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Biomedical subjects

A E Becker

Publications and source records attributed to A E Becker.

At least 55 records · Page 3Linked to original sources
PubMed1998

The surgical anatomy of the left ventricular outflow tract in hearts with ventricular septal defect and aortic arch obstruction.

BACKGROUND: Profound understanding of the left ventricular outflow tract (LVOT) anatomy is crucial to improve surgical results in patients with aortic arch obstruction, ventricular septal defect, and subaortic stenosis. METHODS: We studied the morphology of the LVOT in 32 postmortem hearts with aortic arch obstruction and a ventricular septal defect. In case of subaortic obstruction, the length of the subaortic muscular component was measured anteriorly and posteriorly within the left ventricle. RESULTS: Seven of the 32 hearts had no subaortic stenosis. Nine had aortic override, which caused LVOT narrowing. Sixteen hearts contained a subaortic shelf, downstream to the ventricular septal defect, which deviated into the left ventricle in 15. In 10 of these the shelf was muscular; in 6 it was a fibrous ridge. In cases with a muscular shelf, the posterior part was significantly shorter than the anterior part (p < 0.004). In 9 hearts the LVOT was further narrowed because of the abnormal relationship between the mitral valve and the subaortic shelf. CONCLUSIONS: The present study confirms the complexity of LVOT stenosis in aortic arch obstruction and ventricular septal defect and provides a better understanding of the options to achieve surgical relief.

Aorta, Thoracic↗
PubMed1998

Interventricular communication in complete atrioventricular septal defect.

BACKGROUND: Little attention has been paid to whether the interventricular communication in complete atrioventricular septal defect is different beneath the superior and inferior bridging leaflets, a feature of obvious surgical significance. METHODS: We searched for a defect under the bridging leaflets and examined the valve morphologies in 98 autopsied and 86 surgical patients. Of the overall specimens, 27 were associated with Fallot's tetralogy, and a further 20 had subaortic stenosis, aortic coarctation, or both. In the autopsied specimens, we also measured the degree of deficiency of the ventricular septum. RESULTS: No communication was found under the inferior bridging leaflet in 30% (29 of 98) of the specimens. All 29 hearts except two without such communications showed an undivided inferior leaflet. In contrast, all patients undergoing operation except 1 had a communication beneath both bridging leaflets (p < 0.001). The absence of a communication beneath the inferior leaflet was observed more in hearts with Fallot's tetralogy (seven of 14) or those with subaortic stenosis, aortic coarctation, or both (eight of 18) than in those without associated anomalies (14 of 66; p < 0.01). Those with a communication under the inferior leaflet showed a greater deficiency of the inlet ventricular septum than did those without it (p < 0.001). CONCLUSIONS: In a certain percentage of patients with complete atrioventricular septal defect, there will be no communication under the inferior bridging leaflet. Surgeons should be aware of this possibility, particularly when confronted with a patient with obstruction in either ventricular outlet.

Child↗
PubMed1998

Conotruncal repair for tetralogy of Fallot: midterm results.

OBJECTIVE: Because of the left-sided location of the main atrioventricular conduction axis, the membranous flap can be safely used for closure of the ventricular septal defect in tetralogy of Fallot. METHODS: Conotruncal repair consists of (1) precise closure of the defect using the membranous flap and (2) outflow reconstruction of the right ventricle by a wide monocusp patch. This method has been followed in 233 patients from October 1985 to March 1997. The age of patients ranged from 2 months to 53 years, with a mean of 4.6 years; 44% were younger than 2 years of age, and 11% were less than 12 months of age. RESULTS: A membranous flap was present in 86%, 12% had a muscle bar between the defect and the tricuspid valve, and only 2% had neither a membranous flap nor a muscle bar. There was no early death; two late deaths occurred over a mean follow-up period of 7.3 years. The actuarial survival was 99.1%. No patients required reoperation except for two with residual anomalously connecting pulmonary veins. All 233 patients were in sinus rhythm postoperatively. No patient has had a significant residual defect. The mobility of the polytetrafluoroethylene monocusp was echocardiographically detected in 85% and pulmonary regurgitation was less than mild in 82% at the late phase. The late right and left ventricular pressure ratio was 0.40 +/- 0.14 (n = 30) and the late central venous pressure was 5.6 +/- 2.2 mm Hg (n = 30). CONCLUSION: Conotruncal repair has provided good midterm results with a low central venous pressure, well-reconstructed outflow tract of the right ventricle, no residual defect, and no heart block.

Actuarial Analysis↗
PubMed1998

Morphometric analysis of atrioventricular septal defect with common valve orifice.

OBJECTIVES: We sought to analyze morphometric features of atrioventricular septal defect (AVSD) in autopsy specimens and to consider the developmental implications of obstruction in either ventricular outflow tract. BACKGROUND: Left ventricular outlet obstruction (LVO) is more prevalent in patients with Rastelli type A morphology. When tetralogy of Fallot (ToF) complicates this malformation, there is usually a free-floating superior bridging leaflet. The reasons for these associations are uncertain. METHODS: In 133 hearts with AVSD and common atrioventricular (AV) valve orifice, we measured the degrees of horizontal and anterior deviation of the great arteries from the AV valve, the diameters of the ventricular outlets and the great arteries and the degree of deficiency of the ventricular septum. RESULTS: In Rastelli type A morphology, the great arteries were deviated more leftward than in type C morphology (p < 0.01). Type A hearts also had a relatively small aorta, with a long and narrow subaortic tract. The presence of obstruction in either ventricular outlet was associated with a more oblique arrangement of the great arteries, with the pulmonary trunk being more leftward than in hearts without LVO (p < 0.01). In combination with ToF, the aorta was dextroposed and the pulmonary trunk was located more posteriorly (p < 0.01). No heart with type A morphology showed ToF (p < 0.01). CONCLUSIONS: The geometric arrangement of the great arteries correlated significantly with obstruction in either ventricular outflow tract and with the Rastelli subtypes. Malrotation of the developing outlet septum may be an embryologic factor producing obstruction, with horizontal deviation of the outlets also influencing the morphology of the superior bridging leaflet.

Aorta↗
PubMed1998

Mast cell infiltration in acute coronary syndromes: implications for plaque rupture.

OBJECTIVES: To define the role of mast cells in plaque destabilization. BACKGROUND: Inflammation is an essential feature of human coronary plaques. Macrophages and T lymphocytes are considered to contribute to destabilization of the plaques. The role of mast cells in this setting is less well studied. We therefore counted the mast cells in coronary atherectomy specimens from patients with chronic stable angina, unstable angina and severe unstable angina. METHODS: Patients studied had chronic stable angina (group 1, n=11), "stabilized" unstable angina (group 2; Braunwald's class I and II, n=11) and "refractory" unstable angina (group 3; Braunwald's class III, n=7). Samples of culprit lesions (n=29) were obtained by directional atherectomy, snap-frozen and analyzed immunohistochemically. The numbers of mast cells and T lymphocytes per square millimeter squared were counted and the areas containing macrophages and smooth muscle cells were measured by computed planimetry. RESULTS: We found that the numbers of mast cells and T lymphocytes increased from group 1 through groups 2 to 3. Specimens from group 3 also contained the largest numbers of tumor necrosis factor alpha (TNF-alpha)-positive mast cells and of matrix metalloproteinase (MMP)-9 (92 kD gelatinase)-positive macrophages. CONCLUSIONS: Unstable coronary syndromes are associated with increased numbers of mast cells in culprit lesions. Activated mast cells secrete neutral proteases capable of degrading the extracellular matrix and TNF-alpha, capable of stimulating macrophages to synthesize MMP-9. Our observations suggest that mast cells, in addition to macrophages, contribute to matrix degradation and, hence, to progression of coronary syndromes.

Adult↗
PubMed1998

Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox.

OBJECTIVE: To relate local arterial geometry with markers that are thought to be related to plaque rupture. BACKGROUND: Plaque rupture often occurs at sites with minor luminal stenosis and has retrospectively been characterized by colocalization of inflammatory cells. Recent studies have demonstrated that luminal narrowing is related with the mode of atherosclerotic arterial remodeling. METHODS: We obtained 1,521 cross section slices at regular intervals from 50 atherosclerotic femoral arteries. Per artery, the slices with the largest and smallest lumen area, vessel area and plaque area were selected for staining on the presence of macrophages (CD68), T-lymphocytes (CD45RO), smooth muscle cells (alpha-actin) and collagen. RESULTS: Inflammation of the cap or shoulder of the plaque was observed in 33% of all cross sections. Significantly more CD68 and CD45RO positive cells, more atheroma, less collagen and less alpha-actin positive staining was observed in cross sections with the largest plaque area and largest vessel area vs. cross sections with the smallest plaque area and smallest vessel area, respectively. No difference in the number of inflammatory cells was observed between cross sections with the largest and smallest lumen area. CONCLUSION: Intraindividually, pathohistologic markers previously reported to be related to plaque vulnerability were associated with a larger plaque area and vessel area. In addition, inflammation of the cap and shoulder of the plaque was a common finding in the atherosclerotic femoral artery.

Actins↗
PubMed1998

Retrieval analysis of mechanical heart valves: impact on design and clinical practice.

Explanted mechanical heart valves were examined nondestructively, and the findings were related to guidelines, technical reports, and other information to judge the risk of failure and its possible impact on valve design and clinical practice. Diagnoses for single valves could be made, but risks and rates of failure for patient populations could not be predicted due to insufficient information concerning the manufacturing process and valve and patient numbers. Based on the results of this study and the principle that decisions on recalls and patient counseling must be based on scientific knowledge rather than on wait and see policies, the following is recommended: registration of all implanted valves, follow-up of a large cohort of valve carriers, comparison of wear test results of preimplant and postretrieval valves, maintenance of a reference stock of valves and materials, and submission of failure scenarios to certifying bodies.

Guidelines as Topic↗
PubMed1998

Koch's triangle sized up: anatomical landmarks in perspective of catheter ablation procedures.

Koch's triangle contains the compact part of the atrioventricular node and is anatomically delineated by the Eustachian ridge, the membranous septum, and the insertion of the tricuspid valve. Inferiorly, Koch's triangle ends at the site of the os of the coronary sinus and, in part, is continuous with the sub-Eustachian pouch. Catheter ablation procedures for several types of reentrant tachycardias are based on identifying these anatomical landmarks. Variability in the dimensions of Koch's triangle thus may be clinically relevant. We examined 50 hearts. Anatomical landmarks measured were the Eustachian ridge, the tricuspid valve, the overall length between the membranous septum and the coronary sinus, the width of the coronary sinus, the Eustachian ridge in its roof and the distance to the tricuspid valve, and that of the sub-Eustachian pouch. Individual variations were marked. The mean values (+/- SD) were: Eustachian ridge 29.4 +/- 5.3 mm, tricuspid valve 28.9 +/- 4.5 mm, coronary sinus 10.8 +/- 2.2 mm, Eustachian ridge 3.7 +/- 2.3 mm, space underneath coronary sinus 8.6 +/- 3.4 mm, and sub-Eustachian pouch 26.8 +/- 3.3 mm. The overall length varied between 15 and 38 mm, with a mean of 26.3 +/- 4.5. In conclusion, Koch's triangle shows considerable individual variations in size. Given the fact that the absolute figures for the range in size of the compact atrioventricular node is much less than that of Koch's triangle, these variations have implications for catheter ablation procedures.

Adult↗
PubMed1998

Recent activation of the plaque immune response in coronary lesions underlying acute coronary syndromes.

OBJECTIVE: To discriminate between chronic inflammation and acute activation of the plaque immune response in culprit lesions of patients with acute coronary syndromes. DESIGN: Retrospective study. SETTING: Tertiary referral centre. SUBJECTS: 71 patients having coronary atherectomy were classified according to their ischaemic syndrome: stable angina (n = 23); stabilised unstable angina (n = 18); refractory unstable angina (n = 11); and acute myocardial infarction (n = 19). MAIN OUTCOME MEASURES: Immunohistochemical measurement of interleukin 2 receptor (IL-2R) (CD25) positive cells expressed as a percentage of the total amount of (CD3 positive) T lymphocytes in frozen sections of atherectomy specimens. RESULTS: The number of lesions containing IL-2R (CD25) positive T cells increased with severity of the ischaemic coronary syndrome (stable angina, 52%; stabilised unstable angina, 77.8%; refractory unstable angina, 90.9%; acute myocardial infarction, 89.4%). The percentage of activated T cells (CD25/CD3 ratios x100) increased in lesions associated with refractory unstable angina (7.8%) and acute myocardial infarction (18.5%), compared with those in lesions associated with either chronic stable angina (2.2%) or stabilised unstable angina (3.3%). CONCLUSIONS: An increase in the percentage of IL-2R positive T lymphocytes in culprit lesions of patients with acute coronary syndromes indicates recent activation and amplification of the immune response within plaques. This may result in a burst of inflammatory products with tissue degrading and vasoactive properties and, hence, could initiate or accelerate the onset of an acute coronary event.

Angina Pectoris↗
PubMed1997

Upregulation of angiotensin-converting enzyme during the healing process after injury at the site of percutaneous transluminal coronary angioplasty in humans.

BACKGROUND: Balloon injury models in rat have shown enhanced expression of ACE in the developing neointima. However, neointimal lesions in human coronary arteries are complex due to atherosclerosis and different types of wall laceration. This study was designed to investigate whether ACE is present in the neointima of humans, including patients with restenosis after percutaneous transluminal coronary angioplasty (PTCA). METHODS AND RESULTS: Thirty-seven sites with angioplasty injury, obtained at autopsy, were studied using immunocytochemical techniques. Sites with injury limited to a fibrous plaque and those with injury extending into the media (<2 months after PTCA) showed fibrocellular repair tissue composed mainly of smooth muscle cells that were distinctly positive for ACE. In cellular reactions at the site of injury limited to the atheromatous plaque (<2 months after PTCA), the expression of ACE appeared first in accumulated macrophages; once smooth muscle cells appeared in the repair tissue, they also expressed ACE. At a later stage (3 months after PTCA), the number of cells with ACE expression decreased markedly; from 7 months on, ACE was no longer expressed within the repair tissue. Basically, there were no differences with regard to ACE expression during the healing process after PTCA between segments with and those without angiographic evidence of restenosis. CONCLUSIONS: These results show that PTCA injury in humans results in upregulation of ACE at sites of active repair and, therefore, ACE could play an important role as one of the mediators of the healing process after PTCA.

Aged↗
PubMed1997

Subacute narrowing of the left main coronary artery following directional atherectomy for proximal obstructive coronary artery disease.

Directional atherectomy is an alternative device for treatment of highly eccentric or proximal coronary lesions considered less suitable for balloon angioplasty. We report a patient with exuberant neointimal proliferation, extending into the left main coronary artery, following directional atherectomy of the proximal target site in the left circumflex artery. This observation indicates that patients with mild left main disease have an increased risk to develop this complication following directional atherectomy.

Aged↗
PubMed1997

Hypoplastic aortic arch morphology pertinent to growth after surgical correction of aortic coarctation.

BACKGROUND: Whether a hypoplastic transverse arch will grow after successful coarctectomy remains controversial. METHODS: We studied 15 coarctation specimens with hypoplastic transverse arch. Eight patients were less than 1 month old and 7 were between 1 and 3 months. The diameter and length of the various segments of the aortic arch were measured. The number of elastin lamellae was determined histologically. Collagen density was quantified with a microdensitophotometer. Using immunohistochemistry, we determined alpha-actin-positive smooth muscle cells in the media of the ascending aorta and the hypoplastic transverse arch. RESULTS: Despite a hypoplastic transverse arch, the ascending and descending aorta grew. The absolute number of elastin lamellae in the hypoplastic transverse arch was low, but when expressed as a ratio versus its diameter, this number was high (p < 0.05). Collagen density showed high absolute values in the descending aorta. In the older group, 4 of 7 showed no staining for alpha-actin in the hypoplastic transverse arch, whereas under 1 month of age, only 2 of 8 cases were negative. CONCLUSIONS: The hypoplastic transverse arch is characterized by a relatively high number of elastin lamellae. Fewer alpha-actin-positive cells in the hypoplastic transverse arch occur in older specimens, which could indicate a diminished potential growth.

Actins↗
PubMed1997

Morphologic features of the normal aortic arch in neonates, infants, and children pertinent to growth.

BACKGROUND: The aorta in newborns rapidly adapts by growth to postnatal circulatory conditions. The question arises what structural features are associated with growth and whether differences occur between the various segments. METHODS: Nineteen specimens have been studied: seven from babies less than 1 month, seven from 1 month to 1 year, and five from 1 to 4 years. In each baby the diameter of the aortic segments and its branches were measured. Histologically the number of elastin lamellae was counted, and furthermore, collagen density was quantified at several measurement sites. RESULTS: The diameter of each segment increases rapidly after birth and more so than that of the descending aorta, except for the brachiocephalic artery and its branches and the left common carotid artery, albeit not at the same rate. The ascending aorta is the only segment that shows a decrease in the ratio of elastin lamellae to diameter. Collagen density was always highest in the descending aorta. CONCLUSIONS: These observations show that postnatal growth of the thoracic aorta is associated with distinct structural remodeling soon after birth; these observations are of clinical relevance in case of aortic arch abnormalities.

Aorta, Thoracic↗
PubMed1997

Costimulatory molecules in human atherosclerotic plaques: an indication of antigen specific T lymphocyte activation.

Atherosclerotic plaques contain inflammation, composed largely of macrophages and lymphocytes. A proportion of lymphocytes shows signs of activation, but the question arises whether they are activated in an antigen specific way. The expression of costimulatory molecules-receptors that provide accessory signals during antigen-specific activation is a prerequisite for such a condition. This aspect of inflammation in atherosclerotic lesions has not been investigated. Human arterial segments with diffuse intimal thickening, fatty streaks and atherosclerotic plaques were studied with immuno-single and double staining methods. Macrophages and T lymphocytes were stained with CD68 and CD3, respectively, and pan-B cell markers CD19 and CD22 were also used. Costimulatory molecules B7-1 and B7-2, together with their common ligand CD28, and CD27 with its ligand CD70, were stained with specific monoclonal antibodies. The results show that most T lymphocytes were CD27 positive and that only a subpopulation of these (5-15%) was positive also for B7-1, CD28 and CD70. Macrophages expressed B7-1, B7-2, CD28 and CD70, while macrophages positive for CD28 and CD70 have not been reported yet. The expression of costimulatory molecules was most pronounced in the superficial layers at the fibrous cap, but decreased towards the lipid core. This study shows, therefore, that atherosclerotic plaques provide costimulatory signals generally accepted as a prerequisite for adequate T cell stimulation. In addition, this study reveals that only approximately 5-15% of the lymphocytes appears actively involved in the inflammatory reaction.

Aged↗
PubMed1997

The left ventricular outflow tract in atrioventricular septal defect revisited: surgical considerations regarding preservation of aortic valve integrity in the perspective of anatomic observations.

OBJECTIVE: The anatomy of the left ventricular outflow tract in hearts with atrioventricular septal defect has been widely investigated, but controversies remain regarding detailed aspects of left ventricular outflow tract anatomy in the perspective of operative techniques to either prevent or relieve outflow tract obstruction. METHODS: We investigated 29 postmortem hearts with an atrioventricular septal defect. Measurements were taken of the circumferences and of the widths of the components that make up the outflow tract, that is, the interventricular septum, the superior bridging leaflet, the left ventricular free wall, and the length of the tendinous cords. RESULTS: The circumference of the left ventricular outflow tract immediately underneath the aortic valve was not different from that at the middle part of the outflow tract. Hearts with the partial type defect, characterized by separate atrioventricular orifices, had a smaller outflow tract than those with the complete variety. Although the anatomic constituents that contribute to left ventricular outflow tract obstruction are complex, this study showed that a reduced width of the interventricular septum was most intimately related to narrowing immediately underneath the aortic valve. Obstruction at the middle part of the left ventricular outflow tract was largely caused by reduced width of the interventricular septum together with short tendinous cords. CONCLUSIONS: On the basis of these observations, we recommend detailed investigation of the anatomy of the left ventricular outflow tract immediately underneath the aortic valve, before surgical attempts to relieve outflow tract obstruction, because in some procedures the integrity of the aortic valve will be at stake.

Aortic Valve↗
PubMed1997

Remodeling after myocardial infarction in humans is not associated with interstitial fibrosis of noninfarcted myocardium.

OBJECTIVES: This study was specifically designed to evaluate whether noninfarcted hypertrophic myocardium in patients with end-stage heart failure after myocardial infarction (MI) is associated with an increase in interstitial fibrous tissue. BACKGROUND: Postinfarction remodeling consists of complex alterations that involve both infarcted and noninfarcted myocardium. The question arises whether ventricular dysfunction is due to physical events, such as inadequate myocardial hypertrophy to compensate for increased tangential wall stress, or is caused by the development of progressive interstitial fibrosis in noninfarcted myocardium. METHODS: Fifteen hearts were obtained as cardiac explants (n = 13) or at autopsy (n = 2) from patients with end-stage coronary artery disease. Sixteen normal hearts served as reference hearts. Samples were taken from the left ventricular (LV) wall that contained the infarcted area, the border area and noninfarcted myocardium remote from scar areas. Collagen was quantified biochemically and microdensitophotometrically. Collagen type I and III ratios were analyzed by using the cyanogen bromide method and immunohistochemical staining, followed by microdensitophotometric quantification. RESULTS: In noninfarcted myocardium remote from the scar areas, total collagen levels and collagen type I/III ratios did not differ statistically from those in reference hearts. These observations contrasted with high total collagen content and high collagen type I/III ratios in scar and border areas. CONCLUSIONS: Remodeling of LV myocardium after MI in patients with end-stage heart failure is not necessarily associated with interstitial fibrosis in noninfarcted hypertrophic myocardium remote from scar areas. This finding raises questions regarding therapeutic interventions designed to prevent or retard the development of interstitial fibrosis.

Adult↗