Constrictive pericarditis decades after aortic valve repair

Abstract

Constrictive pericarditis is rare after cardiac surgery, with a time to presentation ranging from 82 days to 204 months. We report a 75-year-old man who underwent aortic valve replacement and developed constrictive pericarditis 21 years later. He underwent a pericardiectomy with pericardial stripping, which confirmed constrictive pericarditis and improved his symptoms.

Constrictive pericarditis after cardiac surgery has a reported incidence of 0.2%. The median time between surgery and presentation was 82 days in one study and 23.4 months in another, while the most extreme cases were up to 204 months. ^{1 , 2} Due to the length of time between surgery and median time to presentation, it can be difficult for the clinician to associate the initial cardiac surgery with the patient’s presentation consistent with constrictive pericarditis.

CASE PRESENTATION

A 75-year-old man had a past medical history of aortic valve replacement with a 21 high-performance St. Jude aortic valve (placed for congenital aortic stenosis due to a bicuspid valve), atrial fibrillation on warfarin, heart failure with preserved ejection fraction, nonalcoholic liver cirrhosis (diagnosed 3 years earlier), and hypertension. He presented with several months of worsening exertional dyspnea, abdominal distension, and fatigue. His vital signs upon presentation were normal, and he had no leukocytosis or jaundice. Physical exam revealed distended jugular veins with prominence of the y descent along with pulsus paradoxus. Computed tomography of his abdomen and pelvis without contrast showed a large right-sided pleural effusion, extensive diffuse pericardial calcification, and gross ascites. A transthoracic echocardiogram showed a left ventricular ejection fraction of 65% to 70%, grade III diastolic dysfunction, decreased left ventricular cavity size, bowing of the ventricular septum to the left, impaired right ventricular systolic function, an enlarged right atrium, an enlarged right ventricle, a dilated inferior vena cava with poor inspiratory collapse, and a mitral valve e′ velocity of 1.68 m/s (Figure 1). Paracentesis was performed with removal of 7.5 L of transudative ascitic fluid. After removal of the fluid, the patient’s symptoms improved. He was diagnosed with cardiac ascites secondary to decompensated right-sided heart failure and thought to also have constrictive pericarditis.

Figure 1.

Transthoracic echocardiogram. (a) Parasternal long axis view during diastole. Note the enlarged right ventricle, bowing of the ventricular septum into the left ventricle, and decreased left ventricular cavity size. (b) The mitral valve, showing increased mitral valve e′ velocity.

The patient subsequently underwent an outpatient right-sided heart catheterization, which showed a right atrial pressure of 18 mm Hg, right ventricular pressure of 60/80 mm Hg with a dip and plateau configuration, left atrial pressure of 30 mm Hg, left ventricular pressure of 103/10 mm Hg, and end diastolic pressure of 25 mm Hg. Approximately 1 month later, he underwent a pericardiectomy with pericardial stripping. In the operating room, the parietal pericardium was noted to adhere to the visceral pericardium with heavy calcium. The calcifications and adhered pericardium were removed. After this, the surgeon noted that his heart function visibly improved and had little constriction. In the immediate postoperative period, he required vasopressors due to cardiogenic and hypovolemic shock thought to be due to dehydration, third spacing, and low albumin. He also developed recurrent high-output pleural effusions, for which he received a pleural catheter. Transthoracic echocardiogram performed approximately 1 month after surgery showed a mildly dilated left atrium, mildly dilated right atrium, normal ventricular septal movement, and normal right ventricular systolic function without evidence of right-sided filling compromise. His symptoms continued to improve, and he was discharged in stable condition to a rehabilitation center.

DISCUSSION

Pericarditis can be acute or chronic. Acute pericarditis lasts <6 weeks; common etiologies include medications, postmyocardial infarction, and viral infections. Chronic pericarditis lasts >6 months and can lead to development of constrictive pericarditis. Etiologies of constrictive pericarditis include past cardiac surgeries, viral infections, radiation, trauma, or uremia. Our patient had no recent viral infections and no history of radiation, trauma, or uremia. Signs and symptoms of chronic pericarditis include elevated jugular venous pressure, pulsus paradoxus, and right heart failure symptoms, such as dyspnea, ascites, hepatomegaly, pitting edema, and pleural effusions. ³ In patients with constrictive pericarditis, the pericardium becomes fibrotic and thickened. This leads to a decrease in compliance of the atria and ventricles, which decreases the blood return, subsequently causing the signs and symptoms described above. While ventricular interdependence is always present, constrictive pericarditis leads to a marked increase of ventricular interdependence due to the increase in right ventricular pressure, causing a decrease in left ventricular end diastolic volume. ⁴

Constrictive pericarditis is suspected on the basis of presenting signs or echocardiography, with the gold standard method of diagnosis being a right-sided heart catheterization. The diagnostic criteria on echocardiography include abnormal ventricular septum motion, a medial mitral annulus e′ velocity >9 cm/sec, and a plethoric inferior vena cava. ⁵ The initial transthoracic echocardiogram in our patient showed all of these diagnostic criteria. Right heart catheterization will classically show an equalization of the diastolic pressures of the right and left ventricle along with a dip and plateau pattern and decrease in cardiac output. ⁶ Our patient had some of these findings on right heart catheterization, but results were not definitive. Definitive treatment is an anterior surgical pericardiectomy extending down to the phrenic nerve. ⁷

Our patient presented with a recent diagnosis of nonalcoholic cirrhosis along with heart failure with preserved ejection fraction. His symptoms included anorexia, dyspnea on exertion, and lower-extremity edema. We believe our patient developed chronic constrictive pericarditis leading to right heart failure and cardiac cirrhosis. Although right-sided heart catheterization was not definitive, due to high suspicion he underwent a pericardiectomy with resolution of his symptoms. In conclusion, constrictive pericarditis after heart surgery can be missed if suspicion is not high enough, especially given the possibility of it happening decades after the original surgery.