Abstract 2810: Assessing the Impact of High-Thrombus Burden Lesion on Myocardial Damage during Primary-Percutaneous Coronary Intervention: a Magnetic Resonance Study
Background: Macroscopically detectable Distal Embolization (DE) during primary-Percutaneous Coronary Intervention (p-PCI), has been shown to enhance myocardial necrosis. High thrombus burden lesion (HTBL) has been identified as the most powerful predictor for this complication. However, little is known about the impact of HTBL on the extent of myocardial necrosis, regardless of angiographic detectable embolization.
Methods: in 241 patients, who underwent p-PCI without mechanical device use within 6 hours from symptom onset, we prospectively assessed the impact of HTBL on infarct size, transmural extent of myocardial necrosis and microvascular damage, using contrast enhanced-magnetic resonance imaging (ce-MR). HTBL was defined by the presence of TIMI-thrombus score ≥ 3 in patent IRA; or cut off occlusion pattern in occluded IRA; or large reference vessel diameter (≥ 3.5 mm)in occluded IRA.
Results: 107 (44.4%) patients showed HTBL, and 134 (55.6%) did not. DE occurred in 25.0% HTBL vs 4.7% no-HTBL patients, respectively (p<0.0001). Tn-I peak was higher in HTBL (140.7 ± 105.3 vs 87.0 ± 99.8 ug/L, p=0.01). At ce-MR, patients with HTBL had larger infarct size (28 ± 15.9% vs 24.6 ± 16.5% p=0.01), more often transmural necrosis (69.2% vs 56.7%, p=0.04) and microvascular damage (35.8% vs 20.8%, p=0.02) compared to patients without HTBL. After excluding cases in whom DE occurred, HTBL patients showed still a trend toward more transmural necrosis (65.1% vs 51.5%, p = 0.08), and more often microvascular damage (18.6 vs 6.8%, p = 0.04).
Conclusion: High-Thrombus Burden Lesion in the setting of p-PCI is related to larger myocardial and microvascular damage as detected by cardiac magnetic resonance, regardless of angiographic detectable embolization. These findings suggest that HTBL may play a role on myocardial damage by both macro and microembolization phenomenon.