Ann Thorac Surg 2002;74:595-597
© 2002 The Society of Thoracic Surgeons
Case report
Coronary obstruction by a calcific pericardial ring
Suresh T. Bhagia, MDa,
Aashish R. Patel, BSa,
George J. Reul, MD*a
a Department of Cardiovascular Surgery, Texas Heart Institute, Houston, Texas USA
Accepted for publication December 5, 2001.
* Address reprint requests to Dr Reul, Department of Cardiovascular Surgery, Texas Heart Institute, 1101 Bates St, Rm O 298H, Houston, TX 77030 USA
e-mail: greul{at}heart.thi.tmc.edu
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Abstract
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We report the unique case of a 62-year-old man whose left anterior descending artery was intermittently obstructed by a heavily calcified pericardial ring. This is a rare case in which a coronary artery has been compressed because of constrictive pericarditis.
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Introduction
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Calcific constrictive pericarditis is believed to be a nonspecific response to chronic inflammation [1]. This form of pericarditis has become increasingly rare, because it is usually due to tuberculosis, which is no longer common in westernized nations. Other possible causes of calcific disease include radiation, rheumatoid disorders, sarcoidosis, and trauma. Whatever its etiology, calcific pericarditis can lead to cardiac tamponade by reducing cardiac diastolic filling, thereby jeopardizing diastolic function.
We describe a patient in whom a calcified constrictive pericardial ring intermittently compressed the left anterior descending coronary artery.
A 62-year-old Asian man started having chest pain in 1982 and was treated with medical therapy, which stabilized his symptoms. In 1987, his cardiac condition worsened, and he complained of pain in his back and both arms. He underwent a cardiac evaluation in Pakistan, where a chest roentgenogram showed calcification around the heart and an electrocardiogram showed a left bundle-branch block (Fig 1).
The patient was treated conservatively with medication by his cardiologist, until December 1999, when he started to have shortness of breath on exertion and increasing pedal edema. In June 2000, he was referred to the Texas Heart Institute for further management.
Upon admission to our hospital, the patient had atrial flutter and congestive heart failure. His condition was initially managed with furosemide, metoprolol, digoxin, amiodarone, and warfarin therapy. Cardiac catheterization revealed a heavily calcified pericardial ring, and coronary angiography showed an indentation in the left anterior descending artery (LAD) [2, 3]. The myocardial compression caused by the dense pericardial calcification occurred during systole; fortunately, the LAD was widely patent during diastole (Fig 2).
The left ventricular ejection fraction was normal. Surgical treatment was contemplated.
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Fig 2. The myocardial compression caused by the dense pericardial calcification during systole. Fortunately, the left anterior descending artery was widely patent during diastole.
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A median sternotomy revealed that the heavily calcified, 1.5-cm-thick pericardium covered the lateral and inferior aspects of the left ventricle, which was deformed into an hourglass shape. Using sharp scissors, we stripped the pericardium from both the right atrium and the right ventricle. We then performed a pericardiectomy on the posterior surface of the heart with the aid of cardiopulmonary bypass. The LAD was released from the calcific ring with a bone cutter and a rongeur [4]. The total cardiopulmonary bypass time was 38 minutes [5]. At the end of the operation, the sternum was closed, and the patient was transferred to the recovery room in stable condition. Postoperatively, amiodarone was administered to treat atrial fibrillation.
The patient was extubated on the 1st postoperative day. Samples of pericardial fluid, pleural fluid, blood, and urine were negative for acid-fast bacilli, fungal organisms, and anaerobic bacilli. Pathologic examination of the surgical specimen showed multiple elongated fragments of bone and calcified material. Microscopic examination revealed extensive fibrosis with focal calcification and no acute inflammation or evidence of malignancy. On the 6th postoperative day, the patient was discharged from the hospital with his heart in sinus rhythm. As of March 2001, he remained in good health.
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Comment
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Pericardial diseases have been of interest since the time of Hippocrates (circa 400 BC) and of Galen (circa 180 AD). In 1696, Giorgio Baglivi vividly described a calcified pericardium as a heart invested in a mortar sheath. In 1852, the term tuberculous pericarditis was coined by the English scientist Rokitansky. In 1893, Sir William Osler noted that tuberculous pericarditis was not always associated with tuberculous lesions. Ryoke and colleagues demonstrated the value of performing a pericardiectomy early, before tuberculosis could spread in the myocardium.
Our patient was from Asia, where tuberculosis is a major health concern. About 2% of tuberculous patients end up with tuberculous pericarditis. The symptoms, signs, and laboratory findings associated with this condition are related to constriction and tamponade instead of pericarditis per se. In our case, microscopic examination of the surgically removed pericardial tissue revealed extensive fibrosis, with focal calcification, but no acute inflammation or malignancy.
Calcification of the pericardium is caused by reduced carbon dioxide tension in the injured tissue, which allows enzymes to release sufficient phosphate to cause precipitation of calcium phosphate. Most tissues consist of 86% calcium phosphate, 13% calcium carbonate, and 1% magnesium phosphate. These calcium salts tend to form hoops, bands, and most often, irregular sheets around the cardiac surface. Although calcification may not necessarily cause clinical constriction, extensive calcification is the most notable characteristic of chronic constrictive pericarditis [6].
In our case, a purified protein derivative (PPD) test yielded a positive result, although the patient had no bacteriologic or pathologic evidence of tuberculosis. Because tubercle bacilli are difficult to isolate with smears and cultures, DNA amplification by means of a polymerase chain reaction is the most conclusive test method available. A negative PPD test result cannot rule out tuberculous pericarditis, however, as 30% of all histologically confirmed cases of tuberculosis are negative for PPD [7].
With chronic constrictive pericarditis, multidrug therapy is often insufficient. The only definitive treatment is surgical, a pericardiectomy yielding the best long-term results. Because the disease process is ongoing, however, inflammatory constriction may recur even after a complete pericardiectomy. Therefore, it is imperative that all pericardiectomy patients be followed up for many years postoperatively to ensure that constriction does not recur.
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Acknowledgments
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The authors cordially thank Ms Virginia Fairchild for providing editorial support and Ms Carol Latta for creating the illustration.
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References
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- Ling L.H., Oh J.K., Breen J.F., et al. Calcific constrictive pericarditis: is it still with us?. Ann Intern Med 2000;132:444-450.[Abstract/Free Full Text]
- Tanaka H., Kadoba K. An unusual case of annular constrictive pericarditis: a "framed heart. " Nippon Kyobu Geka Gakkai Zasshi 1992;40:996-1000.[Medline]
- Iselin M. Calcified constrictive pericarditis in an adolescent. Arch Mal Coeur 1994;86:683-685.
- Casha A. Pericardiectomy using an oscillating saw. Ann Thorac Surg 2000;69:613-614.[Abstract/Free Full Text]
- Shumway N.E., Griepp R.B. Surgical treatment of chronic constrictive pericarditis using cardiopulmonary bypass. J Thorac Cardiovasc Surg 1975;69:236-238.[Abstract]
- Spodnick D.H. Chronic and constrictive pericarditis. New York: Grune and Stratton, 1964:81-100.
- Zukowska H., Zwolinski J. Two cases of tuberculous pericarditis: diagnostic difficulties. Pneumonol Alergol Pol 1993;61:291-294.[Medline]
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