Coronary artery vasoconstriction routinely occurs after percutaneous transluminal coronary angioplasty. A quantitative arteriographic analysis.

Abstract

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 ,ug 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<O.OOl) and compared with the control segment at 30 minutes (p<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 adminlstration 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. (Circulation 1988;78:1323-1334 Despite the widespread application of percutaneous transluminal coronary angioplasty (PTCA) in the treatment of obstructive coronary artery disease, little is known about the early spontaneous changes in coronary artery morphology and vasomotor behavior after this proce-

Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty.

“…Coronary artery vasoconstriction distal to the site of balloon dilatation has been observed after successful PTCA, and has been previously attributed to the release of platelet-derived vasoactive substances at the proximal site of balloon-induced arterial injury (7). This study demonstrates that the severity of this distal vasoconstriction is significantly correlated with lesion severity before PTCA.…”

“…The basic protocol for study has been described in detail previously (7). All patients agreed to proceed with the PTCA and study procedures after being informed of the potential risks and complications, as outlined in a protocol approved by the Institutional Review Board of the Stanford University Medical Center.…”

“…computer assisted edge detection of a digitized cineangiographic image, as has been described in detail in prior reports (7,12). Wellopacified end-diastolic cine frames were selected as described, and magnified (X3.5) with the appropriate coronary segment centered in the image field.…”

Differential Role of K ATP Channels Activated by Conjugated Estrogens in the Regulation of Myocardial and Coronary Protective Effects

“…1 Coronary vasoconstriction is associated with a greater residual stenosis and an increased incidence of restenosis after angioplasty. 2,3 A better understanding of possible mechanisms involved and potential strategies to limit its extent should be sought.…”

Potentiation of the vasospastic response to angioplasty by pretreatment with fluoxetine. A study in the atherosclerotic rabbit.

“…118 Vasospasm after angioplasty has been identified in both animals 19 " 23 and patients. 24 Its contribution to acute vessel closure is suggested by reversal of the acute occlusion in some cases with vasodilators. The mechanism of angioplasty-induced vasospasm is not known, but it may be caused by the release of - 27 Other implicated mechanisms include alterations in vessel wall arachidonate metabolism, 28 adrenergic nerve dysfunction, 29 loss of endothelium-derived relaxation factor (EDRF), 30 and release of endothelin.…”