Acute Right Ventricular Failure After Successful Opening of Chronic Total Occlusion in Right Coronary Artery Caused by a Large Intramural Hematoma
- cardiac tamponade
- coronary artery disease
- coronary occlusion
- percutaneous coronary intervention
- ventricular dysfunction, right
A 76-year-old man with history of critical aortic stenosis was referred for surgical aortic valve replacement. Two months prior, preoperative diagnostic angiogram showed 2-vessel coronary artery disease, including 80% stenosis in midsection of left circumflex (LCX) artery, and serial lesions in the right coronary artery (RCA) with chronic total occlusion (CTO) of the distal segment (Movie I in the Data Supplement; Figure 1A) and significant left to right collateralization. At the time of surgical aortic valve replacement, coronary artery bypass was attempted; however, his saphenous veins were found to be unsuitable to use for bypass. His target vessels were deeply buried into myocardial fat as well. It was the heart team’s decision to bring him back for elective percutaneous coronary intervention (PCI). Unfortunately, 3 weeks after the aortic valve replacement surgery, the patient was admitted to medical service for urosepsis with mild elevation in troponin because of demand ischemia. His transthoracic echocardiogram showed normal left ventricle (LV) function with basal inferior and midseptal wall hypokinesis at this time. Given the elevated troponin and known need to perform complete revascularization, we proceeded to PCI of his 2-vessel disease, including the mid-LCX lesion and the CTO in the large RCA system after he recovered from infection.
Before the PCI, he was maintained on dual antiplatelet therapy with aspirin 81 mg and clopidogrel 75 mg. He was loaded with additional 300 mg of clopidogrel before the procedure. Dual femoral accesses with 6F sheaths were placed, and CTO lesion was treated via antegrade approach. One drug-eluting stent was placed in mid-LCX lesion, and the CTO of RCA was opened with 3 drug-eluting stent (Movie I in the Data Supplement; Figure 1B). CTO lesion length was 50 mm.
Total 12 000 U of unfractionated heparin was used, and highest activated clotting time recorded was 201; no other anticoagulants were used. The procedure was uncomplicated, and the plan was to continue the same dual antiplatelet therapy regimen with aspirin and clopidogrel.
Six hours after the procedure, he developed acute left shoulder and chest pain in the recovery unit. ECG showed ST-segment–elevation in inferolateral leads (Figure 1D). He was loaded with prasugrel and emergently taken back to the catheterization laboratory with assumed in-stent thrombosis. An intra-aortic balloon pump was placed from the right femoral artery before coronary angiography was performed from the right radial artery, which showed patent stents in RCA and LCX and no significant disease in left anterior descending artery (Movie II in the Data Supplement; Figure 1C). There was an acute obstruction of small posterior descending artery, which was treated with balloon angioplasty but the flow could not be restored distally. Limited transthoracic echocardiogram in the cath laboratory showed no evidence of pericardial effusion.
He was transferred to coronary care unit afterward, where he was found to have increasing inotrope requirement, continued chest pain unresponsive to narcotics, and a sharp rise in Troponin I level to >40.0 ng/mL raising concern for ongoing myocardial injury. Moreover, echocardiographic images taken from subcostal view showed a large mass measuring 3.5×6 cm along the space between epicardium and pericardium that resulted in severe compression of right ventricle (RV; Movie III in the Data Supplement; Figure 2, upper left). The mass extended to the LV septum and inferior wall but did not compromise LV systolic function. Serial transthoracic echocardiography demonstrated ongoing enlargement of the mass up to 4×13 cm in size (Movie IV in the Data Supplement; Figure 2, upper right). Fluid inside the mass was organizing, and there was color Doppler evidence of blood flow inside (Movie V in the Data Supplement; Figure 2, lower left). Meanwhile, his liver function and urine output worsened despite medical and mechanical support. He was thus taken to the operating room for hematoma evacuation.
After redo sternotomy and lysis of adhesions of the heart, he was found to have a large intramural hematoma extending from the acute margin of the heart around the apex and onto the LV side of the intraventricular septum (Movie VI in the Data Supplement; Figure 3). Pericardiectomy from phrenic to phrenic was performed to relieve any possible constriction on the RV. Transesophageal echocardiography demonstrated a return of the RV cavity. Because of the recent prasugrel loading and concern for continued space-occupying lesions of the intramural hematoma on the RV, his chest was kept open and was subsequently monitored in cardiac intensive care unit. The chest was closed 2 days later, and subsequently he had an uncomplicated postoperative recovery. He was eventually discharged to a skilled nursing facility. Follow-up transthoracic echocardiography after 6 weeks showed resolution of the intramural hematoma, normal LV size and systolic function with estimated ejection fraction 66%, normal RV size with moderately reduced systolic function, with distal RV free wall adhered to the pericardium. (Movie VII in the Data Supplement; Figure 2, lower right).
Analysis of National Cardiovascular Data Registry has shown that PCI of CTO carries a higher procedural complication compared with non-CTO PCI (1.6% versus 0.8%).1 Steinwender et al2 reported a similar case of intramural RV hematoma after failed attempt to cross the CTO in RCA, resulting in pseudotamponade physiology causing refractory cardiac arrest. Unfortunately, this patient did not survive because of severe hypoxic brain injury secondary to prolonged resuscitation attempts.2 Lee et al3 reported a case of RV hematoma after balloon angioplasty of CTO at distal posterior descending artery and drug-eluting stent placement to posterolateral branch, which spontaneously drained into RV without intervention and the patient did well. In the present case, the initial PCI of LCX and RCA successfully revascularized all the lesions, and the repeat coronary angiography showed no clear evidence of coronary dissection or perforation that were extensively evaluated during the case. There was no incidence of extraluminal wire placement or myocardial staining during the initial PCI. The case itself was one of the least eventful cases, which was done in under 2 hours, including 3 RCA stents, 1 LCX stent, and fractional flow reserve measurement of ramus intermedius (0.84, not intervened). Nevertheless, it is speculated that there was a microperforation of RCA, which was exacerbated by the reloading of antiplatelet therapy and repeat heparinization, as well as possible further mechanical damage during the second angiogram, which may have contributed to rapidly enlarging hematoma. In the setting of recent surgery and pericardial adhesions and inflammation, this likely caused severe compression of RV resulting in RV failure and tamponade physiology in the absence of pericardial effusion. Prompt recognition and treatment for RV failure, discovery of RV hematoma, and timely surgical intervention with relief of constriction were all critical in this patient’s care.
The Data Supplement is available at http://circinterventions.ahajournals.org/lookup/suppl/doi:10.1161/CIRCINTERVENTIONS.116.004674/-/DC1.
- © 2017 American Heart Association, Inc.
- Brilakis ES,
- Banerjee S,
- Karmpaliotis D,
- Lombardi WL,
- Tsai TT,
- Shunk KA,
- Kennedy KF,
- Spertus JA,
- Holmes DR Jr.,
- Grantham JA.