Intima thickness structure during restenosis after aorto-femoral bypass

Intima thickness structure during restenosis after aorto-femoral bypass

Poster session abstracts / A therosclerosis 115 (Suppl.) (1995) $45-$129 P20 Cardiology SI27 P20 CARDIOLOGY 476 478 MRI OF ATHEROSCLEROTIC PLAQUES...

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Poster session abstracts / A therosclerosis 115 (Suppl.) (1995) $45-$129 P20 Cardiology

SI27

P20 CARDIOLOGY 476

478

MRI OF ATHEROSCLEROTIC PLAQUES: WATER T2S ARE SIMILAR IN VIVO AND IN VITRO J.F. Toussaint J.F. Southern, G. Lamuraglia, V. Fuster, H.L. Kantor Mass. Gen. Hosp. Cardiac Unit, Harvard MS, Boston, MA & CEA Orsay, NMR-Center

INTIMA THICKNESS STRUCTURE DURING RESTENOSIS AFTER AORTO-FEMORAL BYPASS B.V. Shekhonin, A.E. Zotikov, A.V. Pokrovsky Cardiology Research Center, flrd Cherepkovskaya str. 15A, 121552 Moscow, and Vishnevsky Institute of Surgery, B Serpukhovskaya str. 27, 113811 Moscow, Academy of Medical Sciences, Russia

13ackground: Collagenous cap thickness is a major factor of atheromatous plaque stability. No technique is presently capable of discriminating this component from the lipid core in vivo. Using :HNMR we have demonstrated that water T2 in vitro is shorter inside the lipid core than in collagenous cap. The aim of this study was to determine T2 in vivo in atherosclerotic plaques at 1.5T. Methods: Three patients were studied before carotid endarterectomy with an ECG gated spin-echo sequence. T2 was determined by a double echo sequence (TE 20 and 55ms, TR = 1 cardiac cycle; slice thickness: 5mm). After surgery, samples were imaged at 37°C, with the same parameters as in vivo. Plaque structure was determined by histology. Results: In vivo and in vitro T2 are shown below. Values are obtained from 10-15 measurements in 3 successive slices (mean -I- SD, in ms). Lipid Core Collagen Cap Meclia In vivo 27.9"±5.8 50.6+9.9 48.4+7.1 In vitro 31.9"±4.7 51.3±8.6 52.7+6.4 "p < 0.001 compared to media and collagenous cap. In vitro values are not significantly different from in vivo values. Adventitia with a short T2 (24.8±4.3) appears as a low intensity layer. Conclusion: At clinical field, water T2's of atherosclerotic plaques are similar in vivo and in vitro: long T2 regions correspond to collagen or media; short T2 to lipid rich regions. 'H-MRI allows the discrimination of atheromatous plaque component in vivo. Improving NMR microscopy in vivo may help to differentiate stable from vulnerable plaques.

The structure of intimal thickness in the area of distal anastamosis after aortofemoral reconstruction was studied using histological and immunohistochemical methods. The above mentioned segments were resected for return reconstruction for patients with thrombosis or restenosis anastamosis. The period from the initial operation ranged from 6 month to 15 years. Intimal thickenings with the structure of a fibrous atherosclerotic plaques were found in the anastamosis area. The peculiarity of this plaques consist in increased amount of type IV collagen around the smooth muscle cells (SMC) and great accumulation of fibrinogen in the subendothelial area. In addition, intimal thickenings free of lipids were detected. Their extracellular matrix contained collagen of I,III,IV,V types and fibronectin. Specifical for this type of intimal thickening was diffuse distribution of collagen type IV and high contents of fibrinogen in extracellular matrix (ECM). In addition to fresh thrombotic masses parietal organizated trombes were found. Besides high concentration of fibrinogen and fibronectin they contained collagen types I,III,IV and V. Diffuse localization of type IV collagen in the connective tissue together with interstitial collagen was detected. Sometimes it was difficult to distinguish the old organized trombotic masses from the intimal thickenings mentioned above. In conclusion, we suggest that hydrodynamic stress in the area of distal anastamosis and high degree of blood coagulation may be considered as a stimulating factor for atherosclerotic progress, intramural thrombosis and/or local intimal thickening.

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THE HISTOLOGY OF THE SUPERFICIAL FEMORAL ARTERY FOLLOWING ENDARTERECTOMY P.D.F. Dodd J.V, Smyth, J. Hoyland', M.G. Walker Manchester Royal Infimary, University of Manchester', England

UNSATISFACTORY MANAGEMENT OF HYPERLIPIDAEMIA IN PATIENTS UNDERGOING CORONARY ARTERY BYPASS GRAFTING T.M. Ooi, A. Cooper, G Jackson Department of Cardiology, Guy's Hospital, London, U.K

The nature of the arterial wall remaining after closed-loop endarterectomy was examined. Conventional, immunohistochemical (IHC), and scanning electron microscopic techniques were used on explanted human superficial femoral artery specimens. We performed closed-loop endarterectomy on samples of occluded superficial femoral artery from patients undergoing bypass procedures. Histological examination included haemotoxy[in/eosin, Masson's trichrome and elastin vav Gieson staining. IHC markers fibronectin, collagen IV, smooth muscle actin, yon Willehrand factor, CD68, plasminogen activator inhibitor I were used. In-situ hybridisation for tissue plasminogen activator was performed. Scanning electron microscopy using an environmental scarming technique which avoids the need for tissue drying was employed. We found that closed-loop endarterectomy produces a consistent plane of cleavage at that level of the internal elastic lamina (IEL) with no retention of sub-intimal smooth muscle. The IEL was well preserved without exception. The residual surface was rich in fibronectin. Restenosis after surgery to peripheral vessels is a major cause of delayed failure in revascularisation procedures. It has been shown that preservation of the IEL is an important factor in this process. The preservation of this layer is a significant finding after closedloop endarterectomy.

Objective: To audit the detection and management of hyperlipidaemia in patients undergoing coronary artery bypass graft surgery (CABG). Method: a prospective and retrospective review of 65 patients who underwent CABG over 2 months. (Prospective review by personal interviews, questionaires, and follow-up by telephone, retrospective review by analyses of case notes, questionaires and contact by telephone) All lipid data were checked on computer database. Results: 1.Forty-three patients in this study were recruited into the study of lipid profile before and after CABG; of these, 15(23%) had undetected hyperlipidaemia, which was defined by patients' unawareness of their abnormal and treatable lipid levels i.e.. total cholesterol and low density liproprotein of greater than 5.2mmol/L and 3.4mmol/L respectively; up to the day of admission for CABG, and absent computer records of lipid profile at Guy's. Hyperlipidaemia would otherwise remain undetected. Of these 15 patients, 7 alleged their lipid profiles were assessed either by their general practitioners or local referring physicians, but were not advised afterwards. 2.Two (3 %) patients with known hypercholestrolaemia, were on lipid lowering therapy which was discontinued on discharge from Guy's after CABG. Because they were recruited into the study of lipid profile, their cholesterol levels were shown to rise to untreated levels by the first post-operative month, clinicians were consequently alerted and lipid lowering therapy restarted. Conclusion: The detection and management of hyperlipidaemia in CABG patients remains unsatisfactory. More detailed post-operative supervision is necessary.