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

Collagen from tissues of the heart valve, the wall of the left auricle, palatine tonsils and periodontium was studied. The material was taken during surgical procedures, performed for therapeutic reasons, in patients with acquired valvular heart disease (avhd) and congenital heart disease. The obtained results pertain to the content of total collagen as well as to its soluble and insoluble fractions. An increase of the soluble collagen fraction, as compared to the insoluble one, provides support for collagen degradation, and this fact has prompted the authors to conclude that collagen plays a part in the etiopathogenesis of a.v.h.d. The authors suggest that estimation of collagen metabolites, and the amount of soluble collagen in tissues, and particularly in palatine tonsils, may be helpful in identifying persons susceptible to a.v.h.d.
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PMID:Collagen content in the heart of patients operated on for valvular heart disease caused mainly by infective endocarditis. 248 61

The effect of chronic hypoxia (barochamber, 8 h per day, 5 days a week, stepwise up to 7000 m) on some cardiac functional and metabolic parameters was compared in rats acclimatized either from the 4th day or the 12th week of postnatal life. Pulmonary hypertension and right ventricular enlargement were found in both age group. Whereas in young hypoxic animals the weight of the right ventricle increased linearly with the right ventricular pressure, in adult high altitude exposed rats this relation could not be proved. High altitude induced significant increase of concentration of collagenous proteins: in adult animals increased collagen III only, in young also collagen I. The changes of the energy metabolism were similar in both age groups: activity of enzymes of the lactate metabolism and glucose phosphorylation increased; on the other hand, catabolism of fatty acids decreased. Chronic hypoxemia significantly influenced also the myocardial metabolism in children with congenital heart disease; the aerobic capacity was decreased both in the atrial and ventricular tissue; atrial changes were even more pronounced. The type of changes was, however, different from the rat heart.
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PMID:The effect of chronic hypoxia on the developing cardiopulmonary system. 252 33

The accumulation of collagen within the myocardium is termed fibrosis. In left ventricular pressure overload a reactive interstitial fibrosis, having distinctive biochemical and structural features, is seen. This reactive fibrosis occurs in the absence of myocyte necrosis, is progressive in nature, and initially is an adaptive response that preserves the force generating capacity, or active (systolic) stiffness, of the hypertrophied myocardium. Later in hypertrophy a reparative (or replacement) fibrosis occurs in response to cell loss, the pathogenesis of which is not clear. Nevertheless, independently of cell loss, interstitial fibrosis can have a detrimental influence on the diastolic and systolic stiffness of the myocardium and can result in pathologic hypertrophy with heart failure. In established hypertrophy with disproportionate collagen matrix remodeling (ie, interstitial heart disease), it would be desirable to retard the continued formation of collagen and, if necessary, degrade collagen fibers that are responsible for impeding the stretching and shortening of muscle fibers. Prevention of interstitial fibrosis in pressure overload hypertrophy with pharmacologic agents with both antihypertensive and antifibrotic properties must also be considered. Future research should address these issues with a view toward developing corrective and preventative forms of therapy. Such advances will require a better understanding of cardiac fibroblast growth, collagen synthesis and the regulation of collagen gene expression in the heart.
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PMID:Myocardial collagen remodeling in pressure overload hypertrophy. A case for interstitial heart disease. 253 16

Composed of type I and III collagens, the valve leaflets, chordae tendineae and collagen matrix of the myocardium form a structural continuum. Synthesized by cardiac fibroblasts, these fibrillar collagens support and tether myocytes to maintain their alignment, whereas their respective tensile strength and resilience resist the deformation, maintain the shape and thickness, prevent the rupture and contribute to the passive and active stiffness of the myocardium. An acquired or congenital defect in this collagen network can lead to abnormalities in myocardial architecture, mechanics or valve function. In the hypertrophic process that accompanies a pressure overload, for example, increased collagen synthesis, fibroblast proliferation and a structural and biochemical remodeling of the matrix are seen. This includes distinctive patterns of reparative and reactive myocardial fibrosis, each of which alters diastolic and systolic myocardial stiffness and may lead to pathologic hypertrophy. Alternatively, a loss of collagen tethers or decline in matrix tensile strength can be responsible for regional or global transformations in myocardial architecture and function seen in the reperfused ("stunned") myocardium and in dilated (idiopathic) cardiopathy. Inherited disorders in the transcriptional and posttranslational processing of collagen can also alter the biophysical properties of the network. Future studies into collagen gene regulation, gene switching events and the control of collagen synthesis and degradation are needed to develop a more complete understanding of the relation between the collagen network and acquired and inherited forms of heart disease and to utilize therapeutics that will prevent, retard or regress abnormal collagen matrix remodeling.
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PMID:Cardiac interstitium in health and disease: the fibrillar collagen network. 265 24

Signal-averaged electrocardiography (ECG) was performed in 38 patients (mean age 38 years, range 15 to 70) with ventricular tachycardia who had no clinical evidence of structural heart disease. Spontaneous ventricular tachycardia was nonsustained in 23 patients and sustained in 15. None of the patients had symptoms of heart failure or ischemic heart disease, and at cardiac catheterization none had significant coronary artery disease or left ventricular wall motion abnormalities. In addition, all patients underwent left and right ventricular endomyocardial biopsy and ventricular stimulation studies. Signal-averaged ECG was performed and late QRS potentials were defined with use of Simson's method. Late QRS potentials were detected in a minority (18%) of patients including 2 of 23 with nonsustained and 5 of 15 with sustained (p = NS) ventricular tachycardia. Fifteen patients (40%) had abnormal endomyocardial biopsy results and these findings were more common in patients with sustained than in those with nonsustained ventricular tachycardia (9 of 15 versus 6 of 23, p less than 0.05). Late potentials were associated with abnormal endomyocardial biopsy findings (6 of 15 versus 1 of 23, p less than 0.01). An increase in fibrous tissue was the most frequent histopathologic abnormality; this increase was quantified by morphometric methods and compared with biopsy findings in normal control subjects. In the control group the proportion of collagen in relation to myocytes was less than 10%. All patients with both late potentials and abnormal biopsy findings had a greater than 15% ratio of collagen to myocytes in at least one specimen and the biopsies revealed marked interstitial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of signal-averaged electrocardiography in relation to endomyocardial biopsy and ventricular stimulation studies in patients with ventricular tachycardia without clinically apparent heart disease. 275 26

In a histological and fine structural study of right atrial biopsy specimens from 31 patients with rheumatic heart disease (RHD), aged 7 to 46 years, and 11 patients with congenital heart disease (CHD), aged 3 to 36 years, nerve fibers or endings were seen by electron microscopy in 11 specimens. There was concurrence of ordinary axons along with terminals bearing pale cholinergic or dark adrenergic synaptic vesicles. Smaller and denser cholinergic vesicles suggested proliferation followed by exhaustion of such nerve endings. The closest proximity of nerve terminal to muscle fiber was about 100 nm. In one RHD specimen a "specific terminal cell" was present between a nerve ending and muscle fiber; in another a possible neuromuscular contact was developing at the surface of a regenerating small muscle fiber with a few myofilaments. Unmyelinated axons amidst increased subendocardial and subepicardial collagen, with prominent fibroblasts and depleted muscle fibers, were seen more frequently in specimens of CHD. Loss of myofibrils and accumulation of mitochondria, with infrequent formation of lipofuscin bodies, characterized degenerating muscle fibers in CHD also, although to a lesser degree than in RHD (reported earlier, 1985). The myocardial blood vessels in CHD tended to have pale swollen endothelial cells and narrowed lumen. The most severely affected cases of CHD were those with (1) a very wide atrial septal defect (ASD), (2) ventricular septal defect (VSD) with vegetations near the defect, (3) infundibular pulmonary stenosis, and (4) Fallot's tetralogy.
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PMID:Fine structure of A: autonomic nerve fibers and terminals in human myocardium; and B: myocardial changes in congenital heart disease. 276 78

Between August 1982 and December 1986, 56 patients survived implantation of an extracardiac valved conduit for complex congenital heart disease. The mean age at operation was 4.2 years (16 days to 24 yrs) and the mean weight was 15.9 kg (2.4 to 93.0 kg). The diagnosis was pulmonary atresia (PA) with ventricular septal defect (VSD) in 13 patients, tetralogy of Fallot in 11, transposition of the great arteries (TGA) with VSD in 8, truncus arteriosus, in 7, complex left ventricular outflow tract obstruction (LVOTO) in 6, complex left atrioventricular valve obstruction in 4, double outlet right ventricle with VSD and subaortic obstruction in 3, univentricular heart with pulmonary stenosis in 2, TGA with LVOTO in 1, and PA with intact ventricular septum in 1. In 35 patients, a preclotted conventional Dacron conduit (CDC) with bioprosthetic valve was used, in 19 patients a collagen-sealed Tascon valved conduit (TC) was implanted, and in 1 patient an aortic homograft was used. In a mean follow-up of 32.5 months (9 to 64 mo), there were two deaths (2/56, 3.6%) that were not related to the conduit. All survivors have been evaluated by two-dimensional and Doppler echocardiography, and 29/56 (51.8%) underwent cardiac catheterization. Nine patients (9/56, 16.1%) underwent successful valved conduit replacement, in seven cases with a nonvalved conduit. There was a significant difference (P = .011) with regard to the incidence of conduit replacement between the group with CDC (2/36, 5.5%) and the group with TC (7/19, 36.8%). Five patients underwent percutaneous transluminal balloon dilatation of the prosthetic conduit, with adequate relief of the gradient in four patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term results after extracardiac valved conduits implanted for complex congenital heart disease. 298 53

The indications for endomyocardial biopsy were evaluated from 116 consecutive cases. The diagnostic value of this invasive but well tolerated procedure was in agreement with data from the literature. An accurate diagnosis, unforseeable in 8% of the patients, was established in 12%. The diagnosis of apparently primary myocardiopathy with ventricular dilatation was confirmed in 45 out of 59 cases; there were 3 cases of myocarditis, 3 cases of restrictive cardiopathy (haemochromatosis, fibroplastic endocarditis) and 1 case of hypertrophic cardiopathy. No tissue abnormality was noted in 6 cases. An accurate diagnosis was obtained by biopsy in 1 case of "eosinophilic lung" without overt cardiac involvement. In malignant diseases treated with anthracyclines in doses reaching maximal theoretical total dosage (30 patients), severe tissue lesions were present in 10% of the cases, incipient haemochromatosis in 16.6% and subendocardial fibrosis in 3.3%. However, total doses of up to 600 mg/m2 could be administered to 90% of the patients. Myocardial lesions could be demonstrated in 1 of 2 patients with collagen disease. Endomyocardial biopsy therefore seems to be justified in myocardiopathies with ventricular dilatation, in some collagen diseases with a tendency to cardiac involvement and to monitor treatment with anthracyclines in total doses higher than the theoretical maximum dosage.
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PMID:[Right intraventricular biopsy. Indications and results. 116 cases]. 315 91

We depict the histologic findings of ventricular aneurysms in 8 patients, 5 with Chagas heart disease and 3 secondary to myocardial infarction. Chagas disease and ischemic cardiopathy are the 2 conditions which show the highest incidence of ventricular aneurysms. The first one averages more than 60% in large series. The second one reveals ventricular aneurysms as a complication of myocardial infarction in 20-25% in large series. Both entities share identical hallmarks, and the same frequency of complications related to the presence of the aneurysms: vgr. sudden death, presence of malignant ventricular arrhythmias, thromboembolism, etc. Several histologic findings help to differentiate both conditions. Inflammatory cells, monocytes, eosinophils and lymphocytes interspersed within myocardial fibers, plus diverse lesions of myocytolysis point to a diagnosis of Chagas disease. We consider scar fibrosis as another capital difference to be observed in aneurysms of chagasic or ischemic origin. Fibrosis of ischemic origin is intense and early depending upon a quick stimulation of collagen I and III during the first days of myocardial infarction. Conversely, in Chagas disease the injury to the myofibrils by immunocomplexes is very slow and consequently collagen response will be slower and with lesser fibrotic response. We have previously considered in other publications this phenomenon after a geometrical-dynamical model have been designed for this purpose.
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PMID:[Histologic correlation of ischemic and chagasic ventricular aneurysms. Relation to physiopathology]. 321 6

Since infective endocarditis may affect individuals without pre-existing valvar heart disease, and Staphylococcus aureus is the organism most commonly involved, the binding characteristics of S aureus to several components of normal vascular endothelium and subendothelium were studied. S aureus adhered specifically to endothelial monolayers (6.08(1.10)%; p less than 0.005), fibronectin (5.43(0.81)%; p less than 0.001), fibrinogen (7.13(1.43)%; p less than 0.001), and acid soluble calf skin collagen (2.38(0.90)%; p less than 0.001). S aureus also adhered specifically to Von Willebrand factor (1.62(0.28)%, p less than 0.001). Protein A containing (Cowan I) and deficient (Wood) strains of S aureus adhered similarly to all surfaces and substrates (NS). Escherichia coli adhered poorly. Immunofluorescence microscopy of preconfluent endothelial cells identified an extensive pericellular fibronectin network at regions of cell to cell contact. Light microscopy showed S aureus binding solely within these regions. Therefore, the ability of S aureus to infect valvar endothelium may be dependent on the presence of a fibronectin receptor. The existence of specific receptor for S aureus on the endothelial cell surface itself remains undetermined.
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PMID:Bacterial tissue tropism: an in vitro model for infective endocarditis. 328 1


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