Summary
In patients with prior coronary artery bypass graft (CABG) surgery, distal coronary perforations are commonly considered to be at low risk for causing cardiac tamponade due to a potential protective role of pericardial adhesions, which obliterate the pericardial space. Loculated effusions can however form in such patients, compressing various cardiac structures and causing hemodynamic compromise. We present two cases of distal coronary perforation in prior CABG patients undergoing chronic total occlusion percutaneous coronary intervention. In the first case a distal coronary perforation was initially observed, resulting in a loculated pericardial effusion that caused ST-segment elevation and death, despite successful sealing of the perforation. In the second case a similar perforation was immediately sealed with a covered stent, followed by uneventful patient recovery. A literature review of coronary perforation leading to hemodynamic compromise in patients with prior CABG surgery revealed high mortality (22%), suggesting that prompt sealing of the perforation is critical in these patients.
Highlights
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Loculated effusions can form in patients with prior CABG suffering coronary perforation.
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This complication is associated with high mortality.
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Prior CABG and pericardial obliteration should not offer reassurance against tamponade.
Introduction
Coronary perforation is a potentially catastrophic complication of percutaneous coronary intervention (PCI) and may occur more commonly when treating complex lesions such as chronic total occlusions (CTO) . Coronary perforations can be classified according to location (main vessel, distal artery, collateral vessel) and severity (using the Ellis classification ), and may require emergent treatment (percutaneous or surgical), in order to prevent or relieve cardiac tamponade .
It is a commonly held belief that patients with prior coronary artery bypass grafting (CABG), or other prior cardiac surgery requiring pericardiotomy, are relatively protected from tamponade due to obliteration of the pericardial space by pericardial adhesions. However, several cases of tamponade have been reported in this setting . A unique manifestation of coronary perforation in prior CABG patients is the development of loculated effusions that have been shown to cause chamber compression, often of the left atrium, and even cardiogenic shock .
We report two cases of distal vessel perforation during CTO PCI in prior CABG patients. In the first case, distal wire perforation was observed leading to a loculated pericardial hematoma along the inferolateral wall of the left ventricle, resulting in death, despite successful sealing of the perforation. In the second case, immediate sealing of a similar perforation was performed using a covered stent and the patient had an uneventful recovery. We also include a review of the literature on coronary perforations leading to hemodynamic compromise in patients with prior CABG.
Case 1
A 71-year-old man with a history of chronic obstructive pulmonary disease and three-vessel CABG presented with worsening dyspnea on exertion and angina. Myocardial perfusion imaging revealed inferior wall ischemia. Coronary angiography revealed patent left anterior descending artery (LAD) with CTO of the distal circumflex and the right coronary artery (RCA, Fig. 1 A ). All previously placed aortocoronary bypass grafts were occluded. The right posterior descending artery (PDA) was a small, diffusely diseased vessel that filled via septal collaterals from the LAD ( Fig. 1 A).
A trial of medical therapy was done for 3 months but the patient continued to have significant exertional dyspnea and angina, and was referred for CTO PCI of the RCA. Bilateral femoral arterial access was obtained with 8F 45-cm long sheaths. The RCA was engaged with an 8F AL 1 guide catheter and the left main coronary artery with an 8F EBU 3.75 guide catheter. Dual injection revealed long occlusion length, blunt proximal cap, and severe calcification and tortuosity. The J-CTO score was 4, suggesting high PCI difficulty . The proximal RCA diameter was 3.5–4.0 mm, indicating that the RCA was a large vessel supplying a sizable territory.
Due to the small size of the PDA, a primary retrograde approach was attempted through septal collaterals, but multiple attempts to cross the collaterals with a Sion (Asahi Intecc, Nagoya, Japan) and Fielder FC (Asahi Intecc) guidewires through a Corsair microcatheter (Asahi Intecc) using both a “surfing” and contrast-guided approach were unsuccessful ( Fig. 1 B).
We then attempted antegrade crossing, initially with a CrossBoss catheter (Boston Scientific, Natick, Massachusetts) that could not advance past the mid RCA, in spite of predilatation with a 1.5 mm balloon. A knuckled Fielder XT guidewire (Asahi Intecc) was advanced to the right posterolateral branch ( Fig. 1 C), and was then redirected into the PDA ( Fig. 1 D). The Fielder XT guidewire entered a branch of the PDA, but a Gaia 2nd guidewire (Asahi Intecc) was advanced using a Twin Pass catheter (Vascular Solutions, Minneapolis, Minnesota) to the PDA ( Fig. 1 E). Using the “double-blind stick and swap” technique with a Stingray balloon and guidewire (Boston Scientific), a Pilot 200 guidewire (Abbott Vascular, Santa Clara, CA) successfully entered the PDA ( Fig. 1 F).
After predilatation perforation of a side branch of the PDA was seen. The contrast did not clear, suggesting the extravasation was contained ( Fig. 2 A ). However, the area of contrast stain appeared to increase after stent implantation was performed ( Fig. 2 B). Transthoracic echocardiography did not demonstrate any effusion ( Fig. 2 C). After a few minutes, the patient developed acute ST-segment elevation ( Fig. 2 D and E). Left main angiography did not demonstrate any change in left main antegrade flow ( Fig. 2 F) and transthoracic echocardiography remained unchanged. Right coronary angiography demonstrated Ellis grade 3 distal perforation ( Fig. 3 A ). A balloon was inflated in the mid RCA to stop antegrade flow ( Fig. 3 B), and given the electrocardiographic changes the patient was emergently intubated. After implantation of 3 coils through a Progreat microcatheter (Terumo, Somerset, NJ) the perforation was sealed ( Fig. 3 C and D). Transesophageal echocardiography demonstrated a loculated effusion along the inferolateral wall of the left ventricle ( Fig. 3 E and F). No collateral flow to the perforate segment from the left anterior descending artery could be seen.
The patient remained hemodynamically stable, although ST-segment elevation persisted. After observation for 60 min in the cardiac catheterization laboratory, he was transferred to the intensive care unit. Upon arrival to the unit he developed pulseless electrical activity and could not be resuscitated; emergent bedside echocardiography did not demonstrate a pericardial effusion, and attempts for pericardiocentesis did not help (draining catheter was likely placed in the right ventricle). The family declined autopsy.
Case 1
A 71-year-old man with a history of chronic obstructive pulmonary disease and three-vessel CABG presented with worsening dyspnea on exertion and angina. Myocardial perfusion imaging revealed inferior wall ischemia. Coronary angiography revealed patent left anterior descending artery (LAD) with CTO of the distal circumflex and the right coronary artery (RCA, Fig. 1 A ). All previously placed aortocoronary bypass grafts were occluded. The right posterior descending artery (PDA) was a small, diffusely diseased vessel that filled via septal collaterals from the LAD ( Fig. 1 A).
A trial of medical therapy was done for 3 months but the patient continued to have significant exertional dyspnea and angina, and was referred for CTO PCI of the RCA. Bilateral femoral arterial access was obtained with 8F 45-cm long sheaths. The RCA was engaged with an 8F AL 1 guide catheter and the left main coronary artery with an 8F EBU 3.75 guide catheter. Dual injection revealed long occlusion length, blunt proximal cap, and severe calcification and tortuosity. The J-CTO score was 4, suggesting high PCI difficulty . The proximal RCA diameter was 3.5–4.0 mm, indicating that the RCA was a large vessel supplying a sizable territory.
Due to the small size of the PDA, a primary retrograde approach was attempted through septal collaterals, but multiple attempts to cross the collaterals with a Sion (Asahi Intecc, Nagoya, Japan) and Fielder FC (Asahi Intecc) guidewires through a Corsair microcatheter (Asahi Intecc) using both a “surfing” and contrast-guided approach were unsuccessful ( Fig. 1 B).
We then attempted antegrade crossing, initially with a CrossBoss catheter (Boston Scientific, Natick, Massachusetts) that could not advance past the mid RCA, in spite of predilatation with a 1.5 mm balloon. A knuckled Fielder XT guidewire (Asahi Intecc) was advanced to the right posterolateral branch ( Fig. 1 C), and was then redirected into the PDA ( Fig. 1 D). The Fielder XT guidewire entered a branch of the PDA, but a Gaia 2nd guidewire (Asahi Intecc) was advanced using a Twin Pass catheter (Vascular Solutions, Minneapolis, Minnesota) to the PDA ( Fig. 1 E). Using the “double-blind stick and swap” technique with a Stingray balloon and guidewire (Boston Scientific), a Pilot 200 guidewire (Abbott Vascular, Santa Clara, CA) successfully entered the PDA ( Fig. 1 F).
After predilatation perforation of a side branch of the PDA was seen. The contrast did not clear, suggesting the extravasation was contained ( Fig. 2 A ). However, the area of contrast stain appeared to increase after stent implantation was performed ( Fig. 2 B). Transthoracic echocardiography did not demonstrate any effusion ( Fig. 2 C). After a few minutes, the patient developed acute ST-segment elevation ( Fig. 2 D and E). Left main angiography did not demonstrate any change in left main antegrade flow ( Fig. 2 F) and transthoracic echocardiography remained unchanged. Right coronary angiography demonstrated Ellis grade 3 distal perforation ( Fig. 3 A ). A balloon was inflated in the mid RCA to stop antegrade flow ( Fig. 3 B), and given the electrocardiographic changes the patient was emergently intubated. After implantation of 3 coils through a Progreat microcatheter (Terumo, Somerset, NJ) the perforation was sealed ( Fig. 3 C and D). Transesophageal echocardiography demonstrated a loculated effusion along the inferolateral wall of the left ventricle ( Fig. 3 E and F). No collateral flow to the perforate segment from the left anterior descending artery could be seen.
The patient remained hemodynamically stable, although ST-segment elevation persisted. After observation for 60 min in the cardiac catheterization laboratory, he was transferred to the intensive care unit. Upon arrival to the unit he developed pulseless electrical activity and could not be resuscitated; emergent bedside echocardiography did not demonstrate a pericardial effusion, and attempts for pericardiocentesis did not help (draining catheter was likely placed in the right ventricle). The family declined autopsy.
Case 2
A 75-year-old man with a prior CABG and medically refractory angina was referred for PCI of a proximal RCA CTO ( Fig. 4 A ). The CTO had a clear proximal cap, approximately 100 mm length, and the distal cap was very calcified and located at the bifurcation of the right posterolateral and right PDA. The PDA filled by septal interventional collaterals from the LAD. Antegrade crossing attempts with a Pilot 200 (Abbott Vascular) and Gaia 2nd (Asahi Intecc) guidewire advanced through a Corsair catheter failed to cross past the highly calcified distal cap. Use of contrast micro-injection (Carlino technique) and multiple stiff guidewires (Confianza Pro 12 and Gaia 3rd, Asahi Intecc) failed to penetrate the distal cap. Retrograde crossing was achieved with a Sion guidewire (Asahi Intecc) through a septal collateral ( Fig. 4 C). Retrograde penetration of the distal cap was extremely challenging but was eventually successful with a knuckled retrograde Pilot 200 guidewire ( Fig. 4 E). Reverse controlled antegrade and retrograde subintimal tracking was performed successfully ( Fig. 4 F) and the retrograde guidewire was externalized ( Fig. 4 G). After stent implantation antegrade flow was restored to the PDA, but a distal vessel perforation was observed in a side branch of the PDA ( Fig. 4 H). A balloon was inflated to stop antegrade flow followed by implantation of a 2.8 × 19 mm Graftmaster Rx stent (Abbot Vascular) through a Guideliner (Vascular Solutions), with sealing of the perforation ( Fig. 4 I). The patient had an uneventful recovery and significant improvement in angina.
