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Year : 2019  |  Volume : 3  |  Issue : 1  |  Page : 17-22

Constrictive pericarditis in association with ischaemic heart disease

Private Practitioner, Shrikrishna Hospital, Aurangabad, Maharashtra, India

Date of Web Publication15-Mar-2019

Correspondence Address:
Rajesh Krishnachandra Shah
Shrikrishna Hospital, 223, Samarthnagar, Aurangabad - 431 001, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_18_18

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Constrictive pericarditis (CP), a not so common condition, has symptoms and signs of heart failure and abnormal echocardiographic findings, such as jerky septal motion. These findings can be mistaken for ischemic heart disease (IHD) if the echocardiographer is inexperienced. Although the etiology of CP can be varied such as idiopathic, postviral, tuberculous, postsurgical, and radiation-induced the final common pathway is the development of fibrous thickening or calcification of the visceral pericardium resulting in pericardial noncompliance, and ultimately requiring surgical intervention. As CP is potentially reversible and surgically curable condition, with improvement in symptoms and quality of life, the diagnosis should not be missed. Here, we present a case in which the diagnosis of CP was made, and subsequently found to have IHD also.

Keywords: Constrictive effusive pericarditis, constrictive pericarditis, ischemic heart disease, pericardium, septal motion

How to cite this article:
Shah RK. Constrictive pericarditis in association with ischaemic heart disease. J Indian Acad Echocardiogr Cardiovasc Imaging 2019;3:17-22

How to cite this URL:
Shah RK. Constrictive pericarditis in association with ischaemic heart disease. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2019 [cited 2023 May 29];3:17-22. Available from: https://jiaecho.org/text.asp?2019/3/1/17/254249

  Introduction Top

Constrictive pericarditis (CP) is not a condition occurring frequently in day-to-day practice. Particularly in the elderly, presenting with signs of the right-sided failure, with echocardiographic signs of abnormal septal motion, one is prejudiced to diagnose it as due to ischemic heart disease (IHD) rather than any other condition. The condition requires a high index of suspicion for not being overlooked. Second, CP and constrictive effusive pericarditis where the effusion may be very small, the diagnosis may be more difficult. Both conditions being surgically curable, with total relief from signs and symptoms and improvement in the quality of life, it is necessary not to overlook the diagnosis.[1],[2]

  Clinical Presentation Top

The patient is a 70 years male, who was on regular follow-up for 3–4 years, for bicuspid aortic valve. In between for 7 and 8 months he was lost to follow-up, and then presented with h/o weakness, breathlessness New York Heart Association Grade II, swelling over the feet and distension of abdomen.

On examination, his pulse rate was 92/min, blood pressure was 124/80 mm Hg, neck veins were full, there was pitting edema over the feet, the liver was 2 cm palpable with free fluid in the abdomen, i.e., all signs of right-sided failure.

The electrocardiogram except for low voltage was unremarkable [Figure 1]. His echocardiography was done which revealed a bicuspid aortic valve, with commissures at 1 and 6 o'clock, and a raphe, due to the fusion of right and noncoronary cusps [Figure 2] and [Video 1]. Parasternal long axis view showed doming of the aortic leaflets, with mild sclerosis. There was a small, anterior and posterior pericardial effusion; the interventricular septum (IVS) motion was jerky. The visceral and parietal pericardium appeared thickened [Figure 3] and [Video 2]. Apical views showed significant shuddering motion of the IVS, with pericardial effusion all around the heart and the pericardium appearing bright and thickened. There was a constant invagination of the right ventricular free wall with color flow mapping showing right ventricular mid cavity turbulence [Figure 4] and [Video 3]. There was mild aortic regurgitation. There was no cardiac tamponade. The inferior vena cava (IVC) was dilated measuring 21 mm and appeared turgid showing no respiratory collapse [Figure 5] and [Video 4]. The hepatic veins showed systolic flow reversal in late diastole [Figure 6] and [Video 5]. The mitral and tricuspid inflow velocities showed more than 30% respiratory variation [Figure 7] and [Figure 8]. The mitral annular tissue Doppler velocities showed annulus reversus with medial 8.2 cm/sec. and lateral 6.9 cm/s, respectively [Figure 9] and [Figure 10].
Figure 1: Preoperative electrocardiogram

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Figure 2: Parasternal short axis view showing bicuspid aortic valve (BAV) with a raphe

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Figure 3: Parasternal long axis view preoperative. LV: Left ventricle, LA: Left atrium, Ao: Aorta, PE: Pericardial effusion

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Figure 4: Preoperative apical 4 chamber view. LV: Left ventricle, RA: Right atrium, RV: Right ventricle, PE: Pericardial effusion

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Figure 5: Preoperative dilated and turgid inferior vena cava (IVC)

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Figure 6: Hepatic vein late diastolic flow reversal

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Figure 7: Mitral inflow velocities showing respiratory variation

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Figure 8: Tricuspid inflow velocities showing respiratory variation. TV: Tricuspid valve

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Figure 9: Mitral lateral annulus tissue Doppler imaging velocities

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Figure 10: Mitral annulus tissue Doppler imaging medial annulus velocity

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Hence, in view of the signs of right-sided failure, the shuddering motion of the IVS, mild pericardial effusion, more than 30% respiratory variation in the mitral and tricuspid velocities, and mitral tissue Doppler annular velocities showing reversal with a dilated, turgid noncollapsing IVC, a confident diagnosis of CP was made, with a differential diagnosis of constrictive effusive pericarditis. The patient was advised computed tomography (CT) scanning, which confirmed the diagnosis with visceral and parietal pericardium thickness of 2–3 mms and 6–8 mms, respectively.

The dilemma now was, whether to give a course of anti-Koch's and steroids, try to tap the fluid, or go ahead with surgery. With these possibilities, the patient was referred to a cardiovascular surgeon for opinion. Pre-operative coronary angiogram revealed, left anterior descending artery lesions at two places. Considering the report, the patient was posted for coronary artery bypass graft surgery (CABG) along with pericardectomy.

The operative findings were suggestive of CP, with severe thickening of the pericardium. The pericardium was removed from the left ventricle, right ventricle, right atrium and pulmonary artery, by sharp and blunt dissection. CABG could not be done due to severe adhesions.

The patient reported for follow-up 15 days later, and a repeat echocardiogram was performed. The parasternal long axis view revealed, markedly decreased IVS shudder, pericardial effusion was still present but less [Video 6]. The apical views also showed reduced IVS shudder, increased left ventricle (LV) cavity, the right ventricle showed mild mid-cavity obstruction [Figure 11] and [Video 7]. There was no respiratory variation in the mitral and tricuspid inflows [Figure 12] and [Figure 13]. The tissue Doppler mitral annular velocities showed normalization, with the lateral and medial annular velocities being 7.3 and 6.5 cm/s, respectively [Figure 14] and [Figure 15]. IVC returned to normal in size with good spontaneous collapse with respiration [Figure 16] and [Video 8]. The aortic regurgitation had increased, and mid right ventricular obstruction reduced. Patient had a remarkable recovery.
Figure 11: Postoperative apical 4 chamber view. LV: Left ventricle, LA: Left atrium, RA: Right atrium, RV: Right ventricle, PE: Pericardial effusion

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Figure 12: Postoperative mitral inflow velocities with no respiratory variation

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Figure 13: Postoperative tricuspid valve inflow velocities with no respiratory variation

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Figure 14: Postoperative lateral mitral tissue Doppler imaging velocity

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Figure 15: Postoperative tissue Doppler imaging medial mitral annulus velocities

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Figure 16: Postoperative inferior vena cava is normal

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  Discussion Top

The true prevalence of CP is unknown. In CP, pericardium becomes noncompliant, forming a stiff covering on the heart, leading to a rapid increase in the intra cardiac pressures in diastole. The patient presents with slowly progressive findings of right-sided failure, namely, the fullness of neck veins, edema feet, palpable liver, and ascites. In 1960 for the first time, the condition of constrictive effusive pericarditis was described. Hancock popularized this definition of constrictive physiology with a coexisting pericardial effusion.[3]

Symptoms of CP overlap those of diverse diseases such as myocardial infarction, aortic dissection, pneumonia, influenza, and connective tissue disorders. This overlap can confuse the most expert echocardiographer. A high level of suspicion of constrictive physiology can help to diagnose CP even when there is a long list of differential diagnosis helping the patient to get timely therapy.[4] Although obtaining a careful history and performing a physical examination remain the cornerstones of evaluation, the different modalities available for confirmation of the diagnosis are Doppler echocardiography, high-resolution CT, cardiac magnetic resonance imaging (MRI), and rarely invasive hemodynamic measurement.[4]

The common causes of CP include:

  • Tuberculosis[5]
  • Incomplete drainage of purulent pericarditis[5]
  • Fungal and parasitic infections[5]
  • Chronic pericarditis[5]
  • Postviral pericarditis[5]
  • Postsurgical[5]
  • Following MI, post-MI[5]
  • In association with pulmonary asbestos.[6]

Effusive-CP is a rare clinical syndrome in which there is constrictive physiology with pericardial effusion, with the constrictive physiology persisting even after drainage of the pericardial fluid. The mechanism of effusive-CP is thought to be the involvement of the visceral pericardium. The hemodynamic definition of this syndrome is the persistent elevation of right atrial, right, and left ventricular diastolic pressures, after the removal of pericardial fluid, thereby reducing the intra-pericardial pressure.[3],[7],[8] It is important to recognize effusive-CP because the routine treatment for CP, i.e., pericardial tapping or a pericardial window may not be effective to relieve the symptoms, as this does not address the visceral pericardium. Therefore, visceral pericardiectomy is indicated for optimal therapy of effusive CP since it is the visceral pericardium that is responsible for the constricting effect.[8]


The normal pericardium is composed of two layers, the tough fibrous parietal pericardium, and the smooth visceral pericardium. Usually, approximately 50 mL of fluid is present in the intra-pericardial space.[9] The normal pericardium is 1–2 mm thick. A pericardial thickness of 3–4 mm or more is considered abnormal. When the pericardium is 4 mm thick, it is very likely to be constrictive pericarditis, and if it is 6 mm the specificity still increases further for the diagnosis of CP.[9] In CP, the normal, thin and compliant parietal and visceral pericardial linings become inflamed, thickened, and fused and ultimately noncompliant.

Effusive-CP is thought to be a continuous process from the early infective pathology to the tamponade physiology with effusion and finally leading to constrictive physiology without effusion, i.e., CP. There has to be a high level of suspicion for this condition when we are dealing with subacute pericarditis or CP with mild effusion.[9] In CP, the later part of the diastole is affected while in conditions with myocardial involvement as in restrictive cardiomyopathy the early part is affected, this is a factor that helps the differentiation of the two conditions.[10]


Echocardiography is the most efficient way to detect an effusion because it has excellent sensitivity and specificity.[11],[12] Unfortunately, no single echocardiographic finding is pathognomonic for constriction. However, when all the echocardiographic findings in conjunction with clinical findings, are evaluated together the diagnosis can be made with quite a certainty.[9] The pathognomonic finding in CP is the respiratory variations seen in the septal motion. This can be detected by either M mode or two-dimensional imaging.[13] The posterior motion of the IVS relative to the less compliant ventricular walls can be appreciated by M-mode and 2D echocardiography as an early diastolic septal notch or “septal bounce.”[14] This septal bounce is considered a finding consistent with constrictive physiology, with sensitivity of 62% and specificity of 93%.[15] Normally in CP, the IVC is plethoric, with no respiratory collapse, this is a sensitive but nonspecific sign of CP.

In expiration, there is reduced right ventricular compliance, and at the same time the left ventricular inflow increases, the increased volume is accommodated by the shift of the IVS to the right. The decreased compliance along with the shift of the IVS is transmitted to the IVC and the hepatic veins causing flow reversal in expiration in diastole.[16] If the Doppler evaluation of the mitral and tricuspid inflow show a respiratory variation to the tune of 25%–30%, it is considered consistent with CP.[17],[18] The incidence of these Doppler related respiratory changes have been reported to be as high as 85% to 90%.[19] Because of lateral wall tethering, the lateral mitral annulus early diastolic tissue Doppler velocity, i.e., the e' wave is often decreased and abnormally lower than the medial e' wave. This is the annulus reversus.[17] This also helps to differentiate from restrictive cardiomyopathy. CT scanning and MRI are considered the procedures of choice for imaging the pericardium.[16]

  Conclusion Top

The case highlights the role of echocardiography in the evaluation of patients with CP and the features that prompted the need for early surgical intervention. Though no specific finding is pathognomonic of CP, if meticulously done, with an illustration of maximal findings, and with the support of the clinical picture one can quite confidently and accurately diagnose the condition.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Geske JB, Anavekar NS, Nishimura RA, Oh JK, Gersh BJ. Differentiation of constriction and restriction: Complex cardiovascular hemodynamics. J Am Coll Cardiol 2016;68:2329-47.  Back to cited text no. 1
Ling LH, Oh JK, Schaff HV, Danielson GK, Mahoney DW, Seward JB, et al. Constrictive pericarditis in the modern era: Evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation 1999;100:1380-6.  Back to cited text no. 2
Hancock EW. Subacute effusive-constrictive pericarditis. Circulation 1971;43:183-92.  Back to cited text no. 3
Shabetai R. Acute viral and idiopathic pericarditis. In: Shabetai R, editor. The Pericardium. New York: Grune & Stratton; 1981. p. 348.  Back to cited text no. 4
Hancock EW. On the elastic and rigid forms of constrictive pericarditis. Am Heart J 1980;100:917-23.  Back to cited text no. 5
Melduni RM, MD. Pericardial Diseases. In: Murphy JG, Lloyd MA, editor. Mayo Clinic Cardiology: Concise Textbook 4th ed. Oxford: Mayo Clinic Scientific Press/Oxford University Press; 2015. p. 718.  Back to cited text no. 6
Goldstein JA. Cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy. Curr Probl Cardiol 2004;29:503-67.  Back to cited text no. 7
Sagristà-Sauleda J, Angel J, Sánchez A, Permanyer-Miralda G, Soler-Soler J. Effusive-constrictive pericarditis. N Engl J Med 2004;350:469-75.  Back to cited text no. 8
Zagol B, Minderman D, Munir A, D'Cruz I. Effusive constrictive pericarditis: 2D, 3D echocardiography and MRI imaging. Echocardiography 2007;24:1110-4.  Back to cited text no. 9
Veress G, Feng D, Oh JK. Echocardiography in pericardial diseases: New developments. Heart Fail Rev 2013;18:267-75.  Back to cited text no. 10
Feigenbaum H, Armstrong W. Pericardial diseases. Feigenbaum's Echocardiography. 6th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2004. p. 260-9.  Back to cited text no. 11
Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357-70.  Back to cited text no. 12
Talreja DR, Nishimura RA, Oh JK, Holmes DR. Constrictive pericarditis in the modern era: Novel criteria for diagnosis in the cardiac catheterization laboratory. J Am Coll Cardiol 2008;51:315-9.  Back to cited text no. 13
Sengupta PP, Mohan JC, Mehta V, Arora R, Khandheria BK, Pandian NG, et al. Doppler tissue imaging improves assessment of abnormal interventricular septal and posterior wall motion in constrictive pericarditis. J Am Soc Echocardiogr 2005;18:226-30.  Back to cited text no. 14
Dal-Bianco JP, Sengupta PP, Mookadam F, Chandrasekaran K, Tajik AJ, Khandheria BK, et al. Role of echocardiography in the diagnosis of constrictive pericarditis. J Am Soc Echocardiogr 2009;22:24-33.  Back to cited text no. 15
Reuss CS, Wilansky SM, Lester SJ, Lusk JL, Grill DE, Oh JK, et al. Using mitral ‘annulus reversus’ to diagnose constrictive pericarditis. Eur J Echocardiogr 2009;10:372-5.  Back to cited text no. 16
Oh JK, Hatle LK, Seward JB, Danielson GK, Schaff HV, Reeder GS, et al. Diagnostic role of Doppler echocardiography in constrictive pericarditis. J Am Coll Cardiol 1994;23:154-62.  Back to cited text no. 17
Hancock EW. Differential diagnosis of restrictive cardiomyopathy and constrictive pericarditis. Heart 2001;86:343-9.  Back to cited text no. 18
von Bibra H, Schober K, Jenni R, Busch R, Sebening H, Blömer H, et al. Diagnosis of constrictive pericarditis by pulsed Doppler echocardiography of the hepatic vein. Am J Cardiol 1989;63:483-8.  Back to cited text no. 19


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16]

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