Emerging strategies for failed percutaneous transluminal coronary angioplasty.

TLDR: The direct intracoronary administration of propranolol or fluorinated hydrocarbons has increased the capacity to prolong inflations by virtue of a decelerated induction of myocardial ischemia, and this overall “tack up” strategy appears to represent the best current approach to the management of abrupt closure.

Abstract: Second only to the problem of restenosis, abrupt closure during percutaneous transluminal coronary angioplasty (PTCA) represents a significant procedural complication. Of the 200,000 PTCA procedures performed in the United States in 1987, abrupt closure occurred in approximately 10,000 patients-resulting in triage to emergency coronary artery bypass surgery in >6,000 patients and >l,OOO deaths.1-3 Current approaches to this problem have been limited. After intracoronary nitroglycerin is given, intracoronary or intravenous thrombolytic therapy has been used in some cases. However, spasm or thrombosis is very rarely the principal cause of abrupt closure. Typically, the inciting event is a complex intimal tear. Definite establishment of the etiology is confounded by the lack of adequate angiographic distinction between thrombus and dissection; our methods for decision-making under these circumstances are relatively crude. A standard approach, which has evolved empirically to “tack up” the tear, is the use of prolonged inflations (2 to 5 minutes), with a larger balloon dilatation catheter (0.5-mm size increase) at low pressure (3 to 5 atmospheres).4 The direct intracoronary administration of propranolol or fluorinated hydrocarbons has increased our capacity to prolong inflations by virtue of a decelerated induction of myocardial ischemia. v Combined with these various pharmacologic interventions, this overall “t.ack up” strategy appears to represent the best current approach to the management of abrupt closure.