No abstract available.
Cholesterol, HDL* ; Coronary Artery Disease* ; Coronary Vessels* ; Fibrinogen*

BACKGROUND: Neointimal ingrowth rather than stent recoil has thought to be important for coronary arterial in-stent restenosis. Intuitively cell migration and extracellular matrix (ECM) formation seems to be important in the pathogenesis of stent restenosis. Therefore, with specific aim of identifying molecules implicated in cell migration and extracellular matrix formation, histopathologic analysis on atherectomized coronary arterial in-stent restenotic tissue was performed. METHODS: In the present study we analyzed 29 atherectomized coronary arterial in-stent restenotic tissue specimens (LAD 14, LCX 5, RCA 10) retrieved (5.7+/-5.4 months after stent deployment) from 25 patients (age 59+/-13, M/F:18/70) in whom restenosis complicated previous revascularization with Palmaz-Schatz stent. Histopathologic analysis was performed after immunostaining. Antibodies against TGF- 1, hyaluronan synthase (HAS) 1, MMP1, MMP9, urokinase type plasminogen activator, PDGF receptor were used for immunostaining. RESULTS: Myxoid tissue characterized by stellate-shaped cells embedded in a loose ECM was present in 20 out of 29 specimens, and tends to decrease over time after stenting. Foci of cell poor area (48-320 cells/mm2) in a microscopic field was present in 17 out of 29 specimens, and tends to increase over time after stenting (13/16 in <4 mo vs. 4/13 in > or =4 mo, p<0.01). Various proportions of specimens show positive stained cells with respect to each antibodies: TGF 1 in 16 out of 20:HAS1 in 10 out of 13:MMP1 in 8 out of 16:MMP9 in 4 out of 13:PDGF receptor in 12 out of 17 specimens. Abundant cells labled with certain antibodies (TGF 1, uPA, PDGF receptor) were frequently found in myxoid tissue. CONCLUSIONS: Myxoid tissue, frequently found in stent restenotic tissue, may be a biologically active tissue in terms of cell migration and of ECM formation. ECM accumulation tends to increase over time after stenting and may be important in pathogenesis of coronary arterial stent restenosis.
Antibodies ; Cell Movement* ; Extracellular Matrix* ; Humans* ; Hyaluronic Acid ; Receptors, Platelet-Derived Growth Factor ; Stents* ; Urokinase-Type Plasminogen Activator

BACKGROUND AND OBJECTIVES: Neointimal ingrowth rather than stent recoil is thought to be important for coronary in-stent restenosis. However only limited pathologic data are available to adress the mechanisms of in-stent restenosis. With the specific aim of measuring cell replication and of assessing cellularity and extracellular matrix (ECM) composition, we analyzed atherectomized coronary arterial in-stent restenotic specimens. METHODS AND RESULTS: In the present study, we analyzed 29 atherectomized coronary arterial in-stent restenotic tissue samples (14 LAD, 10 RCA, and 5 LCX) retrieved from 25 patients (m/f:18/7: age 59+/-13 yr) at 0.5-23 (mean 5.7) months after deployment of Palmaz-Schatz stent. Histopathological analysis of cellular components and ECM was performed using H & E, modified Movat pentachrome, and immunocytochemical staining. Cellular proliferation rate, as estimated by use of antibodies to Ki-67 nuclear antigen showed low proliferation rate with the range of 0-4%, and no positive cells were found in 62% of cases. Myxoid tissue having ECM enriched with versican and hyaluronan was found in 69% of cases, and decreased over time after stenting. Foci of cell poor area were found in 57% of cases, and could be classified into as: (1) containing collagen-rich ECM and (2) containing a proteoglycan-rich ECM. Versican, biglycan, perlecan, and hyaluronan were identified with varying individual distributions in the proteoglycan rich area. Specimens with foci of cell poor area tended to increase over time after stenting (31% in & 4 mo vs. 81% in > or =4 mo after stenting, p<0.01). alpha-smooth muscle actin staining identified the majority of cells as smooth muscle cells (SMC) and occasional macrophages (< or =12 cells per section) were detected by CD68 antibody. CONCLUSIONS: These data suggest that enhanced ECM accumulation rather than cell proliferation may be important mechanisms for stent restenosis. Angioplasty of stent restenosis may therefore fail due to transient compression of this hygroscopic matrix.
Actins ; Angioplasty ; Antibodies ; Biglycan ; Cell Proliferation ; Extracellular Matrix ; Humans* ; Hyaluronic Acid ; Macrophages ; Myocytes, Smooth Muscle ; Proteoglycans ; Stents* ; Versicans

BACKGROUND AND OBJECTIVES: As previously reported, unstable angina is usually related to characteristic coronary artery lesion's morphology analyzed by coronary angiogram. This takes the form of an eccentrically placed convex stenosis with a narrow neck due to one or more overhanging edges or irregular, scalloped borders, or both. Although most studies were done for lesions with high degree stenosis(>50%), recent studies emphasized the role of vulnerability of plaque in acute coronary syndrome and even mild degree stenotic lesions may progress rapidly to evoke acute coronary syndrome. Therefore in this study, we analyzed the morphological characteristics of coronary artery lesions with mild degree stenosis as well as severe stenosis. MATERIALS AND METHODS: We conducted a retrospective study of 96 patients with angina pectoris (42 of stable patients and 54 of unstable patients) who underwent coronary angiography. Each lesions with 25% or greater diameter stenosis were categorized into simple and complex lesion(convex intraluminal obstruction with a narrow neck or irregular borders, diffuse irregularities, ulceration, thrombus). Calcification of coronary artery, extents of lesions were analyzed and stenosis grade and location were categorized by AHA classification. RESULTS: There were no significant differences between the stable angina and unstable angina in risk factors and vessel involvement, numbers of lesions, calcification and total obstruction. In morphologic analysis, complex lesions were more frequent in unstable angina than stable angina (49% vs 33%, p<0.05). The mean of percent diameter stenosis was not signigicantly different between two groups, but severe stenotic lesions with 90% or more stenosis were more frequent in unstable angina (34% vs 22%, p<0.05). Locations of involved vessels were similar between the angina groups. Complex lesions were distributed more frequent in RCA and simple lesions were more in LAD and LCX (p<0.05). CONCLUSIONS: The lesions with both complex morphology and severe degree stenosis are closely implicated in unstable angina.
Acute Coronary Syndrome ; Angina Pectoris ; Angina, Stable ; Angina, Unstable* ; Classification ; Constriction, Pathologic ; Coronary Angiography ; Coronary Vessels* ; Humans ; Neck ; Pectinidae ; Retrospective Studies ; Risk Factors ; Ulcer

We report a case of 86-year-old woman with coronary artery fistula connecting the right coronary artery and left bronchial artery accompanied with cystic lung disease presenting with dyspnea and chest pain. Coronary angiography revealed that right coronary artery was anastomosed with the collaterals of left bronchial artery at the right hilum and tortuously ascended along the aortic arch and descended connecting with left pulmonary lobar artery at a certain site which is faintly opcified showing to and pro phasic movement. Chest CT scan shows the multicystic changes of the left lower lobe of the lung and hypertrophied bronchial artery of left lobar bronchus. Under the diagnosis of coronary artery fistula, hypertensive heart disease and multicystic lung disease, patient's symptoms and signs were improved by conservative treatment without surgical intervention.
Aged, 80 and over ; Aorta, Thoracic ; Arteries ; Bronchi ; Bronchial Arteries* ; Chest Pain ; Coronary Angiography ; Coronary Vessels* ; Diagnosis ; Dyspnea ; Female ; Fistula* ; Heart Diseases ; Humans ; Lung Diseases* ; Lung* ; Tomography, X-Ray Computed

High output heart failure due to congenital arteriovenous fistula is a rare disease and is difficult to treat. A 27 year old man, suffering from dyspnea, palpitation, lower extremity edema, and abdominal distension admitted May, 1987. At admission there were continuous thrill and bruit at left supraclavicular and infraclavicular area. The heart sound was irregular and rapid, and grade IV/VI pansystolic murmur was audible at the apex. Chest PA showed marked cardiomegaly with pleural effusion and notching at superior aspect of left 2nd rib. Selective left subclavian artery angiogram showed extensive congenital arteriovenous fistula at the area of left subclavian artery and its branches. After setrial feeding artery embolization and palliative operation, the fistula size decreased much with clinical improvement.
Adult ; Arteries ; Arteriovenous Fistula* ; Cardiomegaly ; Dyspnea ; Edema ; Fistula ; Heart Failure ; Heart Sounds ; Humans ; Lower Extremity ; Pleural Effusion ; Rare Diseases ; Ribs* ; Subclavian Artery* ; Thorax

No abstract available.
Biomarkers ; Humans ; Myocardial Infarction

BACKGROUND: With the recent development in arterial reconstructive procedure such as percutaneous transluminal coronary angioplasty or atherectomy, the incidence of vascular complications involving femoral artery is increasing due to greater use of larger percutaneous instruments(including arterial sheath) and periprocedural anticoagulant therapy. Femoral pseudoaneurysm requires rapid diagnosis and management to prevent limb ischemia, worsening of the arterial injury or repair of the arterial defect. Recently, accurate diagnosis of these injuries can be made nonivasively with duplex sonography and Doppler color flow imaging, and nonsurgical treatment may be possible by using external compression guided by ultrasound even in patients requiring prolonged anticoagulant therapy. METHOD: Three patients, one undergoing coronary angiography and two undergoing percutaneous transluminal coronary angioplasty, developed expansile groin masses at the vascular access sites diagnosed as femoral artery pseudoaneurysm s by Doppler ultrasound. All patients were hypertensives, taking aspirin and two patients who underwent PTCA received intravenous heparin after procedure. After diagnosis of femoral pseudoaneurysm, all patients underwent mechanical(C-clamp) external compression guided by ultrasound for 3 hours. RESULT: Follow up color flow scans were obtained after 24 hours and in one patients, blood flow in the tract was eliminated but persistent blood flow was observed in two patients who underwent PTCA. Before closure of pseudoaneurysm, one patient needed another 6 hours of ultrasound guided compression and the other needed more 12 hours. All patients were discharged without complication or recurrence of pseudoaneurysm. CONCLUSION: These cases suggest that nonsurgical closure of femoral pseudoaneurysms is feasible even in patients requiring prolonged antiplatelet and anticoagulant therapy.
Aneurysm, False* ; Angioplasty, Balloon, Coronary ; Aspirin ; Atherectomy ; Cardiac Catheterization* ; Cardiac Catheters* ; Coronary Angiography ; Diagnosis ; Extremities ; Femoral Artery ; Follow-Up Studies ; Groin ; Heparin ; Humans ; Incidence ; Ischemia ; Recurrence ; Ultrasonography

There is increasing recognition in medical fields of the importance of behavioral and psychosocial factors in the development of cardiovascular disease. Although the pathogenesis underlying stress-induced atherosclerosis is not well known, inflammation may play a key role. Activation of stress-induced neuroendocrine pathways, such as the hypothalamo-pituitary-adrenal axis, and the sympathetic nervous and renin angiotensin systems, direct neurogenic inflammation may also contribute to the development of stress-induced atherosclerosis.
Atherosclerosis* ; Axis, Cervical Vertebra ; Cardiovascular Diseases ; Inflammation ; Neurogenic Inflammation ; Psychology ; Renin-Angiotensin System

BACKGROUND: We have shown that extracellular matrix (ECM) rather than cell proliferation contributes to in-stent restenosis. Transforming growth factor-beta (TGF-beta), a positive regulator of ECM deposition by vascular cells, may be implicated in in-stent restenosis. We assessed if the blockade of TGF-beta by catheter-based local delivery of an adenovirus expressing a soluble form of TGF-beta type II receptor (AdTbeta-ExR) can inhibit stent-induced neointima. METHODS: AdTbeta-ExR was applied onto a coronary arterial segment of a pig using an Infiltrator(TM), and either of adenovirus expressing beta-galactosidase (AdLacZ) or PBS was applied onto other remote segment of the same pig (n=10). Then, stents (n=20) were deployed in the treated arterial segment. RESULTS: Computer-based morphometric analysis 4 weeks after stenting showed no significant difference in neointima area between the AdTbeta-ExR-infected and control groups (AdLacZ and PBS). However cell density of neointima was significantly increased in the AdTbeta-ExR group compared with control group (3121+/-331 vs 2812+/-183 cells/mm2, p<0.05). Notably, the AdTbeta-ExR group had more extensive CD3 positive T cell infiltration. In addition matrix metalloproteinase (MMP)1 expression and accumulation of hyaluronan was greater in the AdTbeta-ExR group. Cell proliferation rate was significantly increased in the media of the AdTbeta-ExR group compared with control group (2.04+/-1.21% vs 1.18+/-1.06%, p<0.05). CONCLUSION: Blockade of TGF-beta by use of catheter-based local in vivo gene delivery did not alter neointima formation significantly in our porcine coronary artery stent model, however it increased inflammation and pathological changes that could promote lesion formation.
Adenoviridae ; beta-Galactosidase ; Cell Count ; Cell Proliferation ; Constriction, Pathologic* ; Coronary Restenosis ; Coronary Vessels* ; Extracellular Matrix ; Hyaluronic Acid ; Inflammation* ; Neointima* ; Stents ; Transforming Growth Factor beta*