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PubMed2005

Enhanced oxidative stress in coronary heart disease and chronic heart failure as indicated by an increased 8-epi-PGF(2alpha).

The role of oxidation injury as an important factor in the pathophysiology of cardiomyopathy (CMP) has recently gained increasing interest. Semiquantitative analysis for isoprostane, 8-epi-prostaglandin F(2alpha) (8-epi-PGF(2alpha)), and oxidised low-density lipoprotein (ox-LDL) of coronary vascular tissue samples derived from CMP patients revealed an increased extent and intensity of uptake as compared to the respective controls. To evaluate oxidative stress in vivo, we examined plasma, serum, salivary, and urinary 8-epi-PGF(2alpha) in patients with dilated CMP (n=20) and ischemic CMP (n=20) with decreased left ventricular ejection fraction (LVEF). Patients with coronary heart disease (CHD) (n=20) and 20 healthy, age-matched, and sex-matched controls were investigated in parallel. 8-Epi-PGF(2alpha) levels were correlated with the functional severity of heart failure [New York Heart Association (NYHA) classification] and LVEF. 8-Epi-PGF(2alpha) levels were matched according to risk factors (smoking and hypercholesterolemia) and were significantly higher in patients with CMP as compared to healthy controls and patients with CHD in all investigated compartments. A positive correlation between NYHA stages and 8-epi-PGF(2alpha), as well as a negative correlation to LVEF, could be demonstrated in a subgroup analysis. These findings reflect the enhanced oxidation injury in patients with CMP and, to a lesser extent, in CHD as compared to healthy controls, thus highly indicating the relevance of oxidative stress for the pathogenesis and progression of cardiovascular disease.

Adult↗
PubMed1999

The pathophysiology of pulmonary hypertension in congenital heart disease.

Congenital heart disease with increased pulmonary blood flow commonly leads to the development of pulmonary hypertension and increased vascular reactivity. These serious sequelae are associated with the following two major categories of congenital heart defects: those resulting in increased pulmonary blood flow and increased pulmonary arterial pressure and those resulting in increased pulmonary venous pressure. Recent evidence that the pulmonary vascular endothelium is an important determinant of vascular tone has led to the hypothesis that endothelial injury, secondary to congenital heart disease with increased pulmonary blood flow, disrupts these regulatory mechanisms and thereby plays a role in the development of pulmonary hypertension and its associated increased vascular reactivity. In many animal models, endothelial dysfunction is a precursor for smooth muscle dysfunction, and there is an apparent progression from endothelial dysfunction to smooth muscle dysfunction as vascular changes progress. We established a chronic model of pulmonary hypertension with increased pulmonary blood flow in young lambs by placing a systemic-to-pulmonary shunt in utero. In this model, we found significant physiologic and molecular alternations of both the nitric oxide (NO) and endothelin signaling pathways, two important mechanisms by which the endothelium regulates pulmonary vascular tone. These alterations occur extremely early and precede severe anatomic changes. Early endothelial damage may contribute to the development of pulmonary hypertension and its associated enhanced pulmonary vascular reactivity.

Animals↗
PubMed2006

[Gastroesophageal reflux disease and coronary heart disease--coexistence or interrelationship?].

There is the normal coronary artery appearance in 20-30% of coronarographies, made in patients with chest pain and/or positive noninvasive cardiological tests. The simple explanation of this fact is the presence of diseases which may affect coronary perfusion via mechanism independent to the diameter of main coronary arteries. One of them is gastroesophageal reflux disease (GERD). The presence of GERD symptoms in general population concerns about 30-40% of individuals, while non-physiological reflux is stated in 50-65-85% of patients with coronary heart disease (CHD). That means, that GERD is twice more frequent in patients with CHD than in general population. One explanation of the increased frequency of gastroesophageal reflux appearance in patients with CHD is the adverse effect of drugs used in treatment of cardiological diseases. Morover, one of potential mechanisms explaining the influence of esophagal disturbance on the appearance of coronary hipoperfusion may be their common neurological control of the functions. There are three aspects of it: vagal reflexes (esophageal-cardiac reflex), the disturbances of autonomic nervous system balance and changes in visceral pain perception threshold. Visceral reflex can combine GERD and CHD with mechanism of vicious circle: acid gastroesophageal reflux via vagal reflex may cause coronary hipoperfusion, and the products of anaerobic metabolism of cardiomyocytes may cause relaxation of lower esophagus sphincter, facilitating reflux. Additional mechanism connecting GERD and CHD is inflammation caused by Helicobacter pylori infection. The relationship between digestive tract pathology and evolution, as well as progression and complications of atherosclerosis together with similarity of clinical presentation imply the necessity of precise diagnosis of chest pain causes and caution in interpretation of laboratory examination results.

Comorbidity↗
PubMed2005

Toward the etiologies of congenital heart diseases.

Congenital heart disease remains a significant cause of morbidity and mortality. In recent years, significant advances in molecular genetics, improved understanding of morphogenesis, recognition of specific patterning of abnormalities within and between species, and the impact of the Human Genome Project have accounted for these advances. Continued rapid developments in genomics and proteomics are anticipated. Epidemiologic investigations continue to be necessary to assess the influence of the environment on genetics. We are on the threshold of influencing the occurrence of congenital heart diseases.

Heart Defects, Congenital↗
PubMed1993

Dental disease and risk of coronary heart disease and mortality.

OBJECTIVE: To investigate a reported association between dental disease and risk of coronary heart disease. SETTING: National sample of American adults who participated in a health examination survey in the early 1970s. DESIGN: Prospective cohort study in which participants underwent a standard dental examination at baseline and were followed up to 1987. Proportional hazards analysis was used to estimate relative risks adjusted for several covariates. MAIN OUTCOME MEASURES: Incidence of mortality or admission to hospital because of coronary heart disease; total mortality. RESULTS: Among all 9760 subjects included in the analysis those with periodontitis had a 25% increased risk of coronary heart disease relative to those with minimal periodontal disease. Poor oral hygiene, determined by the extent of dental debris and calculus, was also associated with an increased incidence of coronary heart disease. In men younger than 50 years at baseline periodontal disease was a stronger risk factor for coronary heart disease; men with periodontitis had a relative risk of 1.72. Both periodontal disease and poor oral hygiene showed stronger associations with total mortality than with coronary heart disease. CONCLUSION: Dental disease is associated with an increased risk of coronary heart disease, particularly in young men. Whether this is a causal association is unclear. Dental health may be a more general indicator of personal hygiene and possibly health care practices.

Adult↗
PubMed2003

Dietary magnesium intake and the future risk of coronary heart disease (the Honolulu Heart Program).

Magnesium (Mg) deficiency is believed to have adverse cardiovascular consequences that are broad and complex, although an association between dietary Mg intake and the risk of coronary heart disease (CHD) has not been clearly identified. The purpose of this study is to examine the relation between dietary Mg intake and future risk of CHD. Reported findings are based on dietary Mg intake in 7,172 men in the Honolulu Heart Program. Intake of Mg was recorded at baseline examinations that took place from 1965 to 1968 when the men were aged 45 to 68 years. In 30 years of follow-up, 1,431 incident cases of CHD were identified. Within 15 years after dietary assessment, the age-adjusted incidence decreased significantly from 7.3 to 4.0 per 1,000 person-years in the lowest (50.3 to 186 mg/day) versus highest (340 to 1,183 mg/day) quintiles of Mg intake (p <0.001). When adjustments were made for age and other nutrients (singly or combined), there was a 1.7- to 2.1-fold excess in the risk of CHD in the lowest versus highest quintiles (p <0.001). The excess risk ranged from 1.5- to 1.8-fold after further adjustment for other cardiovascular risk factors (p <0.05). Associations between dietary Mg and coronary events occurring after 15 years of follow-up were modest. We conclude that the intake of dietary Mg is associated with a reduced risk of CHD. Whether increases in dietary Mg intake can alter the future risk of disease warrants further study.

Aged↗
PubMed1982

Coeliac disease associated with congenital heart disease.

Six children with congenital heart disease are described in whom poor growth was found to be due to small-bowel villous atrophy; none was in heart failure and only one was severely cyanosed. Growth improved in all 6 on a gluten-free diet. Gluten enteropathy may be more common than is realised in children with congenital heart disease, and jejunal biopsy should be undertaken early in any patient with poor growth and no heart failure to exclude the coexistence of the condition.

Celiac Disease↗
PubMedDate not supplied

HAND proteins: molecular mediators of cardiac development and congenital heart disease.

Congenital heart defects are the clinical manifestation of anomalies in embryonic cardiac development. Such defects occur in distinct regions or chambers of the heart. A molecular framework in which to consider cardiac development and congenital heart disease in a segmental fashion has begun to emerge. dHAND and eHAND are two related basic helix-loop-helix transcription factors that are expressed in a complementary fashion in the developing right and left ventricles, respectively. They are also expressed in the neural crest-derived cardiac outflow tract and aortic arch arteries. Targeted mutations of dHAND and eHAND in mice have revealed novel pathways of organogenesis in mesodermal and neural crest derivatives. dHAND mutants exhibit hypoplasia of the right ventricle, branchial arches, and aortic arch arteries. The distinct nature of cardiac defects in dHAND mutants provides an entry into dissecting molecular pathways governing morphogenesis of specific components of the heart. Congenital heart disease is considered as a defect in segmental development of the heart and the role of dHAND and eHAND in regulating such developmental pathways in normal and abnormal cardiogenesis is examined.

Animals↗
PubMed1990

Mortality from circulatory diseases, especially ischaemic heart disease in sea pilots and boatmen in Sweden 1951-84: a retrospective cohort study.

A cohort of 1455 sea pilots and boatmen employed after 1921 was established. Those identified and alive in 1951 (n = 1323) were linked to the Swedish cause of death register 1951-84. In 21 352 person-years 383 deaths were observed among sea pilots compared with 379.3 expected (SMR = 101;95% CI between 99 and 112) and in 12,127 person-years the observed number of deaths among boatmen was 136, expected 135.9 (SMR = 100) when Swedish men were used as a reference population. For ischaemic heart disease (IHD) (ICD-8: 410-414) the SMR was equal to 96 (obs = 131, exp = 137.2) for sea pilots and 91 (obs = 44, exp = 48.4) for boatmen. No trend over time or geographical differences could be observed. A healthy worker effect could not explain why there was no excess mortality from IHD.

Aged↗
PubMed2006

[Therapeutic angiogenesis for peripheral arterial disease and ischemic heart disease by autologous bone marrow cells implantation].

Postnatal neovascularization was initially thought to result exclusively from the migration and proliferation of pre-existing, fully differentiated endothelial cells (a process referred to as angiogenesis). Several lines of experimental evidence, however, demonstrated that circulating endothelial progenitor cells (EPCs) home to sites of neovascularization and differentiate into endothelial cells in situ in a manner consistent with a process termed vasculogenesis. Moreover, recent clinical study, named as the Therapeutic Angiogenesis Using Cell Transplantation (TACT), has demonstrated the efficacy and safety of autologous implantation of bone marrow-mononuclear cells(BM-MNCs) in randomly allocated patients with ischemic limbs of peripheral arterial diseases. Implantation of BM-MNCs is also applied to patients with no-option angina pectoris, demonstrating the usefulness of this therapy for improvement of symptom, myocardial perfusion, and exercise capacity. Moreover, recent accumulating studies demonstrated the possibilities that transplantation of bone marrow-derived or peripheral blood-derived EPCs enhances neovascularization and improves cardiac function after acute myocardial infarction(AMI). There were no serious adverse effects reported in cell transplantation therapy. Thus, bone marrow-derived cell transplantation therapy has been applied to acute and chronic ischemic heart diseases as well as peripheral arterial diseases, demonstrating the safety and effectiveness of therapeutic angiogenesis.

Bone Marrow Transplantation↗
PubMed2002

Hematological risk factors for coronary heart disease.

Coronary heart disease (CHD) is a leading cause of morbidity and mortality in the developed and developing countries. Several underlying genetic and environmental factors have been implicated in its etiology. Some of the hematological risk factors implicated in the development of coronary heart disease include antithrombin III deficiency, protein C and protein S deficiency, factor V Leiden mutation, prothrombin gene (20210A) mutation hyperhomocystinaemia, elevated factor VIII levels, plasminogen activator inhibitor type 1 and dysfibrinogenaemia. In general, these factors result in thrombosis, thus having a negative effect on the heart and blood vessels. This paper presents an overview of some of the hematological risk factors involved in the development of CHD.

Antithrombins↗
PubMed2003

The impact of hyperhomocysteinemia as a cardiovascular risk factor in the prediction of coronary heart disease.

Coronary heart disease often occurs in the absence of traditional risk factors. Consequently, epidemiological studies exploring novel risk factors are necessary to improve the prediction of coronary heart disease. This study evaluated five promising markers of cardiovascular risk: homocysteine, C-reactive protein, fibrinogen, lipoprotein(a) (Lp(a)), free apolipoprotein(a) (apo(a)) and Lp(a) phenotypes. The study included 135 patients with angiographically confirmed atherosclerosis. The control group consisted of 93 sex- and age-matched individuals. The Mann-Whitney U-test was used for group comparison. New risk factors were evaluated by binary logistic regression. The odds ratios were calculated continuously for homocysteine in dependence on C-reactive protein. Low density lipoprotein (LDL)-cholesterol was nearly identical in controls and patients. Homocysteine, C-reactive protein, fibrinogen, high density lipoprotein (HDL)-cholesterol and Lp(a) discriminated highly significantly between both groups. The continuously calculated odds ratio for homocysteine demonstrated a distinct influence of C-reactive protein. In the group with high C-reactive protein levels, homocysteine levels above 9.6 micromol/l resulted in a markedly elevated risk (odds ratio 12), in the group with C-reactive protein levels below 5 mg/dl, a comparable risk increase was observed at a homocysteine level of 16.6 micromol/l. This data strongly suggests that plasma homocysteine helps identify individuals at risk, especially among those with elevated C-reactive protein levels.

Aged↗
PubMed1994

Deciphering the molecular genetics of congenital heart disease.

Congenital heart diseases are starting to benefit from the major advances provided by the advent of molecular biology methods. It is now possible to identify genes which are responsible for congenital heart diseases. The gene responsible for supravalvular aortic stenosis--an autosomal dominant trait--was cloned last year. It is the elastin gene. DiGeorge and Shprintzen syndromes, conotruncal anomaly face and some cardiac malformations have a common cause: a deletion of the 22q11 region resulting in a monosomy. Although the region of deletion is large, it is possible that monosomy of only one gene results in these conditions. Studies are underway to evaluate the impact of this new genetic factor on the incidence of congenital heart malformations. Studies on familial bundle branch block, and lateralization defect with midline anomalies are soon going to show a chromosomal region with the gene defect. Discovering the genes and their protein products which are implied in the cardiac morphogenesis will definitively change our understanding of these cardiac malformations.

Abnormalities, Multiple↗
PubMed1992

Height: a risk marker for ischaemic heart disease: prospective results from the Caerphilly and Speedwell Heart Disease Studies.

The predictive power of height for future ischaemic heart disease (IHD) was examined in 4860 men from two communities in South Wales and the West of England. At follow-up, men in the shortest fifth of the height distribution had experienced twice as many incident IHD events (fatal and non-fatal myocardial infarction) as was the case for men from the tallest fifth. Adjustment for age, social class and smoking habit failed to alter these relationships significantly. In the data from South Wales, determinants of height were examined; birth rank and number of siblings showed a trend with height. This trend was found only in men whose fathers were manual workers and may be related to inadequate nutrition in the higher birth ranks and larger families. These results support the suggestion that early childhood factors may be relevant to IHD in middle age and possible mechanisms are discussed.

Birth Order↗
PubMed1995

Preventive cardiology and its potential influence on the early natural history of adult heart diseases: the Bogalusa Heart Study and the Heart Smart Program.

Observations from pediatric epidemiology studies over the past 20 years document that atherosclerosis and essential hypertension begin in childhood. Evidence of coronary artery disease and hypertensive cardiovascular renal disease is found and relates strongly to clinical cardiovascular risk factors. Obesity, especially central obesity, and hyperinsulinemia are commonly found, and these cluster with other risk factors. Lifestyles, such as poor eating behavior and tobacco usage, also begin early and influence cardiovascular risk. The implication from these pediatric observations is that intervention should begin early to prevent unhealthy lifestyles and encourage adoption of healthy behaviors. Where adult heart diseases pervade the major part of the United States population and other industrialized cultures, various epidemiologic strategies of prevention are needed. A high-risk, clinical approach can be applied to individuals with heart disease or to individuals with underlying risk factors and their families. Primary and secondary prevention are both important and should be implemented by primary care physicians. A population approach is also needed because of the widespread occurrence of heart disease. A public health approach to prevention can occur through health education and health promotion programs. Physicians should play a role in encouraging prevention for the general population. The future direction of Preventive Cardiology for our nation rests on educating children to adopt and maintain healthy lifestyles. The Bogalusa Heart Study has made a major contribution in providing the background information for that direction.

Adult↗
PubMed1980

The changing face of congenital heart disease. A method for predicting the influence of cardiac surgery upon the prevalence and spectrum of congenital heart disease.

The influence of surgery upon the natural history of congenital heart disease is great. Children with many types of congenital heart lesions are now living to adult life. Most of these children will, however, require continuing medical care, care which traditionally has been given by the pediatrician. We have developed a method by which incidence figures and a knowledge of the natural history may be used to obtain prevalence estimates of congenital heart disease. We estimate that in the United States in 1995 there will be nearly 300,000 children under 21 years old with congenital heart disease; 38 per cent of these will have had one or more surgical procedures. In the last two decades the majority of care for children with congenital heart disease was aimed at the correction of the original lesion; however, we predict that in the next two decades an increasing fraction of medical resources will be directed toward the residua and sequelae of cardiac surgical procedures. This alteration in character of congenital heart disease will affect the patient mix seen by the cardiologist with adult patients as well as that of the pediatrician. For ventricular septal defect, pulmonary stenosis, atrial septal defect, persistent ductus arteriosus, coarctation of the aorta and tetralogy of Fallot, we have estimated the nationwide prevalence and the surgical requirements for 1995. Used with more specific local data on population and birth rate, this model can provide important input into planning the delivery of cardiovascular services.

Adolescent↗
PubMed2005

Relation of low socioeconomic status to C-reactive protein in patients with coronary heart disease (from the heart and soul study).

Low socioeconomic status (SES) is associated with poor health outcomes in patients who have coronary heart disease (CHD). Inflammation is a potential mechanism by which low SES may lead to adverse cardiovascular outcomes, but it is not known whether low SES is associated with inflammation in patients who have CHD. We measured high-sensitivity C-reactive protein (CRP) levels in a cross-sectional study of 985 adults who had CHD. Income and education were determined by self-report. We used ordinal logistic regression to examine the association of income and education with CRP. Of the 985 participants, 390 had high CRP levels (>3 mg/dl). The proportion of participants who had high CRP levels ranged from 30% (103 of 340) in those who had a college degree to 51% (65 of 127) in those who had less than a high school degree (p<0.0001). The proportion of subjects who had a high CRP level ranged from 28% (52 of 183) in those who had annual income>or=$50,000 to 42% (199 of 974) in those who had an annual income<$20,000 (p<0.001). After adjustment for traditional cardiovascular risk factors and other potential confounding variables, lower income and education remained associated with higher CRP levels. In conclusion, low SES is associated with high CRP levels in patients who have CHD. This observation raises the possibility that inflammation may contribute to the adverse cardiovascular outcomes associated with low SES.

Aged↗