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Biomedical subjects

M B Forman

Publications and source records attributed to M B Forman.

At least 37 records · Page 2Linked to original sources
PubMed1991

Reduction of myocardial reperfusion injury by intravenous adenosine administered during the early reperfusion period.

Adenosine influences the function of several cell types thought to be involved in the pathogenesis of myocardial reperfusion injury. We have previously demonstrated that intracoronary administration of adenosine enhances myocardial salvage 24 hours after reperfusion. To determine if these beneficial effects could be obtained during a prolonged period of reperfusion using an intravenous route of administration, 22 closed-chest dogs were subjected to 90 minutes of proximal left anterior descending coronary artery occlusion and 72 hours of reperfusion. Animals randomly received either intravenous adenosine (0.15 mg/kg/min) or an equal volume of Ringer's lactate during the first 150 minutes of reperfusion. The area at risk was defined in vivo with Monastral blue, and infarct size was measured histologically with Mallory's trichrome stain. Serial global and regional ventricular function were determined with contrast ventriculography and analyzed using a computerized radial shortening method. Biopsies were obtained from the central ischemic zone to assess endothelial ultrastructure and capillary obstruction. No significant effects in heart rate or blood pressure were noted during adenosine infusion. Transmural collateral blood flow during ischemia was similar in the groups. Infarct size expressed as a percentage of the anatomical area at risk was significantly less in the adenosine-treated group (35.3 +/- 4.3% in controls versus 17.1 +/- 4.3% in treated animals, p less than 0.01). A progressive decrease in transmural blood flow was noted in control animals during reperfusion, resulting in a significant reduction at 3 hours compared with the preocclusion value (0.69 +/- 0.11 ml/min/g [at baseline versus 0.45 +/- 0.10 ml/min/g at 3 hours, p less than 0.05]). In contrast, flow in adenosine animals at 3 hours was similar to baseline values (0.91 +/- 0.15 ml/min/g at baseline versus 0.98 +/- 0.14 ml/min/g at 3 hours, p = NS) and was significantly higher (p less than 0.05) than the control group. Radial shortening in the ischemic zone was significantly improved at 3 (-2.6 +/- 2.8% in controls versus 11.6 +/- 3.3% in treated animals, p less than 0.01) and 72 hours (5.5 +/- 2.0% in controls versus 17.3 +/- 3.5% in treated animals, p less than 0.01) after reperfusion in treated animals. Electron microscopy showed reduced neutrophil and erythrocyte plugging of capillaries with relative preservation of endothelial cell structure in the adenosine group.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1990

Reduction of myocardial ischemia during percutaneous transluminal coronary angioplasty with oxygenated Fluosol.

The effects of perfusion of an oxygen-carrying perfluorochemical emulsion (Fluosol) in alleviating symptoms of myocardial ischemia during balloon occlusion were examined in a multicenter trial of 245 patients. Severe anginal pain occurred less frequently in patients receiving Fluosol perfusion (21%) than in those receiving routine angioplasty (34%) (p less than 0.05). ST-segment changes at balloon deflation in routine angioplasty patients were significantly greater than in patients who received oxygenated Fluosol perfusion (2.2 +/- 1.2 vs 1.7 +/- 0.9 mm; p less than 0.03). Profound regional wall dysfunction (-561 +/- 224 U) was observed in routine angioplasty patients by 2-dimensional echocardiography. Patients receiving oxygenated Fluosol perfusion, however, maintained near baseline levels of ventricular function (-61 +/- 335 U) during occlusion (p less than 0.0001). Mean global left ventricular ejection fraction was preserved at baseline levels during balloon inflation in patients perfused with oxygenated Fluosol but decreased significantly (p less than 0.001) during occlusion in routine angioplasty patients. A total of 26 complications (19 routine group; 7 perfusion group) was reported. Adverse responses to the perfusate were infrequent, occurring in 1.6 and 2.0% of patients after the test dose and during perfusion, respectively. Thus, transcatheter perfusion with an oxygen-carrying perfluorochemical emulsion is effective in alleviating myocardial ischemia during angioplasty and can be safely administered in this patient population.

Aged↗
PubMed1990

Long-term effects of excision of the mitral apparatus on global and regional ventricular function in humans.

To evaluate the long-term sequelae of mitral valve excision on global and regional wall motion, contrast left ventriculograms from 21 patients with suspected prosthetic mitral valve dysfunction performed 10.4 +/- 2.1 years after mitral valve replacement were analyzed by a computerized radial shortening method. Patients with significant coronary artery disease (greater than 30% stenosis in any vessel) were excluded. In 8 of the 21 patients in whom preoperative ventriculograms were available, regional wall motion was normal before valve replacement. Although average radial shortening (35.6 +/- 4.8% versus 35.3 +/- 3.8%, p = NS) and left ventricular ejection fraction (62.8 +/- 4.2% versus 57.9 +/- 2.8%, p = NS) were unchanged in the preoperative and postoperative studies of these eight patients, radial shortening in the vicinity of insertion of the posteromedial papillary muscle declined significantly (38.4 +/- 6.4% to 20.8 +/- 4.4%, p less than 0.04). Postoperative radial shortening for all 21 patients at the site of insertion of the papillary muscle was also reduced to a significant degree compared with the average radial shortening (32.9 +/- 10.3% versus 17.5 +/- 2.0%, p less than 0.001). The findings demonstrate significant long-term and possibly permanent regional ventricular dysfunction after severing the chordae tendineae during mitral valve replacement.

Female↗
PubMed1990

Intracoronary adenosine administration during reperfusion following 3 hours of ischemia: effects on infarct size, ventricular function, and regional myocardial blood flow.

Previous studies have demonstrated that adenosine significantly enhances myocardial salvage after 90 minutes of regional ischemia. To determine its effect after prolonged ischemia, closed-chest dogs underwent 3 hours of left anterior descending artery occlusion followed by 72 hours of reperfusion. Intracoronary adenosine (3.75 mg/min; at 1.5 ml/min:total volume = 90 ml; n = 10) or an equivalent volume of saline (1.5 ml/min: total volume = 90 ml; n = 9) was infused into the left main coronary artery during the first 60 minutes of reperfusion. Regional myocardial blood flow was assessed serially with microspheres and regional ventricular function was assessed by contrast ventriculography. Infarct size was determined histologically. Light and electron microscopy were utilized to assess neutrophil infiltration and microvascular injury. Adenosine failed to reduce infarct size expressed as a percentage of the area at risk (38.0 +/- 4.9% versus 34.8 +/- 4.6%; p = NS) or to improve regional ventricular function as measured by the radial shortening method (3.2 +/- 1.8% versus 2.2 +/- 3.1%; p = NS) at 72 hours after reperfusion. Vasodilatory effects were not observed in the endo- and midmyocardial regions of the ischemic zone during adenosine administration. This was associated with a similar extent of capillary endothelial changes and neutrophil infiltration in both adenosine-treated and saline control groups. These results suggest that severe functional abnormalities are present in the vasculature after 3 hours of ischemia and that adenosine therapy is ineffective in enhancing myocardial salvage.

Adenosine↗
PubMed1990

Effect of coronary angioplasty on electrocardiographic changes in patients with unstable angina secondary to left anterior descending coronary artery disease.

The effect of semiemergent percutaneous transluminal coronary angioplasty on clinical and electrocardiographic (ECG) variables was assessed in 76 patients with unstable angina secondary to an isolated severe proximal left anterior descending coronary artery stenosis. All patients manifested symmetric T wave inversion in two or more anterior ECG leads. Wall motion abnormalities were present in 37 patients on ventriculography before dilation. Angioplasty was successful in 70 patients (92%), resulting in a reduction in luminal diameter stenosis from 91 +/- 8% to 21 +/- 6%, with no major acute procedure-related complications observed. The other six patients underwent semiurgent (less than 48 h) coronary artery bypass surgery and three patients experienced a myocardial infarction (before bypass surgery in two). Serial ECGs revealed complete resolution of ST-T wave changes in 51% of patients at 14 weeks and in 90% at 28 weeks. In contrast, prolongation of the corrected QT interval, which was present in 16 patients (8%), normalized within 48 h of successful angioplasty. Twelve of these 16 patients with a prolonged QT interval had nonocclusive thrombus formation and poor collateral circulation on angiography. Patients were followed up for 6 to 43 months (mean 23 +/- 10). Angiographic evidence of restenosis was present in 34% of patients, all of whom underwent a successful second or third procedure. One death occurred at 8 months after successful angioplasty. Wall motion abnormalities had completely resolved in 13 of 15 patients who underwent repeat ventriculography, at which time 10 had a normal ECG. This study demonstrates that ECG changes may persist for up to 7 months in patients who undergo successful angioplasty for severe left anterior descending coronary artery disease and unstable angina. Semiemergent angioplasty was associated with a high initial success rate and excellent long-term outcome.

Adult↗
PubMed1990

Enhanced left ventricular contractility in autonomic failure: assessment using pressure-volume relations.

Severe autonomic failure is usually characterized by both supine hypertension and orthostatic hypotension. Inadequate preload reserve, insufficient arterial resistance and abnormal cardiac performance have been postulated to contribute to the hypotension. To clarify these mechanisms, left ventricular performance and contractility were assessed using radionuclide ventriculography and systolic pressure-volume relations when supine and with graded head-up tilt in 11 patients with autonomic failure. Results were compared with those of 12 normal subjects, using phenylephrine infusion for pharmacologic afterload augmentation after autonomic blockade with atropine and propranolol. In a subset of four patients with autonomic failure, systolic pressure-volume relations were similar by both the tilt and phenylephrine methods. In autonomic failure, end-diastolic volume, end-systolic volume and stroke volume decreased with progressive degrees of tilt (p less than or equal to 0.007 for each). The supine radionuclide ejection fraction and cardiac output were similar to those of normal subjects (69% versus 68% and 5.4 versus 4.9 liters/min, respectively, p = NS). However, the slopes of the pressure-volume relations and the supine pressure/volume ratio in autonomic failure were much greater than normal (8.8 versus 2.5, and 6.3 versus 3.6 mm Hg/ml, respectively, p less than or equal to 0.04 for both). The baseline total peripheral resistance was greater than normal (24.9 versus 17.4 mm Hg.min-1/liter, p = 0.01), but the resistance at maximal tilt failed to increase (20.8 +/- 6.1 units). Plasma norepinephrine concentrations were lower than normal. Thus, patients with autonomic failure had hypercontractile left ventricular performance when assessed by pressure-volume relations, and their hearts were well matched to the elevated peripheral resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

The effect of perfluorochemical fluosol-DA (20%) on myocardial infarct healing in the rabbit.

Although the perfluorochemical Fluosol-DA 20% has been shown to reduce myocardial infarct size, its effect on the evolution of infarct healing has not been determined. Rabbits (n = 91) were randomized to ether-oxygenated Fluosol-DA (20 ml/kg) administered intravenously at the time of reperfusion after 30 min of coronary occlusion or no intervention. Animals were sacrificed at 1, 3, 7, and 14 days after infarction. Infarct size was significantly reduced in Fluosol-DA treated animals when compared with controls at one and three days. Infarct thinning was observed at one and three days in both groups. Left ventricular wall thickness in the infarcted area was greater with Fluosol-DA than control at 7 and 14 days. Increasing amounts of foamy macrophages containing perfluorochemical particles were noted in treated animals at 7 and 14 days. No differences were noted in hydroxyproline content between groups. These studies suggest that Fluosol-DA results in persistence of foamy macrophages without significantly altering infarct topography in the temporary occlusion rabbit model.

Analysis of Variance↗
PubMed1990

Prevention of neutrophil-mediated injury to endothelial cells by perfluorochemical.

Myocardial salvage after reperfusion may be limited by neutrophil-mediated microvascular damage. The effect of the perfluorochemical, Fluosol-DA, and its various components on neutrophil adherence, cytotoxicity, and proteolytic enzyme release was examined on sheep large and small vessel endothelial cells in vitro. Cells were studied under normoxic (N) and anoxic conditions (A). Various concentrations of Fluosol (10%, 25%, and 50%) significantly reduced neutrophil adherence under both experimental conditions [mean 22 +/- 3.25% versus 7 +/- 0.8% (N) and 20 +/- 3.2% versus 7.5 +/- 0.9% (A); P less than 0.01]. The perfluorocarbons, perfluorodecalin (PFD), and perfluoro-tripropylamine (PFTP) in a 50 volume/percent concentration exhibited profound effects on adherence, particularly on cells subjected to anoxia (51% and 69% reduction in adherence, respectively; P less than 0.01). No effect on adherence was observed with other components, including the detergent, pluronic F68. A 25% reduction (P less than 0.02) in endothelial cytotoxicity was noted when neutrophils were preincubated with Fluosol. However, pretreatment of endothelial cells with Fluosol did not inhibit neutrophil adherence. Neutrophils stimulated with cytochalasin B and FMLP showed a significant reduction in lysozyme release after incubation with Fluosol (28 +/- 5% versus 17 +/- 4%; P less than 0.01). This study demonstrates that Fluosol significantly attenuates neutrophil adherence, cytotoxicity, and enzyme release in an in vitro model of microvascular injury. It also suggests that prevention of neutrophil-mediated microvascular damage may be an important mechanism whereby Fluosol enhances myocardial salvage after ischemia and reperfusion.

Animals↗
PubMed1990

Myocardial reperfusion injury. Histopathological effects of perfluorochemical.

Regional myocardial ischemic injury progresses as a "wave-front" phenomenon from the endocardium to the epicardium. Myocyte damage can be reversible or irreversible and is dependent on the duration of ischemia. Endothelial cell injury lags behind myocyte injury. Reperfusion of ischemic myocardium can result in the acceleration of endothelial injury with resultant conversion of surrounding reversibly injured myocytes to irreversible damage; this has been termed the "no-reflow" phenomenon. This process can be accelerated by the presence of neutrophils. Agents such as perfluorochemicals and adenosine, which attenuate endothelial injury and inhibit neutrophil infiltration, also reduce infarct size in animal models. Infarct size reduction with perfluorochemical was observed with both intracoronary and intravenous infusion. Infarct healing was not adversely affected except for the persistence of perfluorochemical-laden macrophages. These studies suggest that perfluorochemicals and adenosine might be beneficial adjuvants to thrombolytic therapy in the reduction of reperfusion injury.

Animals↗
PubMed1990

Mechanisms and therapy of myocardial reperfusion injury.

Recent advances in thrombolytic therapy and balloon angioplasty have resulted in reperfusion therapy as a logical maneuver in the treatment of evolving myocardial infarction. The introduction of electrolytes, oxygen, and cellular elements, especially neutrophils, however, into the previously ischemic bed may initiate cellular and biochemical changes that limit the amount of potentially salvageable myocardium (reperfusion injury). Experimental studies have demonstrated that microvascular damage may play an important role in the pathogenesis of this phenomenon. Reperfusion enhances the infiltration of activated neutrophils into the ischemic bed, and neutrophil plugging of capillary lumens in association with extensive disruption of endothelial cells results in a progressive decrease in blood flow (the "no-reflow" phenomenon). Activated neutrophils may potentiate the inflammatory response, produce cellular damage, and reduce capillary blood flow by producing chemoattractants, proteolytic enzymes and reactive oxygen species, and arachidonate products, respectively. Therapeutic strategies that modify the interaction between neutrophils and endothelium have shown promising results in experimental preparations for reperfusion. The administration of both perfluorochemical (Fluosol, Alpha Therapeutic Corp., Los Angeles, California) and adenosine after reperfusion has resulted in enhanced myocardial salvage after 90 minutes of ischemia in the canine model. Histological studies have shown reduced neutrophil infiltration and relative preservation of endothelial cells without neutrophil plugging with both agents. Both adenosine and perfluorochemical have been shown to reduce neutrophil adherence and cytotoxicity to endothelial cell cultures. These findings suggest that suppression of neutrophil activation, especially chemotaxis, might be an ideal step to reduce this component from the inflammatory response in the ischemic myocardium after reperfusion. Clinical trials seem warranted to determine the role of reperfusion injury in limiting myocardial salvage in patients undergoing reperfusion within the first few hours of a thrombotic event.

Adenosine↗
PubMed1989

Emergent coronary angioplasty in the treatment of acute ischemic mitral regurgitation: long-term results in five cases.

Severe mitral regurgitation in the setting of an evolving myocardial infarction is associated with a high operative mortality rate. Five patients with acute severe mitral regurgitation secondary to ischemic posterior papillary muscle dysfunction underwent emergent percutaneous transluminal coronary angioplasty. Two patients were in cardiogenic shock and required intraaortic balloon counterpulsation. Angioplasty resulted in rapid improvement in hemodynamic variables, and all patients were discharged at a mean of 10 days after the procedure. Long-term follow-up study (mean 35 +/- 6 months) revealed normal mitral valve function angiographically and by Doppler echocardiography in four patients. Repeat angioplasty was required in one patient, and another underwent coronary artery bypass surgery without valve replacement for restenosis. One patient developed progressive mitral regurgitation and required elective mitral valve replacement 12 months after angioplasty. These preliminary findings suggest that emergent coronary angioplasty is a useful therapeutic intervention in the treatment of ischemic mitral regurgitation and is associated with a favorable long-term outcome.

Adult↗
PubMed1989

Endothelial and myocardial injury during ischemia and reperfusion: pathogenesis and therapeutic implications.

Early reperfusion remains the most effective way of limiting myocardial necrosis and improving ventricular function in experimental models and human patients. However, the introduction of oxygen and cellular elements, especially the neutrophil, into the ischemic zone may initiate a deleterious cascade of events that limits myocardial salvage after reperfusion. Although the pathogenesis of reperfusion injury remains controversial, recent studies have suggested that the endothelium may play a critical role. Endothelial cells maintain flow in the microcirculation by secreting a number of vasodilatory compounds and substances that prevent plugging of capillaries by inhibiting neutrophil adherence and platelet aggregation. Reperfusion of ischemic myocardium accelerates structural and functional changes in endothelial cells, resulting in a progressive decrease in microcirculatory flow ("no reflow" phenomenon). Numerous studies suggest that activated neutrophils mediate vascular damage by releasing reactive oxygen species and potent proteolytic enzymes. The administration of therapeutic agents that limit endothelial disruption and neutrophil plugging has shown promising results in limiting myocardial reperfusion injury in experimental models.

Animals↗
PubMed1989

Limitation of myocardial reperfusion injury by intravenous perfluorochemicals. Role of neutrophil activation.

Neutrophil activation and infiltration into the ischemic myocardium after reperfusion may limit the amount of salvageable myocardium (reperfusion injury). The effects of intravenous perfluorochemicals (Fluosol-DA) on infarct size, ventricular contractility, and neutrophil function were assessed in an occlusion-reperfusion canine model. Closed-chest dogs were subjected to 90 minutes of left anterior descending artery occlusion followed by 24 hours of reperfusion. Animals were randomized to receive either Fluosol-DA (FDA, n = 8) or Ringer's lactate (CONT, n = 10) intravenously over 30 minutes just before left anterior descending artery reperfusion. Neutrophil demargination and infiltration into the myocardium were assessed in vivo with In111. Neutrophil chemotaxis, superoxide radical production, and lysozyme degranulation were evaluated ex vivo at baseline, 1 hour after occlusion, and 1 hour after reperfusion. Perfluorochemicals significantly reduced infarct size expressed as percent of area at risk (FDA, 7 +/- 4%; CONT, 24 +/- 6%; p less than 0.01). This was associated with positive wall motion in the jeopardized zone of Fluosol-DA animals compared with dyskinesis in control animals (FDA, +4.4 +/- 2.1%; CONT, -1.1 +/- 1.5%; p less than 0.05). Electron microscopy showed reduced neutrophil and erythrocyte plugging of capillaries with relative preservation of endothelial cells in the Fluosol-DA animals. Myocardial blood flow was greater in the ischemic endocardium of Fluosol-DA animals 1 hour after reperfusion (FDA, 1.23 +/- 0.21; CONT, 0.62 +/- 0.08 ml/g/min; p less than 0.01). Neutrophil demargination and infiltration into the ischemic myocardium was reduced in the animals treated with Fluosol-DA. (FDA, 2.5 +/- 0.7 x 10(3); CONT, 14.1 +/- 2.7 x 10(3) neutrophils/g; p less than 0.01). Neutrophil chemotaxis and lysozyme release were also markedly suppressed in the Fluosol-DA groups ex vivo. These results show that intravenous Fluosol-DA significantly reduces reperfusion injury with greater salvage of myocardium and improved left ventricular function. The chief mechanism of action of Fluosol-DA appears to be the suppression of neutrophil function.

Animals↗
PubMed1989

Intracoronary adenosine administered after reperfusion limits vascular injury after prolonged ischemia in the canine model.

Myocardial salvage after reperfusion may be limited by deleterious vascular changes in the previously ischemic microcirculatory bed. This could result in a progressive decrease in blood flow in the capillary bed to potentially viable myocytes (no-reflow phenomenon). The effect of intracoronary adenosine on these changes was assessed in 15 closed-chest dogs subjected to 2 hours of proximal left anterior descending artery (LAD) occlusion followed by 3 hours of reperfusion. Animals randomly received adenosine (n = 8) 3.75 mg/min into the proximal LAD or an equivalent volume of saline (control) (n = 7) for 1 hour after reperfusion. Endothelial-dependent and independent coronary vasodilator reserve was determined using a chronically implanted volume-flowmeter on the mid-LAD at baseline and 1 and 3 hours after reperfusion with acetylcholine and papaverine infusions, respectively, into the proximal vessel. Regional myocardial blood flow was measured serially with radioactive microspheres and regional contractile function with contrast ventriculography. Both agonists produced a significant increase in LAD flow before occlusion. Endothelial-dependent and independent vasodilatory reserve was significantly reduced (p less than 0.05) at 1 and 3 hours after reperfusion in control animals compared with adenosine treatment. A progressive decrease in mid-LAD flow and increase in coronary vascular resistance after reperfusion was observed in control animals (p less than 0.05). The treated group manifested improved regional myocardial blood flow in endocardial regions from the central (0.73 +/- 0.15 versus 0.24 +/- 0.11 ml/g/min; p less than 0.02) and lateral ischemic zones (0.80 +/- 0.15 versus 0.34 +/- 0.12 ml/g/min; p less than 0.05) 3 hours after reperfusion. A significant reduction (p less than 0.05) in endocardial and midmyocardial flow compared with baseline was seen in control animals at 3 hours. Intravascular and interstitial neutrophil infiltration was reduced in adenosine animals and this was associated with relative ultrastructural preservation of endothelial cells. Regional ventricular function in the ischemic zone was improved in the adenosine group 3 hours after reperfusion (13.4 +/- 3.9% versus -5.3 +/- 1.6%; p less than 0.001). This study demonstrates that selective administration of adenosine after reperfusion significantly attenuates functional and structural abnormalities in the microvasculature after prolonged (2 hours) regional ischemia in the canine model. Prevention of microvascular injury and the non-reflow phenomenon by adenosine may preserve reversibly injured myocytes following restoration of blood flow to previously ischemic myocardium.

Adenosine↗
PubMed1988

Myocardial protection by perfluorochemical infusion during transient ischemia produced by balloon coronary occlusion.

To assess the efficacy of the perfluorochemical Fluosol-DA 20% for myocardial protection during repeated periods of balloon occlusion of the left circumflex coronary artery, 25 anesthetized dogs were randomized to receive either oxygenated perfluorochemical, (Fluosol-DA [F]; n = 10) or oxygenated Ringer's lactate (R; n = 6), at the rate of 30 ml/min, during inflation of the balloon. A control group (C; n = 9) received no infusion. A total of eight inflations were performed, each lasting 90 seconds, followed by an equivalent deflation time. Hemodynamics, ECGs, regional myocardial function, and biochemical parameters were studied. Significant differences were noted in ST segment elevation at 90 seconds of inflation in the F (1.5 mm +/- 0.6), C (3.7 mm +/- 0.75), and R (2.9 mm +/- 0.75) groups (F vs C or R p less than 0.05). This was associated with significant improvement in radial shortening in the jeopardized zone at 45 seconds into occlusion in the F group compared to the C and R groups (F = 21.1% +/- 5.1 vs C = 3.5% +/- 4.5 or R = 1.1% +/- 3.2; p less than 0.05). Results of electron microscopy showed reversible changes of ischemia within the mitochondria, and these were most marked in the C and R groups compared to the F group. Endothelial swelling was mild and was present only focally in the R and C groups. Thus perfluorochemicals may enhance the safety and efficacy of balloon angioplasty.

Adenine Nucleotides↗
PubMed1988

A comparison of morphologic and angiographic findings in long-term internal mammary artery and saphenous vein bypass grafts.

Internal mammary artery grafts are currently considered the conduits of choice for myocardial revascularization. Comparisons of long-term morphologic changes in internal mammary artery grafts and saphenous vein grafts and correlation with premortem angiography have not been reported. Eighteen internal mammary artery and 15 saphenous vein grafts that had been in place for 12 to 118 months (mean 56) in 18 patients were removed either surgically or at necropsy and examined histologically. Premortem angiograms were performed within 1 month of histologic study in 15 of these patients. Fibrointimal proliferation was more frequent in internal mammary artery than in saphenous vein grafts 8 [( 44%] of 18 versus 4 [27%] of 15; p = NS). In contrast, atherosclerosis was common in saphenous vein grafts but was extremely rare in internal mammary artery grafts (10 of 15 versus 1 of 18; p = 0.01). A good correlation was noted between the degree of narrowing estimated by angiographic and histologic measurements in both internal mammary artery grafts (d = 0.90) and saphenous vein grafts (d = 0.71). Accelerated atherosclerosis did not occur in internal mammary artery grafts, but was common in saphenous vein grafts. Fibrointimal proliferation was commonly associated with graft narrowing in internal mammary artery grafts and may be an important factor in late graft closure. This study also confirms that internal mammary artery grafts have greater longevity compared with saphenous vein grafts.

Adult↗