Author + information
- Eui Im, MD†,
- Chi Young Shim, MD, PhD†,
- Geu-Ru Hong, MD†,
- Kyung-Jong Yoo, MD‡,
- Young-Nam Youn, MD‡,
- Byung-Chul Chang, MD, PhD‡,
- Yangsoo Jang, MD, PhD†,
- Namsik Chung, MD, PhD† and
- Jong-Won Ha, MD, PhD†,⁎ ()
- ↵⁎Division of Cardiology, Severance Biomedical Science Institute, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul 120-752, Republic of Korea
To the Editor:
Previous reports have shown changes in the etiologic spectrum of constrictive pericarditis, characterized mainly by a declining incidence of tuberculous pericarditis and an increase in cases resulting from cardiac surgery (1). Constrictive physiology (CP) not only is found in patients with symptomatic constrictive pericarditis but is also more commonly observed in post-cardiac surgery patients when assessed with comprehensive echocardiographic examination. However, few data are available with regard to echocardiographically observed post-operative CP. Therefore, the purpose of this study was to investigate the incidence and clinical course of CP observed on post-operative echocardiographic examination in patients who had undergone isolated coronary artery bypass graft (CABG) surgery.
Our study population consisted of 454 consecutive patients who underwent isolated CABG with comprehensive pre- and post-operative transthoracic echocardiography (TTE) at the Severance Cardiovascular Hospital from 2004 to 2006. The patients were divided into 2 groups (the CP group vs. the No-CP group) according to the presence or absence of the following CP findings on post-operative TTE (2): abnormal ventricular septal motion, dilated inferior vena cava, typical respiratory variations in mitral or hepatic venous flow, and preserved or exaggerated early diastolic mitral annular velocity.
Seventy-eight (17%) of 454 patients showed CP on post-operative TTE (Table 1). In the CP group, no patient showed right ventricular dysfunction, and 5 patients (6%) showed severe tricuspid regurgitation. There were no significant differences in preoperative baseline characteristics between the 2 groups. However, on post-operative TTE, which was conducted a median of 7 days (interquartile range [IQR]: 6 to 9 days) after CABG in the CP group and a median of 7 days (IQR: 6 to 9 days) after CABG in the No-CP group (p = 0.863), left ventricular ejection fraction (LVEF) was higher (59 ± 12% vs. 55 ± 13%, p = 0.030), and the frequency of regional wall motion abnormality was lower (36% vs. 51%, p = 0.019) in the CP group. Also, pericardial effusion on TTE was more commonly observed in the CP group (39% vs. 19%, p <0.001). Cardiac multi-detector computed tomography (MDCT) was performed within 1 month after CABG to assess immediate graft patency if possible. Of the patients who performed MDCT, the rate of graft patency and pericardial thickening were similar between the 2 groups. There were no significant differences of post-operative clinical symptoms—including dyspnea, chest pain, peripheral edema, or fever—between both groups.
Multivariate logistic regression analysis was performed to identify factors independently associated with post-operative CP (Table 1). Variables with p value <0.100 from univariate analysis were included in multivariate analysis. However, pre-operative TTE parameters were excluded to avoid collinearity problems with corresponding post-operative TTE values. The presence of post-operative pericardial effusion was independently associated with post-operative CP (odds ratio: 2.64, 95% confidence interval [CI]: 1.52 to 4.58, p = 0.001).
During follow-up (614 ± 357 days vs. 623 ± 292 days after CABG, p = 0.802), the rates of composite clinical events including heart failure, death due to heart failure, constrictive pericarditis, or cardiac tamponade were not different between both groups by the log-rank test (6.0% vs. 4.4%, p = 0.325) (Fig. 1A,Table 1).
Sixty-one patients (78%) of the CP group underwent follow-up TTE (Fig. 1B). Of them, 50 (82%) showed complete resolution of CP a median of 466 days (IQR: 244 to 738 days) after CABG. The other 11 (18%) still showed residual CP until the last follow-up TTE, which was conducted a median of 757 days (IQR: 78 to 1,142 days) after CABG. Of these 11 patients, only 1 progressed to clinically symptomatic constrictive pericarditis with symptoms of dyspnea, engorged jugular veins, friction rub, and thickened pericardium on MDCT. The remaining 10 patients did not have any of these features.
Our study showed that post-operative CP is a relatively common finding (17% after CABG) compared with typical constrictive pericarditis, which is a well-recognized but rare complication after CABG, occurring in 0.2% to 0.3% of patients (3). Comprehensive TTE have contributed significantly to the ability of physicians to easily and reliably detect CP without invasive catheterization or operative findings.
Matsuyama et al. (4) suggested that post-operative pericardial effusion and normal LVEF are predictors of constrictive pericarditis after CABG. They explained that there is continuous violent friction between the pericardium and the beating heart under normal LVEF. This friction can potentially result in pericardial injury, inflammation, and pericarditis. Our study showed similar findings. Post-operative pericardial effusion was identified as a predictor of post-operative CP. In addition, post-operative left ventricular systolic function was more preserved in the CP group by univariate analysis. These findings might explain the role of pericardial friction and resultant pericardial inflammation in the pathogenesis of post-operative CP. Although C-reactive protein and erythrocyte sedimentation rate values during post-operative period were available only in 11 patients of the CP group, all of them had elevated C-reactive protein (7.6 ± 5.9 mg/dl, reference range: 0 to approximately 0.8 mg/dl) and erythrocyte sedimentation rate (62 ± 34 mm/h, reference range: 0 to approximately 15 mm/h).
Most (82%) patients in the CP group showed complete resolution of CP. Only 1 (1%) patient progressed to constrictive pericarditis. Furthermore, clinical event rates of the CP group and the No-CP group were similar during follow-up. These findings support the transient and benign nature of post-operative CP. Because CABG is a traumatic procedure with intraoperative irritation to the pericardium by the physical manipulation of surgeons, this pericardial trauma and previously mentioned pericardial friction can possibly cause pericardial inflammation, which is enough to cause transient CP but not enough to cause constrictive pericarditis. No patient in the CP group showed irreversible pericardial adhesion, fibrosis, or calcification on MDCT. These findings might also explain the transient and benign nature of post-operative CP.
Although follow-up echocardiography was recommended in all patients, 17 (22%) patients with post-operative CP did not have serial follow-up TTE for various reasons. Another limitation is small sample size. However, to the best of our knowledge, this is the first study investigating the incidence and clinical outcome of post-operative CP.
Post-operative CP is relatively common in patients who underwent CABG. However, it is usually transient and benign. Progression to clinically symptomatic permanent constrictive pericarditis is rare. Therefore, conservative management might be warranted for post-operative CP.
Please note: This work was supported by a Korea Science and Engineering Foundation grant funded by the Korean government (M10642120001-06N4212-00110). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation