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At least 199 records · Page 11Linked to original sources
PubMed1994

Estimating clinical morbidity due to ischemic heart disease and congestive heart failure: the future rise of heart failure.

OBJECTIVES: Many developed countries have seen declining mortality rates for heart disease, together with an alleged decline in incidence and a seemingly paradoxical increase in health care demands. This paper presents a model for forecasting the plausible evolution of heart disease morbidity. METHODS: The simulation model combines data from different sources. It generates acute coronary event and mortality rates from published data on incidences, recurrences, and lethalities of different heart disease conditions and interventions. Forecasts are based on plausible scenarios for declining incidence and increasing survival. RESULTS: Mortality is postponed more than incidence. Prevalence rates of morbidity will decrease among the young and middle-aged but increase among the elderly. As the milder disease states act as risk factors for the more severe states, effects will culminate in the most severe disease states with a disproportionate increase in older people. CONCLUSIONS: Increasing health care needs in the face of declining mortality rates are no contradiction, but reflect a tradeoff of mortality for morbidity. The aging of the population will accentuate this morbidity increase.

Female↗
PubMed2001

Cellular cardiomyoplasty with autologous skeletal myoblasts for ischemic heart disease and heart failure.

Cell transplantation to repair or regenerate injured myocardium is a new frontier in the treatment of cardiovascular disease. Even though it is based on many years of pre-clinical studies, much remains to be understood about this methodology, even as it progresses to the clinic. For example, controversies exist over the specific cells to be used, the dosages needed for tissue repair, how cells will affect the electrical activity of the myocardium, and even whether the cells can improve myocardial function after transplantation - all of which are briefly reviewed here. Autologous skeletal myoblasts appear to be the most well studied and best first generation cells for cardiac repair. Yet cardiocytes and, more recently, stem cells have been proposed as cell sources for this technology. Their advantages and limitations are also discussed. Although cellular cardiomyoplasty (cell transplantation for cardiac repair) shows great pre-clinical promise, its future will heavily depend on conducting carefully controlled, randomized clinical trials with appropriate endpoints. Utilizing biologically active cells provides both an opportunity for tissue repair and the potential for not yet understood outcomes. As with any frontier, many pioneers will attempt to conquer it. But also as with any frontier, there are pitfalls and consequences to be considered that may surpass those of previous endeavors. The future thus requires careful consideration and well-designed trials rather than haste. The promise for cell transplantation is too great to be spoiled by ill-designed attempts that forget to account for the biology of both the cells and the myocardium.

Journal Article↗
PubMed1993

[The use of sodium nitroprusside aerosols combined with ultrasound in the combined treatment of patients with ischemic heart disease and heart failure].

Use of sodium nitroprusside aerosol in association with ultrasound in 51 patients with IHD plus cardiac failure (stage I-IIA) allowed to reduce the dosage and side-effects of drugs as compared with a group of patients by routine complex methods. The method may be used for treatment and prophylaxis of initial stages of cardiac failure in IHD patients including those with contraindications to cardiac glycosides.

Adult↗
PubMed2004

Beneficial effects of yoga lifestyle on reversibility of ischaemic heart disease: caring heart project of International Board of Yoga.

OBJECTIVES: Yoga based lifestyle modifications have been earlier shown to be beneficial in coronary artery disease in a small number of patients. We evaluated the role of lifestyle modification based on Yoga techniques, stress management and dietary modifications in retardation of coronary artery disease. METHODS: This prospective, controlled, open trial included angiographically proven coronary artery disease patients (71 patients in study group and 42 patients in control group). They were assessed clinically, by biochemical parameters, stress myocardial perfusion and function studies and coronary angiography and on psychological parameters. The study group patients were given a family based Yoga Programme which included, control of risk factors, dietary modifications and stress management for a period of one year. The patients were assessed at baseline, at frequent intervals and at the end of one year. RESULTS: At the end of one year of yoga training, statistical significant changes (P<0.05) were found in serum total cholesterol (reduction by 23.3% in study group patients as compared to 4.4% in controls); serum LDL cholesterol (reduction of 26% in study group patients as compared to 2.6% in the control group), regression of disease (43.7% of study group patients v/s 31% control group on MPI and 70.4% of study group v/s 28% of control group on angiography) arrest of progression (46.5% study group v/s 33.3% control group on MPI) and progression (9.9% of study group vs 35.7% of controls on MPI, 29.6% of study group v/s 60.0% of controls on angiography). At the end of the study improvement in anxiety scores was concordant with the improvement seen in the MPI. No untoward effects of the therapy were observed. CONCLUSION: Yoga based lifestyle modifications help in regression of coronary lesions and in improving myocardial perfusion. This is translated into clinical benefits and symptomatic improvement.

Adult↗
PubMed2005

[Serum levels of sexual hormones in young and middle-age healthy subjects with risk factors of coronary heart disease and patients with coronary heart disease].

AIM: To study sexual hormones levels in risk of beginning and development of coronary heart disease (CHD) in young and middle-aged (up to 50 years) men and women. MATERIAL AND METHODS: Sexual hormones were studied in 105 patients (53 males and 52 females) aged 25-50 years. Of them, 88 suffered from IHD and 17 had CHD risk factors. Twenty healthy controls were matched by age and gender. LH, FSH, estradiol, testosteron were measured in blood serum by enzyme immunoassay (Elecsys kit, Beringer Mannheim). RESULTS: Young and middle-aged (under 50 years of age) males and females with IHD or its risk factors have changed levels of sexual hormones. CONCLUSION: In IHD male hormones levels increase in women but decrease in men while female hormones increase in men and decrease in women.

Adult↗
PubMed1998

Relation of Helicobacter pylori infection to 13-year mortality and incident ischemic heart disease in the caerphilly prospective heart disease study.

BACKGROUND: Associations have been suggested between Helicobacter pylori seropositivity, cardiovascular risk factors, and ischemic heart disease (IHD). The effect of this common infection on mortality is uncertain. METHODS AND RESULTS: Plasma specimens collected during 1979 to 1983 from 1796 men in Caerphilly, South Wales, were analyzed for IgG antibodies to H pylori. Cause of death and occurrence of incident IHD events were ascertained over an average of 13.7 years from death certificates, hospital records, and ECG changes at 5-yearly follow-up examinations. Seventy percent of men were seropositive. The prevalence of IHD at entry was similar in men with and without H pylori antibodies (odds ratio [OR], 1.10; 95% CI, 0.87 to 1.40). Seropositivity was significantly (P<0.05) associated with poorer socioeconomic status currently and in childhood, shorter stature, and poorer ventilatory function at entry but not with age, smoking, body mass index, blood pressure, total cholesterol, HDL cholesterol, LDL cholesterol, fibrinogen, plasma viscosity, or heat shock protein antibodies. Thirteen-year incidence of IHD was not significantly associated with H pylori (OR, 1.05; 95% CI, 0.80 to 1.39), but there was a stronger relationship with all-cause mortality (OR, 1.46; 95% CI, 1.12 to 1.92) and fatal IHD (OR, 1.54; 95% CI, 1.03 to 2.30). After adjustment for cardiovascular risk factors and both adult and childhood socioeconomic status, ORs were slightly reduced and lost statistical significance (OR=1.32 [95% CI, 0.99 to 1.78] for all-cause mortality and OR=1.52 [95% CI, 0.99 to 2.34] for fatal IHD). CONCLUSIONS: H pylori infection is unlikely to be as strong a risk factor for IHD as some previous studies have suggested, but its relationship to mortality, including fatal IHD, deserves further investigation. The mechanism underlying these associations is unlikely to involve hypertension, circulating lipid profile, fibrinogen, or cross-reacting antibodies to bacterial heat shock proteins.

Helicobacter Infections↗
PubMed2004

T cell mimicry in inflammatory heart disease.

Inflammatory heart diseases such as myocarditis and rheumatic heart disease result from the infiltration of the myocardium or valve with T cells and macrophages that result in scarring of the myocardium or valve and alteration in cardiac function. Our studies of T cells from these diseases have identified cardiac myosin in both rheumatic carditis and myocarditis as an important autoantigen. In rheumatic heart disease, streptococcal M protein specific T cells migrate to valves. By investigating streptococcal M protein and cardiac myosin in the Lewis rat model of myocarditis and valvulitis, T cell mimicry is supported as a potential mechanism in disease. Structural and immunological mimicry between the streptococcal M protein and cardiac myosin is shown directly in the Lewis rat model. Rat T cell lines demonstrate mimicry between cardiac myosin and M protein, and T cells isolated directly from inflammatory lesions in myocarditis respond to streptococcal M protein peptides. Studies in BALB/c mice also support the immunological crossreactivity of T cells primed against cardiac myosin with streptococcal M protein peptides containing cardiac myosin homologies. T cell lines produced from the Lewis rat specific to the cardiac myosin like sequences of streptococcal M protein migrated to the valves after passive transfer of the M protein specific T cell lines. In coxsackieviral myocarditis in the MRL mouse strain, cardiac myosin mimicking M protein peptide NT4 was found to induce tolerance and prevent coxsackieviral induced myocarditis, suggesting T cell mimicry between coxsackievirus and streptococcal M protein, both of which are associated with inflammatory heart disease. T cell mimicry between cardiac myosin and microbial antigens such as the streptococcal M protein may prime the immune system for inflammatory heart disease.

Animals↗
PubMed2001

A model for predicting the future incidence of coronary heart disease within percentiles of coronary heart disease risk.

BACKGROUND: We present a method (The CHD Prevention Model) for modelling the incidence of fatal and nonfatal coronary heart disease (CHD) within various CHD risk percentiles of an adult population. The model provides a relatively simple tool for lifetime risk prediction for subgroups within a population. It allows an estimation of the absolute primary CHD risk in different populations and will help identify subgroups of the adult population where primary CHD prevention is most appropriate and cost-effective. METHODS: The CHD risk distribution within the Australian population was modelled, based on the prevalence of CHD risk, individual estimates of integrated CHD risk, and current CHD mortality rates. Predicted incidence of first fatal and nonfatal myocardial infarction within CHD risk strata of the Australian population was determined. RESULTS: Approximately 25% of CHD deaths were predicted to occur amongst those in the top 10 percentiles of integrated CHD risk, regardless of age group or gender. It was found that while all causes survival did not differ markedly between percentiles of CHD risk before the ages of around 50-60, event-free survival began visibly to differ about 5 years earlier. CONCLUSIONS: The CHD Prevention Model provides a means of predicting future CHD incidence amongst various strata of integrated CHD risk within an adult population. It has significant application both in individual risk counselling and in the identification of subgroups of the population where drug therapy to reduce CHD risk is most cost-effective.

Actuarial Analysis↗
PubMed1990

[Therapeutic principles in pulmonary heart disease and right heart insufficiency].

Until now the pathomechanism of pulmonary heart disease is insufficiently elucidated. Therefore, at present, rational therapeutical concepts are possible only in chronic obstructive lung diseases. Without any modification, the principle of comprehensive treatment of the basic pulmonary disease remains valid. In the symptomatic therapy of the pulmonary heart disease, in first place the long-term oxygen therapy becomes mandatory. Treatment with vasodilatory drugs remains in the long-term activity disappointing. Reasonable expectations are directed to clinical trials of angiotensin-converting-enzyme-inhibitors. Cardiac glycosides remain reserved for manifest cardiac failure. The stabilization of the acid-base-balance is of great importance for the efficacy of treatment. The decision on the use of additives depends upon a critical evaluation of the actual clinical state and upon the consideration of the risks from polymorbidity.

Combined Modality Therapy↗
PubMed2003

Elevated circulating levels of inflammatory cytokines and bacterial endotoxin in adults with congenital heart disease.

Chronic heart failure is a state of immune activation, and endotoxin is a potential trigger for cytokine production. Our aim was to study whether immune activation and endotoxemia occur in adults with congenital heart disease. We prospectively measured tumor necrosis factor (TNF)-alpha, soluble TNF receptors (sTNFR-1, sTNFR-2), interleukin-6, interleukin-10, endotoxin, and soluble CD14 levels in 52 consecutive adults with congenital heart disease (age 34 +/- 2 years [mean +/- SEM]) and 18 healthy controls (age 31 +/- 1 years). A variety of congenital heart lesions were studied: single ventricle physiology (n = 15), systemic right ventricle (n = 7), tetralogy of Fallot (n = 20), and "other" congenital heart disease (n = 10). Patients were subgrouped into asymptomatic (New York Heart Association [NYHA] class I, n = 11), mild (NYHA class II, n = 30), and moderate/severe (NYHA class III/IV, n = 11) categories. Patients had elevated TNF and interleukin-6 levels compared with controls (TNF 2.8 vs 2.1 pg/ml, p <0.05; interleukin-6 8.5 vs 5.7 pg/ml, p <0.001). TNF levels were higher in patients with moderate/severe symptoms compared with patients who were asymptomatic or had mild symptoms (p <0.05). Soluble TNFR-1 levels related directly to the degree of systemic ventricular impairment (p <0.05). There were no significant differences in sTNFR-1, sTNFR-2, interleukin-10, or sCD14 levels between patients and controls. Endotoxin levels were greater in patients with congenital heart disease versus controls (0.40 vs 0.26 endotoxin units/ml, p <0.0001). Thus, adults with congenital heart disease have elevated levels of inflammatory cytokines and bacterial endotoxin, which relate to functional status. Congenital heart disease in adults may be amenable to novel anti-inflammatory therapies in selected patients.

Adult↗
PubMed2005

Cellular therapy with autologous skeletal myoblasts for ischemic heart disease and heart failure.

Cardiomyocytes are final differentiated cells that lose the ability to regenerate. Autologous cellular transplantation for cardiac repair has recently emerged as a promising new approach for end-stage heart failure that avoids the risk of immune rejection and ethical problems. Skeletal myoblasts (or satellite cells) are committed progenitor cells located under the basal lamina of adult skeletal muscle; they are committed to multiply after injury. They are highly resistant to ischemia and possess a considerable potential for division in culture. The cardiac milieu might alter the developmental program of grafted myoblast and facilitate their conversion to the slow-twitch phenotype, which is capable of performing cardiac work. We have used autologous cultured myoblast grafts for mouse and rat myocardial infarction in more than 200 cases. From these grafting experiments, it has been shown that cultured autologous myoblast grafting is a useful technique in the treatment of ischemic heart failure. This chapter offers a step-by-step guide to a successful research project on cultured myoblasts for the treatment of myocardial infarction, as well as a set of special techniques for yielding large numbers of skeletal myoblasts and studying postimplantation myocardial repair.

Animals↗