Changing outcomes and treatment strategies for wire induced coronary perforations in the era of bivalirudin use.
OBJECTIVE
The objective of this study is to analyze the clinical outcomes and treatment strategies of coronary wire perforations (WPs) in the era of heparin use compared to the era of bivalirudin use.


BACKGROUND
Percutaneous coronary intervention (PCI) advances have led to progressive decrease in complications. Therefore, complex coronary lesions such as chronic total occlusions and calcified lesions are being attempted with stiff/hydrophilic wires with resultant higher incidence of coronary WP.


METHODS
A single-center retrospective data analysis of coronary perforation (CP) for the last 4 years with review of coronary angiograms was done and WPs were identified. A simple classification scheme based on angiographic appearance of CP was made: Type I ("myocardial stain," with no frank dye extravasation) and type II ("myocardial fan," with dye extravasation to pericardial cavity or cardiac chambers).


RESULTS
Overall incidence of CP was 0.49% (82/16,859). Of these 50 (61%) were caused by WP; 30 occurred with heparin use (Group A) and 20 with bivalirudin use (Group B). WPs always occurred in type B2/C lesions (100%) and commonly with use of hydrophilic guidewires (70%). Major adverse cardiac events and cardiac tamponade were frequent in group A (50%) and none in group B (0%); P < 0.01. All WP in group B responded to stopping anticoagulation and prolonged balloon inflation, while group A type II perforations frequently required additional interventions (pericardiocentesis, coil embolization).


CONCLUSIONS
Cardiac tamponade and major adverse cardiac events from WPs were less frequent with bivalirudin use compared to heparin use. This beneficial effect of bivalirudin may be explained on the basis of its short half-life and reversible thrombin inhibition property. Therefore, bivalirudin may offer a safer alternative for anticoagulation in complex PCI.
Kini
Annapoorna S
AS
Cardiac Catheterization Laboratory of the Cardiovascular Institute, Mount Sinai Hospital, New York, New York 10029-6754, USA.
Rafael
Oana C
OC
Sarkar
Kunal
K
Rajdev
Sanjay
S
Jakkula
Madhavi
M
Mares
Angelica M
AM
Kaplish
Dheeraj
D
Krishnan
Prakash
P
Kim
Michael C
MC
Sharma
Samin K
SK
D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects* / Q000295:instrumentation / Q000401:mortality; D000925:Anticoagulants / Q000009:adverse effects*; D021721:Balloon Occlusion; D002305:Cardiac Tamponade / Q000000981:diagnostic imaging / Q000209:etiology / Q000401:mortality / Q000628:therapy*; D002932:Cineangiography; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000628:therapy*; D003331:Coronary Vessels / Q000293:injuries*; D005260:Female; D006493:Heparin / Q000009:adverse effects*; D006494:Heparin Antagonists / Q000627:therapeutic use; D006629:Hirudins / Q000009:adverse effects*; D017052:Hospital Mortality; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology; D010446:Peptide Fragments / Q000009:adverse effects*; D020519:Pericardiocentesis; D011994:Recombinant Proteins / Q000009:adverse effects; D012042:Registries; D012189:Retrospective Studies; D016896:Treatment Outcome; D014950:Wounds, Penetrating / Q000000981:diagnostic imaging / Q000209:etiology / Q000401:mortality / Q000628:therapy*
D000925:Anticoagulants; D006494:Heparin Antagonists; D006629:Hirudins; D010446:Peptide Fragments; D011994:Recombinant Proteins; D006493:Heparin; C074619:bivalirudin