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Biomedical subjects

B T Baxter

Publications and source records attributed to B T Baxter.

At least 19 recordsLinked to original sources
PubMed1996

Incidence and histologic characteristics of blebs in patients with abdominal aortic aneurysms.

PURPOSE: Aortic blebs-focal outpouchings within aortic aneurysms-may contribute to their eventual rupture. In this study we determine the incidence of aortic blebs and describe their microscopic features. METHODS: Computed tomographic scans of the abdominal aorta were obtained in 188 patients with aortic diameters measuring > or = 3 cm and were independently evaluated by a radiologist. The number and location of blebs were recorded, and each was measured with calipers. Sixteen blebs, with an adjacent uninvolved aneurysmal segment of aorta, and tissue from two patients with ruptured aneurysms were examined by light microscopy and immunohistochemical analysis. Specimens from six blebs and five aneurysms were examined for alpha 1 (I) procollagen messenger RNA by in situ hybridization. RESULTS: Twenty blebs, ranging in size from 5 to 30 mm (mean, 12 +/- 7 mm), were detected in 11% (20 of 188) of computed tomographic scans. Blebs were observed in 10% (11 of 111) of patients with aortic diameters between 3.0 and 4.9 cm, 10% (6 of 61) of patients with aneurysms between 5.0 and 6.9 cm, and 19% (3 of 16) of patients with aortic diameters > or = 7 cm. Histologically, the major difference between the aneurysmal aortic wall and blebs was found in the media. In aneurysmal aortas, the media consisted of multiple layers of fragmented elastic lamellae, whereas the number of elastic tissue elements along the circumference of the blebs progressively decreased; only a few isolated fragments of elastic tissue were present at the apices. Histologic evidence of rupture was evident in two specimens. A chronic inflammatory cell infiltrate composed of T and B lymphocytes, plasma cells, and macrophages, common to both the aneurysmal and the blebs, was most prominent in the adventitia of aneurysmal tissue, but involved both the media and adventitia of the blebs. In situ hybridization demonstrated the presence of alpha 1 (I) procollagen messenger RNA in four of the five aneurysm segments that were evaluated, compared with only one of six blebs. CONCLUSIONS: Blebs were discovered in aneurysms of all sizes; their frequency appeared to be unrelated to aneurysm size. The presence of inflammatory cell infiltrates and absence of alpha 1 (I) procollagen messenger RNA in five of six blebs suggest that a local imbalance of matrix degradation and repair plays a role in the cause of these lesions. Attenuation of the aortic wall accompanying the formation of blebs may predispose these sites to rupture.

Aorta, Abdominal↗
PubMed1996

Platelet-derived growth factor is a cofactor in the induction of 1 alpha(I) procollagen expression by transforming growth factor-beta 1 in smooth muscle cells.

PURPOSE: Depending on the derivation of vascular smooth muscle cells (SMC), transforming growth factor-beta 1 (TGF-beta 1) has variable effects on proliferation and expression of extracellular matrix. Relatively little is known about TGF-beta 1's effects on human arterial SMC. Therefore, we sought to determine the effects of TGF-beta 1 on human arterial SMC proliferation and 1 alpha(I) procollagen expression. The mechanisms by which TGF-beta 1 regulate type I procollagen expression were also investigated. METHODS: SMC cultures were established from the aorta of transplant donors. Serial doses of TGF-beta 1 were applied, and cellular proliferation assessed by cell counting and tritiated thymidine incorporation. Total cellular ribonucleic acid (RNA) was analyzed by reverse transcription-polymerase chain reaction and Northern blot for changes in 1 alpha(I) procollagen and platelet-derived growth factor (PDGF)-A transcripts. RESULTS: In a dose-dependent manner, TGF-beta 1 inhibited SMC proliferation despite early induction of PDGF-A mRNA. After a delay of 24 hours, TGF-beta 1 increased 1 alpha(I) procollagen expression by 36% compared with control. PDGF-neutralizing antibodies blocked the TGF-beta 1-mediated upregulation of type I procollagen, although PDGF alone had no effect on matrix expression. CONCLUSION: The results indicate that TGF-beta 1 is a potent inhibitor of human arterial SMC proliferation that has a moderate effect on 1 alpha(I) procollagen transcripts. Despite inducing PDGF-A gene expression, TGF-beta 1 is not a mitogen in adult human arterial SMC. TGF-beta 1 regulates SMC type I procollagen expression partly by inducing PDGF-A as a co-factor.

Adult↗
PubMed1995

Localization of aortic disease is associated with intrinsic differences in aortic structure.

PURPOSE: While localization of atherosclerosis and aneurysms to the infrarenal aorta has been attributed, in part, to hemodynamic factors, anatomic differences between the proximal and the distal aorta may also be important. Our purpose was to determine the changes in content and organization of major structural proteins (elastin and collagen) throughout the normal human aorta. METHODS: Biochemical analysis for desmosine-isodesmosine (elastin) and hydroxyproline (collagen) content was done by HPLC on complete 1-cm transverse rings removed from the ascending and descending thoracic aorta and abdominal supraceliac, suprarenal, and midinfrarenal aorta. Elastin and collagen content was normalized to lumenal surface area and compared by ANOVA: Light microscopy and optical micrometry were used to determine changes in intimal, medial, and adventitial thickness and number of elastin lamellae at each level. RESULTS: Both collagen/cm2 and elastin/cm2 decrease from the proximal to distal aorta. Collagen content did not differ among the three abdominal segments, but there was a 58% decrease in elastin between the suprarenal and the infrarenal aorta. The proportion of elastin and collagen does not differ throughout the aorta except in the infrarenal aorta where there is decreased elastin relative to collagen. CONCLUSION: Collagen and elastin in the distal aorta bear an increased load as compared to the proximal aorta. The infrarenal aorta differs biochemically and histologically from the remainder of the aorta. A decrease in infrarenal elastin without a corresponding decrease in collagen may effect the compliance and integrity of the distal aorta. These anatomic differences may be important in predisposing the infrarenal aorta to atherosclerosis and aneurysm formation.

Adult↗
PubMed1995

Transforming growth factor-beta 1 inhibits human arterial smooth-muscle cell proliferation in a growth-rate-dependent manner.

BACKGROUND: Proliferation of arterial smooth-muscle cells is central in the development of both atherosclerosis and intimal hyperplasia. The cytokine transforming growth factor-beta 1 (TGF-beta 1) is known to have variable effects on smooth-muscle cell proliferation. Using human arterial smooth-muscle cells, we sought (1) to define the serum concentrations required to maintain cellular proliferation; and (2) to define the effects of TGF-beta 1 on smooth-muscle cell proliferation. METHODS: Smooth-muscle cell cultures were established from the normal aorta of transplant donors. Cells were grown to subconfluent and confluent densities, then incubated in either serum-free media, or 1% or 10% fetal bovine serum (FBS) enhanced media. Cellular proliferation was assayed by cell counting at 24, 48, and 96 hours to establish growth rate. Identical experiments with the addition of recombinant human TGF-beta 1 (5 ng/mliters) were also performed. Studies were done in triplicate for each group, and results expressed as the mean +/- SE. Groups were compared by analysis of variance. RESULTS: In subconfluent cultures, only smooth-muscle cells in 10% FBS proliferated, whereas growth arrest occurred in serum-free media and 1% FBS. In confluent cultures, cells in all media conditions proliferated. TGF-beta 1 had an inhibitory effect in actively proliferating cultures. There was a positive correlation between the inhibitory effects of TGF-beta 1 and smooth-muscle cell growth rate (r = .65; P = 0.005). CONCLUSIONS: When confluent, human arterial smooth-muscle cells continue to proliferate after serum deprivation, suggesting that these cells are capable of conditioning their own medium. TGF-beta 1 inhibits smooth-muscle cell proliferation in a growth-rate-dependent manner. These data suggest that TGF-beta 1 may have a growth-regulatory role in vascular disease by counteracting states of arterial smooth-muscle cell proliferation.

Aorta↗
PubMed1995

Management of synchronous renal cell carcinoma and aortic disease.

BACKGROUND: We have noted a significant incidence of renal cell carcinoma (RCC) detected during evaluation for aneurysmal and aortoiliac occlusive disease. The approach to synchronous malignancy and aortic disease (staged versus concurrent resection) is controversial, as is the management of incidental RCC (partial versus radical nephrectomy). PATIENTS AND METHODS: We reviewed our experience with incidental RCC in patients undergoing aortic reconstruction between 1991 and 1994. Ninety-seven patients underwent aortic reconstruction for aneurysmal (72), occlusive (20), or embolic disease (5) during the time frame under review. All were men. Of the 80 preoperative computerized tomographic (CT) scans obtained, 7 (9%) demonstrated renal lesions suspicious for RCC. All lesions were explored and excised by partial or radical nephrectomy before heparinization and completion of the planned aortic procedure. RESULTS: The overall mortality rate was 3%. None of the deaths occurred in patients undergoing combined procedures. Four partial and three radical nephrectomies were performed. Of the 7 renal lesions, 2 were complex cysts and 5 were RCC. Both patients with complex cysts were treated with wedge resection. One patient required surgical drainage of a wound abscess after partial nephrectomy. No significant differences were found between preoperative (1.4 +/- 0.1 mg/dL) and postoperative (1.8 +/- 0.2 mg/dL) creatinine levels following combined procedures. On follow-up CT scans done at 6-month intervals (mean follow-up 24 months), no evidence exists of recurrence, metastasis, or graft infection. CONCLUSIONS: This patient population demonstrated an unexpectedly high prevalence of incidental RCC (5 or 80 CTs, 6%). No increase in mortality was found when RCC and aortic disease were treated at the same operation. While partial nephrectomy was associated with one wound infection in this series, it is an effective treatment for small incidental RCC and may avoid unnecessary nephrectomy in patients with benign disease. Base on the high incidence of RCC in this population, we recommend exploration of all suspicious lesions. Nephrectomy can be performed safely in the same setting as aortic reconstruction. Because underlying renal dysfunction is not uncommon in patients with aneurysmal and aortoiliac occlusive disease, nephron-sparing surgery should be considered.

Aged↗
PubMed1995

Pathogenesis of aneurysms.

We now know our past concepts of AAA pathogenesis to be oversimplified and inaccurate. In fact, the metabolic activity of the aneurysm wall is markedly increased in comparison with normal aorta. It has become clear that AAAs result not from passive dilatation, but from a complex remodeling process involving both the synthesis and degradation of matrix proteins. Our understanding of this process has been advanced by applying molecular biology techniques. Although elastin fragmentation and medial attenuation remain the most striking histological features of AAA tissue, experimental and clinical evidence suggests that the adventitia, which is predominantly collagen, is capable of maintaining the dimensional stability of the aorta in the absence of the medial elastin network. Thus, although factors that result in fragmentation and attenuation of elastin may be important in the etiology of AAA, factors regulating the balance of collagen synthesis and degradation likely determine the rate of AAA progression. The resident inflammatory cells in AAA undoubtedly play an important pathological role in aortic dilatation. Thus, understanding the interaction between aortic mesenchymal cells (smooth muscle cells and fibroblasts) and inflammatory cells (lymphocytes and macrophages) should allow for the identification of genetic factors that predispose to AAA. In addition to the possibility of early identification of patients at risk for AAA, new insights into AAA pathogenesis might allow for development of pharmacological strategies for inhibiting expansion of small AAA.

Aorta, Abdominal↗
PubMed1994

Elastin is increased in abdominal aortic aneurysms.

The decrease in elastin concentration in abdominal aortic aneurysm (AAA) has been ascribed to elastolysis. The discordant response of the elastin and collagen genes in AAA suggests a different explanation: dilution of elastin because of higher levels of synthesis of collagen and other matrix proteins. The purpose of this study was to determine circumferential content of elastin, collagen, and total protein in aneurysmal (AAA), atherosclerotic, and normal (NL) infrarenal aorta. Standard serial extraction techniques of complete 1-cm rings of midinfrarenal aortic tissue were used to remove soluble protein, calcium, and lipids. Hydroxyproline (collagen), desmosine/isodesmosine (elastin), and total amino acid (total protein) content were determined by amino acid analysis. Means values (+/- SEM) were compared by ANOVA. Circumferential content of desmosine/isodesmosine was increased 2.5-fold in AAA compared to NL (P < 0.05). Collagen and total protein were increased 5.7- and 4.7-fold, respectively (P < 0.05). There was a high degree of correlation between circumference and collagen content (r = 0.89). These data demonstrate that significant synthesis of matrix proteins accompanies aortic dilatation. While both elastin and collagen are increased, there is a much greater increase in circumferential collagen content than elastin content. These data do not preclude proteolysis as a factor in AAA but suggest that the decrease in elastin concentration results from dilution of elastin by a greater increase in the synthesis of other matrix proteins and that synthesis is an important factor in AAA formation.

Adult↗
PubMed1994

Abdominal aortic aneurysms are associated with altered matrix proteins of the nonaneurysmal aortic segments.

PURPOSE: Abdominal aortic aneurysms (AAA) are associated with diffuse arteriomegaly and peripheral aneurysms, suggesting a generalized process. Elastin and collagen are the key structural proteins of the aorta, and their relative content is markedly altered in tissue from AAA. Our purpose was to investigate elastin and collagen content in the proximal, nonaneurysmal segments of aortas with infrarenal AAA. METHODS: After extraction of lipid, calcium, and soluble proteins, hydroxyproline (collagen) and desmosine-isodesmosine (elastin) contents were determined by high-performance liquid chromatography in the ascending and descending thoracic, supraceliac, and suprarenal aorta. By repeated measures of analysis of covariance, collagen was found to be increased throughout the aorta in AAA as compared with normal aorta or aorta with atherosclerotic occlusive disease. This difference remained significant when adjustments were made for group differences in age and degree of atherosclerosis. This increase in collagen content results in a dilutional decrease in elastin concentration. These data demonstrate that the same matrix protein alterations found in AAA tissue occur throughout the aorta, differing only in magnitude in the aneurysmal and nonaneurysmal segments. These data suggest that aneurysm formation may related to alterations in the regulation of elastin and collagen.

Adult↗
PubMed1994

Pseudoaneurysm of the external carotid artery following radical neck dissection and irradiation: a case report and review of the literature.

A 54-year-old man developed a pseudoaneurysm of the left external carotid artery 8 years after concluding treatment for squamous cell carcinoma of the tongue. Treatment included radiation therapy, radical neck dissection and a myocutaneous pectoralis major flap. Percutaneous transcatheter embolization resulted in thrombosis of the pseudoaneurysm. A review of the literature yielded only six other reported cases of pseudoaneurysm of the external carotid artery proper.

Aneurysm↗
PubMed1993

Limb-threatening ischemia complicated by perigenicular infection.

When graft infection or infection of the medial leg or popliteal fossa precludes a standard approach to revascularization of the ischemic leg, the literature suggests amputation may be the most prudent course because of excessive perioperative mortality and morbidity of attempts to reestablish axial flow. The purpose of this study is to define the outcome of revascularization when limb-threatening ischemia is complicated by perigenicular infection. Of 1020 infrainguinal reconstructions performed since 1984, nine (0.9%) presented with limb-threatening ischemia and graft or wound infections involving the popliteal fossa (6) or medial thigh or calf wounds (3) which precluded standard revascularization in the five women and four men. Risk factors for infection included diabetes mellitus (5/9), wound hematoma at initial operation (2/9), and intravenous drug abuse (1/9); Staphylococcus aureus was the predominant organism in all infected wounds and two popliteal fossa infections. The other deep infections grew group D streptococci, Enterococcus, and Salmonella. Extra-anatomic reconstruction was performed from the femoral (7) and iliac vessels (2) extending to the below-knee popliteal (2), the anterior tibial (4) and the peroneal (3) arteries using vein (5), and PTFE (4) in a lateral tunnel which avoiding the plane of the infection. Postoperative complications included MI (1), early graft thrombosis (2), and osteomyelitis of the femur (1); there were no deaths. With a mean follow-up of 19 months (3-57 months), primary graft patency was 66% and secondary patency was 78%, resulting in salvage of 66% of extremities at risk. These data demonstrate the safety and efficacy of extra-anatomic reconstruction for maintaining axial flow when limb-threatening ischemia is complicated by perigenicular infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Rational approach to postoperative transfusion in high-risk patients.

An appropriate threshold for transfusion in patients with coronary artery disease has not been defined. Our purpose was to determine: (1) the effects of preoperative volume loading; (2) postoperative function and oxygen delivery (DO2); (3) an appropriate transfusion threshold based on observed DO2 in high-risk patients undergoing abdominal aortic aneurysm (AAA) repair, bypass of aortoiliac disease (AOD), distal bypass, or carotid endarterectomy (CEA). Preoperative volume loading increased cardiac output (CO) in all groups by 15% to 22%. Postoperative CO was unchanged from optimal preoperative values except in the CEA group, in which it decreased. Systemic vascular resistance decreased in the AAA and AOD groups. The decrease in postoperative DO2 in all groups (25% to 31%) was related to a decrease in hemoglobin. Despite marginal (less than 11 mL/kg/min) postoperative DO2 in more than a third of patients, there was no compensatory increase in CO. Thus, after optimization of function by volume loading, red cell transfusion may be the only way to increase DO2. Hemoglobin levels of 10 to 12 g/dL may be required for adequate DO2 when ventricular function is markedly impaired.

Aortic Aneurysm, Abdominal↗
PubMed1993

Elastin and fibrillin mRNA and protein levels in the ontogeny of normal human aorta.

Elastin associated microfibrils (EAMF) are ubiquitous connective tissue structures that are believed to provide tensile strength and flexibility to numerous tissues. In this study the ontogeny of EAMF in normal human aorta was examined using immunohistochemical analysis of fibrillin, an EAMF component, and mRNA levels of fibrillin and elastin. Specimens of infra-renal aorta from ages 11 months to 44 years were obtained following organ procurement. Decreasing amounts, as judged by computer digitized image analysis, of immunoreactive fibrillin when compared to elastin auto-fluorescence were observed in aortic sections with increasing age. Elastase treatment would un-mask the anti-fibrillin reactive epitope reinforcing the suggestion that EAMF act as a "scaffold" for elastin deposition. Northern and dot blot hybridizations demonstrated a decrease in relative fibrillin message levels with increasing age. The abundance of fibrillin in relation to elastin may suggest a role for EAMF independent of their association with elastin.

Actin Cytoskeleton↗
PubMed1993

Soluble factors modulate changes in collagen gene expression in abdominal aortic aneurysms.

BACKGROUND: Although increased procollagen gene expression and synthesis have been implicated in the progression of abdominal aortic aneurysms (AAA), factors modulating this change have not been identified. Furthermore, it is not known whether the increase in AAA procollagen expression is specific to this disease or also occurs in tissue affected by atherosclerotic occlusive disease (AOD). If paracrine rather than autocrine factors are responsible for increased gene expression in AAA, this effect should be transferable to target smooth muscle cells through conditioned media. Our objectives were to determine 1 alpha (I) procollagen messenger RNA levels in AOD tissue compared with normal and AAA and to determine whether differences noted in tissue procollagen gene expression could be transferred through conditioned media from normal, AOD, and AAA tissues to target smooth muscle cells in primary culture. METHODS: Normal, AOD, and AAA tissue was used for tissue RNA extraction or was minced and washed with serum-free media (4 degrees C) x 30 minutes and the media applied to human aortic smooth muscle cells (SMC) in primary culture for 36 hours. Total RNA from tissue and SMC exposed to conditioned media was analyzed by Northern and dot blot analysis for 1 alpha (I) procollagen. RESULTS: Relative tissue 1 alpha (I) procollagen levels were not increased in AOD (0.23 +/- 0.05) as compared with normal (0.17 +/- 0.03); both were decreased compared with AAA (0.53 +/- 0.07; p < 0.01). The 1 alpha (I) procollagen levels in SMC exposed to conditioned media from AAA (1.73 +/- 0.15) were increased (p < 0.05) compared with AOD (1.10 +/- 0.12) and normal (1.16 +/- 0.16). CONCLUSIONS: There is no increase in tissue AOD procollagen gene expression. The ability to transfer the same relative patterns of gene expression from tissue to target SMC with conditioned media suggests that paracrine, rather than autocrine, factors modulate procollagen expression in AAA tissues.

Adult↗
PubMed1992

Elastin content, cross-links, and mRNA in normal and aneurysmal human aorta.

Although elastin depletion is thought to be an etiologic factor in abdominal aortic aneurysm, little is known about its transcription and posttranslational modification in normal and diseased human aorta. Our objectives were to quantify total elastin and elastin cross-links (desmosine/isodesmosine [DID]) and to determine if elastin mRNA was detectable in the disease-prone infrarenal aorta from patients with abdominal aortic aneurysm and a comparative group with no aneurysmal diseases. After preliminary extraction and thermolysin digestion, content of DID and the elastin tetrapeptide, valine-alanine-proline-glycine (VAPG), were determined by high-performance liquid chromatography. Tissue mRNA was studied by Northern blot analysis. Mean values (+/- SE) were compared by Student's t test. The proportion of insoluble elastin was markedly decreased in abdominal aortic aneurysm tissue (1.3% +/- 0.04% vs 12% +/- -2.8%; p less than 0.001). There was no difference in the small percentage of elastin solubilized during extraction in abdominal aortic aneurysm (5.3% +/- 1%) and no aneurysmal disease (6.0% +/- 1.2%; p = 0.71) tissues. The DID concentration of insoluble elastin was not different for abdominal aortic aneurysm and no aneurysmal disease tissue (0.18% +/- 0.07 vs 0.18 +/- 0.05 nm DID/nm VAPG; p = 0.97). On the basis of VAPG content, only 26% +/- 4% of the sodium hydroxide insoluble residue from abdominal aortic aneurysm was elastin; the predominate protein(s) was high in polar amino acids. Elastin mRNA was detectable in all tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Collagen and elastin gene expression in aortic aneurysms.

BACKGROUND: The decreased elastin concentration found in abdominal aortic aneurysms (AAAs) may result from a differential synthetic response wherein elastin gene expression fails to increase in parallel with type I procollagen (COL I) gene expression. The purpose of this study is to determine tissue mRNA levels for elastin and COL I in AAAs compared with levels in normal, age-matched aorta and to determine the relationship between aging and COL I gene expression. METHODS: Total RNA exacted from normal infrarenal aortic tissue (n = 7) and AAA (n = 10) tissue was subjected to Northern analysis. Mean values for COL I, elastin, and alpha-tubulin mRNA levels were compared by use of the Student t test. Age and COL I mRNA levels were analyzed by regression analysis. RESULTS: COL I mRNA was increased significantly in AAAs (1.18 +/- 0.13) compared with normal aortas (0.14 +/- 0.05). A commensurate increase in elastin mRNA (AAAs, 0.11 +/- 0.02, vs normal aortas, 0.39 +/- 0.2) was absent. There was no correlation between age and COL gene expression. CONCLUSIONS: The decreased elastin concentration relative to collagen in AAAs may be explained, in part, by the changes in message level of elastin and collagen. The enhanced COL I gene expression in AAAs is unrelated to age.

Aging↗
PubMed1991

Aneurysm or occlusive disease--factors determining the clinical course of atherosclerosis of the infrarenal aorta.

Atherosclerosis of the infrarenal aorta results in distinct clinical entities--aortoiliac occlusive disease (AOD) and abdominal aortic aneurysm (AAA). Although loss of collagen has been implicated in AAA, collagen accumulation plays a role in AOD. In vivo collagen-gene expression can be assessed using complementary DNA for collagen types I and III alpha-chains. The purpose of this study is to compare total collagen (type I + III) and collagen types I and III messenger RNA in AAA, AOD and normal aorta. Specimens were collected from the infrarenal aorta during operation for AOD (n = 7), AAA (n = 7), autopsy, or organ procurement (normal; n = 7). Northern transfer analysis of total RNA was used to compare mRNA levels for type I and III collagen. After preliminary extraction, specimens were hydrolyzed for hydroxyproline analysis used to calculate total collagen (type I + III). Relative levels of type I (pro-a1[1]) mRNA were greater in both AOD (0.77 +/- 0.35) and AAA tissue (0.94 +/- 0.24; p = 0.6) than in normal aorta (0.02 +/- 0.03). Type III (pro-a1[III]) mRNA levels were also greater in AOD (2.52 +/- 0.19; p = 0.09) and AAA tissue (3.15 +/- 1.3) than in normals (0.97 +/- 0.47). Total collagen concentration was increased in AOD (45.6% +/- 3.1% dry weight; p less than 0.05) but not AAA tissue (27.8% +/- 4%) when compared to normal aorta (34.7% +/- 2.3%). Collagen type I and III gene expression is greater in older, diseased aorta, yet collagen accumulated only in AOD. This implies a similar synthetic response in both AOD and AAA. Thus, proteolytic degradation in AAA appears to determine collagen content and possibly the clinical course of the atherosclerotic process.

Aged↗