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Substantial evidence of postangioplasty vasoconstriction is available, both at the dilated site and distal to balloon injury, demonstrating its frequent occurrence. It is likely that even mild or moderate vasoconstriction at the site of balloon injury may create flow turbulence, promoting platelet aggregation and contributing to thrombotic vessel closure. The regulation of arterial smooth muscle tone is a complex process and should be distinguished from elastic recoil, which occurs at the site of balloon injury due to passive elastic properties of the artery, generally immediately after balloon deflation. The contribution of a variety of messengers generated by humoral, neurogenic, myogenic, and endothelium-derived factors in this regulatory process has been implicated. The possible mechanisms of post-percutaneous transluminal coronary angioplasty vasoconstriction at the dilated site (local) and in segments of coronary artery beyond the dilated site (distal) are reviewed in this article.

Purpose: The ability of three different intravascular stents (Gianturco-Roubin, Palmaz-Schatz, and CV Rad), and two different metals (stainless steel and tantalum) to resist vasoconstriction was evaluated in an intact artery ex vivo model., Materials and Methods: Stents were deployed in 21 rabbit thoracic aortae and five dog carotid arteries, which were constricted with phenylephrine and serotonin, respectively. Vasoconstriction was measured with the use of high-frequency ultrasonic imaging., Results: The maximal vasoconstriction of the control segment was 37.7% +/- 2.6 with rabbit aortae and 36.3% +/- 4.1 with dog carotid arteries, while the average maximal constriction for all segments in which stents were placed was 5.7% +/- 1.1 (P < .01). The maximal constriction of the Gianturco-Roubin stainless steel stent was 9.4% +/- 2.7 versus 7.9% +/- 1.6 with the tantalum version (P = .65). Both designs showed somewhat greater constriction compared with either the Palmaz-Schatz (3.3% +/- 0.9) or the CV Rad (1.4% +/- 1.1) stents., Conclusions: Although all of the stents tested substantially resist arterial vasoconstrictive forces, the Palmaz-Schatz and CV Rad stents resist vasoconstriction to a greater degree than the Gianturco-Roubin stents. Tantalum and stainless steel stents of the same design (Gianturco-Roubin) appear similar in their ability to resist vasoconstrictive forces.

Objectives: This study was designed to describe the clinical effects of ultrasound energy on guide-wire-induced arterial vasoconstriction., Background: We have previously shown that ultrasound energy (20 kHz) delivered by a wire probe produces dose-dependent, endothelium-independent smooth muscle relaxation capable of reversing both receptor-mediated and voltage-dependent vasoconstriction in vitro., Methods: A high intensity, low frequency ultrasound catheter system was used to recanalize total occlusions in the superficial femoral arteries of two patients. After recanalization, the proximal residual stenoses were each less than 15%. However, distal arterial vasospasm was found angiographically in a popliteal artery of one patient and in an anterior tibial artery of another. Subsequently, the ultrasound catheter probe was advanced to the sites of arterial vasospasm (diffuse in one, focal in one)., Results: After 30 and 90 s, respectively, of exposure to ultrasound energy with a frequency of 19.5 kHz, peak tip amplitude of 111 microns and power output at the transducer of 25 W, the vasospasm resolved in each arterial segment., Conclusions: Our findings are the first reported clinical cases documenting that catheter-delivered low frequency, high intensity ultrasound induces arterial vasodilation at the site of vasoconstriction. These biologic effects appear to be relatively unique for an angioplasty device and may have potential clinical importance.

To determine whether percutaneous transluminal coronary angioplasty (PTCA) increases coronary artery luminal dimensions by stretching and injuring ("paralyzing") the smooth muscle of the arterial wall, we prospectively analyzed spontaneous changes and then intracoronary nitroglycerin-induced changes in segmental coronary artery diameters during the first 30 minutes after uncomplicated single-vessel PTCA in 10 patients. Five additional patients received intravenous nitroglycerin throughout the procedure to determine whether nitroglycerin could prevent vasoconstriction after PTCA. All of the patients were maintained on oral doses of diltiazem and aspirin at the time of the study. Coronary arteriography was performed at 2, 5, 15, and 30 minutes after PTCA and then 3 minutes after 300 micrograms i.c. nitroglycerin. Quantitative measurements (computerized edge-detection) were performed at each time, in coronary segments centered in the dilated segment, distal to the dilated segment, and in a control vessel not manipulated with the balloon catheter or guidewire. Progressive vasoconstriction (defined as a loss of diameter that was reversed by intracoronary nitroglycerin) was observed after PTCA in the dilated and distal segments (10 of 10 patients) but not in the control segment. The vasoconstriction in the dilated segment at 30 minutes (mean, 30 +/- 4%) was highly statistically significant compared with vasoconstriction at 2 and 5 minutes after PTCA (p less than 0.001) and compared with the control segment at 30 minutes (p less than 0.005). There was no significant loss of diameter after PTCA in the dilated segment in the five patients who received intravenous nitroglycerin. In conclusion, 1) spontaneous coronary artery vasoconstriction after PTCA occurs routinely at and distal to the site of balloon dilatation despite pretreatment with aspirin and calcium channel blockers; 2) coronary artery vasoconstriction after PTCA is rapidly reversed by intracoronary nitroglycerin and can be prevented by the continuous administration of intravenous nitroglycerin during and after the procedure; 3) these results are incompatible with the hypothesis that PTCA improves coronary luminal dimensions by arterial "paralysis"; and 4) these findings have implications concerning the etiology and prophylaxis of abrupt vessel closure after PTCA.

We have developed a novel method combining two-dimensional ultrasonic imaging and computerized edge detection to study the vasomotor responses of isolated arterial vessels to various pharmacological agents. Using this in vitro system, we studied the contraction and relaxation of rabbit aorta, respectively, to phenylephrine and acetylcholine. Quantification of these drug-induced changes in vessel wall diameter was achieved by computerized edge detection processing of the two-dimensional ultrasonic vessel wall images. Resolution of this imaging system was determined to be +/- 0.27 mm. Dose-response curves obtained via this new method showed a high degree of correlation with data obtained by classical tissue bath techniques using ring segments. Two-dimensional ultrasonic imaging combined with computerized edge detection is a new and sensitive method to study vasoreactivity of whole, isolated arterial vessels to pharmacological agents.

To determine whether balloon angioplasty can provoke arterial vasoconstriction independent of platelet aggregation and neurogenic input, we studied the spontaneous vasomotor effects of balloon dilatation in isolated, perfused whole-vessel segments of rabbit aorta and pig carotid artery. Freshly dissected rabbit thoracic aortas were mounted in a muscle bath-perfusion chamber, perfused with physiologic saline solution at 70 mm Hg, and allowed to equilibrate. The proximal or distal half of the aortas were dilated with either a "large" (5 mm, 31-51% stretch beyond relaxed diameter) or a "small" (4 mm, 5-16% stretch) balloon angioplasty catheter with the other half of the vessel serving as the control. A similar series of experiments were performed in pig carotid arteries using "large" (6 or 8 mm, 48-90% stretch) balloon catheters. The spontaneous vasomotor effects of balloon angioplasty were examined with long-axis, high-frequency ultrasonic imaging combined with computerized edge detection image processing to measure changes in segmental internal vessel diameters. Additional experiments were carried out in rabbit aortas to determine the roles of the endothelium, extracellular calcium, indomethacin, ibuprofen, and calcium-channel blockade in modulating angioplasty-induced vasoconstriction. Significant arterial vasoconstriction was observed in the balloon angioplasty segments after dilatation with 5-mm balloons but not with 4-mm balloons. After dilatation with 5-mm balloons, the angioplasty segments' cross-sectional areas decreased by an average of 31% versus 4% for the nondilated (control) segments (p less than 0.0001). Similar postangioplasty vasoconstriction was observed in the pig carotid arteries (decrease in minimal vessel cross-sectional area of 41% [angioplasty segment] versus 2% [control segment]) (p less than 0.005). This angioplasty-induced vasoconstriction was prevented by endothelial denudation before angioplasty, removal of extracellular calcium, and pretreatment with indomethacin or ibuprofen. The vasoconstriction was only partially inhibited by calcium channel blockade with verapamil. These findings demonstrate that stretch-pressure-induced arterial vasoconstriction may occur after balloon angioplasty, independent of platelet aggregation and neurogenic input. This angioplasty-induced vasoconstriction appears to be mediated by an endothelially derived cyclooxygenase product(s).

The coronary response to acetylcholine was evaluated in 10 patients who had had cardiac transplantation 1 to 8 years earlier and in 4 patients who did not undergo transplantation. All 14 patients had no angiographic evidence of fixed coronary arterial narrowing. Acetylcholine was infused in 10-fold increasing concentrations (10(-6) to 10(-2) M) into the midpoint of the left anterior descending coronary artery by an infusion catheter. Administration was terminated when either vasoconstriction was noted at fluoroscopy or when the maximal acetylcholine concentration was reached. Vascular responses were evaluated by quantitative angiography. All 14 patients had a decrease in coronary lumen size in response to acetylcholine. The mean percentage of vasoconstriction was 37 +/- 24% (p less than 0.001). Combined infusion of nifedipine and the maximal vasoconstricting dose of acetylcholine did not result in a significant reversal of coronary vasoconstriction in all 10 cardiac transplantation patients. It was concluded that acetylcholine is a potent coronary vasoconstrictor in patients who had cardiac transplantation and possibly lacks vasodilating effects in most normal patients without angiographic evidence of coronary artery disease, thus suggesting that acetylcholine might not be a suitable pharmacologic agent for testing endothelial cell integrity.