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PubMed2005

Depression and heart rate variability in patients with stable coronary heart disease: findings from the Heart and Soul Study.

CONTEXT: Depression is associated with low heart rate variability (HRV) in patients following myocardial infarction, suggesting that alterations in the autonomic nervous system may contribute to the adverse cardiac outcomes associated with depression. Whether depression is associated with low HRV in patients with stable coronary heart disease (CHD) is not known. OBJECTIVE: To examine the association between major depression and 24-hour HRV in patients with stable CHD. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional study of 873 outpatients with stable CHD recruited from outpatient clinics in the San Francisco Bay Area, California. MAIN OUTCOME MEASURES: Major depression was assessed using the Computerized National Institute of Mental Health Diagnostic Interview Schedule. Heart rate variability was measured by 24-hour ambulatory electrocardiography. RESULTS: A total of 195 participants (22%) had major depression. Overall, we observed no association between depression and HRV as measured by time domain or frequency domain variables. Mean HRV was similar in participants with and without depression (all P values >.10), and participants with depression were no more likely than those without depression to have low HRV (all P values >.10). CONCLUSIONS: We found no evidence of an association between depression and HRV in 873 outpatients with stable CHD. These findings raise questions about the potential role of HRV in the association between depression and cardiovascular disease.

Aged↗
PubMed1999

Lewis blood group phenotype as an independent risk factor for coronary heart disease (the NHLBI Family Heart Study).

In the Copenhagen Male Study, men with Lewis blood group phenotype Le(a-b-) were found to have increased risk for coronary heart disease (CHD); such a relation has not been confirmed in men, and has not been evaluated in women. In the NHLBI Family Heart Study, we determined the Lewis blood type of 1,620 white subjects (790 male and 830 female subjects). The Lewis(a-b-) phenotype was found in 142 subjects (8.8%), 6.3% of subjects from randomly chosen families and 9.7% of subjects from families found to be at high risk for CHD. A history of CHD was present in 39.1% of men with Le(a-b-) versus 27.2% of men with other Lewis types; for women, the corresponding numbers were 12.3% versus 9.4%, respectively. In multivariate analysis, adjusting for age, sex, and risk group, the odds ratio for CHD was 2.0 (95% confidence interval = 1.2 to 3.1) for Le(a-b-) versus other Lewis groups. Mean values for body mass index, blood pressure, total cholesterol, low-density lipoprotein and high-density lipoprotein cholesterol, glucose, insulin, homocysteine, and fibrinogen were not significantly different between Le(a-b-) subjects and others, but triglycerides (p = 0.002) were higher in the Le(a-b-) subjects. However, inclusion of all risk factors in multivariate analysis did not diminish the increased risk for CHD associated with the Le(a-b-) phenotype. We conclude that the Le(a-b-) phenotype is associated with an increased risk for CHD; its effect does not appear to act predominantly through conventional cardiovascular risk factors. At present, mechanisms of effect are unknown.

Adult↗
PubMed2005

The 'geneticisation' of heart disease: a network analysis of the production of new genetic knowledge.

Genetic science is making ever-expanding claims about the (mal)functioning of the body. The 'geneticisation' of health and medicine is extending from rare single gene conditions to more common multi-factorial disease, such as heart disease. The dominant behavioural and socio-spatial explanations of heart disease are now being challenged by genetic claims of deterministic biological causes. This paper builds an account of the transformation of heart disease in the new genetics era, by applying actor network theory (ANT) to the production of genetic knowledge of one aspect of heart disease-hypertension-within a medical genetics laboratory in Glasgow, Scotland. Using this approach, the paper shows that there is no straightforward geneticisation of heart disease. Instead, there is a contested, complex and uncertain understanding of heart disease as genetic, a product of the many people, technologies, natural elements and spaces involved in the network of genetic science knowledge making. The paper concludes that a 'critical' ANT could be developed that acknowledges the inherent unevenness of the network, and connects genetic and socio-spatial explanations of heart disease.

Causality↗
PubMed2005

Are remnant-like particles independent predictors of coronary heart disease incidence? The Honolulu Heart study.

BACKGROUND: Remnant-like particles have been proposed as a new risk factor for coronary heart disease (CHD). This is the first long-term prospective investigation of the relationship between remnant-like particles and a cardiovascular disease outcome in healthy men. METHODS AND RESULTS: A cohort of 1156 Japanese-American men aged 60 to 82 from the Honolulu Heart Program was followed for 17 years. During that period 164 incident cases of CHD were identified. In multivariate Cox regression analyses, baseline remnant-like particle cholesterol (RLP-C) and triglyceride (RLP-TG) levels were significantly related to CHD incidence independently of nonlipid cardiovascular risk factors and of total cholesterol or high-density and low-density lipoprotein cholesterol levels. Total triglyceride levels were an independent predictor of CHD incidence. However, in models including RLP and triglyceride level simultaneously, neither variable was significant when adjusted for the other. This finding can be attributed to the strong correlation between RLP-C and RLP-TG levels and total triglycerides. When individuals with normal triglyceride levels (n=894) were separated from those with elevated triglycerides (n=260), the association between RLPs and CHD relative risk was only significant for the group with elevated triglyceride levels. CONCLUSIONS: RLP levels predicted CHD incidence independently of nonlipid risk factors and of total cholesterol or high-density and low-density lipoprotein cholesterol levels. However, RLP levels did not provide additional information about CHD incidence over and above total triglyceride levels. Therefore, this study does not support the need for testing of remnants in men if measures of fasting triglycerides are available.

Aged↗
PubMed1998

Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group.

CONTEXT: Observational studies have found lower rates of coronary heart disease (CHD) in postmenopausal women who take estrogen than in women who do not, but this potential benefit has not been confirmed in clinical trials. OBJECTIVE: To determine if estrogen plus progestin therapy alters the risk for CHD events in postmenopausal women with established coronary disease. DESIGN: Randomized, blinded, placebo-controlled secondary prevention trial. SETTING: Outpatient and community settings at 20 US clinical centers. PARTICIPANTS: A total of 2763 women with coronary disease, younger than 80 years, and postmenopausal with an intact uterus. Mean age was 66.7 years. INTERVENTION: Either 0.625 mg of conjugated equine estrogens plus 2.5 mg of medroxyprogesterone acetate in 1 tablet daily (n = 1380) or a placebo of identical appearance (n = 1383). Follow-up averaged 4.1 years; 82% of those assigned to hormone treatment were taking it at the end of 1 year, and 75% at the end of 3 years. MAIN OUTCOME MEASURES: The primary outcome was the occurrence of nonfatal myocardial infarction (MI) or CHD death. Secondary cardiovascular outcomes included coronary revascularization, unstable angina, congestive heart failure, resuscitated cardiac arrest, stroke or transient ischemic attack, and peripheral arterial disease. All-cause mortality was also considered. RESULTS: Overall, there were no significant differences between groups in the primary outcome or in any of the secondary cardiovascular outcomes: 172 women in the hormone group and 176 women in the placebo group had MI or CHD death (relative hazard [RH], 0.99; 95% confidence interval [CI], 0.80-1.22). The lack of an overall effect occurred despite a net 11% lower low-density lipoprotein cholesterol level and 10% higher high-density lipoprotein cholesterol level in the hormone group compared with the placebo group (each P<.001). Within the overall null effect, there was a statistically significant time trend, with more CHD events in the hormone group than in the placebo group in year 1 and fewer in years 4 and 5. More women in the hormone group than in the placebo group experienced venous thromboembolic events (34 vs 12; RH, 2.89; 95% CI, 1.50-5.58) and gallbladder disease (84 vs 62; RH, 1.38; 95% CI, 1.00-1.92). There were no significant differences in several other end points for which power was limited, including fracture, cancer, and total mortality (131 vs 123 deaths; RH, 1.08; 95% CI, 0.84-1.38). CONCLUSIONS: During an average follow-up of 4.1 years, treatment with oral conjugated equine estrogen plus medroxyprogesterone acetate did not reduce the overall rate of CHD events in postmenopausal women with established coronary disease. The treatment did increase the rate of thromboembolic events and gallbladder disease. Based on the finding of no overall cardiovascular benefit and a pattern of early increase in risk of CHD events, we do not recommend starting this treatment for the purpose of secondary prevention of CHD. However, given the favorable pattern of CHD events after several years of therapy, it could be appropriate for women already receiving this treatment to continue.

Aged↗
PubMed2004

The significant effect of diabetes duration on coronary heart disease mortality: the Framingham Heart Study.

OBJECTIVE: The risk of coronary heart disease (CHD) in type 2 diabetes is two- to threefold higher than in the general population, but the effect of diabetes duration on CHD risk has not been well characterized. We hypothesized that duration of diabetes is an important predictor of incident CHD among people with diabetes. RESEARCH DESIGN AND METHODS: The duration of diabetes (fasting glucose > or =126 mg/dl, random glucose > or =200 mg/dl, or use of an oral hypoglycemic agent or insulin) was assessed in participants with diabetes in the original and offspring cohorts of the Framingham Heart Study. Only subjects with diabetes diagnosed between the ages of 30 and 74 years, without a history of ketoacidosis, and free of cardiovascular disease at the baseline evaluation were included. Cox proportional hazards models were used to estimate the hazard ratio of incident CHD events and mortality over a 12-year follow-up period; models were adjusted for known CHD risk factors. RESULTS: Among 588 person-exams with diabetes (mean age 58 +/- 9 years, 56% men), there were 86 CHD events, including 36 deaths. After adjustment for age, sex, and CHD risk factors, the risk of CHD was 1.38 times higher for each 10-year increase in duration of diabetes (95% CI 0.99-1.92), and the risk for CHD death was 1.86 times higher (1.17-2.93) for the same increase in duration of diabetes. CONCLUSIONS: Duration of diabetes increases the risk of CHD death independent of coexisting risk factors. Further research is necessary to understand the pathophysiology of this increased risk.

Adult↗
PubMedDate not supplied

[B group vitamin metabolism in duodenal ulcer disease, hypertension, and ischemic heart disease].

No differences were found in the rate of metabolism of vitamins B1, B2, B6 and niacin either in healthy persons or in patients with duodenal ulcer, hypertension of the 2nd degree and with ischemic heart disease as shown by excretion of riboflavin, 4-pyridoxylic acid, 1-methyl nicotinamide and thiamin with urine which correlated with concentration of these vitamins and their coenzyme forms in blood plasma and erythrocytes. Dependence of these vitamins excretion with urine on their concentration in blood and the vitamins content in food appear to demonstrate similar consumption of vitamins B in the persons studied; at the same time, evaluation of the vitamins consumption in the patients with these forms of pathology should be performed using the criteria suitable for healthy persons. Dissimilar rates of metabolism of these vitamins described in literature might be related to differences in nutrition as well as to the use of nonspecific techniques for estimation of the vitamins. Besides, initial consumption of vitamin B2 was not sometimes considered, but deficiency in riboflavin caused considerable impairments of vitamin B6 and niacin metabolism.

Adolescent↗
PubMed2004

Heart disease, clinical proteomics and mass spectrometry.

Heart disease is the leading cause of mortality and morbidity in the world. As such, biomarkers are needed for the diagnosis, prognosis, therapeutic monitoring and risk stratification of acute injury (acute myocardial infarction (AMI)) and chronic disease (heart failure). The procedure for biomarker development involves the discovery, validation, and translation into clinical practice of a panel of candidate proteins to monitor risk of heart disease. Two types of biomarkers are possible; heart-specific and cardiovascular pulmonary system monitoring markers. Here we review the use of MS in the process of cardiac biomarker discovery and validation by proteomic analysis of cardiac myocytes/tissue or serum/plasma. An example of the use of MS in biomarker discovery is given in which the albumin binding protein sub-proteome was examined using MALDI-TOF MS/MS. Additionally, an example of MS in protein validation is given using affinity surface enhanced laser desorption ionization (SELDI) to monitor the disease-induced post-translational modification and the ternary status of myocyte-originating protein, cardiac troponin I in serum.

Albumins↗
PubMed1985

The significance of psychosocial factors in predicting coronary disease in patients with valvular heart disease.

Several prognostic indices for predicting various aspects of coronary artery disease were significantly improved by the inclusion of psychosocial factors. 218 patients with valvular heart disease who had undergone routine coronary arteriography before valve replacement were studied in terms of cigarettes smoked, family history of ischaemic heart disease, HDL:cholesterol ratio, angina, sex, blood pressure and four psychosocial characteristics (i.e. social support, work stress, life events and Type A behavior). It was found that the psychosocial factors improved the preoperative predictive power of significant coronary artery disease on four criteria: previous history of hypertension, previous history of myocardial infarction, signs of peripheral vascular disease and ECG evidence of myocardial infarction.

Angina Pectoris↗
PubMed1980

[Familial history of coronary heart diseases and high blood pressure in relation to the prevalence of risk factors, and the incidence of coronary heart diseases. The Paris Prospective Study (author's transl)].

In the Paris Prospective Study, 7 484 men from the same professional group, 43 to 54 years old, have been followed for six and a half years. The incidence of coronary heart diseases (CHD) has been studied among those free of CHD at entry, in relation to parental history of CHD and high blood pressure (HBP), obtained by interview. In the presence of paternal history of CHD, the relative risk is 1.5, and in the presence of paternal history of HBP, the relative risk is 2 (after exclusion of the subjects with HBP). The following risk factors: age, blood pressure, cholesterol, diabetes, and cigarette smoking can explain but a small part of the higher risk. Maternal history of CHD or HBP is not associated with a higher risk. It is shown that the "classical" risk factors, paternal history of CHD, and paternal history of HPB all contribute independently to the risk of CHD. The simultaneous presence of the last two is associated with a relative risk of 3.

Cholesterol↗
PubMed1977

Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta.

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.

Animals↗
PubMed1999

Lipoprotein(a)-cholesterol and coronary heart disease in the Framingham Heart Study.

BACKGROUND: Increased plasma lipoprotein(a) [Lp(a)] concentrations have been reported to be an independent risk factor for coronary heart disease (CHD) in some prospective studies, but not in others. These inconsistencies may relate to a lack of standardization and the failure of some immunoassays to measure all apolipoprotein(a) isoforms equally. METHODS: We measured plasma Lp(a)-cholesterol [Lp(a)-C] in a Caucasian population of offspring and spouses of the Framingham Heart Study participants, using a lectin-based assay (LipoproTM). We compared the prevalence of increased Lp(a)-C to the presence of sinking pre-beta-lipoprotein (SPB). We also related Lp(a)-C concentrations to the prevalence of CHD risk in the entire population. RESULTS: The mean (+/- SD) Lp(a)-C concentration in the Framingham population (n = 3121) was 0.186 +/- 0.160 mmol/L, with no significant gender or age differences. The mean Lp(a)-C concentrations in the absence or presence of SPB were 0.158 +/- 0. 132 mmol/L and 0.453 +/- 0.220 mmol/L, respectively (P <0.0001). The mean Lp(a)-C concentration in men with CHD (n = 156) was 0.241 +/- 0. 204 mmol/L, which was significantly (P <0.001) higher, by 34%, than in controls. The odds ratio for CHD risk in men with Lp(a)-C >/=0. 259 mmol/L (>/=10 mg/dL), after adjusting for age, HDL-cholesterol, LDL-cholesterol, smoking, diabetes, blood pressure, and body mass index, was 2.293 (confidence interval, 1.55-3.94; P <0.0005). Lp(a)-C values correlated highly with a Lp(a)-mass immunoassay [ApotekTM Lp(a); r = 0.832; P <0.0001; n = 1000]. CONCLUSIONS: An increased Lp(a)-C value >/=0.259 mmol/L (>/=10 mg/dL) is an independent CHD risk factor in men with a relative risk of more than 2, but was inconclusive in women. Lp(a)-C measurements offer an alternative to Lp(a)-mass immunoassays and can be performed on automated analyzers.

Age Factors↗
PubMed2003

Hepatic lipase mutations,elevated high-density lipoprotein cholesterol, and increased risk of ischemic heart disease: the Copenhagen City Heart Study.

OBJECTIVES: We investigated associations between single nucleotide polymorphisms (SNPs) in the hepatic lipase promoter, levels of high-density lipoprotein (HDL), and risk of ischemic heart disease (IHD). Our primary hypothesis was that these SNPs associate with IHD after adjustment for HDL levels. BACKGROUND: Hepatic lipase influences HDL metabolism, and may thus affect reverse cholesterol transport and consequently risk of IHD. METHODS: We genotyped 9,121 white subjects aged 20 to 93 years from the Copenhagen City Heart Study, 456 of whom had incident IHD, as well as 921 Danish patients with IHD for the -216, -480, and -729 SNPs in the hepatic lipase promoter. RESULTS: Frequencies of wild-type, triple heterozygotes, and triple mutation homozygotes in the general population were 61%, 33%, and 5%, respectively. Compared with wild-type, HDL cholesterol levels were 4% (0.06 mmol/l) and 10% (0.15 mmol/l) higher in heterozygotes and mutation homozygotes; the equivalent values for apolipoprotein A1 were 3% and 7% higher. In prospective and case-control studies, mutation homozygotes versus wild-type had relative risk (RR) and odds ratio (OR) for IHD of 1.5 (95% confidence interval [CI]: 1.0 to 2.2) and 1.4 (CI: 1.1 to 1.9) when adjusted for age, gender, and HDL cholesterol. In individuals with the epsilon43 apolipoprotein E genotype, RR and OR for IHD in mutation homozygotes versus wild-type was 2.9 (CI: 1.5 to 5.6) and 2.0 (CI: 1.2 to 3.2). CONCLUSIONS: Hepatic lipase promoter SNPs are associated with increased HDL cholesterol and, paradoxically, an increased risk of IHD after adjustment for HDL cholesterol, and particularly in individuals with apolipoprotein E epsilon43 genotype. Implications are that increased HDL levels may in certain situations be not protective, but rather associated with increased IHD risk.

Adult↗
PubMed2001

Lipid metabolism in the heart--contribution of BMIPP to the diseased heart.

Lipid contributes greatly in cardiac metabolism to produce high energy ATPs, and is suggested to be related to the progression and deterioration of heart disease. It is fortunate that the I-123-betamethyliodophenylpentadecanoic acid (BMIPP) imaging technique is now available in determining heart condition, but we must be cautious about the interpretation of images obtained with this new tracer. From the uptake of BMIPP into the cell to breakdown and catabolism of it, there exist so many critical enzymatical pathways relating to the modification of BMIPP imaging. In clinical evaluation, the image will be translated as the integral effects of these pathways. In other words, we must be aware of these critical pathways regulating lipid metabolism and modifying factors in order to correctly understand BMIPP imaging. Lipid transport is affected by the albumin/FFA ratio in the blood, and extraction with membrane transporter proteins. Fatty acid binding protein (FABP) in the cytosole will play an important role in regulating lipid flux and following metabolism. Lipid will be utilized either for oxidation, triglyceride or phospholipid formation. For oxidation, carnitine palmitoil transferase is the key enzyme for the entrance of lipid into mitochondria, and oxidative enzymes such as acyl CoA dehydrogenase (MCAD, LCAD, HAD) will determine lipid use for the TCA cycle. ATPs produced in the mitochondria again limit the TG store. It is well known that BMIPP imaging completely changes in the ischemic condition, and is also shown that lipid metabolical regulation completely differs from normal in the very early phase of cardiac hypertrophy. In the process of deteriorating heart failure, metabolical switching of lipid with glucose will take place. In such a different heart disease conditions, it is clear that lipid metabolical regulation, including many lipid enzymes, works differently from in the healthy condition. These lipid enzymes are regulated by nuclear factor peroxisome proliferator-activated receptors (PPAR) just like a conductor of an orchestra. Most of the regulating mechanisms of the PPAR are still unknown, but reduction of this nuclear factor is shown in the process of decompensated heart failure. This review is based by mostly on our fundamental and Japanese clinical data. BMIPP has been used clinically in abundant cases in Japan. In such situations, further correct information on lipid metabolism, including BMIPP, will contribute to the understanding of deteriorating heart disease and its prognosis.

Animals↗