Long-term human vein graft contractility and morphology: a functional and histopathological study of retrieved coronary vein grafts.

Vasoreactivity of 11 coronary artery vein bypass grafts and 13 human saphenous veins was examined. Isometric tension studies were performed in response to potassium chloride (110 mmol/l), noradrenaline (10(-9)-10(-4) mol/l), serotonin (10(-9)-10(-4) mol/l) and histamine (10(-8)-10(-2) mol/l). After precontraction with noradrenaline (10(-5) mol/l), the response to acetylcholine (10(-8)-10(-4) mol/l) and the calcium ionophore A23187 (10(-8)-10(-4) mol/l) was also assessed. Results are given as mean(s.e.m.). Compared with saphenous veins, vein grafts showed decreased sensitivity to noradrenaline (1.7(0.5) versus 0.4(0.1) mumol/l, P = 0.01), no change in sensitivity to serotonin (55(18) versus 37(15) mumol/l, P > 0.05) and supersensitivity to histamine (3.2(0.9) versus 30.1(13.2) mumol/l, P = 0.01). Vein grafts had a decreased maximal contraction to potassium chloride (1.1(0.3) versus 5.5(0.8) g, P = 0.0001), noradrenaline (1.2(0.3) versus 4.1(0.8) g, P = 0.005), histamine (1.2(0.3) versus 4.5(0.8) g, P = 0.003) and serotonin (0.7(0.2) versus 5.7(0.6) g, P = 0.0002) compared with saphenous vein. Precontracted vein grafts did not relax in response to acetylcholine; in contrast, saphenous vein relaxed in a dose-dependent manner to a maximal relaxation of 22(3) per cent. Both saphenous vein and vein graft relaxed in response to A23187. Vein graft intimal thickness was approximately fourfold greater than that of saphenous vein (540(110) versus 136(30) microns). Scanning electron microscopy of vein and vein graft revealed an intact endothelium. Coronary artery vein grafts are capable of responding to various contractile agonists; these response are notably different from those of saphenous vein and there is a loss of endothelium-dependent relaxation. Even at a late stage vein grafts are not inert but are functional conduits with an abnormally responsive endothelium and a less potent, but significantly altered, smooth muscle contractile profile.

Increased concentrations of angiotensin-converting enzyme in the intimal hyperplasia of experimental vein grafts.

Local renin and angiotensin-converting enzyme (ACE) activity were recently implicated in development of intimal hyperplasia after vascular injury, but little is known about the local responses of angiotensin I/II (AI/AII) and local ACE activity in vein graft physiology. The activity of the local ACE system of experimental vein grafts was examined in this study. The right carotid artery was divided and bypassed in 21 New Zealand White rabbits, using the right external jugular vein. The left external jugular vein was used as a control. Veins and vein grafts were harvested after 14 days. Rings from both vessels were studied in vitro under isometric tension, and dose-response curves to AI and AII were obtained. AI responses were also measured in the presence of captopril. The tissue concentrations of ACE in both vessels were estimated by spectrophotometry and were localized by immunohistochemistry. The responses of the veins to AI and AII were multiphasic, whereas the responses of vein grafts were sigmoid-shaped. Incubation of vein grafts with captopril significantly decreased the sensitivity to AI (p < 0.0001). Immunohistochemical localization identified ACE in the endothelial layer of the veins and vein grafts, but also at a greater density in the intimal hyperplasia of the vein graft. The concentration of ACE was 1.92 +/- 0.16 U/g (wet weight; mean +/- SEM, n = 9) in vein grafts and 1.39 +/- 0.05 U/g in the veins (38% increase, p < 0.05, n = 9).(ABSTRACT TRUNCATED AT 250 WORDS)

Argon beam coagulation compared with cryoablation of ventricular subendocardium.

The Argon Beam Coagulator uses radiofrequency energy to excite argon gas that may be used for ventricular ablation. The effects of power level and number of applications of the Argon Beam Coagulator were compared wtih cryothermia. Ten mongrel dogs underwent cardiac extirpation. The endocardial surfaces of 5 hearts were used for the creation of lesions using the Argon Beam Coagulator at five power levels with either one or two applications. Five hearts were used for endocardial and epicardial lesions using cryothermia (15-mm-diameter probe at -70 degrees C) for 1, 2, 3, or 4 minutes. The Argon Beam Coagulator lesions showed an increase in depth with increasing power levels (2.25 +/- 1.05 mm at 50 W to 6.64 +/- 0.75 mm at 150 W) and number of applications (maximum depth of 6.64 +/- 0.75 mm with one application, 11.2 +/- 1.1 mm with two applications). Cryothermia lesions were similar in depth regardless of duration or site of application (range, 6.1 to 10.2 mm). Both techniques resulted in homogeneous and well-demarcated lesions. These data show that the Argon Beam Coagulator results in discrete endocardial lesions, which may be created quickly and reproducibly. This may be a useful alternative for the operative ablation of endocardial scar in the treatment of ventricular tachycardia.

Early and late outcome following deployment of a new flexible tantalum intracoronary stent in dogs.

A new radiopaque, highly flexible balloon-expandable tantalum stent was tested. Thirty-six of 40 stents were successfully deployed percutaneously in the coronary arteries of 31 dogs. The dogs were given aspirin before, intravenous heparin during, and aspirin alone after the procedure. One dog died at 24 hours because of coronary occlusion following traumatic implantation. Four dogs were put to death early, revealing re-endothelialization by 9 days. Eleven dogs were put to death from 2 weeks to 9 months during long-term follow-up, showing all vessels widely patent with the stent uniformly embedded within a stable neointimal layer. Follow-up arteriography showed patency in all remaining stents up to 1 year, with no perforation or aneurysm formation. Four stents were placed into canine peripheral arteries and were removed percutaneously after deployment. Pathology revealed no significant trauma to involved vessels. This tantalum stent exhibits feasibility of percutaneous deployment, early neointimal formation, low thrombogenicity on long-term aspirin therapy alone, and patency up to 1 year in this canine model.

Saphenous vein endothelium-dependent relaxation in patients with peripheral vascular disease.

In vitro vasomotor responses of saphenous veins of 15 patients undergoing peripheral vascular bypass procedures were studied. Vessels were harvested by standard techniques, sectioned into 4 mm rings, and suspended in organ baths under isometric tension. Stimulation with cumulative doses of norepinephrine revealed a -logED50 of 6.85 +/- 0.12 M and maximal tension of 8.64 +/- 1.77 g. Patient characteristics suggesting high maximal response (by univariate analysis) included male sex (male 11.69 +/- 2.49 g versus female 5.08 +/- 1.69 g; p = 0.058). Intact and denuded rings were additionally tested for endothelium-dependent relaxation following submaximal norepinephrine precontraction. The vessels relaxed in response to acetylcholine (maximal relaxation 31.1 +/- 10.7% at 1 x 10(-6) M), calcium ionophore A23187 (85.3 +/- 11.8% at 1 x 10(-5) M), and sodium nitroprusside (150.8 +/- 15.2% at 1 x 10(-5) M), but only acetylcholine relaxation was completely endothelium-dependent. Calcium ionophore A23187 relaxation was partially dependent on the endothelium while sodium nitroprusside relaxation was entirely endothelium-independent. Negligible relaxation was observed in response to adenosine diphosphate (ADP) (12.1 +/- 12.8% at 1 x 10(-5) M) while histamine and serotonin caused additional contraction only. We concluded that, in patients undergoing vascular surgical procedures, the saphenous vein (1) demonstrates variable contractile function which appears to be greater in males following spinal anesthesia, and (2) exhibits moderate endothelium-dependent relaxation in response to acetylcholine and calcium ionophore A23187 but not to ADP, histamine, or serotonin.

Correlation of the complete version of the Selvester QRS scoring system with quantitative anatomic findings for multiple left ventricular myocardial infarcts.

The correlation between myocardial infarct size estimated by the complete version of the Selvester QRS scoring system and that documented by pathoanatomic studies has been reported for single anterior, inferior and posterolateral infarcts. Although previous studies described electrocardiographic changes in patients with multiple infarcts, no quantitative documentation of the ability of such changes to estimate the total amount of left ventricular infarction has been reported. This study of 32 patients with anatomically documented multiple infarcts shows a significant correlation between QRS-estimated and anatomically documented sizes (r = 0.44; p = 0.01), which is less than that previously reported for single infarcts in the anterior, inferior and posterolateral locations. Several of the 54 electrocardiographic criteria were never satisfied. Criteria for posterior infarction were seldom present, suggesting "cancellation effect" of coexisting anterior infarction. These results will be the basis for future modification of QRS criteria for estimating myocardial infarct size.

The effect of interstitial air on the in vitro thrombogenicity of ePTFE vascular grafts.

Gas trapped in the interstices of the biomaterials used for vascular prostheses causes thrombosis, and the process of eliminating this gas is known as denucleation. An apparatus was developed for testing in the in vitro effects of denucleation on 4 mm I.D. expanded polytetrafluoroethylene (ePTFE) Vitagraft (Johnson and Johnson). The apparatus was designed to ensure that neither the blood nor the grafts came in contact with air. Blood from a single donor was incubated with control and denucleated grafts for 5, 10, 15, 20, and 30 minutes. The thrombus volume in the graft lumen was measured with a computer assisted videometric system. Little thrombus formed by 5 or 10 minutes, but there was less thrombus in the denucleated graft than in the control graft at all times. The differences were statistically significant at 15 and 20 minutes (p < 0.05). Denucleation nearly doubled the thrombus formation time. Thrombus was more adherent to denucleated grafts than to control grafts. These results are consistent with in vivo observations in the rat where denucleation decreased thrombus formation and increased patency duration.

Myointimal thickening in experimental vein grafts is dependent on wall tension.

This study examines the relative contributions of intraluminal pressure, blood flow, wall tension, and shear stress to the development of myointimal thickening in experimental vein grafts. To study these different hemodynamic parameters, several experimental models were created in 30 New Zealand White rabbits separated into six groups: common carotid interposition vein grafts harvested at 4 weeks (VG-4) or 12 weeks (VG-12), common carotid-linguofacial vein arteriovenous fistulas harvested at 4 weeks (AVF-4) or 12 weeks (AVF-12), AVFs with partial outflow obstruction harvested at 4 weeks (AVFobs), and combination VG-AVFs in series harvested at 4 weeks (VGAVF). Blood pressure and flow in the graft or vein were measured by use of a transducer-tipped pressure catheter and electromagnetic flow meter. At harvest, veins were perfusion-fixed and proximal, middle, and distal sections were subjected to computerized morphometric analysis. Vein grafts were characterized by a high mean pressure (VG-4, 51 +/- 4; VG-12, 62 +/- 3 mm Hg), low mean flow (VG-4, 17 +/- 1; VG-12, 16 +/- 4 ml/min), large luminal area (VG-4, 19.7 +/- 2.4; VG-12, 19.3 +/- 3.9 mm2), high wall tension (VG-4, 17.0 +/- 1.5; VG-12, 19.5 +/- 2.4 x 10(3) dyne/cm), low shear stress (VG-4, 0.75 +/- 0.13; VG-12, 0.96 +/- 0.38 dyne/cm2), and a high degree of myointimal thickening (VG-4, 5.89 +/- 0.90; VG-12, 4.72 +/- 0.83 mm2). Arteriovenous fistulas were characterized by a low mean pressure (AVF-4, 5 +/- 1, AVF-12, 6 +/- 2 mm Hg), elevated blood flow (AVF-4, 82 +/- 16; AVF-12, 82 +/- 17 ml/min), small luminal area (AVF-4, 2.43 +/- 0.58; AVF-12, 7.14 +/- 2.68), low wall tension (AVF-4, 0.62 +/- 0.19; AVF-12, 0.89 +/- 0.24 x 10(3) dyne/cm), elevated shear stress (AVF-4, 108 +/- 32; AVF-12, 71 +/- 50 dyne/cm2), and decreased myointimal area (AVF-4, 1.18 +/- 0.26; AVF-12, 1.90 +/- 0.55 mm2). The addition of outflow obstruction to AVFs (AVFobs) resulted in elevated pressure (48 +/- 2 mm Hg), decreased flow (17 +/- 4 ml/min), larger luminal area (8.71 +/- 2.31 mm2), elevated wall tension (10.3 +/- 1.7 x 10(3) dyne/cm), and a degree of myointimal thickening approaching that of vein grafts (3.79 +/- 0.66 mm2).(ABSTRACT TRUNCATED AT 400 WORDS)

Chronic ACE inhibition reduces intimal hyperplasia in experimental vein grafts.

Intimal hyperplasia is an important factor in the pathophysiology of vein graft failure. Local renin-angiotensin systems recently have been shown to modulate the development of intimal hyperplasia in arteries after intimal injury. The effect of chronic angiotensin-converting enzyme (ACE) inhibition on the development of intimal hyperplasia in experimental vein grafts was examined in this study. Ten New Zealand White rabbits received 10 mg/kg of captopril daily in their drinking water. One week later the right carotid artery was divided and bypassed with the reversed right external jugular vein in these rabbits and in 10 matched controls. Captopril was continued for 28 days after operation, when all the grafts were harvested. Five grafts from each group were perfusion fixed, and the intimal thickness in the proximal, middle, and distal segments was determined. Rings from the remaining grafts (n = 20 in each group) were studied in vitro under isometric tension, and their responses to norepinephrine (NE), histamine (HIST), serotonin (5-HT), angiotensin I (AI), and angiotensin II (AII) was measured. The intimal thickness of the proximal, middle, and distal segments of the captopril-treated grafts were significantly less than controls, being reduced in all segments by approximately 40% (p less than 0.0001). With regard to vasoreactivity, the captopril-treated grafts were hypersensitive to 5-HT (control ED50 5.5 +/- 0.5 X 10(-7) mol/L vs. captopril-treated 1.1 +/- 0.2 X 10(-6) mol/L; p less than 0.005) although the maximal response was significantly reduced (control 1.6 +/- 0.3 g vs. captopril-treated 0.8 +/- 0.1 g; p less than 0.05). There were no differences in sensitivity between control and captopril-treated rings with respect to NE, HIST, AI, or AII. Four of the ten captopril-treated segments, however, failed to respond to AI, and the maximal active tension of the responders was significantly reduced (control 0.47 +/- 0.06 g vs. 0.20 +/- 0.05 g; p less than 0.02). These results suggest that ACE is involved in the modulation of vein graft intimal hyperplasia, and that ACE inhibitors may have therapeutic applications in patients undergoing vein bypass procedures.

Effects of distention and short-term grafting on vasoreactivity in rabbit external jugular veins.

The relative effects of distention, intraluminal pressure, and wall tension on venous smooth muscle and endothelial cell function were examined in 40 external jugular veins from New Zealand white rabbits. Vein grafts (n = 5) were interposed in the common carotid artery and explanted after 10 minutes. Distended veins were inflated in vitro with modified Krebs' solution at 37 degrees C for 10 minutes at pressures of either 20 mm Hg (D-20; n = 5) or 80 mm Hg (D-80; n = 5). Externally supported veins (ES-80; n = 5) were inflated at 80 mm Hg pressure, but distention was prevented by covering with a 3 mm internal diameter polytetrafluoroethylene sleeve. Bradykinin-induced in vitro maximal tension was attenuated significantly in vein grafts (0.13 +/- 0.04 g) and D-80 rings (0.27 +/- 0.07 g) compared with D-20 rings (1.20 +/- 0.14 g), ES-80 rings (0.99 +/- 0.13 g), or nondistended control rings (n = 40; 1.19 +/- 0.10 g; p less than 0.001). The attenuation in contraction in the vein graft and D-80 groups was nonspecific (i.e., similar results were obtained with respect to other smooth muscle agonists). Contractile function was inversely associated with wall tension, the product of pressure and radius (r2 = 0.7438; p = 0.06). In contrast, there were no differences in endothelium-dependent or endothelium-independent relaxation among the five groups. It is concluded that, in this experimental system, (1) venous smooth muscle function is significantly attenuated after short-term in vitro distention or grafting although endothelial function is largely preserved, and (2) the decrement in contraction is due to elevated wall tension.

Systemic hypertension alters vasomotor function in experimental vein grafts.

Hypertension is an established risk factor for atherosclerosis, a disease that is important in the pathophysiology of vein graft failure. Hypertension can also alter arterial vasoreactivity. The vasomotor function and histologic characteristics of autogenous vein grafts in hypertensive rabbits were assessed in this study. Hypertension was induced in 13 male New Zealand white rabbits by use of the Goldblatt one clip two kidney method. The right carotid artery was divided and bypassed with the reversed right external jugular vein 7 days later in these animals and in 13 normotensive controls. Blood pressure and renal function were assessed serially, and all the grafts were harvested after 28 days. Three grafts in each group were examined by light microscopy. The responses of the remaining grafts to norepinephrine, histamine, serotonin, and angiotensin II were determined in vitro under isometric tension. Endothelium-dependent relaxation to acetylcholine and calcium ionophore (A23187) was assessed in precontracted grafts. The mean arterial pressure was significantly increased after the Goldblatt procedure was performed. Intimal hyperplasia was observed in both groups, but the grafts in the hypertensive groups showed increased adventitial and medial fibrosis and a reduced number of vasa vasora. The grafts in the hypertensive rabbits were hypersensitive to all agonists as indicated by a significant reduction in their median effective dose values, and their maximal responses to all agonists were also significantly reduced. No graft relaxed in response to acetylcholine, and whereas precontracted grafts in normotensive rabbits had a maximal relaxation of 24% +/- 6% of precontraction with A23187, this was absent in the grafts in the hypertensive rabbits. The results suggest that angiotensin-induced hypertension may adversely affect vein graft patency by inducing hypersensitivity to physiologically important agonists and reducing the effect of receptor-independent endothelium-derived relaxation on vasomotor tone.

Alterations in serotonergic receptor expression in experimental vein grafts.

Rabbit external jugular veins, normally unresponsive to serotonin (5-HT), develop a constrictive response when grafted into the arterial circulation. The mechanisms responsible for this alteration were examined in this study. The right external jugular vein was grafted into the right carotid artery in 37 New Zealand white rabbits. The vein grafts were harvested at 3, 7, 9, 14, and 28 days after operation; contralateral external jugular veins were harvested at 9 days in six animals. Rings of these vessels were mounted under isometric tension, and dose-response curves to 5-HT were obtained. None of the grafts harvested at day 3 responded to 5-HT. All the grafts harvested from day 7 through day 28 constricted to 5-HT. The maximal response increased from 258 +/- 30 mg at 7 days to 734 +/- 108 mg at 28 days. No change occurred in the sensitivity to 5-HT with time. The increase in maximal response was paralleled by a linear increase in percent intimal area (intimal area/intimal + media areas) from 11.6% +/- 2.1% at 3 days to 48.7% +/- 1.9% at 28 days. Preincubation with ketanserin, a 5-HT2 and alpha 1-adrenergic antagonist, produced a concentration-dependent rightward shift in the 5-HT dose-response curve. The median effective dose for 5-HT increased progressively from 1.9 +/- 0.3 x 10(-6) mol/L (in the absence of ketanserin) to 6.1 +/- 1.7 x 10(-5) mol/L (ketanserin 8 x 10(-7) mol/L; p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Functional and morphologic endothelial damage in rabbit external jugular veins stored in heparinized normal saline.

Previous studies have demonstrated that vein storage in normal saline leads to significant mechanical morphological, and biochemical aberrations. However, little information is available regarding the functional damage that occurs. The purpose of this study was to evaluate the effect of saline storage on venous smooth muscle and endothelial function. Segments of ten external jugular veins from male New Zealand White rabbits were placed nondistended in either modified Krebs solution at 37 degrees C (Krebs-stored, KS) or heparinized normal saline at room temperature (saline-stored, SS) for 1 h. Segments 4 mm in length were then simultaneously studied in vitro under isometric tension. There was no difference in maximum tension or sensitivity to either bradykinin or histamine. Acetylcholine-induced relaxation in KS segments was not significantly different from relaxation in a historical cohort of nonstored segments (nonstored 87.4 +/- 1.0% vs. KS 84.5 +/- 2.0%; p = NS). However, there were significant attenuations in SS segment endothelium-dependent relaxation in response to both acetylcholine (KS 84.5 +/- 2.0% vs. SS 76.4 +/- 2.7%, p less than 0.02) and adenosine diphosphate (KS 47.9 +/- 2.9% vs. SS 40.6 +/- 3.7%, p less than 0.002). Relaxant responses to sodium nitroprusside (endothelium-independent) were not significantly different in the two groups (KS 94.6 +/- 1.6% vs. SS 95.7 +/- 2.2%; p = NS). Electron microscopic evaluation of SS segments revealed endothelial cell disruption with cellular edema and loss of intact junctions.(ABSTRACT TRUNCATED AT 250 WORDS)

Morphologic and morphometric analyses of rat femoral arteries after crush injury.

Replantation after crush amputation has a relatively low success rate. An arterial crush injury was produced in rats under a range of pressure (8.5 to 2,551 g/mm2) and durations (10 to 60 minutes). The degrees of vessel injury and thrombus formation were evaluated as functions of both crush force and duration, and the healing process was followed for 8 weeks. Crushing resulted in morphologic damage to the arterial wall but did not impair patency. Damage was directly proportional to crush pressure and duration. Intimal denudation caused flat platelet adhesion but no thrombus formation or thrombosis. Re-endothelialization was completed by 2 weeks. Intimal hyperplasia appeared at 1 week and consisted of endothelia in the most luminal layers and smooth muscle in the deeper layers. the internal elastic lamina was intact in all specimens and was thought to minimize platelet aggregation on the arterial wall after denudation of the intima.

Optimal temperature for preservation of donor myocardium.

The ideal method for the preservation of donor hearts for transplantation is unclear. To assess the optimal temperature for donor myocardium preservation, the recovery of isolated canine hearts (n = 20) exposed to 4 hours of either standard ice-chest hypothermia (0-4 degrees C) or constant moderate hypothermia (12 degrees C) were compared. Functional and metabolic data were acquired before hypothermia and every 30 minutes during 3 hours of reperfusion with oxygenated blood. Mean end-systolic pressure-volume slopes were 2.11 +/- 0.06 and 2.09 +/- 0.06 mm Hg/ml for ice-chest hypothermia and constant moderate hypothermia, respectively (p = NS), which were unchanged from control. All y intercepts during reperfusion were decreased compared with control (p = 0.002) without any differences between groups. End-diastolic pressures were greater than control throughout the reperfusion period for both groups (p = 0.02), but there was a difference in change of end-diastolic pressures with time between groups (p = 0.04). Dry/wet ratios were similar after preservation and reperfusion in both groups. ATP recovered to control levels during reperfusion for both groups although energy charge ratios were greater for hearts exposed to constant moderate hypothermia (p = 0.007). These data indicate that intracellular energy stores are well maintained by preservation using either technique. Changes in function appear to be related to altered compliance irrespective of preservation temperature. These data suggest that a wide range of temperatures may be acceptable for donor heart preservation.

Sensitivity of a set of myocardial infarction screening criteria in patients with anatomically documented single and multiple infarcts.

A subset of 3 screening criteria (Q wave greater than or equal to 30 ms in lead aVF, any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV in lead V2, and R wave greater than or equal to 40 ms in V1) has been proposed to identify single nonacute myocardial infarcts. Cumulatively, these 3 criteria achieved 95% specificity, and 84 and 77% sensitivities for inferior and anterior myocardial infarcts, respectively, among patients identified by coronary angiography and left ventriculography. This study establishes the true sensitivities of the set of screening criteria in 71 patients with anatomically proven single myocardial infarcts and 32 patients with multiple myocardial infarcts. In the single inferior infarct group, the aVF criterion was 90% sensitive. The V2 criterion (any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV) was 67% sensitive in the single anterior infarct group. No single criterion proved sensitive in identifying a posterolateral infarct. The set of screening criteria performed just as well for multiple infarcts as it did for single infarcts, with a cumulative sensitivity of 72%. The overall sensitivity of the screening set in the 103 patients in all groups was 71%.

Correlation of clinical history with quantitative histology of lower extremity atheroma biopsies obtained with the Simpson atherectomy catheter.

The purpose of this study was to compare the histologic variability of atheromas resected from patients with various risk factors for vascular disease. Twenty-seven plaques obtained using the Simpson atherectomy catheter were studied. The results of this light and electron microscopic study indicate that patients with diabetes mellitus had increased numbers of smooth muscle cells in their plaques (P less than 0.05) and a trend toward denser, less fatty connective tissue matrix (P less than 0.07) when compared with non-diabetics, and that female diabetics had more smooth muscle cells in their plaques than male diabetics (P less than 0.05). The female patients, regardless of risk factors, had more smooth muscle cells in their plaques than male patients (P less than 0.004). Patients with poor distal runoff had more neovascularization of plaque (P less than 0.001). Tobacco use and age did not have statistically significant correlations with histologic patterns.

Histopathologic examination of material from angioplasty balloon catheters used in vivo in human coronary arteries.

Reports on vascular pathology post-PTCA in both human and animal coronary vessels have revealed medial and intimal cracks and tears, thrombus formation, platelet accumulation, and loss of endothelial cells. The extent and type of damage can currently be assessed in vivo at the macro level by means of coronary artery angiography. However, this technique cannot define vessel wall characteristics at the cellular level. Our hypothesis is that vessel wall material may adhere to the balloon and thus provide a source for coronary artery cytological investigation in vivo. Ten balloon catheters were evaluated to discern any material which was dislodged from the coronary artery and which remained attached to the balloon catheter or guide wire. Our results indicate that angioplasty catheter balloons frequently have adherent collagen, endothelial cells, organized thrombus, and plaque with obvious cholesterol clefts, that can be retrieved and examined histologically. We conclude that material is often dislodged from the plaque during PTCA. In addition, plaque material removed by the balloon catheter offers an unusual opportunity to analyze the morphologic characteristics of cells from the human coronary artery in vivo.

Normal endothelial function and decreased vasoreactivity of experimental arterial grafts.

During autogenous vascular grafting endothelial cell damage inevitably occurs. In this study we examined the functional and morphologic integrity of experimental arterial grafts. The right external iliac artery was grafted into the right carotid artery of 12 male New Zealand white rabbits. The left external iliac artery was used as the control artery. Four weeks after surgery, isometric tension studies were performed on rings of control artery and arterial graft. Control arteries and arterial grafts precontracted with norepinephrine demonstrated endothelium-dependent relaxation of 28.3% +/- 5.6% and 16.1% +/- 1.7%, respectively, in response to acetylcholine (5 x 10(-6) mol/L). Both control arteries and arterial grafts contracted in response to norepinephrine, histamine, and serotonin. The median effective dose (ED50) of norepinephrine was 4.1 +/- 1.3 x 10(-7) mol/L for control arteries and 62.1 +/- 17.9 x 10(-7) mol/L for arterial grafts (p less than 0.005). Similarly, arterial grafts were less sensitive to histamine; the ED50 of histamine for control arteries was 4.6 +/- 1.3 x 10(-7) mol/L and 51.4 +/- 13.0 x -7 mol/L for arterial grafts (p less than 0.005). In contrast, reactivity to serotonin was unaltered. The ED50 was 4.1 +/- 1.3 x 10(-7) mol/L for control arteries and 4.5 +/- 1.3 x 10(-7) mol/L for arterial grafts. Scanning and transmission electron microscopy revealed a largely intact endothelial surface. These data are markedly different from our previous findings with vein grafts in which serotonin supersensitivity was associated with an absence of endothelium-mediated relaxation to acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Peripheral artery atherectomy: description of technique and report of initial results.

Percutaneous transluminal atherectomy has been developed for treatment of peripheral artery stenoses. The atherectomy catheter is inserted through a sheath, and the resection window of the catheter is positioned adjacent to the vascular stenosis. The balloon is inflated, and the motor-driven cutting blade advanced. The balloon is then deflated, the catheter withdrawn, and the atheromatous material, which resembles the resected material of an endarterectomy, removed from the catheter. This process is repeated until the resection provides an adequate lumen. To date, 12 arterial lesions (three common iliac, two external iliac, four superficial femoral, and three popliteal artery) in ten patients have been resected with excellent angiographic results. The conditions of seven patients who underwent atherectomy for relief from claudication were improved by the criteria of ankle/arm ratios and/or claudication distance. Three patients successfully underwent atherectomy for limb salvage. More data on long-term patency and restenosis rates are needed before the ultimate role of atherectomy in the management of peripheral artery disease can be determined.