Involvement of the left ventricle is of primary importance in constrictive pericarditis.
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A case of constrictive pericarditis that occurred 4 months after CABG is reported. After undergoing CABG the patient developed pneumopericardium with a subsequent pericardial effusion, which were successfully treated with steroids and diuretics and the patient was discharged asymptomatic. About 3 months later easy fatiguability, abdominal bloating and pedal edema appeared, prompting him to undergo a thorough examination, which revealed the presence of constrictive pericarditis. At that time the graft was shown to remain patent. Eight months post CABG pericardial stripping was performed through a median sternotomy with confirmation of a fall in the CVP and PAP (diastolic) intraoperatively. Towards postoperative day 3, however, the CVP rose again with reappearance of abdominal bloating. Hence, cardiac catheterization was performed once again. The RV pressure tracing showed dip and plateau, and reoperation was performed. Pericardial stripping performed on the lateral and supradiaphragmatic sides of the left ventricle via a left anterior thoracotomy brought about a satisfactory hemodynamic improvement.
The current status of constrictive pericarditis is reviewed with regard to its etiology, physical signs, electrocardiographic findings, and hemodynamic features. Angiographic aspects are also presented. The role and limitations of M-mode echocardiography in this disease are emphasized. The value of other noninvasive studies such as measurement of systolic time intervals, myocardial scanning, and high-speed echocardiography is described. Emphasis is placed on the invasive and noninvasive methods that may be useful in separating restrictive cardiomyopathy from constrictive pericarditis. Methods of treatment, indications for pericardial resection, and the current operative results are commented on briefly.
OBJECTIVES: This study sought to examine the value of analyzing Doppler echocardiographically derived tricuspid regurgitation signals during respiration in relation to the diagnosis of constrictive pericarditis. BACKGROUND: A physiologic hallmark of constrictive pericarditis is enhanced ventricular interdependence, which produces reciprocal changes in right and left ventricular filling and ejection dynamics during the respiratory cycle. It was hypothesized that these changes could be detected noninvasively by analyzing Doppler echocardiographically derived tricuspid regurgitation signals and that this information could assist in noninvasively diagnosing constrictive pericarditis. METHODS: Simultaneous Doppler echocardiography and catheterization studies of the right and left sides of the heart with high fidelity pressure manometers were performed in 5 patients with surgically confirmed constrictive pericarditis and 12 patients (control subjects) with heart failure due to other causes. RESULTS: Changes observed in tricuspid regurgitation Doppler echocardiographic variables from onset to peak inspiration in patients with constrictive pericarditis were significantly different from those in control subjects. Mean (+/- SD) percent change in maximal tricuspid regurgitation velocity was 13% +/- 6% and -8% +/- 7% in the constrictive pericarditis and control groups, respectively (p < 0.0001); mean percent change in tricuspid regurgitation signal duration was 18% +/- 2% and -2% +/- 7%, respectively (p < 0.0001); mean percent change in tricuspid regurgitation time velocity integral was 27% +/- 15% and -10% +/- 12%, respectively (p < 0.0001). CONCLUSIONS: Respiratory changes in Doppler echocardiographically derived tricuspid regurgitation peak velocity and velocity duration are increased in patients with constrictive pericarditis and may be helpful in diagnosing this condition noninvasively.
Twenty-four cases of the constrictive pericarditis were operated on pericardiectomy from 1966 to 1990. One case died because of massive bleeding, LOS, and respiratory failure immediately after the operation. A long-term follow up study was performed up to 27 years (mean 13.1 years) in other cases. Ten cases died during the follow up period (cardiac: 6, non cardiac: 4). Five cases of the cardiac deaths had major complications: tabes dorsalis, chronic respiratory failure, pacemaker implantation, mitral regurgitation, emergency operation at high age (78 years old). The survival rates of 5, 10, and 15 years were 85%, 67%, and 58.2%, respectively (Kaplan-Meier). All of survival cases are now in NYHA I or II class in satisfactory. We concluded that pericardiectomy is a very effective treatment for constrictive pericarditis but a more careful follow up is required especially in cases complicated with other major problems because cardiac function is not so recovered as normal level after surgery due probably to readhesion and fibrotic changes of the myocardium.
Two patients underwent pericardiectomy for postirradiation constrictive pericarditis. Both had received radiotherapy (more than 6,000 rads) for treatment of Hodgkin's disease 17 (patient 2) and 20 years (patient 1) earlier. At the time of operation, the patients were in New York Heart Association functional class III-IV or IV. Preoperative catheterization showed the following pressures for patients 1 and 2, respectively: right atrial, 30 and 14 mm Hg; right ventricular end-diastolic, 28 and 14 mm Hg; wedge, 29 and 13 mm Hg; and left ventricular end-diastolic, 27 and 14 mm Hg. Complete epicardiectomy and pericardiectomy was attempted in both patients. However, hospital mortality was 100%; patient 1 died of multiorgan failure after six days, and patient 2 died of biventricular failure after 3 months. A review of the literature revealed 44 cases of pericardiectomy for postirradiation constrictive pericarditis and a late survival rate of less than 50%. The poor results in these patients compared with patients having pericardiectomy for other reasons seem to be due mainly to the various kinds of radiation-induced damage to the heart as a whole, including untimely coronary artery disease, myocardial fibrosis, atrioventricular conduction disturbances, and valve dysfunction, with the result that complete relief by epicardiectomy and pericardiectomy may not be technically feasible.
A case of constrictive pericarditis intimately involving patch electrodes of the automatic implantable cardioverter-defibrillator is described. Typical clinical and hemodynamic findings for constrictive pericarditis were noted 15 months after lead installation. Additionally, chest x-ray examination revealed a severe crumpling deformity of the patch electrodes. Thoracotomy was performed and revealed marked fibrous reaction surrounding both surfaces of each patch electrode. Histologic examination revealed fibrous tissue with multinucleated giant cells, consistent with a foreign body reaction. The patient had complete resolution of signs and symptoms of constrictive pericarditis after removal of the patch electrodes and pericardial stripping. Constrictive pericarditis from implanted patch electrodes appears to be an uncommon complication of the automatic implantable cardioverter-defibrillator and should be considered in patients with one or more patch electrodes and other signs of constrictive pericarditis.