A latent profile analysis of the typology of bulimic symptoms in an indigenous Pacific population: evidence of cross-cultural variation in phenomenology.

BACKGROUND: Previous efforts to derive empirically based eating disorder (ED) typologies through latent structure modeling have been limited by the ethnic and cultural homogeneity of their study populations and their reliance on DSM-IV ED signs and symptoms as indicator variables. METHOD: Ethnic Fijian schoolgirls (n=523) responded to a self-report battery assessing ED symptoms, herbal purgative use, co-morbid psychopathology, clinical impairment, cultural orientation, and peer influences. Participants who endorsed self-induced vomiting or herbal purgative use in the past 28 days (n=222) were included in a latent profile analysis (LPA) to identify unique subgroups of bulimic symptomatology. RESULTS: LPA identified a bulimia nervosa (BN)-like class (n=86) characterized by high rates of binge eating and self-induced vomiting, and a herbal purgative class (n=136) characterized primarily by the use of indigenous Fijian herbal purgatives. Both ED classes endorsed greater eating pathology and general psychopathology than non-purging participants, and the herbal purgative class endorsed greater clinical impairment than either the BN-like or non-purging participants. Cultural orientation did not differ between the two ED classes. CONCLUSIONS: Including study populations typically under-represented in mental health research and broadening the scope of relevant signs and symptoms in latent structure models may increase the generalizability of ED nosological schemes to encompass greater cultural diversity.

The association between sports participation and athletic identity with eating pathology among college-aged males and females.

The current study examined associations among sports participation (SP), athletic identity (AI), weight status, and eating pathology, and whether these relations differed by gender. Data come from male and female first-year college students who participated in the Tufts Longitudinal Health Study (TLHS) between 1999-2007 (N=712). Relations among SP, AI, actual and perceived weight statuses, Eating Disorders Inventory (EDI) subscale scores, and indices of body shape concern and restrictive eating were examined with hierarchical ordinary least squares (OLS) regression. Associations between SP and eating pathology among females were moderated by perceived weight status. By contrast, relations between males' EDI subscales scores and SP were moderated by ethnicity, as well as by actual weight status. Our findings support that sports participation alone neither promotes nor protects against eating pathology among males and females.

Naturalistic study of course, effectiveness, and predictors of outcome among female adolescents in residential treatment for eating disorders.

Few empirical data address naturalistic outcomes of residential eating disorder (ED) treatment. Study aims were to evaluate course, effectiveness, and predictors of outcome in a residential treatment program. We evaluated 80 consecutively admitted female adolescents with the SCID-IV. Primary outcomes were treatment completion, subsequent readmission, clinical global impressions, and changes in body weight. Mean length of stay was 51 days, and 80% of patients were discharged according to treatment plans. Mean expected body weight (EBW) for AN patients increased from 80% to 91%. Patients reported significant improvements in ED symptoms, depression, and quality of life. Low admission %EBW and previous psychiatric hospitalizations were associated with premature termination. Overall, findings support that residential treatment is largely acceptable to patients, and that residential care may provide an opportunity for substantive therapeutic gains.

Mental health training for secondary school teachers in Haiti: a mixed methods, prospective, formative research study of feasibility, acceptability, and effectiveness in knowledge acquisition.

BACKGROUND: Engagement and training of educators in student mental health holds promise for promoting access to care as a task sharing strategy but has not been well-studied in low-income regions. METHODS: We used a prospective and convergent mixed methods design to evaluate a customized school mental health 2½ day training for teachers in rural Haiti (n = 22) as the initial component of formative research developing a school-based intervention to promote student mental health. Training prepared teachers to respond to student mental health needs by providing psychoeducational and practical support to facilitate access to care. We examined level of participation and evaluated feasibility, acceptability, and perceived effectiveness by calculating mean scores on self-report Likert-style items eliciting participant experience. We examined effectiveness of the training on improving mental health knowledge and attitudes by comparing mean scores on an assessment administered pre- and post-training. Finally, we examined self-report written open-ended responses and focus group discussion (FGD) interview data bearing on perceived feasibility, acceptability, and effectiveness to contextualize participant ratings of training and to identify recommendations for enhancing the utility of mental health training locally for educators. RESULTS: Mean scores of knowledge and attitudes significantly improved between the pre-test and post-tests; e.g., knowledge improved from 58% correct at baseline to 68% correct on the second post-test (p = 0.039). Mean ratings of the training were favorable across all categories and FGD data demonstrated widespread participant endorsement of training acceptability and effectiveness; participants recommended extending the duration and number of training sessions. CONCLUSIONS: Findings support feasibility, acceptability, and a limited scope of effectiveness of brief mental health training for secondary school teachers in Haiti. Further development of approaches to engage teachers in promoting school mental health through training is warranted.

Colocalisation of intraplaque C reactive protein, complement, oxidised low density lipoprotein, and macrophages in stable and unstable angina and acute myocardial infarction.

BACKGROUND: C reactive protein (CRP), an important serum marker of atherosclerotic vascular disease, has recently been reported to be active inside human atherosclerotic plaques. AIMS: To investigate the simultaneous presence of macrophages, CRP, membrane attack complex C5b-9 (MAC), and oxidised low density lipoprotein (oxLDL) in atherectomy specimens from patients with different coronary syndromes. METHODS: In total, 54 patients with stable angina (SA; n = 21), unstable angina (UA; n = 15), and myocardial infarction (MI; n = 18) underwent directional coronary atherectomy for coronary lesions. Cryostat sections of atherosclerotic plaques were immunohistochemically stained with monoclonal antibodies: anti-CD68 (macrophages), anti-5G4 (CRP), aE11 (MAC), and 12E7 (oxLDL). Immunopositive areas were evaluated in relation to fibrous and neointima tissues, atheroma, and media. Quantitative analysis was performed using image cytometry with systematic random sampling (percentage immunopositive/total tissue area). RESULTS: Macrophages, CRP, MAC, and oxLDL were simultaneously present in a higher proportion of fibrous tissue and atheroma of atherectomy specimens from patients with UA and MI compared with SA (p<0.05). Quantitative analysis showed significantly higher mean percentages of macrophages in plaques from patients with MI (44%) than UA (30%; p<0.01) and SA (20%; p<0.001). Significantly higher mean percentages of CRP were also seen in MI (25%) and UA (25%) compared with SA (12%; p<0.05). CONCLUSIONS: The presence of CRP, complement, and oxLDL in a high proportion of plaque tissue from patients with unstable coronary artery disease implies that these surrogate markers have important proinflammatory effects inside atherosclerotic plaques. This may increase vulnerability to plaque rupture and thrombosis, with subsequent clinical sequelae.

Reversing the direction of paced ventricular and atrial wavefronts reveals an oblique course in accessory AV pathways and improves localization for catheter ablation.

BACKGROUND: The purpose of this study was to determine how often accessory atrioventricular (AV) pathways (AP) cross the AV groove obliquely. With an oblique course, the local ventriculoatrial (VA) interval at the site of earliest atrial activation (local-VA) and the local-AV interval at the site of earliest ventricular activation (local-AV) should vary by reversing the direction of the paced ventricular and atrial wavefronts, respectively. METHODS AND RESULTS: One hundred fourteen patients with a single AP were studied. Two ventricular and two atrial pacing sites on opposite sides of the AP were selected to reverse the direction of the ventricular and atrial wavefronts along the annulus. Reversing the ventricular wavefront increased local-VA by >/=15 ms in 91 of 106 (91%) patients. With the shorter local-VA, the ventricular potential overlapped the atrial potential along a 17.2+/-8.5-mm length of the annulus. No overlap occurred with the opposite wavefront. Reversing the atrial wavefront increased local-AV by >/=15 ms in 32 of 44 (73%) patients. With the shorter local-AV, the atrial potential overlapped the ventricular potential along an 11.9+/-8.9-mm length of the annulus. No overlap occurred with the opposite wavefront. Mapping during longer local-VA or local-AV identified an AP potential in 102 of 114 (89%) patients. Catheter ablation eliminated AP conduction in all 111 patients attempted (median, 1 radiofrequency application in 99 patients with an AP potential versus 4.5 applications without an AP potential). CONCLUSIONS: Reversing the direction of the paced ventricular or atrial wavefront reveals an oblique course in most APs and facilitates localization of the AP potential for catheter ablation.

Elevated levels of oxidized low density lipoprotein show a positive relationship with the severity of acute coronary syndromes.

BACKGROUND: There is accumulating data that acute coronary syndromes relate to recent onset activation of inflammation affecting atherosclerotic plaques. Increased blood levels of oxidized low density lipoprotein (ox-LDL) could play a role in these circumstances. METHODS AND RESULTS: Ox-LDL levels were measured in 135 patients with acute myocardial infarction (AMI; n=45), unstable angina pectoris (UAP; n=45), and stable angina pectoris (SAP; n=45) and in 46 control subjects using a sandwich ELISA method. In addition, 33 atherectomy specimens obtained from a different cohort of patients with SAP (n=10) and UAP (n=23) were studied immunohistochemically for ox-LDL. In AMI patients, ox-LDL levels were significantly higher than in patients with UAP (P<0.0005) or SAP (P<0.0001) or in controls (P<0.0001) (AMI, 1.95+/-1.42 ng/5 microgram LDL protein; UAP, 1.19+/-0.74 ng/5 microgram LDL protein; SAP, 0.89+/-0.48 ng/5 microgram LDL protein; control, 0.58+/-0.23 ng/5 microgram LDL protein). Serum levels of total, HDL, and LDL cholesterol did not differ among these patient groups. In the atherectomy specimens, the surface area containing ox-LDL-positive macrophages was significantly higher in patients with UAP than in those with SAP (P<0.0001). CONCLUSIONS: This study demonstrates that ox-LDL levels show a significant positive correlation with the severity of acute coronary syndromes and that the more severe lesions also contain a significantly higher percentage of ox-LDL-positive macrophages. These observations suggest that increased levels of ox-LDL relate to plaque instability in human coronary atherosclerotic lesions.

Collateral blood supply to the myocardium at risk in human myocardial infarction: a quantitative postmortem assessment.

The relation between the type and size of myocardial infarcts and collateral development was studied in postmortem human hearts with a new approach that allows quantification of vascular beds. The coronary arteries were perfused with radioactive microspheres and were visualized by injecting a barium-gelatin mixture. The collateral supply was assessed in 6 reference hearts without infarction, 4 hearts with a transmural infarct and 12 hearts with a total of 16 subendocardial infarcts. The distribution pattern of microspheres in hearts in the reference group did not differ significantly from that in hearts with a transmural infarct but was significantly different (p less than 0.01) from that in hearts with a subendocardial infarct, which had a much greater number of microspheres in the collateral-dependent area. Moreover, the lateral zone of myocardium at risk--defined as the area containing viable myocardium but within the distribution zone of the occluded artery--was small in hearts with a transmural infarct (less than or equal to 2 mm), but showed a much wider range in hearts with a subendocardial infarct. This study strongly suggests that collateral vessels play an important role during the development of myocardial infarction, both in determining infarct type (transmural versus subendocardial) and in preserving the viability of the lateral zone of the myocardium at risk.

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.

Long-term follow-up of idiopathic mitral valve prolapse in 300 patients: a prospective study.

A prospective long-term follow-up study was made of 300 patients with idiopathic mitral valve prolapse, diagnosed by clinical, cineangiographic and echocardiographic criteria. There were 136 male and 164 female patients, ranging in age from 10 to 87 years (mean 42.2). The study included all patients with primary mitral valve prolapse, irrespective of clinical condition at the onset, and excluded only those patients with "secondary" mitral valve prolapse attributable to an accompanying established disorder. The average follow-up period was 6.1 years (range 6 months to 20 years). Two patients died of a noncardiac cause. The clinical condition of 153 patients remained stable. In 27 patients a supraventricular tachycardia occurred that was readily controlled with medication and caused no serious clinical complications. In 20 patients signs of mitral regurgitation appeared, but the patients remained clinically asymptomatic. Serious complications developed in 100 patients. Sudden death, most likely due to ventricular fibrillation, occurred in three patients; documented ventricular fibrillation was seen in two. Ventricular tachycardia developed in 56 patients, but in all instances the rhythm disorder was managed effectively and durably with medication. Infective endocarditis occurred in 18 patients, 4 of whom died during treatment and 6 of whom needed mitral valve replacement. The remaining eight patients suffer from severe mitral regurgitation that will require surgery in the near future. Twenty-eight patients underwent mitral valve operation because of progressive regurgitation. Cerebrovascular accidents occurred in 11 patients, but lifelong treatment with coumarin derivatives or antiplatelet aggregation agents was not considered necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Isolated mitral valve prolapse: chordal architecture as an anatomic basis in older patients.

Ten patients with an average age of 58 years underwent valve replacement because of isolated mitral valve prolapse with severe regurgitation. None had clinical evidence of Marfan's syndrome or another systemic disease that would indicate that a primary connective tissue disorder was the cause of the prolapse. All 10 patients had a dome configuration of the posterior leaflet and one or more ruptured chordae related to it. The gross morphology of the resected specimens revealed marked deviations in chordal branching and the pattern of anchoring in each of the 10 cases, rendering the most severely affected parts of the leaflets less well supported. Similar changes occurred at sites remote from the principal abnormality. Microscopically, the dominant tissue change was myxomatous transformation within the affected leaflets and chordae with secondary changes at both atrial and ventricular surfaces. These findings could indicate that insufficient chordal support may have promoted the development of the floppy valve through a process of chronic undue and unbalanced stress on the valve tension and closure apparatus. The resultant degeneration of the connective tissues, histologically expressed as myxomatous transformation, may underlie stretching and thus redundance of the leaflets and eventually rupture of chordae. It is suggested that this sequence of events be considered as a possible pathogenetic mechanism of isolated mitral valve prolapse, particularly in the subset of aged patients.

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.

Left atrial isomerism associated with asplenia: prenatal echocardiographic detection of complex congenital cardiac malformations.

Complex congenital heart disease with suspected isomerism of the atria was diagnosed in two fetuses of 20 and 29 weeks' gestation using two-dimensional and M-mode scanning techniques. The first pregnancy was terminated at 21 weeks' gestation and stillbirth occurred at 31 weeks' gestation in the second pregnancy. At postmortem examination, a thoracoabdominal discordancy was found; the spleen was absent and the arrangement of the abdominal vessels was as anticipated for asplenia, but the thoracic situs revealed a bilateral right-sided arrangement with left isomerism of the atria. The heart, otherwise, showed complex abnormalities as anticipated for asplenia.

The neonatal heart has a relatively high content of total collagen and type I collagen, a condition that may explain the less compliant state.

OBJECTIVES: This study evaluated the extent of the collagen network in neonatal heart muscle and whether the type I/type III collagen ratio is the same as in the adult heart. BACKGROUND: The functional integrity and the stress-strain relation of heart muscle depends largely on the extracellular collagen matrix. The question therefore arises whether the altered compliance of the neonatal heart could relate to the developmental state of collagen and, in particular, the distribution of types I and III collagen. Type I collagen mainly provides rigidity and type III collagen elasticity. METHODS: Specimens from the left lateral wall of the left ventricle of human hearts (immature to full term, n = 23; 3 weeks to 12 years, n = 17) were used to determine the total collagen amount, using the hydroxyproline assay. Similar left ventricular specimens of human hearts (fetal to mature, n = 20; 2 months to 1.5 years, n = 6) were fixed in formalin, paraffin embedded and stained with Sirius red F3BA for total collagen. The ratio of total collagen to total protein was quantified spectrophotometrically. Frozen sections of left ventricular myocardium (immature to mature, n = 17; 4 months to 12 years, n = 10) were stained with antibodies raised against types I and III collagen. Antibody titration was done on human leiomyoma tissue with a known type I/type III collagen ratio. The endomysial collagen types were quantified using a spectrophotometer and expressed as a ratio. Adult human myocardium (n = 10) was used as reference. RESULTS: The study showed that the total amount of collagen increases with age. However, the ratio of total collagen to total protein and the ratio of type I to type III collagen were very high in hearts of the very young. During development, a gradual decrease occurred, with the total collagen/total protein ratio reaching normal levels at approximately 5 months after birth and the type I/type III collagen ratio stabilizing at a much later age. CONCLUSIONS: These findings suggest that the relative high content of collagen, related to the myocytes, and the high ratio of type I to type III collagen provide the substrate for a rigid, less compliant heart in neonates.

Is the Watanabe heritable hyperlipidemic rabbit a suitable experimental model for percutaneous transluminal coronary angioplasty in humans? A light microscopic, immunohistochemical and ultrastructural study.

OBJECTIVES: This study was designed to assess an experimental model for the study of mechanisms that underlie restenosis after percutaneous transluminal coronary angioplasty. BACKGROUND: The Watanabe heritable hyperlipidemic (WHHL) rabbit lacks the receptor for low density lipoproteins, produces atherosclerotic lesions very similar to those in humans and, therefore, could serve as a suitable model. METHODS: Percutaneous transluminal angioplasty was performed on the left subclavian artery of 10 homozygous rabbits. The animals were killed at a few hours or 3, 7, 14 or 28 days after the procedure. The artery was fixed by perfusion, and the site of angioplasty was examined by both light and electron microscopy with the use of conventional and immunohistochemical staining techniques. RESULTS: Angioplasty had caused a flap-like or dissecting tear into the media. At day 3, cells within the preexisting media adjacent to the injury had the ultrastructural characteristics of synthetic smooth muscle cells. At day 7, spindle cells at the site of injury stained either negative or very weakly positive with a marker for actin; ultrastructurally, these cells had the synthetic phenotype. At day 14, the spindle cells showed a mix of contractile and synthetic phenotypes. The surface was partially covered by endothelial cells. At day 28, the dominant cell type was the contractile smooth muscle cell and the surface was completely covered by endothelial cells. CONCLUSIONS: Both the injury and the response to injury after percutaneous transluminal angioplasty were almost identical to that seen in humans after coronary angioplasty. Thus, the WHHL rabbit appears to be an appropriate experimental model for use in further studies.

Ventricular tachycardia in the infarcted, Langendorff-perfused human heart: role of the arrangement of surviving cardiac fibers.

Electrophysiologic and histologic studies were performed on Langendorff-perfused human hearts from patients who underwent heart transplantation because of extensive infarction. In nine hearts, 15 sustained ventricular tachycardias could be induced by programmed stimulation. In all hearts, mapping of epicardial and endocardial electrical activity during tachycardia was carried out. Histologic examination of the infarcted area between the site of latest activation of one cycle and the site of earliest activation of the next cycle revealed zones of viable myocardial tissue. In two hearts in which the time gap between latest and earliest activation was small, surviving myocardial tissue constituted a continuous tract that traversed the infarct. In three other hearts in which the time gap was large, surviving tissue consisted of parallel bundles that coursed separately over a few hundred micrometers, then merged into a single bundle and finally branched again. The direction of the fibers within the bundles was perpendicular to the direction of the activation front in that area. A similar type of inhomogeneous anisotrophy and activation delay was found in an infarcted papillary muscle removed from one of the explanted hearts and studied in a tissue bath during basic stimulation. Histologic examination of this preparation revealed that the delay was caused by a zigzag route of activation over branching and merging bundles of surviving myocytes separated by connective tissue.

Plaque inflammation in restenotic coronary lesions of patients with stable or unstable angina.

OBJECTIVES: To evaluate immunohistochemically various parameters of inflammation in coronary atherectomy specimens obtained from restenotic culprit lesions of patients presenting with either stable or unstable angina (UA). BACKGROUND: There is no information regarding the relationship between atherosclerotic plaque inflammation and the severity of the coronary syndromes in patients with restenotic coronary lesions. METHODS: A total of 37 patients with either stable angina or UA underwent directional coronary atherectomy for restenotic coronary lesions. Cryostat sections of atherectomy specimen were immunohistochemically stained with monoclonal antibodies CD68 (macrophages [MACs]), CD3 (T-lymphocytes) and alpha-actin (smooth muscle cells [SMCs]). Smooth muscle cell contents and MAC contents were planimetrically quantified as the percentage immunopositive tissue area of the total tissue area. T-lymphocytes were counted at 100-X magnification throughout the entire section and expressed as number of cells per mm2. RESULTS: Restenotic coronary lesions of patients with UA or stable angina showed no significant difference in SMC areas (31.9%+/-16.3% vs. 38.5%+/-18.8%, respectively; p = NS). However, restenotic coronary lesions of patients presenting with unstable angina contained significantly more MACs (24.4%+/-15.1% vs. 10.5%+/-5.8%, p = 0.001) and T-lymphocytes (18.8 cells/mm2+/-15.1 cells/mm2 vs. 8.6 cells/mm2+/-9.8 cells/mm2; p = 0.034) than patients with stable angina. CONCLUSIONS: These results suggested that inflammation appears to affect plaque instability in restenotic coronary lesions resulting in unstable coronary syndromes.

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.

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.

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.