This study examines the relative contributions of intraluminal pressure, blood flow, wall tension, and shear stress to the development ofmyointimal 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 c.omputerized morphometric .analysis•. Vein grafts were characterized by a high mean pressure (VG-4, 51 ± 4; VG-12, 62 ± 3 nim Hg), low

A cryosurgical instrument was used to ablate atrioventricular conduction. The procedure was carried out in 20 dogs and subsequently in three patients with drug resistant, life-threatening supraventricular tachycardias. In patients, the cryosurgical unit lowered the temperature of the His bundle area to 0 degrees C, effecting complete but reversible heart block. Rewarming resulted in resumption of normal atrioventricular conduction. The His bundle region then was cooled to -60 degrees C; complete heart block was produced with two or more 90-120 second freezes. Postoperative evaluations revealed persistent atrioventricular conduction block. The lesion showed no tendency to rupture, form aneurysm, or interfere with valvular function. In the clinical cases, postoperative studies demonstrated a stable pacemaker arising proximal to the branching portion of the His bundle. A potential application of the cryosurgical technique might be ablation of sites of dysrhythmia (i.e., ectopic foci, re-entry circuits, accessory pathways).

Enzymatic estimates of myocardial infarct size based on plasma levels of MB creatine kinase (MB-CK) were

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.