Biomedical subjects

Pamela Somers

Publications and source records attributed to Pamela Somers.

7 recordsLinked to original sources

PubMed2006

Histopathology of calcific aortic valve stenosis.

Calcific aortic valve stenosis is the most common and increasing heart valve disease in the western world. In the last 30 years, diagnosis and management were revolutionized by the development of cardiac catheterisation, echocardiography, cardiac surgery, and medication. Recently, new strategies were introduced for aortic valve replacement using more sophisticated bioprosthetic heart valves. Moreover, tissue-engineered heart valves are under development to improve management strategies. In this article we review the current morphological and histopathological findings in the progression of calcific aortic valve stenosis. This is, to our understanding, important to contribute to the knowledge of fundamental management strategies of this disease.

Aortic Valve Stenosis↗

PubMed2006

Histological evaluation of autophagic cell death in calcified aortic valve stenosis.

BACKGROUND AND AIM OF THE STUDY: Calcification in aortic valves is the most common valvular lesion in western populations. This event is correlated with cellular degeneration in the valvular cusps, although there is no exact evidence how these cells die: this requires further exploration. METHODS: Twelve human severely calcified aortic valves obtained during cardiac surgery were studied by semi-quantitative analysis, and results compared with data from 12 human control aortic valves obtained during autopsy. Tissue analysis was by hematoxylin and eosin and Alcian blue staining. Detection of neurons was by immunohistochemical staining of PGP9.5 and neurofilament. In order to detect autophagy, an immunohistochemical staining for ubiquitin was used. The TUNEL technique was used to detect apoptosis. Co-localization of Alizarin red with ubiquitin labeling was performed on non-decalcified aortic valves. RESULTS: Hematoxylin and eosin staining showed moderate to severe mineralization in 10 of 12 patients in the surgical group, but in only one of 12 in the autopsy group. No significant observations were made with regard to PGP9.5 and neurofilament staining. Moderate to severe ubiquitin labeling was found initially in the majority of the surgical resection group (9/12) compared to a minority in the autopsy group (1/12). TUNEL-positive labeling was very rare and found mostly at the endothelial layer of the valvular cusps. CONCLUSION: Immunohistochemical methods showed the main cell death mechanism involved in the calcification of aortic leaflets to be autophagy rather than apoptosis. These findings suggest that autophagic cell death might play a role in the release of matrix vesicles in early degenerative aortic valves, thereby attracting inflammatory cells, and this could eventually lead to mineralization.

Aged↗

PubMed2005

Influence of intracoronary attenuation on coronary plaque measurements using multislice computed tomography: observations in an ex vivo model of coronary computed tomography angiography.

Assessment of attenuation (measured in Hounsfield units, HU) of human coronary plaques was performed using multislice computed tomography (MSCT) in an ex vivo model. In three ex vivo specimens of left coronary arteries in oil, MSCT was performed after intracoronary injection of four solutions of contrast material (400 mgI/ml iomeprol). The four solutions were diluted as follows: 1/infinity, 1/200, 1/80, and 1/20. All scans were performed with the following parameters: slices/collimation 16/0.75 mm, rotation time 375 ms. Each specimen was scored for the presence of atherosclerotic plaques. In each plaque the attenuation was measured in four regions of interest for lumen, plaque (non-calcified thickening of the vessel wall), calcium, and surrounding (oil surrounding the vessel). The results were compared with a one-way analysis of variance test and were correlated with Pearson's test. There were no significant differences in the attenuation of calcium and oil in the four solutions. The mean attenuation in the four solutions for lumen (35+/-10, 91+/-7, 246+/-18, 511+/-89 HU) and plaque (22+/-22, 50+/-26, 107+/-36, 152+/-67 HU) was significantly different between each decreasing dilution (p<0.001). The mean attenuation of lumen and plaque of coronary plaques showed high correlation, while the values were significantly different (r=0.73; p<0.001). Intracoronary attenuation modifies significantly the attenuation of plaques assessed with MSCT.

Cadaver↗

PubMed2005

Influence of increasing convolution kernel filtering on plaque imaging with multislice CT using an ex-vivo model of coronary angiography.

PURPOSE: To assess the variability in attenuation of coronary plaques with multislice CT-angiography (MSCT-CA) in an ex-vivo model with varying convolution kernels. MATERIALS AND METHODS: MSCT-CA (Sensation 16, Siemens) was performed in three ex-vivo left coronary arteries after instillation of contrast material solution (Iomeprol 400 mgI/ml, dilution: 1/80). The specimens were placed in oil to simulate epicardial fat. Scan parameters: slices 16/0.75 mm, rotation time 375 ms, feed/rotation 3.0 mm, mAs 500, slice thickness 1 mm, and FOV 50 mm. Datasets were reconstructed using 4 different kernels (B30f-smooth, B36f-medium smooth, B46f-medium, and B60f-sharp). Each scan was scored for the presence of plaques. Once a plaque was detected, the operator performed attenuation measurements (HU) in coronary lumen, oil, calcified and soft plaque tissue using the same settings in all datasets. The results were compared with T-test and correlated with Pearson's test. RESULTS: Overall, 464 measurements were performed. Significant differences (p<0.05) were found for the mean attenuation of lumen (B30f/B36f, B30f/B60f, B36f/B46f, B36f/B60f, and B46f/B60f), oil (B30f/B36f, B30f/B46f, B30f/B60f, B36f/B46f, and B46f/B60f), calcium (all kernels), and plaque (B30f/B36f, B30f/B46f, B30f/B60f, and B46f/B60f) using 4 different kernels. The attenuation values (mean+/-SD) within the lumen (246+/-6, 215+/-13, 248+/-5, and 270+/-7), oil (-123+/-3, -127+/-1, -121+/-6, and -127+/-4), calcified plaque tissue (703+/-334, 739+/-364, 817+/-381, and 1181+/-503), and soft plaque tissue (134+/-56, 111+/-49, 120+/-56, and 102+/-41) showed high correlation (p<0.001) when attenuation of all structures were compared in different kernels. CONCLUSIONS: Use of sharper convolution kernels significantly increases the attenuation of the calcium within coronary plaques and reduces the attenuation of soft plaque tissue.

Aged↗

PubMed2004

Smooth muscle cell hypertrophy in varicose veins is associated with expression of estrogen receptor-beta.

Varicose veins are characterized by dilated and thickened vein walls. This study examined whether the changes that occur in varicose veins are associated with smooth muscle cell (SMC) hypertrophy, cellular proliferation or apoptosis. Moreover, the association between SMC hypertrophy and the expression of the estrogen receptor-beta (ERbeta) was investigated. Varicose veins were obtained from male patients during vascular stripping surgery (n = 11) and nonvaricose veins during coronary bypass surgery, also from male subjects (n = 12). The cellular volume of the SMC in both the longitudinal and circular layer of the vessel wall was measured using stereological methods. Apoptosis was detected using the TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling) technique. SMC proliferation and ERbeta expression were investigated by immunohistochemistry. Neither in the longitudinal nor in the circular layer of the varicose vein wall were signs of apoptosis or proliferation present. However, the mean cellular volume of the SMC in the circular layer of the varicose veins was strongly increased (5,291 +/- 363 microm3) as compared to non-varicose veins (2,812 +/- 212 microm3, p < 0.001). Moreover, ERbeta expression in the circular layer of varicose veins (63 +/- 4%) significantly differed from nonvaricose veins (39 +/- 4%; p = 0.001). Interestingly, the SMC volume correlated with ERbeta expression (r = 0.71, p < 0.001). These data show that cell death or proliferation of SMC do not, or only rarely, occur in varicose veins. However, remodeling of varicose veins can mainly be attributed to increased volumes of the SMC of the circular layer and this increase correlates with ERbeta expression.

Adult↗

PubMedDate not supplied

The histopathology of varicose vein disease.

Varicosity is a complex venous pathology affecting the lower extremities. The exact etiology and physiopathology of varicose vein disease remain, however, unclear. Several theories exist from incompetence of the valves to a disturbance of the smooth muscle cells (SMC) and extra-cellular matrix (ECM) organization providing a weakness of the venous wall. Multiple studies have been performed to explain the underlying mechanisms of varicosity inducing alterations in the expression patterns of the endothelium, SMC, and ECM. In that respect, most attention has been focused on the alteration of the endothelium due to blood stasis and hypoxia inducing migration/proliferation of the medial SMC into the intima. Also, studies in the deformation of the ECM induced by alterations of the expression patterns of the metalloproteinases (MMP) and their inhibitors (TIMPs) have been put forward to explain the etiology of varicosity. However, less attention has been paid to the hormonal changes that occur during pregnancy and menopause, crucial factors to be involved in the etiology of varicosity. Since alteration of the estrogen receptor-b (ERb) expression could enhance directly the cellular volume of SMC and thus the disorganization of the contractile-elastic units, hypertrophy of SMC must be accounted a pivotal role that could induce the weakness of the venous wall. Altogether, this review summarizes an overview of the latest findings of varicosity with respect to the histopathological changes of the different cellular components of the varicose vein wall related to functional and morphologic alterations.

Endothelium, Vascular↗

PubMedDate not supplied

Autophagy as mechanism for cell death in degenerative aortic valve disease.

Once degenerative aortic valve disease becomes symptomatic, valve replacement is necessary for prognostic and symptomatic reasons. In elderly patients, symptoms of degenerative aortic valve can often be doubtful. Therefore, it is difficult but important to distinguish patients who need surgery from those who do not. Estimation of the rate of the progression of this disease can be helpful herein because one needs to bear in mind that aortic valve degeneration is an active process, which can influence the rate of progression. Recently, autophagy was discovered as a mechanism of cell death in different cardiovascular diseases such as atherosclerosis, aortic valve degeneration, heart failure and at regions around heart infarctions. Thus understanding autophagy in all its details can be helpful to contribute insights into the cell death machinery of cardiovascular diseases. This could open ways for inhibition of cell death in cardiovascular disease and possibly define targets for future drug design.

Aortic Valve↗