Male Coronary Heart Disease Patients Research Articles

Small LDL-Cholesterol is Superior to LDL-Cholesterol for Determining Severe Coronary Atherosclerosis

Recent evidence suggests that small dense low-density lipoprotein (sd-LDL) particles are more atherogenic than large-LDL in spite of their lower cholesterol content. This study aimed to determine whether sd-LDL-cholesterol (sd-LDL-C) is superior to LDL-C as a biomarker of coronary heart disease (CHD). LDL particle size determined by gradient gel electrophoresis and sd-LDL-C concentrations quantified by heparin-magnesium precipitation were compared between 482 stable CHD patients and 389 non-diabetic subjects without CHD who were not receiving any lipid-lowering drugs. Both male and female CHD patients had significantly smaller LDL particles and lower large-LDL-C concentrations (estimated by subtracting the sd-LDL-C concentration from the LDL-C concentration), and significantly higher sd-LDL-C concentrations than the control subjects. LDL-C concentrations were modestly higher and sd-LDL-C concentrations were significantly higher in 258 patients with angiographically documented severe CHD than in the patients with mild CHD irrespective of treatment by LDL-lowering drugs and history of myocardial infarction and/or coronary revascularization. Large-LDL-C concentrations, in contrast, were similar between the two groups. Multivariate logistic regression analysis revealed that sd-LDL-C levels were significantly associated with severe CHD independently of LDL-C. sd-LDL-C levels are more powerful than LDL-C levels for the determination of severe stable CHD.

Relationship between testosterone and indexes indicating endothelial function in male coronary heart disease patients

To investigate the relationship between androgen level and the indexes indicating endothelial function in male patients with coronary heart disease (CHD). We registered the following data for 106 50-70-year-old men: age, weight, blood lipid, including total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol and triglyceride, whether a smoker, sugar levels, blood pressure, free testosterone (FT), vascular cell adhesion molecule-1 (VCAM-1) and the intima-media thickness (IMT) of common carotid artery, common carotid diameter, maximum velocity in systolic phase, minimum velocity in diastolic phase and resistant index. Among the 106 men, 51 were patients with CHD. The relationships between FT level, VCAM-1 concentration and IMT were examined, respectively, using a stepwise linear regression technique among all the 106 men. There was no statistical difference in terms of age, blood pressure, whether a smoker, sugar levels, HDL-C, minimum velocity in diastolic phase, resistant index between male CHD patients and controls; whereas results for weight, total cholesterol, low density lipoprotein cholesterol, triglyceride, VCAM-1 and IMT of male CHD patients were higher than those of controls; FT level and maximum velocity in systolic phase were lower. It was found that among all the objects, FT level was inversely correlated with IMT and VCAM-1 concentration. FT level was inversely correlated with VCAM-1 concentration and IMT which are indicators of endothelial function.

Lipid-altering efficacy of switching from atorvastatin 10 mg/day to ezetimibe/simvastatin 10/20 mg/day compared to doubling the dose of atorvastatin in hypercholesterolaemic patients with atherosclerosis or coronary heart disease

This randomised, double-blind study evaluated the efficacy and safety of ezetimibe/simvastatin (EZE/SIMVA) 10/20 mg tablet compared to doubling the atorvastatin (ATV) dose in hypercholesterolaemic patients with atherosclerotic or coronary heart disease (CHD). The study group included 435 male and female CHD patients (aged >or=18 years) who had not achieved their low-density lipoprotein cholesterol (LDL-C) goal of <2.50 mmol/l while on a stable dose of ATV 10 mg for >or=6 weeks. After a 1-week diet/stabilisation period, patients with LDL-C >or=2.50 mmol/l and <or=4.20 mmol/l were randomised (1:1) to EZE/SIMVA 10/20 mg/day (n = 221) or ATV 20 mg/day (n = 214) for 6 weeks. The primary efficacy objective was to determine the per cent reduction from baseline in LDL-C at week 6. EZE/SIMVA 10/20 mg produced significantly greater mean per cent changes from baseline in LDL-C compared with ATV 20 mg (-32.8 vs. -20.3%; p </= 0.001). A significantly greater proportion of patients achieved an LDL-C goal <2.50 mmol/l with EZE/SIMVA than ATV (77.9 vs. 51.9%; p <or= 0.001). Significant improvements in total cholesterol (-20.3 vs. -13.0%), non-high-density lipoprotein cholesterol (non-HDL-C) (-27.9 vs. -17.0%), apolipoprotein B (-23.4 vs. -14.7%) and HDL-C (1.8 vs. -0.4%) were observed after switching to EZE/SIMVA 10/20 mg for 6 weeks (p < 0.05 for all parameters). EZE/SIMVA 10/20 mg was generally well tolerated, with an overall safety profile similar to that of ATV 20 mg. EZE/SIMVA 10/20 mg produced superior lipid-altering efficacy by dual inhibition of cholesterol synthesis and intestinal absorption compared with doubling the dose of ATV from 10 to 20 mg.

Childhood adversities experienced by working-aged coronary heart disease patients

Objective The aim of this study is to investigate associations between childhood adversities and coronary heart disease (CHD). Methods This was a case-control study based on a postal questionnaire addressed to randomly selected working-aged Finns, and response rate was 39% ( N=15,477). The sample comprised 319 CHD patients. Four age- and gender-matched controls were selected for every patient. The participants were asked in six questions to think about their childhood adversities. Results Fear of some family member and someone in the family being seriously or chronically ill were more common during childhood among working-aged CHD patients than among controls. Likewise, among female CHD patients, serious conflicts in the family and someone in the family having had alcohol problems and, among male CHD patients, long-lasting financial problems were more common than among controls. Odds ratios (OR) varied between 1.27 and 2.66. Adjustment for education had no influence among women, but it had an influence among men. Upon adjustment for conventional risk factors (smoking, obesity, and hypertension), the association mostly disappeared. A family member having been seriously or chronically ill was statistically significant after full adjustment among both genders. Conclusion Working-aged CHD patients have experienced more dramatic events during their childhood than did the control population. This issue cannot be solved in doctors' offices. Health-promoting social policies are of vital importance.

Effects of a health advocacy, counselling, and activation programme on depressive symptoms in older coronary heart disease patients

To describe the effects of a health advocacy, counselling, and activation programme on depressive symptoms among older coronary heart disease (CHD) patients. A randomised, controlled intervention study in Lieto, South-western Finland. Older (65 years and older) patients with CHD were randomly divided into an intervention group (IG) (n = 116) and a control group (CG) (n = 106). Outcome measures comprised changes in depressive symptoms (Zung Self-rating Depression Scale, ZSDS). Depressive symptoms tended to decrease in IG and to increase in CG among men scoring 45 ZSDS sum points or more at baseline. The differences of the changes between IG and CG were significant in favour of IG. No similar changes were found among women. A health advocacy, counselling, and activation programme aimed to increase knowledge about CHD, social activities, contacts, roles, support, and exercising was effective in reducing depressive symptoms among male CHD patients suffering from a moderate or high amount of depressive symptoms.

The short-term effects of a hostility-reduction intervention on male coronary heart disease patients.

This preliminary study examined the effects of a hostility-reduction intervention on patients with coronary heart disease (CHD). Twenty-two high-hostile CHD men were matched on age and hostility and then randomly assigned to a hostility intervention (N = 10) or an information-control group (N = 12). Patients were reassessed immediately and 2 months posttreatment on hostility (with self-report and structured interview) and resting blood pressure. The intervention's overall effect size was moderately strong (d' = .62). Intervention patients reported at both reassessments and were observed at follow-up to be less hostile than controls. At follow-up, intervention patients had significantly lower diastolic blood pressure (DBP) than controls. Finally, reductions in hostility were significantly and positively correlated with reductions in DBP. Replication with a larger sample and CHD outcomes is recommended.

A Synergistic Effect of Serotonin Transporter Gene Polymorphism and Smoking in Association with CHD

Serotonin induces vasoconstriction in the presence of atherosclerotic lesions. Platelets acquire serotonin from the extracellular space by serotonin transporter and release it following aggregation. There is a functional polymorphism in the serotonin transporter (5-HTT) gene promoter associated with transcriptional efficacy and plasma serotonin levels. To examine whether the polymorphism is associated with coronary heart disease (CHD) in the Japanese, we analyzed 144 male CHD patients with an onset age before 65 and 222 apparently healthy men. The L allele was observed significantly more frequently in the CHD patients (26%) than in the control subjects (19%); the odds ratio was 1.48 (p <0.03). A significant interaction between the polymorphism and smoking was observed for CHD (p = 0.03), suggesting that the two have a synergistic effect on CHD. Odds ratio of the combination of the L allele and smoking was 1.95 (p <0.003). The 5-HTT gene promoter polymorphism may play a role in susceptibility to CHD, particularly when it is combined with smoking.

Facial expression and the affective component of cynical hostility in male coronary heart disease patients.

This study describes the affective component of hostility as measured by the Cook-Medley Hostility Scale (Ho; W. Cook & D. Medley, 1954) by examining the relationship between facial expressions of emotion and Ho scores in 116 male coronary heart disease patients. Patients underwent the videotaped Type A Structured Interview, from which facial expressions were later coded using the Facial Action Coding System. They also completed the Cook-Medley Ho scale. Facial expression of the emotion of contempt was significantly related to Ho scores; anger expression was not. Also, there was a significant interaction between hostility and defensiveness, wherein low-defensive, highly hostile people showed substantially more contempt expression than others. The implications of these findings for the construct validity of Ho and for identifying clinically important subtypes of hostility are discussed.

Facial expression and the affective component of cynical hostility in male coronary heart disease patients.

Facial expression and the affective component of cynical hostility in male coronary heart disease patients.

Fractional esterification rate of cholesterol in high density lipoprotein (HDL) can predict the particle size of low density lipoprotein and HDL in patients with coronary heart disease

Fractional esterification rate of cholesterol in high density lipoprotein (HDL) (FER HDL) can predict the size distribution and physicochemical characteristics of HDL in plasma. In the present study, we investigated the correlation of FER HDL with the particle size of low density lipoprotein (LDL) (LDL-size) in 111 patients (81 males and 30 females) with coronary heart disease (CHD). The correlations of FER HDL and LDL-size with conventional lipid and lipoprotein parameters were also studied. FER HDL was closely associated with LDL-size (males: r=−0.618, females: r=−0.629, P<0.001). Plasma levels of TG, HDL-cholesterol (HDL-C), HDL 2-cholesterol (HDL 2-C) and apo B were also associated with LDL-size in male CHD patients ( r=−0.534, 0.314, 0.358, and −0.482, P<0.01 or 0.001), while plasma levels of TG and apo B were associated with LDL-size in female patients ( r=−0.350 and −0.348, P<0.05). In a stepwise multiple regression analysis, FER HDL alone accounted for 38 and 40% of the variability in LDL-size in male and female CHD patients, respectively. Other parameters accounted for an additional 6–10%. With respect to the relation between FER HDL and HDL subfractions, FER HDL related only to HDL 2-C (males: r=−0.640, females: r=−0.652, P<0.001). This result suggests that FER HDL is better able to predict the presence (or absence) of large HDL, rather than that of small HDL. All these data taken together, suggest that FER HDL is a useful tool to predict the particle size of both LDL and HDL, even in CHD patients.

Coronary heart disease and depression in the elderly--a population- based study

Growing interest is nowadays focused on the quality of life of elderly people who survive with chronic diseases. Coronary heart disease (CHD) is one of the most common diseases among the elderly and may have an unfavourable impact on the patient's emotional well-being. We aimed to describe the prevalence of depression and the occurrence of depressive symptoms among elderly CHD patients, with a special emphasis on the relations between depression and the severity of CHD, and to find out the possible association between CHD and depression. The study was carried out at the health centre of the municipality of Lieto, in south-west Finland. The study population consisted of 488 community-dwelling men and 708 women, over 64 years old, from among whom the participants with CHD (89 men and 73 women) were selected, and for whom 178 male and 146 female sex- and age-matched controls (free of CHD) were drawn from the population. CHD patients were selected on the basis of the presence of angina pectoris or a past myocardial infarction. Depressive symptoms were measured with the Zung Self-rating Depression Scale. Depression was described in relation to the severity of dyspnoea and chest pain among patients. The associations between depression and age, health, health behaviour, drugs, functional ability and social, psychosocial and environmental factors were analysed by logistic regression analyses. The prevalence of depression was 29% among male patients and 20% among female patients. Depression was significantly more common among male CHD patients than among male controls (P = 0.011). Among women, depression was not associated with CHD. Earlier, depression had gone undiagnosed among many CHD patients and controls, especially male patients. Among male CHD patients, depression was associated with more severe dyspnoea, but no similar association was found among female CHD patients. Among men the occurrence of CHD, physical disability, widowhood or divorce, and among women previous clinical depression, physical disability and the use of angiotensin-converting enzyme (ACE) inhibitors, were associated with depression. Depression is common among patients with CHD. It seems that CHD is not an independent factor in the aetiology of depression among the elderly. The association of CHD with depression among men is explained by the acute or chronic psychic stress caused by CHD. It may be that the more complicated the patient's CHD, the more probable is the presence of depression.

Impact of polymorphisms in the alpha- and beta-fibrinogen gene on plasma fibrinogen concentrations of coronary heart disease patients

Despite many investigations in a variety of experimental settings, uncertainty remains concerning the size of the genetic contribution to plasma fibrinogen levels. We used the polymerase chain reaction to amplify the polymorphic sites for the restriction enzymes TaqI in the α-fibrinogen gene and HaeIII, HindIII and BclI in the β-fibrinogen gene. Three hundred and eighty-four male coronary heart disease patients were investigated. Two alleles for each enzyme (+ or − designating, respectively, the presence or absence of the cutting site) were detected. The HaeIII and HindIII cutting sites were in complete linkage disequilibrium. A small but significant increase in fibrinogen level was associated with the rare cutting sites of HaeIII HindIII , BclI and TaqI. At all polymorphic sites homozygosity for the frequent alleles was associated with about 0.20 g/l lower plasma fibrinogen concentrations than heterozygosity at the respective sites (p < 0.05). The frequencies and natures of the rare alleles were as follows: TaqI (+) 0.28, HaeIII HindIII (−) 0.22 and BclI (+) 0.17. Mean fibrinogen levels in patients heterozygous for each of the four polymorphisms were 0.47 g/l greater than in subjects homozygous for the frequent allele at each cutting site ( HaeIII HindIII + −, TaqI + −, BclI + ÷ fibrinogen level 3.58 g/l (n = 32); HaeIII HindIII + +, TaqI − −, BclI − ÷ fibrinogen level 3.11 g/l (n = 99), p = 0.003). Each polymorphism accounted for between 0.5 and 1.4% of the overall variance in fibrinogen concentration. Together, the polymorphisms in HaeIII, HindIII and TaqI explained 5.8% of overall variance, a proportion equivalent to that explained by age, smoking and body mass index (5.5%). In conclusion, there is a hereditary component to plasma fibrinogen concentrations in men. Individuals predisposed to increased fibrinogen levels can be detected using restriction fragment length polymorphisms.

Effects of age, lipoproteins, and hemostatic parameters on the role of homocyst(e)inemia as a cardiovascular risk factor in men.

Previous studies have identified moderately elevated plasma concentrations of homocyst(e)ine as an independent risk factor for coronary heart disease (CHD). The atherogenicity of homocyst(e)ine has mostly been attributed to its effects on endothelial cells, platelets, and the hemostatic system. In this case-control study of 199 male CHD patients and 156 age-matched control subjects, we analyzed the role of homocyst(e)ine as a cardiovascular risk marker in the context of traditional risk factors as well as of plasma fibrinogen, plasminogen, and viscosity. Both univariate and multivariate regression analyses revealed that homocyst(e)ine levels were significantly correlated with age, fibrinogen, and plasma viscosity in both study groups. Geometric mean homocyst(e)ine levels by univariate analysis were significantly higher in patients than in control subjects (8.9 versus 7.8 mumol/L, P < .001). This difference remained significant on multiple logistic function analysis after being adjusted for body mass index, systolic blood pressure, serum cholesterol, and high-density lipoprotein cholesterol but not after additional adjustment for fibrinogen. By contrast, geometric mean fibrinogen levels after adjustment for homocyst(e)ine levels were significantly different between patients and control subjects (296.4 versus 230.8 mg/dL, P < .001). Within the group of CHD patients, both fibrinogen and homocyst(e)ine significantly increased in parallel with the number of stenosed coronary vessels. We conclude that hyperhomocyst(e)inemia is an independent coronary risk factor and that its interrelation with fibrinogen levels merits further study.

Glutamine/histidine polymorphism in apo A-IV affects plasma concentrations of lipoprotein(a) and fibrin split products in coronary heart disease patients.

A glutamine/histidine polymorphism at residue 360 in apolipoprotein (apo) A-IV that generates two electrophoretically detectable isoforms, apo A-IV-1 and apo A-IV-2, affects the plasma concentration of lipoprotein(a) (Lp[a]) in a healthy population. To verify this unexpected association we analyzed the effect of the apo A-IV polymorphism on Lp(a) serum concentrations in 275 male coronary heart disease patients. Allele frequencies of apo A-IV-1 and apo A-IV-2 were 0.917 and 0.083, respectively. In addition, apo A-IV-1/2 heterozygotes showed a 30% lower geometric mean concentration of Lp(a) than apo A-IV-1/1 homozygotes in this study. The relative frequency of Lp(a) concentrations > 20 mg/dl was significantly increased by a factor of 2.25 in apo A-IV-1/1 homozygotes. Other lipid parameters were not significantly affected by this apo A-IV polymorphism. Because of the relations between Lp(a) and the fibrinolytic system, we also analyzed the effect of the apo A-IV polymorphism on hemostatic variables. Apo A-IV-1/2 heterozygosity was associated with a 70% higher geometric mean plasma concentration of D-dimer, i.e., proteolytic fragments of cross-linked fibrin. Plasma concentrations of prothrombin fragments F1 + F2, fibrinogen, plasminogen, and plasminogen activator inhibitor-1 were unaffected. In conclusion, our results indicate a hitherto unappreciated role of the apo A-IV gene or a closely linked locus for the regulation of Lp(a) metabolism and hemostasis and also possibly for atherosclerosis and thrombosis.

Determination of apolipoprotein B in apolipoprotein CII/CIII-containing lipoproteins by an immunoenzymmetric assay.

A solid phase sandwich immunoenzymmetric assay is described for the determination of apolipoprotein B in apolipoprotein CII- and/or CIII-containing lipoproteins (chylomicron remnants, VLDL, IDL). During a first incubation step the particles containing apolipoproteins CII and/or CIII are bound to antibodies against these components, while the antibodies are immobilised on microtitre plate wells. After washing, anti-apolipoprotein B is added in a second incubation step. Finally peroxidase-labelled anti-sheep IgG reacts with the bound anti-apolipoprotein B, thus allowing the quantification of complexes containing both B and CII/CIII apolipoproteins. The amounts of these complexes were correlated with total cholesterol, triacylglycerols, HDL- and LDL-cholesterol, apolipoproteins AI and B, as well as with age and sex of the subject. A total of 258 individuals was studied, including patients with lipid metabolism disorders, patients with manifest coronary heart disease, and healthy controls. The assay described in this article was compared with radial immunodiffusion after pretreatment of samples. The immunoenzymmetric assay was easier and faster to perform and had a lower detection limit than the classical VLDL apolipoprotein B determination using ultracentrifugation. Furthermore, it could be performed directly on native serum. Most importantly, the study revealed elevated apolipoprotein CII/CIII-B levels in coronary heart disease patients of both sexes compared with normal subjects. Furthermore, in male coronary heart disease patients a negative correlation was found between the concentrations of apolipoprotein CII/CIII-B and HDL-cholesterol. These results suggest a delayed VLDL-HDL exchange of lipids and proteins in these patients which results in an accumulation of atherogenic apolipoprotein B-containing VLDL and IDL.

Interactive effects of behavior and reproductive hormones on sex differences in risk for coronary heart disease.

It is well known that women in the United States, as in most industrialized countries in the world, are protected from coronary heart disease (CHD), relative to men. It is thought that this protection is by and large due to the effects of female reproductive hormones (i.e., estrogens) on lipid and lipoprotein metabolism and blood pressure, although women's relatively low rates of cigarette smoking are also thought to play a role. However, epidemiological studies that statistically adjust for sex differences in lipids, blood pressure, and smoking status cannot explain sex differences in CHD morbidity and mortality. Also, inconsistent with a simple main-effect model of reproductive hormones are data showing elevated risk of myocardial infarction and stroke among women who use oral contraceptives. Men who are prescribed estrogens have elevated risk of CHD, and case-control studies show that male CHD patients have elevated estradiol, compared to controls. This article suggests that simple main-effect models of female protection from CHD are inadequate. It argues that reproductive hormones are important determinants of protection from CHD, in interaction with behavioral characteristics. It also demonstrates that reproductive hormones can influence behavioral characteristics and that behavioral characteristics can influence the effects of reproductive hormones on CHD risk factors.