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Biomedical subjects

Vera Demarchi Aiello

Publications and source records attributed to Vera Demarchi Aiello.

17 recordsLinked to original sources
PubMed2006

Value of adenosine infusion for infarct size determination using real-time myocardial contrast echocardiography.

BACKGROUND: Myocardial contrast echocardiography has been used for determination of infarct size (IS) in experimental models. However, with intermittent harmonic imaging, IS seems to be underestimated immediately after reperfusion due to areas with preserved, yet dysfunctional, microvasculature. The use of exogenous vasodilators showed to be useful to unmask these infarcted areas with depressed coronary flow reserve. This study was undertaken to assess the value of adenosine for IS determination in an open-chest canine model of coronary occlusion and reperfusion, using real-time myocardial contrast echocardiography (RTMCE). METHODS: Nine dogs underwent 180 minutes of coronary occlusion followed by reperfusion. PESDA (Perfluorocarbon-Exposed Sonicated Dextrose Albumin) was used as contrast agent. IS was determined by RTMCE before and during adenosine infusion at a rate of 140 mcg.Kg(-1).min(-1). Post-mortem necrotic area was determined by triphenyl-tetrazolium chloride (TTC) staining. RESULTS: IS determined by RTMCE was 1.98 +/- 1.30 cm2 and increased to 2.58 +/- 1.53 cm2 during adenosine infusion (p = 0.004), with good correlation between measurements (r = 0.91; p < 0.01). The necrotic area determined by TTC was 2.29 +/- 1.36 cm2 and showed no significant difference with IS determined by RTMCE before or during hyperemia. A slight better correlation between RTMCE and TTC measurements was observed during adenosine (r = 0.99; p < 0.001) then before it (r = 0.92; p = 0.0013). CONCLUSION: RTMCE can accurately determine IS in immediate period after acute myocardial infarction. Adenosine infusion results in a slight better detection of actual size of myocardial damage.

Adenosine↗
PubMed2006

Atrioventricular septal defect with intact septal structures presenting as left atrioventricular valvar insufficiency.

We describe the findings in a six-year-old girl who presented with signs of left atrioventricular valvar insufficiency. The echocardiogram showed a common atrioventricular junction, intact atrial and ventricular septal structures. At surgery, the left-sided atrioventricular valve was found to be tri-foliate, and corrected by valvoplasty. To the best of our knowledge, this is the first case of atrioventricular septal defect with common atrioventricular junction and intact septal structures diagnosed during life.

Cardiac Surgical Procedures↗
PubMed2006

Complete repair in total atrioventricular canal defect with cyanosis.

Atrioventricular septal defects account for 4% of congenital cardiac malformations and over 50% of cardiac defects seen in Down syndrome. Clinical presentation is marked by congestive heart failure early in infancy. Cyanosis is rarely found in infants and suggests irreversible pulmonary hypertension or associated cardiac defects as tetralogy of Fallot, double outlet right ventricle, Ebstein anomaly, persistent left superior vena cava draining in the left atrium (Barbero Marcial, personal communication). Children with Down's syndrome is particularly difficult to assess because they often suffer from upper airways obstruction, which may contribute to the increased pulmonary vascular resistance determined at cardiac catheterization. This association of factors becomes a challenge for operability and, we will report one such case.

Cyanosis↗
PubMed2004

Chest pain in an adult with truncus arteriosus communis.

We present a case of an adult patient with truncus arteriosus communis and secondary pulmonary hypertension. He had chest pain and sudden death due to cardiac tamponade caused by intramural-limited dissection and rupture of the common trunk.

Adult↗
PubMed2004

Sequential histologic analysis of the myocardium after dynamic cardiomyoplasty: a study based on right ventricular endomyocardial biopsies.

Although dynamic cardiomyoplasty may promote clinical amelioration and mild improvement in left ventricular function in selected patients, whether cardiac reverse remodeling occurs after the procedure is not clear. We did not find histologic differences among right ventricular endomyocardial biopsy specimens taken before and after the surgery at 3 time periods. This result suggests that the procedure has no effect on the microscopic structure of the right ventricular myocardium. However, because reverse remodeling does not necessarily occur concomitantly in both ventricles, our conclusion cannot be extrapolated to the left ventricular chamber.

Adult↗
PubMed2004

Evolutional aspects of children and adolescents with surgically corrected aortic coarctation: clinical, echocardiographic, and magnetic resonance image analysis of 113 patients.

OBJECTIVE: The goals of this study were to determine the prevalence of hypertension and recoarctation in operated children and teenagers and to integrate clinical and imaging technique data. METHODS: One hundred thirteen infants and children (ages 14 years or less) were retrospectively divided into 3 groups according to the age at operation and the surgical technique: 79 underwent resection with end-to-end anastomosis; 14 had patch enlargement; 13 had subclavian flap aortoplasty; and 7 had other techniques performed. The mean age at operation was 3.95 +/- 4.17 years and the mean follow-up period was 4.62 +/- 4.90 years. Each patient was clinically examined and Doppler echocardiography was performed in 112 patients. Sixty-six patients underwent magnetic resonance imaging. Diameters of aortic arch were measured at 4 levels; the ratios between each one and descendent aorta diameters were calculated. Qualitative variables and associations were studied by Fisher exact test or chi-squared test. Comparisons of measurements in different groups were performed using variance analysis, with tests of selective contrasts (nonparametric tests). The level of statistical significance was <.05. RESULTS: The prevalence of hypertension and recoarctation was 38% and 14%, respectively. No statistical difference was found among the age groups. In 65 patients who underwent magnetic resonance imaging, the transverse aortic arch was hypoplastic in 31 (47%) patients; 41 (63%) had stenosis at the site of anastomosis (ratio < 0.9). CONCLUSION: Hypoplasia of transverse aortic arch was highly prevalent. These data suggest that hypoplastic aortic arch should be corrected concomitantly with coarctation.

Adolescent↗
PubMed2003

Coinfection with Mycoplasma pneumoniae and Chlamydia pneumoniae in ruptured plaques associated with acute myocardial infarction.

OBJECTIVE: To study atheromas, Mycoplasma pneumoniae (M. pneumoniae), and Chlamydia pneumoniae (C. pneumoniae). METHODS: C. pneumoniae was studied with immunohistochemistry and M. pneumoniae with in situ hybridization (ISH), in segments of coronary arteries (SCA) as follows: group A - thrombosed ruptured plaques (TRP) of 23 patients who died due to acute myocardial infarction (AMI); group B - 23 nonruptured plaques (NRP) of group A patients; group C - NRP of 11 coronary patients who did not die due to AMI; and group D - 11 SCA from patients with dilated cardiomyopathy or Chagas' disease without atherosclerosis. RESULTS: The mean number of C. pneumoniae+ cells/400x in groups A, B, C, and D was, respectively, 3.3 +/- 3.6; 1.0 +/- 1.3; 1.2 +/- 2.4; and 0.4 +/- 0.3; and the percentage of M. pneumoniae area was, respectively, 3.9 +/- 3.5; 1.5 +/- 1.6; 0.9 +/- 0.9; and 0.4 +/- 0.2. More M. pneumoniae and C. pneumoniae were found in of group A than in group B (P<0.01). Good correlation was seen between the area of the vessel and the M. pneumoniae area in the plaque (r = 0.46; P=0.001) and between C. pneumoniae+ cells and CD4+ T lymphocytes (r = 0.42; P<0.01). The number of C. pneumoniae+ cells correlated with CD20+ B cells (r=0.48; P<0.01). CONCLUSION: M. pneumoniae and C. pneumoniae are more frequently found in TRP correlate with the intensity of the inflammation and diameter of the vessel (positive remodeling).

Aged↗
PubMed2003

Endomyocardial fibrosis in infancy.

The patient was a 4-month-old infant, who underwent persistent ductus arteriosus interruption with titanium clips at the age of 13 days and, since the age of 2 months, had crises of hypoxia and hypertonicity. After clinical investigation, the presence of pulmonary hypertension was confirmed and left ventricular inflow tract obstruction was suspected. The patient underwent surgical treatment at the age of 4 months, during which right and left ventricular endocardial fibrosis was identified. The fibrosis was resected, but the infant had an unfavorable clinical evolution with significant diastolic restriction and died on the sixth postoperative day. Anatomicopathological and surgical findings suggested endomyocardial fibrosis, although that pathology is very rare at the patient's age.

Endomyocardial Fibrosis↗
PubMed2003

Left ventricular remodeling in hearts with tricuspid atresia: morphologic observations and possible basis for ventricular dysfunction after surgery.

OBJECTIVES: This study was undertaken to assess the pattern of left ventricular hypertrophy, the myocardial capillary network, and the extracellular matrix in hearts with tricuspid atresia. METHODS: We examined 32 hearts with tricuspid atresia and 27 normal hearts from control subjects with similar age and sex distribution. Wall thickness, inlet length, and outlet length were obtained from the left ventricle. Immunohistochemical staining for von Willebrand factor was used to label myocardial capillaries. By means of computer-assisted morphometry, the following data were obtained from the inlet, apex, and outlet of the left ventricle: transverse myocyte diameter, myocyte nuclear volume fraction, capillary volume fraction, interstitial fibrous volume fraction, and endocardial thickness. RESULTS: The wall thickness in affected hearts was not different from that in control hearts. The left ventricular outlet length was significantly greater in the malformed hearts (P =.005). The myocyte diameter did not differ from that in control hearts. The capillary volume fraction was decreased in the malformed hearts (P <.001). The interstitial fibrous deposition was greater in the malformed hearts at all sites analyzed (P <.001). Fibrosis was greater in the inlet and apex (P =.004) and also in the subendocardial half of the ventricular wall than in the subepicardial half. According to a logistic regression model, age was the only variable associated with the probability of occurrence of fibrosis. CONCLUSIONS: Our findings in hearts with tricuspid atresia possibly represent chronically induced volume overload in the presence of ischemia, rather than a typical model of volume overload. A decreased capillary volume fraction may indicate a greater susceptibility to ischemia. Fibrous deposition probably occurs early in life.

Age Factors↗
PubMed2003

Morphology of the internal elastic lamina in arteries from pulmonary hypertensive patients: a confocal laser microscopy study.

The development and progression of pulmonary hypertension lesions involve continuous remodeling of the arterial wall, including the extracellular matrix components. The integrity of the internal elastic lamina may represent a barrier to cell migration and formation of intimal proliferative lesions. Some patients with congenital cardiac shunts develop precocious intimal occlusive lesions,whereas others evolve with isolated medial hypertrophy. We studied the 2-D and 3-D morphology of the internal elastic lamina of peripheral pulmonary arteries to search for any difference regarding the type of histological lesion. Fifteen lung biopsies collected for diagnostic purposes from patients with congenital shunts and 6 control lungs (mean ages, 15.8 and 14.7 mo) were studied using the confocal laser scanning microscope, under predetermined conditions of laser intensity, brightness and contrast. We measured the thickness of the internal elastic lamina and determined the number of gaps and projections of elastic tissue towards the medial and intimal layers. The mean internal elastic lamina thickness was significantly higher in arteries from cases with isolated medial hypertrophy when compared with controls and to those with proliferative lesions (P <.05). The number of gaps of the internal elastic lamina was higher in arteries >100 micro m in diameter from the group with intimal lesions when compared to the cases presenting with isolated hypertrophy, but did not differ from the controls. There was a positive linear correlation between the external arterial diameter and the thickness of the internal elastic lamina (r =.74, P <.001) in cases presenting isolated medial hypertrophy. The increased thickness and smaller number of gaps of the internal elastic lamina may act as a barrier that prevents smooth muscle cell migration in patients with pulmonary hypertension without intimal proliferative lesions. On the other hand, a greater number of gaps does not represent, by itself, unrestrained migration, because controls also showed fenestrated laminae.

Biopsy↗
PubMed2002

A possible role for complement in the pathogenesis of chronic chagasic cardiomyopathy.

The membrane attack complex (MAC) of complement participates in several inflammatory and proliferative processes by releasing pro-inflammatory cytokines and growth factors from target cells. Chronic Chagasic cardiomyopathy (CCH) is a parasitic dilated cardiopathy, characterized by severe fibrosis and inflammation, which differs from idiopathic dilated cardiomyopathy (DCM). Trypanosoma cruzi, the pathogenic organism of CCH, is a strong complement activator and can also induce alternative pathway activation by mammalian cells. This study explored whether the myocardium in CCH patients has increased MAC deposition, an expression of complement activation, compared to DCM patients. MAC was semi-quantified in endomyocardial human samples (29 CCH subjects, 18 DCM subjects, and four controls) by immunohistochemistry. MAC was present in the sarcolemma of 38% of CCH, 5.5% of DCM (p<0.02), and 0% of controls, and in interstitial inflammatory cells of CCH. No difference was observed in the expression of the complement regulatory protein CD59, indicating that increased MAC deposition is likely to be the result of complement activation rather than decreased protection. It is proposed that the increased MAC deposition found in CCH, but not in DCM or controls, may help to explain the diffuse myocardial fibrosis and inflammation characteristic of the disease.

Adult↗
PubMedDate not supplied

Decreased numbers of T-lymphocytes and predominance of recently recruited macrophages in the walls of peripheral pulmonary arteries from 26 patients with pulmonary hypertension secondary to congenital cardiac shunts.

INTRODUCTION: In the primary form of pulmonary hypertension (PH), the involvement of inflammation in the physiopathology of the vascular lesions is well established. Its role in secondary PH is yet to be investigated. We quantified the inflammatory cells on the walls of peripheral pulmonary arteries from patients with congenital heart shunts. METHODS: Twenty-six lung biopsies from patients with increased pulmonary flow and 10 lung fragments from control participants were examined. B-lymphocytes (CD20), T-lymphocytes (CD3), recently recruited macrophages (MAC387) and granulocytes (CD15) were quantified by area of the adventitia in arteries >50 microm. An index of inflammatory cells infiltrating the medial and intimal layers was also determined. RESULTS: There was no difference in the sum of densities of adventitial inflammatory cells between the groups. A prevalence of MAC387-labeled cells was detected in the PH group and of CD3-labeled cells in the controls. There was a lower density of T-lymphocytes in the PH group (P<.004). Patients with intimal proliferative lesions showed prevalence of MAC387-labeled cells (P=.004). PH participants showed a higher index of MAC387-labeled cells infiltrating the arterial medial and intimal layers (P<.001). CONCLUSION: The predominance of recently recruited macrophages in the PH group is compatible with ongoing inflammatory reaction in the arterial walls. This could be related to the pathogenesis of the vascular lesions, as a consequence of cytokines produced by the inflammatory cells. The smaller number of adventitial T-lymphocytes in patients with congenital shunts can reflect an impairment of their immune response.

Antigens, CD20↗