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Biomedical subjects

G D Angelini

Publications and source records attributed to G D Angelini.

At least 199 records · Page 11Linked to original sources
PubMed1992

Overcoming perioperative spasm of the internal mammary artery: which is the best vasodilator?

After mobilization, vasospasm often reduces flow through the internal mammary artery. An established method of relaxing the artery and increasing flow is to wrap it in a papaverine-soaked swab. To our knowledge the ability of other topical vasodilators to overcome spasm of the internal mammary artery has not been studied clinically. In 50 patients in whom the left mammary artery was used for myocardial revascularization, we have investigated the effect of five agents on internal mammary artery free flow. The agents investigated were normal saline, papaverine, nifedipine, glyceryl trinitrate, and sodium nitroprusside. Under controlled hemodynamic conditions, free flow was measured before any pharmacologic intervention and a median of 18.5 minutes after the pedicle had been sprayed with one of the five agents. Normal saline produced a small increase in flow from a median of 23 ml/min (range 17 to 88) to 38 ml/min (20 to 84) (not significant), whereas a significant increase occurred with papaverine, from 25 (16 to 78) to 43 ml/min (34 to 112) (p less than 0.01). Nifedipine and glyceryl trinitrate raised free flow by almost threefold, from 23 (14 to 66) to 71 ml/min (45 to 118) and from 23 (14 to 58) to 62 ml/min (46 to 126), respectively (both p less than 0.001). Sodium nitroprusside, however, with an increase in flow from 26 (10 to 58) to 108 ml/min (46 to 196), 250% over control, proved to be more effective than nifedipine and glyceryl trinitrate (p less than 0.05). We therefore recommend the topical use of sodium nitroprusside to relieve perioperative spasm of the internal mammary artery.

Administration, Topical↗
PubMed1992

Time-course of medial and intimal thickening in pig venous arterial grafts: relationship to endothelial injury and cholesterol accumulation.

With use of an established model of pig saphenous vein grafts in the carotid artery, the time-course of the following changes was related: (1) medial and intimal size by morphometry of transverse sections, (2) cell number by deoxyribonucleic acid concentration, (3) cell density by deoxyribonucleic acid concentration per milligram wet weight and by counting nuclei in transverse sections, (4) endothelial morphology by scanning electron microscopy, and (5) cholesterol concentration. In the first week after grafting, medial and intimal thickening occurred associated with an increase in cell number. Between 1 and 4 weeks after grafting, further rapid medial and intimal thickening occurred with no further increase in cell number but with a reduction in cell density, which suggested that cell migration, hypertrophy, and the laying down of extracellular matrix were responsible. Between 4 and 39 weeks after grafting, a slower increase in medial and intimal size occurred, associated with a parallel increase in cell number and no further change in cell density. The endothelium of grafts showed only localized abnormalities, including loss of cells and leukocyte adhesion, either 1 or 4 weeks after grafting. Cholesterol concentration was slightly elevated 1 week after grafting but returned to values similar to those in vein by 4 weeks after grafting. Distention to 600 mm Hg during surgical preparation of vein for grafting resulted in lower graft patency after either 1 or 4 weeks and caused significant medial and endothelial injury. Distention did not, however, affect changes in medial or intimal size, deoxyribonucleic acid, or cholesterol concentration caused by grafting. We conclude that three processes contribute to medial and intimal thickening, namely: (1) an initial phase of rapid smooth muscle cell proliferation, (2) smooth muscle cell migration, hypertrophy, and synthesis of extracellular matrix, and (3) a late phase of slower smooth muscle cell proliferation. The incomplete late suppression of smooth muscle cell proliferation occurs despite regeneration of a morphologically intact endothelium and in the absence of progressive cholesterol accumulation.

Anastomosis, Surgical↗
PubMed1991

Winner of the ESVS prize 1990. Smooth muscle cell proliferation in response to injury in an organ culture of human saphenous vein.

The principal cause of late vein graft occlusion is intimal smooth muscle cell proliferation, the underlying basis of which remains an enigma. Early theories implicating platelet activation now appear untenable since intimal proliferation progresses after endothelial repair, and is little influenced by antithrombotic treatments. We developed an organ culture of human saphenous vein to investigate the basis of intimal proliferation in a preparation which preserved the anatomical relationships of endothelium, smooth muscle and extracellular matrix. Tissue viability remained high during culture for up to 14 days and intimal smooth muscle proliferation occurred. The removal of endothelium reduced intimal thickening in cultured veins from 26 +/- 5 to 6 +/- 3 microns and also reduced the number of intimal cells/mm labelled with [3H]-thymidine from 12 +/- 4 to 3 +/- 1 (both p less than 0.01, n = 10). Surgical preparation of vein resulted in significant injury to medial smooth muscle cells, which was only partially reversed during culturing. Surgical preparation did not affect intimal proliferation, but stimulated medial proliferation from 3 +/- 1 to 32 +/- 9 [3H]-thymidine-labelled cells/mm (p less than 0.01, n = 11). These experiments reveal evidence for proliferation enhancing factors derived from endothelium and injured smooth muscle cells, which probably participate in intimal proliferation in vein grafts. Inhibiting their action may therefore present new possibilities for therapy.

Awards and Prizes↗
PubMed1990

A fiber-optic retractor for harvesting the internal mammary artery.

A retractor for exposure and dissection of the internal mammary artery incorporating a fiber-optic transillumination system is presented. The device, which can be converted to a standard sternal retractor, has also proved valuable in improving illumination during procedures on the mitral valve and in facilitating dissection of fibrous adhesions from the anterior surface of the heart at reoperation.

Cardiac Surgical Procedures↗
PubMed1990

Adverse hemodynamic effects and echocardiographic consequences of pericardial closure soon after sternotomy and pericardiotomy.

The acute hemodynamic and echocardiographic effects of pericardial closure on cardiac function were studied in 11 pigs during steady-state anesthesia and ventilation. Observations were made after sternotomy, both while the pericardium was open and after it had been closed, and then after closure of the chest, after the pericardium had been reopened by removing the pericardial suture through the chest wall. In five pigs, further observations were made when a suture was tightened to close the pericardium while the chest remained closed. Closure of the pericardium when the chest was open reduced cardiac output by 14% and mean stroke volume by 19% (both p less than 0.05). Systemic vascular resistance increased by 15% when the pericardium was closed while the chest was open (NS), and increased by 19% when it was closed while the chest was closed (p less than 0.05). Heart rate did not change significantly, and the systemic blood pressure was maintained (-8%, NS). All these effects were reversed by opening the pericardium. Intrathoracic epicardial echocardiographic monitoring of the left ventricle showed that its end-diastolic dimension increased (by 11%, p less than 0.05) when the pericardium was opened. After chest closure, paradoxical motion of the interventricular septum was consistently demonstrated only during ventilation, and it was not related to whether or not the pericardium was open. This study suggests that cardiac function may be impaired by pericardial closure after cardiac surgery because of some degree of constriction of the heart chambers, although acute circulatory responses compensate for the mild decrease in stroke volume. Monitoring of blood pressure alone cannot document the subtle circulatory changes induced by pericardial closure, and therefore it is not a reliable guide to decisions of whether to close the pericardium or leave it open in individual patients.

Animals↗
PubMed1990

Intimal proliferation in an organ culture of human saphenous vein.

This study investigated whether intimal proliferation, the characteristic feature of the response of human saphenous vein to arterial implantation, also occurs in organ culture. Vein segments were maintained for 14 days in medium supplemented with 30% fetal bovine serum. Tissue viability (measured by adenosine triphosphate [ATP] concentration) decreased only 20% from 280 +/- 20 to 220 +/- 20 nmol/g wet weight. In veins prepared for culturing, endothelial loss (approximately 20%) was confined to near the cut edges. Cultured veins retained an endothelial layer in the initially undamaged areas, while the initially injured areas became covered by a mixture of endothelial and vascular smooth muscle cells. Autoradiography in conjunction with scanning electron microscopy showed the presence of proliferating cells on the intimal surface. Transverse sections of cultured veins showed the development of a new intima containing vascular smooth muscle cells identified by immunocytochemistry with anti-alpha-actin. There were also endothelial cells identified with Ulex europaeus lectin arranged in capillarylike structures. Pulse or continuous labeling of cultures with [3H]thymidine showed that proliferating cells were confined to the new intima and suggested that the smooth muscle cells in this layer arose from both immigration and proliferation. The results demonstrate that intimal proliferation occurs in organ culture of human saphenous veins.

Adult↗
PubMed1990

Preparation of the internal mammary artery.

The internal mammary artery is the best currently available conduit in coronary artery bypass surgery. It is a living arterial graft with intact smooth muscle and its efficiency as a conduit therefore depends to a large extent on the way it is mobilized and prepared for grafting. This article discusses the anatomical, technical and pharmacological aspects of the surgical preparation of the internal mammary artery for coronary grafting.

Humans↗
PubMed1990

Distention promotes platelet and leukocyte adhesion and reduces short-term patency in pig arteriovenous bypass grafts.

A pig model of autologous saphenous vein to common carotid artery bypass grafting was developed. An end-to-end anastomotic technique led to lower middle graft and distal turbulence. Saphenous veins were surgically prepared with or without distention at 600 mm Hg, implanted into the arterial circulation, and removed 2 hours later. Medial integrity was then assessed by adenosine triphosphate/adenosine diphosphate concentration ratio, and endothelial integrity, leukocyte and platelet adhesion by scanning electron microscopy. In grafts made with undistended vein adenosine triphosphate/adenosine diphosphate concentration ratio was not significantly lower (3.0 +/- 0.1, n = 32) than in freshly isolated vein (3.3 +/- 0.1, n = 26), endothelial cover was 98% +/- 1%, n = 6, and there was little platelet or leukocyte adhesion. In distended grafts adenosine triphosphate/adenosine diphosphate concentration ratio was reduced to 2.2 +/- 0.2 (n = 7, p less than 0.005), endothelial cover was reduced to 38% +/- 14% (n = 6, p less than 0.001), and there was extensive platelet and leukocyte adhesion to exposed subendothelium. In separate experiments graft patency measured at 1 to 5 weeks was significantly greater (96%, n = 25) when undistended vein was used than when distended vein was used (64%, n = 25, p less than 0.005). The data show that distention leads to medial and endothelial damage and that this is associated with increased platelet and leukocyte adhesion and with reduced early patency.

Adenosine Diphosphate↗
PubMed1989

Late postoperative cardiac tamponade presenting as dysphagia.

A case of late cardiac tamponade seen with progressive dysphagia 15 days after aortic valve replacement is reported. The diagnosis was confirmed echocardiographically and successful pericardiocentesis was followed by immediate alleviation of the dysphagia.

Aortic Valve↗
PubMed1989

Severe stenotic scar contracture of the Microvel Hemashield right-sided extracardiac conduit.

We report 2 patients who developed severe scar contracture of a Microvel Hemashield valveless right-sided extracardiac conduit implanted 14 months earlier. In both cases, the diameter of the conduit was reduced along its entire length, with the prosthetic material plicated inward by retraction and organization of connective fibrous tissue on either side of the conduit.

Blood Vessel Prosthesis↗
PubMed1989

Post-infarction ventricular septal defect: the importance of right ventricular coronary perfusion in determining surgical outcome.

Mortality from a post-infarction ventricular septal defect (VSD) can be reduced by surgery, selection for which would be helped by knowledge of factors affecting the postoperative prognosis. We reviewed our 9-year experience (1978-1987) of 40 surgically treated patients, comparing preoperative characteristics in those who died postoperatively (n = 15, 37%) and those who survived (n = 25, 63%), all still alive. Sex, age, infarct size as assessed by peak serum creatine kinase values, left ventricular end-diastolic pressure and pulmonary/systemic flow ratio (2.9 +/- 0.2 vs 3.1 +/- 0.3) were similar. Survivors had a lower incidence of inferior infarct than those who died (6, 24% vs 9, 60%, P less than 0.05), a lower incidence of cardiogenic shock (7, 28% vs 10, 67%, P less than 0.05), less elevation of right ventricular end-diastolic pressure (10.1 +/- 0.9 vs 14.7 +/- 1.0 mm Hg, P less than 0.01) and less impairment of right ventricular coronary supply as determined by a coronary angiography-derived myocardial score (0.9 +/- 0.3 vs 4.7 +/- 0.7, P less than 0.001). The data suggest that right ventricular coronary perfusion influences prognosis. The proposed angiographic score may help to identify preoperatively those patients most likely to benefit from surgery.

Cardiac Catheterization↗
PubMed1989

Surgical preparation impairs release of endothelium-derived relaxing factor from human saphenous vein.

Release of endothelium-derived relaxing factor was measured from freshly isolated human saphenous vein and from vein subject to routine surgical preparation for coronary artery bypass grafting. Surgical preparation led to a significant decline in endothelium-derived relaxing factor release as compared with freshly isolated vein, and these changes were associated with loss of endothelial coverage. Storage of freshly isolated vein in blood but not in Hartmann's solution also resulted in a decline in maximally stimulated endothelium-derived relaxing factor release that was not associated with loss of endothelium. Reduced production of endothelium-derived relaxing factor, a potent vasodilator and inhibitor of platelet adhesion and aggregation, may be implicated in the etiology of early vein graft thrombosis.

Animals↗