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

The objective of this study was to determine the accuracy of administrative data (by use of hospital discharge codes) for measuring comorbidity in patients with heart disease. One thousand seven hundred and sixty-five medical records of subjects admitted to hospital for AMI, unstable angina, angina pectoris, chronic IHD or heart failure were reviewed. The number and types of comorbidities were determined from the medical records (regarded as the "gold standard"). These were compared with the 10 discharge codes obtained from the hospital administrative records (referred to as the "administrative data"). The rate of false-negative and false-positive comorbidity diagnoses were determined. Twenty of the 21 comorbidities studied were underreported in the administrative data. For these 20 comorbidities, the median false-negative rate was 49.5% and ranged from 11% for diabetes to 100% for dementia. False-positive rates were low, less than 1.5%, except for chronic arrythmia (4.8%) and hypertension (4.2%). Mean percent agreement was high, ranging from 88% for hypertension to 100% for AIDS/HIV. Administrative data based on hospital discharge codes consistently underestimate the presence of comorbid conditions in our population. This has implications for administrators when estimating mortality, length of stay and disability. Researchers also need to be aware when using administrative data based on hospital discharge codes to assess subject's comorbidities that they may be widely underreported.
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PMID:Accuracy of administrative data to assess comorbidity in patients with heart disease. an Australian perspective. 1143 9

Currently it is the hope of both patients and investigators that human progenitor cells and stem cells can be widely used to replace dysfunctional cells within a tissue. It is speculated that such cells may prove to have the potential to treat or cure a myriad of diseases, including Parkinson's and Alzheimer's diseases, heart disease, diabetes, stroke, spinal cord injuries, and burns. A major goal in this area of research is to identify potential new sources for the isolation of progenitor cells or stem cells, without raising the ethical issues involved in embryonic stem cell research. Despite the widespread and well-established use of amniotic fluid cells in routine prenatal genetic testing, current knowledge about the origin and properties of these cells is limited. A wide variety of different origins has been suggested for the mixture of cells within amniotic fluid. Recent observations on cell cultures from amniotic fluid and on amniotic epithelial cells provide evidence that they may represent new sources for the isolation of cells with the potency to differentiate into different cell types. Are these cells suitable for use as primary cell systems for basic research? Do these cells provide a new source for research on stem cell biology? Can amniotic fluid cells be used to develop new approaches in tissue engineering? In this article the authors review the current state of knowledge about these cells, focusing on these questions.
Med Sci Monit 2002 Nov
PMID:Amniotic fluid cells and human stem cell research: a new connection. 1244 90

Selenium is an essential trace element that is an integral part of many proteins, with catalytic and structural functions. The antioxidant properties of some selenoproteins, such as glutathione peroxidase, may be particularly important in carcinogenesis and heart disease. The content of selenium in food depends on the selenium content of the soil where the plants are grown or the animals are raised. Moreover, the metabolism of selenium is determined by its dietary form: some forms are better utilized than others. Therefore, wide variations have been found in selenium status in different parts of the world. In animal studies, selenium deficiency is associated with cardiomyopathy and sudden death, as well as reduced T-cell counts and impaired lymphocyte proliferation and responsiveness. Abnormalities in liver function, brain, heart, striated muscle, pancreas and genital tract have also been reported. In humans, selenium deficiency has been implicated in the etiology of cardiovascular disease and other conditions in which oxidative stress and inflammation are prominent features, but there is still only limited evidence from epidemiological and ecological studies for this, and the therapeutic benefit of selenium administration in the prevention and treatment of cardiovascular diseases remains insufficiently documented. Interventions studies are currently in progress to assess the benefits of selenium supplements in primary and secondary prevention of atherosclerosis. The results to date are inconclusive and further controlled trials are needed.
Med Sci Monit 2003 Jan
PMID:The controversy surrounding selenium and cardiovascular disease: a review of the evidence. 1255 53

Coronary artery disease is the leading cause of death for both men and women in the United States. While its incidence in men has been long appreciated, the impact on women has been underestimated for many years. This is in part because coronary artery disease generally appears later in women, the incidence increasing after the onset of the female menopause. There are approximately 8 million women living with heart disease in this country; almost 400.000 died from it in 1999 compared to almost 42.000 from breast cancer. Yet many women feel that cancer is more likely to be a cause of mortality. This review examines the common misperception of the prevalence of coronary artery disease in women and examines contributing risk factors such as hypertension, elevated serum cholesterol, diabetes mellitus and cigarette smoking. It considers access to care and diagnosis, both non-invasive and invasive, of coronary artery disease specifically as it pertains to women. Treatment options, ranging from medical management, through cardiac catheterization and percutaneous catheter based intervention, to coronary artery bypass surgery are discussed. In addition is included a section addressing the controversial issue of estrogen and its role in the incidence and treatment of heart disease in women.
Med Sci Monit 2003 Jun
PMID:Womens heart health series: a mini-symposium. 1459 47

It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholesterolemia in experimental animals and prevent carotid vascular disease (associated with stroke) in humans. The concomitant development of myocardiopathy and coronary vascular lesions or coronary and carotid artery intimal medial thickening by catecholamine toxicity is reflected by the frequent primary presentation of patients with catecholamine-secreting pheochromocytoma with cardiovascular disease, ie, hypertension arrhythmias, AMI, SCD, CHF, and vascular disease, which represents a clear example of the primary deleterious impact of catecholamines on the entire cardiovascular system causing adrenergic cardiovascular disease. Thus, like myocardiopathy, CAD and atherosclerosis in general may be the consequences of or a complication of catecholamine actions rather than its putative cause. This report shows how prophylactic bretylium not only prevents arrhythmias but prevents myocardial necrosis, shock, CHF, maintains or restores normal contractility, and lowers mortality in AMI patients by inducing adrenergic blockade.
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PMID:Prevention of ventricular fibrillation, acute myocardial infarction (myocardial necrosis), heart failure, and mortality by bretylium: is ischemic heart disease primarily adrenergic cardiovascular disease? 1535 32

Hypertrophic obstructive cardiomyopathy (HOCM) is a common inheritable cardiac disorder that can lead to symptoms of dyspnea, angina pectoris, and syncope. Symptomatic patients are usually treated with negatively inotropic agents, such as beta-blockers, calcium channel blockers, or disopyramide. However, up to 10% of patients with outflow pressure gradient are unresponsive to medical therapy. Until the early 1990s, surgical myectomy represented the standard treatment for patients with HOCM and drug-refractory symptoms. More than one decade ago, alcohol septal ablation (ASA) was introduced as a less invasive alternative therapy for symptomatic HCM patients with obstruction. ASA is performed through a percutaneous approach, in which 1-3 ml of absolute alcohol is introduced into the septal branch to create a controlled septal infarction of the basal interventricular septum. This procedure results in relief of symptoms, a decrease in the pressure gradient, and improvement in left ventricular diastolic function. A randomized controlled trial is needed to compare ASA and surgical myectomy in order to determine which technique provides maximal benefit.
Med Sci Monit 2007 Apr
PMID:Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: a review of the literature. 1739 60

We applied Bayesian methods to estimate excess mortality rates by selected causes of death for decedents with diabetes compared to those without diabetes in North Dakota and assessed changes in the excess rate between 1992-1998 and 1999-2003. We report the probability (Pr) of a rate decrease in the age-adjusted excess rate and considered the evidence strong if the probability was 0.90 or higher. Among men with diabetes, the evidence was strong for a probable decrease in excess rate for heart disease (8.7 per 1000 to 6.5), cerebrovascular disease (1.2 per 1000 to 0.75) and arterial disease (0.24 per 1000 to 0.08). Among women with diabetes, the evidence was strong for a probable decrease in excess rates for the overall (total) rate (17.8 per 1000 to 12.6), for heart disease (6.1 per 1000 to 4.4), IHD (4.4 per 1000 to 3.1), cerebrovascular disease (1.4 per 1000 to 0.5), arterial disease (0.17 per 1000 to 0.10) and cancer (2.1 per 1000 to 1.3) as underlying cause of death. The data reflect a high likelihood that cause-specific excess mortality is decreasing for men, and especially for women, with diabetes.
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PMID:Reductions in excess mortality rates among people with diabetes by selected cause of death. 1841 4

The syndrome of heart failure in adult non-congenital heart disease patients includes myocardial disease and ventricular dysfunction. In the presence of congenital abnormalities the cause of heart failure is often multi-factorial and can be a result of the underlying anomaly, surgical intervention, or ventricular dysfunction. Despite the possible clinical similarities, the two conditions are fundamentally different. In congenital heart disease the neurohormonal system is already abnormal even in the absence of clinical manifestations of heart failure and, in many cases, exercise intolerance is related to cyanosis. The approach to heart failure management in the two etiologies might be similar. Preventative attempts to preserve ventricular function in coronary or valve disease parallels early reparative therapy in congenital heart disease Pharmacological therapy is common for the two conditions, despite the limited number of evidence-based recommendations for congenital diseases. In drug-resistant patients, cardiac electrical resynchronization is an established therapy for treating ventricular asynchrony in non-congenital heart failure sufferers, but has only recently been adopted in selected congenital cases. Due to this, congenital heart disease patients are managed in highly specialized unites in close cooperation with cardiologists and surgeons. The ideal follow-up protocol for such patients remains to be determined, particularly in those individuals with subclinical signs of residual cardiac dysfunction. Heart Fail Monit 2008;6(1):2-8.
Heart Fail Monit 2008
PMID:Congenital heart disease and heart failure. 1860 16

If lithium therapy is required during pregnancy or lactation, serum lithium monitoring may be indicated in the newborns. In the neonatal population, however, blood samples are often obtained with a sampling device containing lithium heparin. Given the infrequent nature of lithium measurement in the neonatal population, a risk of oversight on the use of these lithium-containing devices for lithium measurements exists. Two such neonatal cases are reported, which may have been mismanaged if the measured levels of lithium were not suspected to be spurious. Patient 1 was a 3-day-old infant with a congenital heart disease born at 31 weeks' gestation to a mother on lithium. After a surgical repair, because of a potential need to monitor lithium in the infant's serum during breastfeeding, a remaining sample of apparently serum from a previous blood testing on day 1 of life was measured for lithium as a baseline value. Despite the lack of toxic signs, the result showed a toxic lithium level of 4.19 mmol/L. Lithium levels in follow-up samples were 0.11 mmol/L (day 4) and undetectable (day 6). Patient 2 was a full-term infant exposed to maternal lithium throughout the fetal life and breastfeeding. Serum lithium at day three of life in a hospital was undetectable, but after discharge, the lithium concentrations increased to 1.1 mmol/L on day 18, with no sign of lithium toxicity or renal dysfunction. This raised a possibility of significant exposure through breastfeeding, but later they were found to be spurious due to the use of lithium-containing devices. Separate investigation of effects of sampling devices on lithium levels indicated that levels of >3 mmol/L were possible if a sampling volume of blood was substantially small compared with the capacity of a tube containing lithium heparin [corrected]
Ther Drug Monit 2008 Dec
PMID:A pitfall of measuring lithium levels in neonates. 1905 75

Chronic mild dehydration has been associated with several diseases, including fatal IHD and stroke. It has been suggested that hydration through total fluid intake (or water) is inversely associated with IHD or stroke mortality. The objective of the present study was to evaluate the relationship between total fluid (and specific beverage) intake and IHD or stroke mortality in the Netherlands Cohort Study (NLCS). In 1986, 120,852 participants aged 55-69 years were enrolled into the NLCS. Mortality data were collected over a 10-year follow-up period. Analysis was done through a case-cohort approach, and it was based on the subjects without a history of heart disease, stroke or diabetes at baseline. A total of 1789 IHD mortality cases and 708 stroke mortality cases occurred during the follow-up. Higher total fluid consumption was not associated with either IHD mortality or stroke mortality in men or women. When analysing specific beverages, a positive association between coffee consumption (increment 270 ml/d) and IHD mortality was observed in men (hazard ratio (HR) 1.09, 95% CI 1.00, 1.18), while an inverse relationship was observed in women (HR: 0.88, 95% CI 0.78, 1.00). For tea consumption (increment of 253 ml/d), an inverse relationship with IHD mortality was observed in men (HR: 0.91, 95% CI 0.83, 1.00). No association with water intake was observed. In the study population, fresh water consumption was very low. In conclusion, total fluid intake was not associated with IHD or stroke mortality in either men or women. Coffee consumption was inversely associated with IHD mortality in women only, while a higher tea intake was associated with lower IHD mortality in men only.
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PMID:Total fluid and specific beverage intake and mortality due to IHD and stroke in the Netherlands Cohort Study. 2045 12


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