A 52‐year‐old man with a history of heavy alcohol use was admitted for cellulitis and chronic edema attributed to cirrhotic liver disease. Exam findings included significant peripheral edema, ascites, and jugular venous distention. A CT scan of the abdomen demonstrated a mildly cirrhotic liver with no signs of portal hypertension. Laboratory studies found no impairment of hepatic synthetic function. Incidental cardiac images obtained during the CT scan revealed the finding of coarse pericardial calcification and compression of the ventricular system suggestive of constrictive pericarditis. A 2‐D echocardiogram, heart catheterization, and cardiac MRI were subsequently performed. Numerous findings supported the diagnosis of chronic calcific constrictive pericarditis, including septal bounce and respiratory variation in LV inflow, equalization of diastolic pressures, calcification of the visceral and parietal pericardium, and an enlarged IVC. The patient subsequently underwent pericardial stripping. Intraoperatively the heart was found to be encased in concretelike calcifications. Preoperative pulmonary artery pressures were 40/27, and immediate postoperative pressures were improved to 27/12. One month postoperatively, the patient's clinical condition was markedly improved, with a 46‐pound weight loss, diminished peripheral edema, no neck vein distention, and a near‐scaphoid abdomen.
Patients with constrictive pericarditis presenting with ascites are often thought to have cirrhosis. The main clue to a cardiac etiology is marked elevation in jugular venous pressure, as cirrhosis is characterized by normal jugular venous pressures in the absence of tense ascites. In constrictive pericarditis, the heavily fibrosed or calcified pericardium restricts diastolic filling, which results in elevation and equilibrium of diastolic pressures in all 4 cardiac chambers. Over the course of years, chronic diastolic heart failure develops, characterized by prominent edema, ascites, and passive hepatic congestion. Calcific pericarditis (concretio cortis) is rare in the United States because tuberculosis incidence has decreased. Causes of constrictive pericarditis include idiopathic or viral, postcardiac surgery, radiation therapy, postinfectious, malignancy, uremia, and connective tissue diseases. Further history revealed that our patient had acute renal failure in 1994, requiring temporary hemodialysis. I suspect he may have had uremic pericarditis.
This case demonstrates chronic right‐sided diastolic heart failure due to calcific pericarditis, Moreover, this case is an example of representativeness bias; numerous prior examiners assumed the commonality between this patient's clinical presentation and that of innumerable similar patients, namely, that an alcoholic will develop cirrhosis and fluid retention. All failed to identify the significance of the neck vein distention and heart failure out of proportion to the liver impairment
R. Paretti, University of Michigan, employee.
To cite this abstract:Paretti R. The Concrete Heart. Abstract published at Hospital Medicine 2009, May 14-17, Chicago, Ill. Abstract 182. Journal of Hospital Medicine. 2009; 4 (suppl 1). https://www.shmabstracts.com/abstract/the-concrete-heart/. Accessed September 16, 2019.