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

A 2 MHz continuous waveform non-invasive ultrasound doppler system has been used in the present investigation. With the aid of the audio signals of the frequency shifts, the ultrasound probe was positioned on the external chest so that the axis of the incident ultrasonic beam coincided with the direction of the maximum velocity vectors of the mitral jet. The frequency shifts due to the mitral jet were frequency analyzed and the time course of the maximum frequency shift was determined. The time course of the maximum mitral jet velocity was then determined from the doppler equation and the time course of the mitral pressure gradient from an orifice equation. The usefulness of the technique was evaluated by studying 25 patients with mitral stenosis and 10 without heart disease. The patients with mitral stenosis were studied during cardiac catheterization and the ultrasound data, the pulmonary artery wedge pressure, and the left ventricular pressure were recorded simultaneously. A table is presented where the gradient determined with the ultrasound technique, deltaPU, is compared with the gradient determined from the pressure tracing, deltaPM. Averaged over the 25 patients studied, deltaPU was 1.7 mmHg smaller than deltaPM at 0.08 sec diastolic time and 1.8 mmHg smaller at 0.25 sec diastolic time. The findings in the patients without heart disease differed distinctly from those in the patients with mitral stenosis. The investigation demonstrated that the non-invasive ultrasound technique can be used with confidence to gain an impression of the magnitude of the mitral pressure gradient. The findings also suggest that deltaPU represents the actual pressure gradient more accurately than deltaPM. Another investigation is proposed to assess the accuracy of the technique more completely.
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PMID:Determination of pressure gradient in mitral stenosis with a non-invasive ultrasound Doppler technique. 93 70

One hundred consecutive cases of rheumatic fever and rheumatic heart disease who were seen at Department of Pediatrics. Ramathibodi Hospital were reviewed. Particular attention was given to the pattern and the outcome of the cardiac status of the patients. The high incidence of severe carditis and tight mitral stenosis was similar to most reports from other developing countries. There was a poor prognosis for the cardiac status of those who came late, had more than valvular lesions, were in congestive heart failure, or had preexisting heart disease and atrial fibrillation. In spite of this, 6 patients had no evidence of heart disease after being followed up for less than 5 years.
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PMID:Juvenile rheumatic fever and rheumatic heart disease at Ramathibodi Hospital, Thailand. 102 12

Fetal cardiac activity was monitored with an external ultrasound transducer in two patients with clinical class III heart disease due to severe mitral stenosis complicated by pulmonary hypertension, undergoing open heart surgery with cardiopulmonary bypass in the 2nd trimester of pregnancy. Fetal distress was detected in one patient, who had mitral valvuloplasty, and was corrected by increasing the rate of blood flow, and the other patient had a mitral valve replacement but no fetal distress was noted. The postoperative course of both mothers and fetuses was uneventful.
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PMID:Fetal monitoring during maternal cardiac surgery with cardiopulmonary bypass. 112 21

A case of aneurism of the left ventricle, confirmed by ventriculogram, associated to an inactive rheumatic cardiopathy with a pure mitral stenosis is presented. Since none of the usual causes that have been reported were found to explain the aneurism of the left ventricle; the possibility of the aneurism resulting from residual myocardiac fibrosis produced by the rheumatic myocarditis is suggested.
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PMID:[Aneurysm of the left ventricle associated with inactive rheumatic heart disease. Report of a case]. 115 9

Two cases of polycythaemic chorea are described, both of which were complicated by severe heart disease. The first was a child with patent ductus arteriosus and coarctation of the aorta causing severe cyanosis and secondary polycythaemia. Chorea began intermittently at an early age, becoming continuous by his fifth birthday. The second was a middle-aged male with tight mitral stenosis and a story of paralytic chorea in his teens. Polycythaemia rubra vera was eventually diagnosed two years after mitral valvotomy, some seven years after the onset of chorea.
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PMID:Chorea, polycythaemis, and cyanotic heart disease. 118 93

In 167 patients with congenital and acquired heart disease (ventricular septum defect (VSD), atrial septum defect (ASD), mitral stenosis (MS), mitral insufficiency (MI), combined mitral stenosis and insufficiency (MV) aortic stenosis (AS), aortic insufficiency (AI), combined aortic stenosis and insufficiency (AV), idiopathic hypertrophic subaortic stenosis (HOK) hemodynamic measures (arterial pressure, right and left heart pressures, cardiac output, cardiac index, stroke volume, cardiac work), left ventricular volumes (endiastolic volume, endsystolic volume, ejection fraction, regurgitant flow) and diastolic pressure-volume relationships (on the basis of diastolic pressure-volume changes) were determined during routine right and left heart catheterization and left ventriculography. 1...
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PMID:[Hemodynamics, left ventricular volumes and compliance in 167 patients with congenital and acquired heart disease (author's transl)]. 120 78

Relative regional ventilation and perfusion were measured with xenon-133 in 16 seated patients with pure or predominant mitral stenosis (group 1) and in 12 patients with chronic pulmonary congestion due to left-sided heart disease without mitral stenosis (group 2). The apex-base perfusion gradient was abnormally reduced and often reversed in group 1 patients. There was a significant negative correlation between perfusion gradient and mean pulmonary capillary pressure in both groups, but for a given elevation of pulmonary capillary pressure the perfusion gradient tended to be greater (i.e., less abnormal) in group 2. The regression line of perfusion gradient on pulmonary capillary pressure indicated that perfusion gradient had a value of zero (indicating reversal of the perfusion gradient) at a mean pulmonary capillary pressure of 26 mm Hg in group 2 but at only 18 mm Hg in group 1. Relative lower zone ventilation was abnormally reduced in group 1 and there was a significant negative correlation between ventilation gradient and pulmonary capillary pressure in group 1 but not group 2 patients. Comparison of the distribution of slowly inhaled small volume boluses, large volume boluses, and inspiratory capacity breaths of 133Xe suggested that the lower zone hypoventilation was due mainly to closure of peripheral airways but that selectively increased resistance and reduced compliance in the lower zones may contribute in some patients. Both ventilation and perfusion were reduced at the lung bases in group 1 patients, and between regions nonuniformity of relative ventilation/perfusion was significantly less than normal. Although ventilation distribution was relatively normal in group 2 patients, they also had significantly less regional ventilation/perfusion nonuniformity than normal subjects.
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PMID:Regional lung function in chronic pulmonary congestion with and without mitral stenosis. 124 16

Rheumatic heart disease contributes to significant cardiac morbidity and mortality in India. The disease predominantly affects the valvular endocardium culminating in crippling valvular deformities, preferentially involving the mitral valve which may be severely affected in children and young adults. This appears to be unique to India and has been termed juvenile mitral stenosis. It is characterized by cardiomegaly, refractory congestive heart failure, and marked by elevated pulmonary vascular pressures and a progressive, fulminant clinical course. Autopsies of patients dying of rheumatic heart disease revealed that the mitral valve was most commonly afflicted either alone or in combination with the aortic and tricuspid valves in 31.6% and 52.8%, respectively. Organic involvement of the tricuspid valve was documented in 38.4% of cases. The extent and severity of the disease process was most marked in the mitral valve, followed by the aortic and tricuspid valves. Mitral valves showed various degrees of calcification, moderate or severe calcification being observed in 36.4%. Chronic inflammatory cell infiltration was observed in both calcified and non-calcified valves. The phenotypic profile of the inflammatory cells by immunohistochemical staining revealed a significant number to be T-helper/inducer lymphocytes. Lungs from cases of mitral stenosis exhibited prominent vascular and parenchymal changes. Pulmonary vessels revealed moderate to marked medial hypertrophy of the medium sized branches of the pulmonary artery. Dilatation lesions were also seen in a few cases. The most striking parenchymal change was the prominent smooth muscle in the bronchoalveolar walls. The extent and severity of the vascular and parenchymal changes were more marked in juvenile patients. The presence of inflammatory cells in cases of chronic heart disease reflects a possible ongoing insult/injury to some persistent antigenic stimulus by beta hemolytic streptococcal antigens that have primed the various target tissues. Further study of surface characteristics of various mesenchymal cells may help in understanding the nature and pathogenesis of this serious cardiac problem.
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PMID:Chronic rheumatic heart disease in India: a reappraisal of pathologic changes. 134 Dec 28

Atrial fibrillation is associated with potentially life-threatening strokes. Anticoagulation with warfarin or aspirin reduces the risk of embolic events in patients with chronic atrial fibrillation and mitral valve stenosis or other underlying heart disease. In patients with acute onset of atrial fibrillation, anticoagulation is not necessary before cardioversion. However, in patients with chronic atrial fibrillation, anticoagulation should be started three weeks before cardioversion and continued for four weeks after the return of normal sinus rhythm. Quinidine remains the agent most commonly used for medical cardioversion in patients who are hemodynamically stable. If a patient is hemodynamically unstable or the atrial fibrillation is not corrected with drug therapy, direct-current electrical cardioversion has a high success rate. Antiarrhythmic (quinidine) therapy is often continued indefinitely to help maintain sinus rhythm.
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PMID:Atrial fibrillation: current therapeutic approaches. 135 Jul

Pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently it has been shown that the wall stresses become very large when the capillary pressure is raised, and in anaesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mm Hg and above. The changes include breaks in the capillary endothelial layer, alveolar epithelial layer, and sometimes all layers of the wall. The strength of the thin part of the capillary wall can be attributed to the type IV collagen in the extracellular matrix. Stress failure of pulmonary capillaries results in a high-permeability form of oedema, or even frank haemorrhage, and is apparently the mechanism of neurogenic pulmonary oedema and high-altitude pulmonary oedema. It also explains the exercise-induced pulmonary haemorrhage that occurs in all racehorses. Several features of mitral stenosis are consistent with stress failure. Overinflation of the lung also leads to stress failure, a common cause of increased capillary permeability in the intensive care environment. Stress failure also occurs if the type IV collagen of the capillary wall is weakened by autoantibodies as in Goodpasture's syndrome. Neutrophil elastase degrades type IV collagen and this may be the starting point of the breakdown of alveolar walls that is characteristic of emphysema. Stress failure of pulmonary capillaries is a hitherto overlooked and potentially important factor in lung and heart disease.
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PMID:Stress failure of pulmonary capillaries: role in lung and heart disease. 809 42


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