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

We examined trends in heart disease (HD) mortality and the delivery of cardiac in Olmsted County, MN. Between 1979 and 1994, women experienced 51% of the total number of HD (ICD9 codes 390-398,402,404-429) deaths (3095). Age-adjusted HD mortality rate declined from 123 per 100,000 (95%CI 102, 144) in 1979 to 81 (67,95) in 1994. The risk ratio (RR) of HD death in 1994 compared to 1979 was 0.69 for women vs 0.53 for men (P = 0.06). This equates to a decline in HD mortality of 2.5%/y in women and 4.2%/y in men. The decline in HD mortality was less pronounced in older age groups (P < 0.001), reflecting a shift of the burden of HD towards women and the elderly. Compared to men, there was less use of stress tests among women, of cardiology visits after stress testing, and of cardiac procedures among women presenting to the emergency room with unstable angina. Further studies are needed to examine causal links between these trends.
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PMID:Sex differences in the epidemiology and outcomes of heart disease: population-based trends. 1045 11

To determine the role of immune responses in the etiology of coronary angioplasty, the distribution of blood lymphocytes and levels of soluble immune factors in sera of patients with primary unstable angina were determined at pre and post coronary angioplasty. Our data showed (1) an increase in the numbers of lymphocytes bearing lymphocyte activating gene-3 (LAG-3) and CD40 in the blood and (2) an increase in levels of sIL2-R and sVCAM-1 in the sera of patients with unstable angina, compared with normal subjects. In contrast, there were no changes in these values in blood or sera of patients shortly after coronary angioplasty. However, levels of sCD8 in the sera of patients, which were similar to those of normal subjects, significantly increased post coronary angioplasty. These results indicate that peripheral blood lymphocytes of patients with unstable angina are immunologically activated and are producing soluble factors which may allow their interaction with endothelial cells in areas of inflammation. This may play a role in antigen presentation and T-B cell interactions which can lead to potentiation of heart disease.
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PMID:Lymphocyte activation in angina pectoris. 1052 93

The diagnosis coronary artery disease is classically based on patient's symptoms and morphology, as analyzed by angiography. The importance of risk factors for the development of coronary atherosclerosis and disturbance of coronary vasomotion is clearly established. However, microembolization of the coronary circulation has also to be taken into account. Microembolization may occur as a single or as multiple, repetitive events, and it may induce inflammatory responses. Spontaneous microembolization may occur, when the fibrous cap of an atheroma or fibroatheroma (Stary i.v. and Va) ruptures and the lipid pool with or without additional thrombus formation is washed out of the atheroma into the microcirculation. Such events with progressive thrombus formation are known as cyclic flow variations. Plaque rupture occurs more frequently than previously assumed, i.e. in 9% of patients without known heart disease suffering a traffic accident and in 22% of patients with hypertension and diabetes. Also, in patients dying from sudden death microembolization is frequently found. Patients with stable and unstable angina show not only signs of coronary plaque rupture and thrombus formation, but also microemboli and microinfarcts, the only difference between those with stable and unstable angina being the number of events. Appreciation of microembolization may help to better understand the pathogenesis of ischemic cardiomyopathy, diabetic cardiomyopathy and acute coronary syndromes, in particular in patients with normal coronary angiograms, but plaque rupture detected by intravascular ultrasound. Also, the benefit from glycoprotein IIb/IIIa receptor antagonist is better understood, when not only the prevention of thrombus formation in the epicardial atherosclerotic plaque, but also that of microemboli is taken into account. Microembolization also occurs during PTCA, inducing elevations of troponin T and I and elevations of the ST segment in the EKG. Elevated baseline coronary blood flow velocity, as a potential consequence of reactive hyperemia in myocardium surrounding areas of microembolization, is more frequent in patients with high frequency rotablation than in patients with stenting and in patients with PTCA. The hypothesis of iafrogenic microembolization during coronary interventions is now supported by the use of aspiration and filtration devices, where particles with a size of up to 700 microns have been retrieved. In the experiment, microembolization is characterized by perfusion-contraction mismatch, as the proportionate reduction of flow and function seen with an epicardial stenosis is lost and replaced by contractile dysfunction in the absence of reduced flow. The analysis of the coronary microcirculation, in addition to that of the morphology and function of epicardial coronary arteries, and in particular appreciation of the concept of microembolization will further improve the understanding of the pathophysiology and clinical symptoms of coronary artery disease.
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PMID:Coronary microembolization--its role in acute coronary syndromes and interventions. 1060 63

Acute cardiac events involving coronary symptoms, elevated enzyme levels, and electrocardiographic changes without the development of Q waves often result in higher rates of reinfarction and unstable angina than do more severe myocardial infarctions. The incidence of these non-Q wave events is on the rise, possibly because of earlier detection and treatment of heart disease. Familiarity with the characteristics and management of the condition, therefore, is more important than ever.
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PMID:Non-Q wave myocardial infarction. Assessment and management of a unique and diverse subset. 1068 10

The validity and reliability of the SF-36 has been studied in 185 patients hospitalized with suspected ischemic cardiopathy, classified into four groups (AMI, unstable angina, nonischemic cardiologies, and absence of cardiologies). The validity of the construct has been analyzed by means of the association of the SF-36 with sociodemographic and clinical variables, and with diagnostic groups. The correlation of the subscales with GHQ-28 scores and the factorial structure have been studied. Internal consistency was measured by Cronbach's alpha and the item-internal consistency and item-discriminant validity. The validation result was as expected, although the scores were significantly lower in patients with unstable angina, only in the PF, VT, and GH subscales. The correlations with the GHQ-28 were high for MH and VT. The internal consistency was high (Cronbach's alpha 0.72-0.94). Factorial analysis identified eight factors, with the "anxiety" component of subscale MH remaining as an independent factor. These results suggest that the SF-36 is a useful scale for the differentiated clinical forms of ischemic cardiopathy, with the additional capability of reflecting the level of anxiety in these patients.
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PMID:Validity and reliability of the SF-36 Health Survey Questionnaire in patients with coronary artery disease. 1078 66

The strong association between severe coronary stenosis and collateral growth continues to be a paradigm in this field of investigation. The present study was based on the hypothesis that angiogenic growth factors are produced by ischemic cardiac tissue, are diffusible and more concentrated in pericardial fluid, and accelerate the growth of vascular smooth muscle cells (VSMC). Pericardial fluid from 17 patients with stable or unstable angina or acute myocardial infarction (group A) and from 10 patients with nonischemic heart disease (group B) were collected at the time of open heart surgery. Cultured human aortic VSMC were plated at the third passage at a density of 5x10(3)/100 microl and allowed to attach for 24 h. The 3-day growth assay was preceded by 72 h of growth arrest with 0.4% fetal calf serum (FCS). Growth was restarted by the addition of 90 microl of medium containing 0.4% FCS, and 1O microl of each pericardial fluid. Cell counts on triplicate wells were performed using a dimethylthiazol (MTT) method on days 0 and 3. The effect of pericardial fluid on the growth of VSMC was evaluated as a ratio (R) of cell numbers on day 3 to those on day 0. The concentration of basic fibroblast growth factor (bFGF) in pericardial fluid was measured by an enzyme-linked immunosorbent assay. The concentration of bFGF in pericardial fluid of group A was 633+/-127 pg/ml, and significantly (p=0.003) higher than that of group B (86+/-23 pg/ml). R in group A was 2.29+/-0.18 and significantly (p=0.019) higher than that in group B (1.68+/-0.11). The level of bFGF positively correlated with R (p=0.009). These findings indicate that pericardial fluid from patients with ischemic heart disease contains some substances that mediate collateral development, and bFGF might be one of them.
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PMID:Pericardial fluid from patients with ischemic heart disease accelerates the growth of human vascular smooth muscle cells. 1092 76

In centers without hemodynamic laboratories the quality of medical care may be suboptimal since the unavailability of these technologies may reduce medical experience in the treatment of heart disease, mostly in acute coronary syndromes, and may increase the need for referring some patients to other hospitals. The problem will be of great relevance in the case of expansion of the aggressive approach in the treatment of acute ischemic syndromes such as acute myocardial infarction and unstable angina. The impelling need for small centers of improving medical care may promote the spontaneous and uncontrolled proliferation of hemodynamic laboratories. The high number of hemodynamic laboratories may lead to a low institutional volume and, as a consequence, may negatively influence the outcome of coronary intervention and increase health care costs. The experience of operators and the costs are probably more relevant as regards angioplasty than coronary angiography. Therefore we propose the implementation of departments of interventional hemodynamic laboratories including different hospitals: diagnostic laboratories will be allocated in hospitals with coronary care units, while interventional laboratories will be allocated in referring hospitals.
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PMID:[A new organization model for hemodynamic cardiology diagnosis and intervention cardiology]. 1121 80

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

Over several decades, a large body of evidence has emerged to suggest that depressive disorder is a risk factor for heart diseases, both aetiologically and prognostically. Several large, prospective, longitudinal studies have examined the relationship between depression and the development of coronary artery disease (CAD); they reveal that the relationship is significant and independent of conventional risk factors. Prognostic studies have shown that depression is associated with two to three times higher mortality after myocardial infarction, unstable angina or coronary artery bypass grafting, and in patients with stable CAD compared with such patients without depression. Depression also has been found to increase mortality and morbidity in patients with heart failure, regardless of its aetiology. Such adverse associations persist after adjustment for conventional prognostic risk factors. Despite all of these findings, depressed patients with heart disease are less likely to be recognised clinically as being depressed than those patients who have depression but no heart disease. The very limited evidence available from pharmacological clinical trials raises concern about the safety of antidepressants in CAD and heart failure. In addition, no research has addressed whether the treatment of depression in patients with heart disease will improve their prognosis.
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PMID:Depression and heart disease: evidence of a link, and its therapeutic implications. 1182 2

We performed a prospective study to describe the broad spectrum of causes of chest pain in patients presenting to the emergency department and to compare the diagnoses in referred patients, self-referred patients and patients rushed in by ambulance. The final diagnosis in a consecutive case series of 578 chest pain patients was established after discharge from the hospital. The underlying disorders were grouped into cardiac, respiratory, gastro-oesophageal disorders, musculoskeletal pathology, somatization disorders, other diseases and unknown. For comparison of the frequencies of the disease categories the Chi-squared test was used. Out of 578 patients, 161 (27.9%) were self-referred, 369 (63.8%) were referred by the general practitioner and 48 (8.3%) were rushed in by ambulance. Cardiac diseases represented 51.7% of the cases, myocardial infarction and unstable angina 19% and 12.8% respectively Cardiac diseases were statistically significantly less common in self-referred patients (p<0.0005). Pulmonary diseases encompassed 14.2% of the population, followed by somatization disorders (9.2%), musculoskeletal pathology (7.1%) and other causes (4.3%). In 11.1% of the cases no definite final diagnosis could be established. Somatization disorders were significantly more frequent in self-referred and ambulance patients. Cardiac and pulmonary problems are the most frequent underlying disorders in acute chest pain patients in the emergency department. Somatization disorders and musculoskeletal pathology represented respectively 19.1% and 14.8% of the non-cardiac causes. The referral pattern influenced significantly the distribution of the disease categories with more cardiac and less psychiatric disorders in referred patients.
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PMID:Chest pain in the emergency department: the broad spectrum of causes. 1198 92


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