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

Sneddon's syndrome consists of livedo reticularis and cerebral vascular accidents with no evidence of systemic disease responsible for the livedo. The syndrome has been assimilated to a subgroup of systemic lupus erythematosus (SLE) with presence of antibodies directed against phospholipids. Recently, a significant increase in the frequency of cardiac valve diseases has been demonstrated in some SLE patients with livedo reticularis, cerebral vascular accidents and antiphospholipid antibodies. We report the case of a 26-year old woman who had been presenting for 6 years with idiopathic livedo reticularis. Her history was remarkable for the occurrence of 2 cerebral ischaemic accidents at the ages of 23 and 26 years, generalized convulsive seizures at 22 years, and hypertension of pregnancy with 2 miscarriages. Biopsy of the livedo showed normal histological patterns, but electron microscopy detected an obliterating endothelial proliferation and endothelial cells with numerous Weibel-Palade bodies. Laboratory signs of SLE, as well as antiphospholipid antibodies were absent. At the age of 26 years, cardiac abnormalities were heard at auscultation for the first time, and echocardiography showed that they were due to a fairly loose mitral stenosis. According to Burton's criteria our patient had all the typical features of Sneddon's syndrome. The finding of mitral stenosis--an emboligenic cardiopathy that is potentially responsible for cerebral vascular accidents--raises the problem of its relationship with Sneddon's syndrome. The association does not seem to be fortuitous, since our case is very similar to the cases of SLE or antiphospholipid antibody syndrome associated with cardiac valve lesions. However, this case is particular in that 6 years after the onset of the disease there was still no sign of SLE and of antiphospholipid antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Livedo reticularis, cerebrovascular disorders and mitral disease: a new cause of Sneddon's syndrome?]. 208 86

Pregnant patients with heart disease seen between 1980 and 1985 were studied. The incidence of heart disease in pregnancy was 1.3%. Rheumatic heart disease was the commonest lesion (78%), followed by congenital heart disease (18.7%). In the rheumatic heart disease group, mitral stenosis was the commonest lesion (71.54%), and patients who had been or were operated on for their heart disease had less severe dyspnoea and fewer complications. The mode of delivery and the foetal and maternal mortality did not differ significantly in operated and non operated patients.
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PMID:Pregnancy with heart disease. Experience at Postgraduate Institute of Medical Education and Research, Chandigarh. 209 24

Heart disease is the most important nonobstetric cause of maternal death; however, most young women with heart disease do well during pregnancy. If the physician is uncertain of the effects of pregnancy on a particular heart condition, needless restrictions may be imposed. The main hazards are: pulmonary edema when it occurs suddenly in mitral stenosis; pulmonary hypertension (because pulmonary vascular disease tends to be exacerbated by pregnancy); infective endocarditis (this is rare); and fulminating peripartum cardiomyopathy. The practical management of the pregnant patient with various concomitant heart conditions (congenital heart disease, pulmonary hypertension, rheumatic heart disease, anticoagulants and artificial valves, constrictive pericarditis, kyphoscoliosis, Marfan's syndrome, mitral prolapse, hypertrophic cardiomyopathy, dilated cardiomyopathy, infective endocarditis, and arrhythmias) is discussed. An absolute indication for therapeutic abortion is severe pulmonary vascular disease; discretionary indications include 'chronic thromboembolic pulmonary hypertension,' cardiomyopathies (depending on the hemodynamic disturbance), and Marfan's syndrome.
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PMID:Cardiovascular disease in pregnancy. 218 16

The capability of transesophageal (TEE) versus transthoracic (TTE) echocardiography as a diagnostic tool in clinical practice was prospectively examined in 86 consecutive cases. A conclusive diagnosis was possible in 95% with TEE, whereas the same result was achieved in 48% by TTE. Specifically, TEE provided a conclusive diagnosis in 14 of 16 cases of infective endocarditis, while TTE gave this result in 4 of the 16 cases (p less than 0.001). Similarly, TEE allowed a conclusive diagnosis in 11 of 11 instances of aortic dissection, while TTE gave this indication in two cases (p less than 0.001). TEE was similarly effective in eight of eight cases of atrial thrombi, whereas TTE gave the diagnosis in three of eight cases (p less than 0.01). In five subjects with intracardiac masses, TEE gave a conclusive diagnosis in all five, whereas TTE was able to diagnose conclusively in one subject (p less than 0.02). In seven patients with mitral regurgitation, TEE gave the conclusive diagnosis in all seven and TTE was able to provide this information in four (p = NS). TEE was able to provide a conclusive diagnosis in four patients with aortic insufficiency, and TTE gave the same information in two of the four (p = NS). In 14 patients with prosthetic valve dysfunction, TEE gave the diagnosis in 12 and TTE gave it in eight patients (p = NS). Both methods gave a conclusive diagnosis in 13 out of 13 cases of mitral stenosis (p = NS). Also, TEE provided a conclusive diagnosis in eight of eight patients with adult congenital heart disease and TTE gave this information in four (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of transesophageal echocardiography to patient diagnosis and treatment: a prospective analysis. 222 May 45

The risk for systemic embolization was studied in 272 patients without mitral stenosis or prosthetic valves who were referred to the echocardiography laboratory with atrial fibrillation (AF). During a mean follow-up period of 33 months (range less than 1 to 83), 27 (10%) patients had a systemic embolic event, which was cerebral in 23 patients (85%) and peripheral in 4 (15%). In the analysis of individual variables, the risk of embolization was increased by female sex, underlying heart disease and left atrial size greater than or equal to 4.0 cm, but not by age, hypertension or type of AF (paroxysmal vs chronic). In multivariable analysis, left atrial size greater than or equal to 4.0 cm was the single strongest predictor of increased risk for embolization (p less than 0.001), but female sex (p = 0.014) and underlying heart disease (p = 0.027) also contributed. When each of these 3 factors was assigned 1 point in a risk score, embolic events were found to occur in none (0%) of 24 patients with a risk score of 0, in 2 (3%) of 83 patients with a risk score of 1, in 13 (11%) of 118 patients with a risk score of 2 and in 12 (26%) of 47 patients with a risk score of 3. The score allows patients with AF and without mitral stenosis to be stratified into high-, medium- and low-risk groups for systemic embolization. Such information could be useful in decision making for anticoagulation in patients with AF.
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PMID:Risk for systemic embolization of atrial fibrillation without mitral stenosis. 233 Aug 96

A review of cardiac admissions to the Ethio-Swedish Children's Hospital from January 1981 to December 1988 revealed 365 cases. Patients were included in the study if they had clinical, laboratory and echocardiographic (M, 2D-Modes, doppler) proofs of the specific disease entity. One hundred and ten patients were eligible. This accounted for 0.65% of all admissions (N = 16,905). Rheumatic heart disease accounted for 54.5% (N = 60), congenital heart disease for 35.5% (N = 39), and acquired heart disease of nonrheumatic origin for 10% (N = 11) or cardiac admissions. Of patients with rheumatic heart disease, the mitral valve was involved in 41.7% (N = 25). Pure mitral stenosis was seen in 8.3% (N = 5). Ventricular septal defect was seen in 33.3% (N = 13) of patients with congenital heart disease. The mean hospital stay for patients with rheumatic heart disease was 35.4 days, and 24.7 days for patients with congenital heart. As rheumatic heart disease predominates, methods for decreasing its incidence are discussed.
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PMID:Profile of cardiac diseases in Ethiopian children. 236 44

To clarify whether the formation of thrombi could be induced by atrial fibrillation itself or by factors predisposing to atrial fibrillation such as mitral stenosis, plasma D-dimer levels (cross-linked fibrin degradation products) were measured in 73 patients without atrial fibrillation (Group 2). In Group 1, 49 of the 73 patients had factors predisposing to atrial fibrillation such as valvular heart disease, and the remaining 24 had lone atrial fibrillation. In Group 2, 16 patients had organic heart disease and the remaining 5 had a chest pain syndrome. The plasma D-dimer level was significantly higher in Group 1 (150 +/- 19 ng/ml) than in Group 2 (61 +/- 3 ng/ml) (p less than 0.01, mean +/- standard error of the mean). In both groups, there were no significant differences in plasma D-dimer level between patients with and without organic heart disease (146 +/- 18 versus 156 +/- 46 ng/ml in Group 1; 61 +/- 4 versus 59 +/- 10 ng/ml in Group 2). These findings indicate that atrial fibrillation itself may be more important than factors predisposing to atrial fibrillation in the development of intracardiovascular clotting.
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PMID:Increased intracardiovascular clotting in patients with chronic atrial fibrillation. 237 15

Contents and molecular forms of human atrial natriuretic peptide (hANP) in right and left auricle were analyzed by reverse phase high liquid chromatography (RP-HPLC), coupled with radioimmunoassay for hANP. Analyses were done with auricles taken from 4 autopsied cases without heart disease, and 13 patients with heart disease. Both right and left auricular hANP contents in patients with heart disease were higher than those obtained at autopsy. In patients with mitral stenosis (MS) or mitral regurgitation (MR) who have left atrial pressure and/or volume overload, hANP contents in left auricle were higher than those in right auricle. In addition, three types of molecular forms of hANP, (gamma) type, (alpha, beta, gamma) type, (beta, gamma) type, were observed in both right and left atrium. In patients with MS or MR, (beta, gamma) type or (alpha, beta, gamma) type which have beta-hANP immunoreactivity were observed in 8 out of 9 in patients in left auricle, however, in 4 out of 9 patients in right auricle. Our results suggested that the difference of contents and molecular forms of hANP may reflect the pathophysiological role in heart diseases.
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PMID:[Contents and molecular forms of human atrial natriuretic peptide in right and left auricle in patients with heart disease]. 252 68

Long-term follow-up of the amplitude of fibrillatory waves (f waves) on the standard electrocardiograms 0.6 +/- 3.3 yr, up to 20 yrs) was performed in 45 patients with chronic stable atrial fibrillation (24 men and 21 women, average age 60.2 +/- 11.5 yrs). The patients were divided into three groups on the basis of the underlying heart disease. Seventeen patients with mitral stenosis were classified as the MS group, 11 with hypertensive heart disease, old myocardial infarction, and aortic insufficiency as the HD group, and 17 without apparent heart diseases as the no heart disease (NHD) group. The f wave amplitude was measured at lead V1 according to the technique employed by Peter. The initial f wave amplitudes of the MS group (0.24 +/- 0.12 mV, mean +/- SD) and of the HD group (0.19 +/- 0.08 mV) were significantly larger than that of the NHD group (0.13 +/- 0.08 mV, p less than 0.05). The f wave amplitudes were significantly decreased during the observation period in each group, and the terminal f wave amplitudes (expressed as the percent of the initial f wave amplitude) were 61 +/- 34% in MS group, 59 +/- 26% in the HD group and 67 +/- 34% in the NHD group. In the NHD group, there was no significant difference in the terminal f wave amplitude between the cases with (n = 10) and without (n = 7) maintenance dose of digitalis. These results showed the apparent reduction of the f wave amplitude with perpetuation of this arrhythmia, and suggested that maintenance doses of digitalis had little effect on this process.
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PMID:[Long-term follow-up of the f wave amplitude in chronic atrial fibrillation]. 261 99

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co
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PMID:Pulmonary and pleural complications of cardiac disease. 268 66


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