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BackgroundCoronary artery perforation (CAP) is a potentially lethal complication of percutaneous coronary intervention. We report on the incidence, clinical characteristics, and management of iatrogenic coronary perforations based on an 11‐year single‐center experience.Methods and ResultsFrom February 9, 2005, through November 20, 2016, 150 CAP cases were identified from our percutaneous coronary intervention database of 21 212 procedures (0.71%). Mean age of CAP patients was 66±11 years, and 62.7% were male. Treated lesion type was B2/C in 94.6%, and 31.3% were chronic total occlusions. Nonworkhorse guidewires were applied in 74.3%. CAP types were Ellis type I in 2.9%, Ellis type II in 40.4%, Ellis type III in 54.8%, and Ellis type III cavity spilling in 1.9%. CAP treatment was conservative (including prolonged balloon inflation) in 73.3%. Covered stents, coiling, and fat embolization were used in 24.0%, 0.7%, and 2.0%, respectively. Pericardiocentesis for tamponade was required for 72 patients (48.0%), of whom 28 were initially unrecognized. Twelve patients (12.7%) required emergency cardiac surgery to alleviate tamponade. Periprocedural myocardial infarction occurred in 34.0%, and in‐hospital all‐cause mortality was 8.0%. All‐cause mortality accrued to 10.7% at 30 days and 17.8% at 1 year.ConclusionsCAP is a rare complication of percutaneous coronary intervention, but morbidity and mortality are considerable. Early recognition and adequate management are of paramount importance.

Aims Successful epicardial reperfusion with primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) can paradoxically evoke myocardial reperfusion injury, which may be signalled by temporally associated ventricular arrhythmias (VAs). We correlated reperfusion VA 'bursts' with final infarct size (IS) in patients with restored TIMI 3 flow following PCI for anterior STEMI. Methods and results All 128 anterior STEMI patients with final TIMI 3 flow had continuous 24 h digital 12-lead ECG with simultaneous Holter recording initiated prior to PCI, and Day 7/discharge SPECT imaging IS assessment. Angiography, SPECT imaging, continuous ST recovery, and quantitative rhythm analyses were performed. Reperfusion VA bursts were defined against patient-specific background VA rates and timed as concomitant with or following first angiographic TIMI 3 flow restoration associated with > or =50% stable ST recovery; they were then correlated with IS and global left ventricular ejection fraction (LVEF) at Day 7/discharge. Bursts occurred in 81/128 (63%) patients and were significantly correlated with larger IS and worse LVEF (median: 21.0 vs. 10.0%, P < 0.001; 35.5 vs. 46.5%, P < 0.001, respectively). In multivariable analyses that adjusted for known predictors of IS, the association of bursts with larger IS remained significant; similar results were seen for worse LVEF. Conclusion Reperfusion VA bursts predict larger IS despite TIMI 3 flow restoration with > or =50% stable ST recovery following PCI for anterior STEMI. Well-characterized reperfusion VAs may provide a novel biomarker of reperfusion injury.

Ventricular arrhythmia bursts temporally associated with TIMI 3 flow restoration and stable ST-segment recovery (reperfusion VA bursts) can be precisely defined in subjects with anterior STEMI and may constitute a unique electric biosignal of myocellular response to reperfusion.

Background: Fractional flow reserve (FFR)-guided treatment has been demonstrated to improve percutaneous coronary intervention (PCI) results. However, little is known on the long-term impact of low post-PCI FFR. Methods: This is a large prospective all comers study evaluating the impact of post-PCI FFR on clinical outcomes. All patients undergoing successful PCI were eligible for enrollment. FFR measurements were performed immediately after PCI when the operator considered the angiographic result acceptable and final. No further action was undertaken based on the post-PCI result. Suboptimal post-PCI FFR was defined as FFR<0.90. The primary end point was major adverse cardiac events, a composite of cardiac death, any myocardial infarction, or any revascularization at 2-year follow-up. Secondary end points were target vessel revascularizations and stent thrombosis and the separate components of the primary end point. Results: A total of 1000 patients were enrolled. Post-PCI FFR was successfully measured in 1165 vessels from 959 patients. A poststenting FFR<0.90 was observed in 440 vessels (37.8%). A total of 399 patients had at least 1 vessel with FFR<0.90 post-PCI. At 2-year follow-up, a patient level analysis showed no association between post-PCI FFR and major adverse cardiac event (hazard ratio [HR], 1.08 [95% CI, 0.73–1.60], P =0.707), cardiac death (HR, 1.55 [95% CI, 0.72–3.36], P =0.261), any myocardial infarction (HR, 1.53 [95% CI, 0.78–3.02], P =0.217). A vessel level analysis showed a higher rate of target vessel revascularization (HR, 1.91 [95% CI, 1.06–3.44], P =0.030) and a tendency toward higher rate of stent thrombosis (HR, 2.89 [95% CI, 0.88–9.48], P =0.081) with final post-PCI FFR<0.90. Conclusions: Suboptimal post-PCI FFR has only a moderate impact on major adverse cardiac event but coronary arteries with a post-PCI FFR<0.90 have a higher rate of target vessel revascularization.