information regarding the goals, efficacy, and safety of dyslipidemia treatment among dialysis patients. Given the strong evidence of risk reduction and the benefits of lipid-lowering treatment in the nondialysis population, the emerging consensus is that dialysis patients should be treated aggressively for dyslipidemia to an LDL-C goal below 100 mg/dl. Although physicians and patients may be reluctant to add medications because of concerns about polypharmacy, potential decreased compliance, and increased cost, the use of agents such as sevelamer that can serve multiple functions, including phosphate control, lipid lowering (decreased LDL-C and total cholesterol), and anti-inflammatory effects (decreased high-sensitivity C-reactive protein), should be explored and considered for patients who would benefit from such treatment.
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PMID:Impact of dyslipidemia in end-stage renal disease. 1293 88


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