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Biomedical subjects

A E Becker

Publications and source records attributed to A E Becker.

At least 73 records · Page 4Linked to original sources
PubMed1997

Non-destructive assessment of 62 Dutch Björk-Shiley convexo-concave heart valves.

OBJECTIVE: Non-destructive assessment of 62 Björk-Shiley convexo-concave heart valves in view of the risk of fracture and possible detection of defects by means of X-ray or acoustics. METHODS: Scanning electron microscopy and stereomicroscopy of an unselected sample of valves, representing approximately 70% of the valves explanted between 1991 and 1996. Mean duration of implantation was 10.7 +/- 1.9 years. RESULTS: Six of the 62 valves had a fracture with disk escape. Of the remaining 56 valves, 11 (19.6%) had a single-leg fracture and seven (12.5%) showed a crack. Valves, 24 (42.8%), revealed no significant defect. After 4600 days of implantation, large valves (i.e. > or = 29 mm) showed a 6.7 time increase in the risk of crack or single-leg fracture compared with smaller valves (OR 6.7, 95% CI 1.8-24.6, P = 0.04). In a small in-vitro experiment with single-leg fracture, rapid smearing occurred, resulting in strut leg separation upon some movement. CONCLUSIONS: After approximately 400 x 10(6) cycles, 42.5% of the retrieved intact valves was without significant defect, while 32% had a serious prefracture defect. Time evolution from defect to fracture remains unpredictable. Also, detection of prefracture defects, including single-leg fracture, remains difficult, because a "well-detectable' fracture with dislocation is just a brief condition. However, technical knowledge can enhance the epidemiological and manufacturing information used for clinical decision making.

Equipment Failure Analysis↗
PubMed1997

Mitral valve prolapse and ventricular arrhythmias: observations in a patient with a 20-year history.

INTRODUCTION: Ventricular arrhythmias are a common feature in patients with mitral valve prolapse. In an attempt to determine the origin and underlying electrophysiologic mechanism, we describe a patient with ventricular fibrillation, exercise-induced ventricular tachycardia (VT), and, at the time of diagnosis, prolapse of the posterior mitral valve leaflet without mitral regurgitation. METHODS AND RESULTS: Treatment with beta-blockade and diphenylhydantoin prevented the occurrence of malignant ventricular arrhythmias for more than 17 years. Discontinuation of the therapy resulted in an immediate reappearance of the VT, which, despite the marked enlargement of the left ventricle (secondary to development of severe mitral valve regurgitation), had a strikingly similar morphology. For hemodynamic reasons, the patient was finally selected for valve replacement. Detailed pre-, peri-, and postoperative studies were performed, including administration of flunarizine, body surface mapping, construction of perioperative epicardial and endocardial maps, and studies of the excised muscles in vitro. CONCLUSIONS: Delayed afterdepolarization-induced triggered activity is the mechanism of VT in this mitral valve prolapse patient. The trigger is provided by isolated ventricular premature complexes elicited by a different electrophysiologic mechanism, possibly reentry, which is related to stretch and presumably to fibrosis of the papillary muscles.

Adult↗
PubMed1997

The Watanabe heritable hyperlipidemic rabbit is a suitable experimental model to study differences in tissue response between intimal and medical injury after balloon angioplasty.

The study evaluates whether the Watanabe heritable hyperlipidemic (WHHL) rabbit is an adequate model to study mechanisms that underlie differences in tissue response after postangioplasty injury. Postangioplasty studies of human coronary arteries have revealed that healing and restenotic processes differ depending on whether the laceration is limited to the atherosclerotic plaque or whether injury extends into the media. Forty-five homozygous WHHL rabbits underwent percutaneous transluminal angioplasty of the left subclavian artery. The inflated arterial segment was studied histologically at 3, 7, 14, 28, and 56 days, using conventional and immunohistochemical techniques to identify macrophages, smooth muscle cell (SMC) phenotypes, and cell proliferation. Electron microscopy was done to study reendothelialization. There were marked differences in response between those segments with medial injury and those with injury limited to the atherosclerotic plaque tissues. The latter category shows a distinct retardation in redifferentiation of SMCs, confirming previous observations in human coronary arteries. In these segments, moreover, cell proliferation occurred mainly in macrophages and spindle cells. Medial injury showed a more florid fibrocellular response, as in human coronary arteries, with cell proliferation initially confined to areas with dedifferentiated SMCs in the preexistent media and, once neointimal tissue was formed, among spindle cells also. The similarities with the repair processes encountered in postangioplasty human coronary arteries suggest that the WHHL rabbit is an adequate model to study differences in the response related to different types of angioplasty injury.

Angioplasty, Balloon↗
PubMed1996

C-type natriuretic peptide in human coronary atherosclerotic lesions.

BACKGROUND: C-type natriuretic peptide (CNP) belongs to the natriuretic peptide family and is considered to have regulatory effects on vascular tone and smooth muscle growth. Since these features play a role in atherogenesis, the presence of CNP at such sites was studied. METHODS AND RESULTS: Thirty-three coronary artery segments were harvested at autopsy: 10 normal, with diffuse intimal thickening, and 23 atherosclerotic lesions. Samples were snap-frozen and processed for immunohistochemical staining. For the identification of CNP, a mouse monoclonal antibody (KY-CNP-1) was used. 1A4, EBM-11 (CD68), and von Willebrand factor antibodies were used to stain smooth muscle cells, macrophages, and endothelial cells, respectively. CNP is present in several cell types. Normal arterial segments show CNP-positive endothelial cells. Hypercellular atherosclerotic lesions show distinct CNP positivity of smooth muscle cells and macrophages but a decrease in positivity of endothelial cells. Advanced atherosclerotic lesions contain CNP-positive macrophages, but the smooth muscle cells within the fibrous cap and the surface endothelial cells are almost all CNP-negative. CONCLUSIONS: These observations suggest that CNP has functional significance in atherogenesis.

Adolescent↗
PubMed1996

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success.

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.

Adult↗
PubMed1996

Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics.

BACKGROUND: Previous work has demonstrated that cells with AV nodal-type action potentials are not confined to Koch's triangle but may extend along the AV orifices. The aim of this study was to examine the histological and electrophysiological characteristics of this tissue. METHODS AND RESULTS: Studies were performed in isolated, blood-perfused dog and pig hearts. Microelectrode recordings revealed cells with nodal-type action potentials around the tricuspid and mitral valve rings. These cells were found within 1 to 2 mm of the valve annuli. A zone of cells with intermediate action potentials, approximately 1 cm wide, separated cells with nodal-type action potentials from cells with atrial-type action potentials in the body of the atria. In cells with nodal-type action potentials, adenosine caused a reduction in action potential amplitude (49 +/- 2 versus 33 +/- 2 mV, mean +/- SE; P < .001), upstroke velocity (2.5 +/- 0.2 versus 2.0 +/- 0.2 V/s, P < .05), and duration (150 +/- 4 versus 96 +/- 8 ms, P < .001). The light microscopic appearance of AV junctional cells was similar to that of myocytes in the body of the atrium. A polyclonal antibody raised against connexin-43 bound to atrial and ventricular tissue but not to the AV junctional tissue or AV nodal region. The absence of connexin-43 correlated with the sites of cells with nodal-like action potentials. With pacing techniques, the AV junctional tissue in the region of the posterior AV nodal approaches could be electrically dissociated from atrial, AV nodal, and ventricular tissue. AV nodal echoes were induced with ventricular pacing in three dog hearts. In each case, retrograde conduction was through the slow pathway, and anterograde conduction was through the fast pathway. During echoes, activation of AV junctional cells preceded atrial activation during retrograde slow pathway conduction, but these cells were not activated during anterograde fast pathway conduction. CONCLUSIONS: AV junctional cells around both annuli are histologically similar to atrial cells but resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin-43. The light microscopic appearance of AV junctional cells is a poor guide to their action potential characteristics. The AV junctional cells in the posterior AV nodal approaches appear to participate in slow pathway conduction. These cells may be the substrate of the slow "AV nodal" pathway.

Action Potentials↗
PubMed1996

A newly recognized autosomal dominant limb girdle muscular dystrophy with cardiac involvement.

Sixty-five members of three families with limb girdle muscular dystrophy (LGMD) underwent neurological, cardiological, and ancillary investigations. Thirty-five individuals were diagnosed as having slowly progressive autosomal dominant LGMD. Symmetrical weakness started in the proximal lower limb muscles, and gradually upper limb muscles also became affected. Early contractures of the spine were absent. Contractures of elbows and Achilles tendons were either minimal or late. Serum creatine kinase activity was normal to moderately elevated. Electromyogram and muscle biopsy were consistent with a mild muscular dystrophy. Cardiological abnormalities, found in more than one-half the patients, included dysrhythmias and atrioventricular (AV) conduction disturbances presenting as bradycardia, syncopal attacks necessitating pacemaker implantation, and sudden cardiac death. There was a significant relation between the severity of AV conduction disturbances and age. In nearly all patients, neuromuscular symptomatology preceded cardiological involvement. The early recognition of this previously not described, autosomal dominant LGMD with life-threatening cardiac involvement offers an opportunity for therapeutic intervention.

Adolescent↗
PubMed1996

The use of enhanced polymer one-step staining reagents for immunoenzyme double-labelling.

The newly developed peroxidase-labelled Enhanced Polymer One-Step (EPOS) reagents were applied, together with an unlabelled primary mouse antibody, in a multistep double-labelling protocol. Enzyme label reporter combinations consisted of either peroxidase and alkaline phosphatase in red and blue, respectively, or beta-galactosidase and alkaline phosphatase in turquoise and red, respectively. The latter enzyme combination was introduced using a rabbit antiperoxidase antibody and an enzyme-labelled anti-rabbit immunoglobulin antibody. The multistep procedure was tested using five different antibody combinations on cryostat and Carnoy- or formalin-fixed, paraffin-embedded sections. In each instance, clear and distinct labelling was obtained, either with the two antigens at separate sites, or with an overlap in distribution. In the latter situation, the sites of co-localization were marked by mixed colours, which were distinct and readily discriminated from the two basic colours.

Animals↗
PubMed1996

Three-dimensional echocardiography of normal and pathologic mitral valve: a comparison with two-dimensional transesophageal echocardiography.

OBJECTIVES: This study was done to ascertain whether three-dimensional echocardiography can facilitate the diagnosis of mitral valve abnormalities. BACKGROUND: The value of the additional information provided by three-dimensional echocardiography compared with two-dimensional multiplane transesophageal echocardiography for evaluation of the mitral valve apparatus has not been assessed. METHODS: Thirty patients with a variety of mitral valve pathologies (stenosis in 8, insufficiency in 12, prostheses in 10) and 20 subjects with a normal mitral valve were studied. Images were acquired using the rotational technique (ever 2 degrees), with electrocardiographic and respiratory gating. From the three-dimensional data sets, cut planes were selected and presented in both two-dimensional format (anyplane echocardiography) and volume-rendered dynamic display. The data were compared with the original multiplane two-dimensional images. Different features of the mitral valve apparatus were defined and graded by three observers for clarity of visualization and confidence of interpretation as 1) inadequate, 2) sufficient, or 3) excellent. RESULTS: All the techniques provided good visualization of the mitral valve (mean global scores +/- SD for multiplane, anyplane and volume-rendered echocardiography were 2.22 +/- 0.34, 2.24 +/- 0.26 and 2.30 +/- 0.25, respectively). With volume-rendered echocardiography, the mitral valve apparatus was scored higher in pathologic than in normal conditions (2.38 +/- 0.24 vs. 2.16 +/- 0.21, p < 0.002). The spatial relationships between the mitral valve and other structures, leaflet mobility, commissures and orifice were scored higher by volume-rendered echocardiography. Prostheses were evaluated equally well by the three methods. Multiplane and anyplane echocardiography were superior for the evaluation of leaflet thickness, subvalvular apparatus and annulus. CONCLUSIONS: Transesophageal three-dimensional echocardiography facilitates imaging of some features of the mitral valve apparatus and provides additional information for comprehensive assessment of mitral valve abnormalities.

Echocardiography↗
PubMed1996

Expression of platelet derived growth factor B chain and beta receptor in human coronary arteries after percutaneous transluminal coronary angioplasty: an immunohistochemical study.

OBJECTIVE: To evaluate whether expression of platelet derived growth factor B (PDGF-B) protein is associated with expression of its receptor protein in human coronary arteries after angioplasty and to identify cells involved. BACKGROUND: PDGF is considered an important growth factor in the repair process of the vessel wall after angioplasty. In situ hybridisation has revealed expression of PDGF-A and -B chain messenger ribonucleic acid (mRNA) in human coronary arteries at sites of postangioplasty injury. METHODS: Target and non-target sites of eight coronary arteries were studied immunohistochemically for PDGF-B and PDGF-beta receptor proteins in relation to macrophages, T lymphocytes, smooth muscle cells, and HLA-DR positive cells. RESULTS: The PDGF-B and PDGF-beta receptor proteins were expressed in areas with distinct repair, containing alpha actin negative spindle cells, macrophages and, at later stages, alpha actin positive smooth muscle cells as well. When the neointima was composed mainly of alpha actin smooth muscle cells, PDGF-B expression was rare and PDGF-beta receptor expression was negative. CONCLUSIONS: There is expression of PDGF-B and PDGF-beta receptor proteins at sites of postangioplasty repair in human coronary arteries. The associated cells are mainly macrophages and alpha actin negative spindle cells; the latter may be dedifferentiated smooth muscle cells. A link between PDGF expression and the postangioplasty time interval suggests a relation with cell differentiation as part of the maturation of the repair tissue. Mutual expression of both the growth factor and its receptor protein strongly suggests that in humans a PDGF mediated repair process occurs, with involvement of smooth muscle cells and macrophages.

Aged↗
PubMed1996

Clinically stable angina pectoris is not necessarily associated with histologically stable atherosclerotic plaques.

OBJECTIVE: To investigate the extent of plaque inflammation in culprit lesions of patients with chronic stable angina. DESIGN: Retrospective study. SETTING: Amsterdam reference centre. SUBJECTS: 89 consecutive patients who underwent directional coronary atherectomy, 58 of whom met the following inclusion criteria: chronic stable angina (Canadian Cardiovascular Society classification 1-3 (group 1, n = 28)); unstable angina (Braunwald class II (group 2, n = 18)); unstable angina (Braunwald class III (group 3, n = 12)). INTERVENTIONS: Directional atherectomy in patients with angina pectoris. MAIN OUTCOME MEASURES: Tissue areas of culprit lesions occupied by inflammatory cells and smooth muscle cells related to clinically defined ischaemic syndrome. RESULTS: Areas (% of total surface area (mean (SEM)) rich in smooth muscle cells were larger in patients with chronic stable angina (group 1, 51.2 (20.9)) than in those with unstable angina (group 2, 42.1 (20.5); group 3, 29.5 (19.4)) (1 v 2 and 2 v 3, NS; 1 v 3, P < 0.004). Macrophage rich areas were significantly smaller in patients with stable angina (group 1, 21.8 (11.9)) than in those with unstable angina (group 2, 31.5 (14.6); group 3, 46.4 (16.7)) (1 v 2, P < 0.02; 2 v 3, P < 0.02; 1 v 3, P < 0.001). Mean numbers of T cells per mm2 were as follows: group 1, 17 (9.4); group 2, 25 (15.9); group 3, 41 (30.6) (1 v 2, P 0.04; 2 v 3, P 0.07; 1 v 3, P < 0.001). Areas with HLA-DR positive cells showed the same pattern as macrophages and T cells and were smaller in stable (29.9 (12.4)) than in unstable angina (group 2, 40.4 (17.6); group 3, 52.4 (12.0)) (1 v 2, P < 0.02; 2 v 3, P < 0.05; 1 v 3, P < 0.001). CONCLUSION: The inverse relation between the extent of inflammatory activity in plaque tissues of culprit lesions and the clinical stability of the ischaemic syndrome supports the concept that reduction of inflammation favours plaque stabilisation. At the same time, the considerable overlap between groups indicates that patients with clinically stable angina do not all have histologically stable plaques.

Angina Pectoris↗
PubMed1996

In situ detection of platelet-derived growth factor-A and -B chain mRNA in human coronary arteries after percutaneous transluminal coronary angioplasty.

Experimental studies have shown that platelet-derived growth factor (PDGF) plays a role in wound-healing processes after angioplasty. In humans, after percutaneous transluminal coronary angioplasty (PTCA), this has not yet been documented. Six coronary arteries of five patients who died after PTCA were studied. The angioplasty sites were sliced serially, and the slices were studied using immunocytochemistry and in situ hybridization. Monoclonal antibodies were directed against muscle actin, vimentin, macrophages, and endothelium. In situ hybridization was performed using a synthetic oligonucleotide probe complementary to the PDGF-A and -B chain mRNAs. The identification of cells was based on a comparison with immune-stained sections. Positive autoradiographic signals for PDGF-A and -B chain mRNAs were found at the site of the PTCA injury and related to areas that contained macrophages, spindle cells, smooth muscle cells, and endothelial cells of neovascularization. In humans, both PDGF-A and -B chain mRNAs are expressed at sites of PTCA injury. The expression relates to the reparative response, and it appears that the cells involved are macrophages, spindle cells, smooth muscle cells, and endothelial cells of neovascularization. This is the first study to document the expression of PDGF-A and -B mRNAs at sites of repair in human coronary arteries after PTCA. It suggests strongly that PDGF is involved in the repair process after PTCA.

Aged↗
PubMed1996

Multiple labeling in electron microscopy: its application in cardiovascular research.

The heart is a muscular pump kept together by a network of extracellular matrix components. An increase in collagens, as in chronic congestive heart failure (CHF), is thought to have a negative effect on cardiac compliance and, thus, on the clinical condition. Conventional electron microscopy allows for the study of cellular and extracellular components and scanning electron microscopy (SEM) can put these structures in three-dimensional perspective. However, in order to study extracellular matrix components in relation to cells, immunoelectron microscopy is superior. We have used this technique in our studies on heart failure. Heart specimens were fixed in 4% paraformaldehyde and 0.1% glutaraldehyde in sodium cacodylate buffer, dehydrated by the method of progressive lowering of temperature and embedded in LR Gold plastic. Immunolabeling could be achieved with different sized gold-conjugated secondary antibodies or protein-A gold conjugates. Depending on the objective, ultra small gold (USG) conjugates or a regular probe size can be used. Labeling efficiency could be increased by bridging antibodies. The double and triple staining procedures were based on single staining methods using one- and two-face labeling. The choice of antibodies and gold conjugates depended on the objectives. Immunoelectron microscopy, using multiple labeling, allowed a detailed study of the organization of the extracellular matrix and its relationship with cardiac myocytes. This may prove to be a useful tool for the study of chronic heart failure.

Actins↗
PubMed1995

Chronic congestive heart failure is associated with a phenotypic shift of intramyocardial endothelial cells.

BACKGROUND: There is evidence that patients with chronic congestive heart failure have endothelial cell-related abnormalities of the peripheral circulation and the coronary microvasculature. For that reason, we have studied the phenotypic expression of endothelial cells in hearts of patients with congestive heart failure. METHODS AND RESULTS: We studied cardiac explants (n = 19) and autopsy hearts (n = 5) of patients with chronic congestive heart failure caused by either a dilated cardiomyopathy (n = 12) or ischemic heart disease (n = 12) and compared them with normal hearts (n = 12). The antigenic expression obtained with several endothelial cell markers (factor VIII-related antigen, EN-4, Ulex europaeus agglutinin-1 (UEA-1), PAL-E, endoglin, and endothelin) and adhesion molecules (intercellular adhesion molecule [ICAM], vascular cell adhesion molecule [VCAM], or E-selectin) was compared by use of immunohistochemical techniques. On the basis of the initial findings, the number of PAL-E- and EN-4-positive vessels was counted. The incidence of PAL-E-positive vessels per area was quantified and related to the percentage of heart muscle cells and the total number of vessels per area. In control hearts, endothelial cells rarely were positive for PAL-E. In hearts of patients with ischemic cardiomyopathies, there was distinct staining with this marker. Hearts of patients with dilated cardiomyopathies showed a marked increase in the number of PAL-E-positive endothelial cells. Vessels with a muscular media were PAL-E-negative. Two-sample analysis revealed a statistically significant difference between hearts with dilated cardiomyopathies and ischemic cardiomyopathies (P < .01), between hearts with dilated cardiomyopathies and control hearts (P < .01), and between hearts with ischemic cardiomyopathies and control hearts (P < .01). Endoglin and ICAM were positive but nondiscriminating. Endothelin, VCAM, and E-selectin were negative. CONCLUSIONS: A phenotypic shift in endothelial antigen expression of the coronary microvasculature occurs in both ischemic hearts and hearts with dilated cardiomyopathies, as revealed by PAL-E, compared with control hearts. The change may relate to compensatory mechanisms in long-standing chronic heart failure.

Adult↗
PubMed1995

Nature of coarctation in hypoplastic left heart syndrome.

The study was designed to establish the underlying pathology of aortic coarctation in hypoplastic left heart syndrome. Aortic coarctation in patients with hypoplastic left heart syndrome is a significant problem when a Norwood procedure or heart transplantation is performed. Previous reports have claimed that the obstruction was merely a branch-point phenomenon and that ductal tissue was absent. Five heart specimens with hypoplastic left heart syndrome and aortic coarctation were examined histologically. The distal segment of the aortic arch, together with the arterial duct, were dissected and processed en bloc. The blocks were sectioned parallel to the longitudinal axis of the aortic arch. In 4 hearts the coarctation was in the preductal position. Ductal tissue encircled the aortic lumen and extended into the aorta both proximally and distally from the ductal orifice. The fifth case showed medial thickening of the aortic wall in the preductal position, but without ductal tissue. The arterial duct showed histologic characteristics of persistent patency. Our observations suggest that aortic coarctation in the preductal position in hypoplastic left heart syndrome is caused by the extension of ductal tissue. The findings may have an impact on clinical strategies for hypoplastic left heart syndrome.

Angioplasty, Balloon↗
PubMed1995

Autologous glutaraldehyde-treated pericardial valved conduit: an experimental study.

Extracardiac conduits in the form of allografts and synthetic tubes containing heterograft valves have been used widely in the management of ventricular outflow abnormalities and for establishing ventriculoarterial continuity. These procedures are limited by long-term calcification as well as by formation of neointimal peel, necessitating reoperation. In an effort to continue the search for an alternative conduit, we designed and evaluated a valved sinus-bearing conduit fashioned out of autologous pericardium treated with glutaraldehyde. The construction of the conduit is described. The results of implantation of these conduits in 12 sheep showed no progression of gradients, fresh regurgitation, or evidence of wall or cusp calcification 9 months after implantation.

Animals↗
PubMed1995

Dilated cardiomyopathy is associated with an increase in the type I/type III collagen ratio: a quantitative assessment.

OBJECTIVES: The aim of this study was to quantify total collagen and the type I/type III collagen ratio and their localization in hearts with dilated cardiomyopathy. BACKGROUND: Patients with dilated cardiomyopathy have an increase in intramyocardial fibrillar collagen. Types I and III are the main constituents and have different physical properties that may affect cardiac compliance. METHODS: Nineteen hearts with dilated cardiomyopathy were studied (17 cardiac explants, 2 hearts obtained at autopsy) and compared with reference hearts. Total collagen was determined by hydroxyproline analysis. Collagen types I and III were analyzed using the cyanogen bromide method and immunohistochemical analysis followed by microdensitophotometric quantification. Localization of collagen types I and III was established at the light and electron microscopic levels. Immunoelectron microscopy provided information regarding their localization. RESULTS: Total collagen and the collagen type I/type III ratio were increased in hearts with dilated cardiomyopathy (p < 0.05). Electron microscopy showed a diffuse increase in collagen fibrils in the endomysium; the perimysium showed an inhomogeneous increase. Collagen fibrils were thicker, and fibrous long-spacing collagen occurred in the endomysium. Immunoelectron microscopic findings confirmed an increase in type I collagen. CONCLUSIONS: Hearts with dilated cardiomyopathy have a statistically significant increase in the collagen type I/type III ratio. The changes occur in the endomysium and perimysium, although with differences in distribution. These changes in intramyocardial collagen may be clinically relevant because they may affect cardiac rigidity and, therefore, eventually may render the heart less compliant. Further studies are needed to evaluate at what point in the course of the disease these changes appear.

Adolescent↗