A 77-year-old man presented to the office complaining of exertional chest pain. His past history was unremarkable. An echocardiogram revealed akinesia at the RCA territory with preserved left ventricular ejection fraction (LVEF) and no pericardial effusion. The patient was admitted for further evaluation, and coronary angiography (CAG) revealed diffuse three-vessel disease, with a right coronary artery (RCA) chronic total occlusion (CTO) with thrombolysis in myocardial infarction (TIMI) grade 0 flow and collateral flow from septal branches. PCI at the RCA CTO lesion was complicated by Ellis classification type II microchannel perforation during right ventricular (RV) branch wiring proximal to the lesion for additional support during CTO wiring (Figure 1). After prolonged balloon inflation at the RCA, no continued contrast extravasation was seen, and the perforation was thought to have resolved. CTO PCI was completed without any further complications, and the patient remained stable throughout the procedure.
Thoracic computed tomography (CT) angiography taken the day after PCI showed no contrast extravasation, and only minimal pericardial effusion was detected. A follow-up echocardiogram was obtained, and there was no visible pericardial effusion and no other remarkable interval changes. The patient was discharged, free from symptoms, and follow-up echocardiograms and chest CT scans obtained one week and two months after PCI detected no remarkable interval change.
Seven months after PCI, the patient complained of progressive dyspnea and abdominal distension and was admitted for further evaluation. The patient's symptoms prompted a follow-up CAG, which revealed no new lesions or in-stent restenosis. Also, no extravasation was noted at the previously perforated RV branch. Echocardiographic findings demonstrated a slightly increased amount of pericardial effusion and inferior vena cava (IVC) plethora, but otherwise no definite constrictive physiology was yet apparent. Laboratory findings were non-specific. Since the overall clinical picture suggested the possibility of progressive CP, he was discharged on 20 mg of prednisolone, 0.6 mg of colchicine, and diuretics.
The patient visited the emergency room two weeks after discharge due to worsening abdominal distension and dyspnea. At presentation, his blood pressure was 95/60 mmHg and heart rate was 70 beats/min. His physical exam was remarkable for grade 2 pitting edema at the lower extremities, a marked jugular venous pulse, pericardial friction rub on ascultation, and a distended abdomen with shifting dullness. Laboratory findings included mildly elevated liver enzymes, with aspartate aminotransferase at 56 U/L and alanine aminotransferase at 64 U/L, and total bilirubin 1.3 mg/dl. A follow-up echocardiogram revealed pericardial thickening and adhesion at the apex and RV anterior wall, along with scanty pericardial effusion. Intraventricular septal bouncing and respiratory mitral and tricuspid valve inflow variability suggested constrictive pericarditis (Figure 2, Supplementary Video S1). Additionally, global hypokinesia resulted in a decreased LVEF of 39%. Large amounts of pleural effusion and ascites were apparent on CT scans of the chest and abdomen, the latter of which was identified as transudate by paracentesis (Figures 3A,B). Unfortunately, due to the patient's instability, right heart catheterization could not be performed.
The patient underwent surgery due to increasing oxygen requirements and hemodynamic instability. Intraoperative findings revealed a thickened (5 mm) and slightly adhesive pericardium without calcifications, and a dark bloody effusion was drained after opening of the pericardium (Figure 3C). Radical pericardiectomy was performed on the anterior, diaphragmatic, and posterior pericardium under cardiopulmonary bypass, and the operation was concluded without major complications. Pathology was negative for tuberculosis, and was unremarkable except for thick fibrosis without evidence of active inflammation. After the operation, the patient experienced significant relief from symptoms such as abdominal distension and dyspnea. Postoperative care was uneventful, and the patient was discharged on diuretics. Minimal remaining septal bouncing was noted on a follow-up echocardiogram two months after surgery, but no other indicators of constrictive physiology were observed. The patient occasionally complains of intermittent chest pain, but is otherwise stable at outpatient follow-up, two years after the surgery. The patient's timeline is presented in Table 1.