European Journal of Echocardiography Advance Access originally published online on March 30, 2008
European Journal of Echocardiography 2008 9(4):591-594; doi:10.1093/ejechocard/jen112
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Restrictive cardiomyopathy versus constrictive pericarditis: making the distinction using tissue Doppler imaging
1 Westmead Private Cardiology, Suite 1, Corner Darcy and Mons Road, Westmead, NSW 2145, Australia
2 Westmead Private Hospital, Corner Darcy and Mons Road, Westmead, NSW 2145, Australia
3 Westmead Hospital, Hawkesbury Road, Westmead, NSW 2145, Australia
4 Department of Medicine, The University of Sydney, NSW 2006, Australia
5 Liverpool Hospital, Elizabeth Street, Liverpool, NSW 2170, Australia
6 Department of Medicine, The University of New South Wales, NSW, Australia
Received 9 January 2008; accepted after revision 9 February 2008; online publish-ahead-of-print 30 March 2008.
* Corresponding author. Tel: +61 02 9687 0866. E-mail address: stoodley{at}tpg.com.au
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Abstract |
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Although the primary cause of constrictive pericarditis is entirely different to that of restrictive cardiomyopathy, the two often present with very similar clinical findings. As such, making the distinction between the two is a diagnostic challenge. We report a case that highlights how tissue Doppler imaging may simplify the distinction between pericardial constriction and myocardial restriction.
Keywords: Restrictive cardiomyopathy; Constrictive pericarditis; Tissue Doppler imaging
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Case report |
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A 57-year-old female with a past history of tuberculosis was referred for cardiac consultation. She presented with a history of atypical chest pain and dyspnoea on exertion. Her recent symptoms included mild orthopnoea, intermittent episodes of increasing pedal oedema, and right upper quadrant discomfort associated with difficulty in breathing.
Previous medical history of significance was the diagnosis of constrictive pericarditis 5 years earlier. Cardiac surgical consultation at that time advised against operative intervention due to the comparatively high operative risk and minimal symptoms at the time. There was no history of hypertension, diabetes, hypercholesterolaemia, or ischaemic heart disease.
On examination, a pulse of 76/min and blood pressure of 110/70 mmHg were recorded. A 12-lead electrocardiogram demonstrated sinus rhythm with evidence of T wave inversion in leads V1–V3 and biphasic T waves in the precordial leads V4–V6. Kussmaul's sign was positive. The jugular venous pulse was visible 6 cm above the sternal angle during quiet respiration. Auscultation of the chest revealed a normal first heart sound and a split second heart sound with a loud pulmonary component. The abdomen was slightly distended and the liver edge was palpable 6 cm below the costal margin.
Transthoracic echocardiography revealed normal left ventricular (LV) and right ventricular (RV) dimensions and systolic function, though a pronounced ‘septal bounce’ was noted. There was moderate-to-severe biatrial enlargement (Figure 1) with displacement of the interatrial septum towards the left side on inspiration. The inferior vena cava was dilated, with no respiratory variation. Significant patchy pericardial thickening was seen on two-dimensional imaging (Figure 2), particularly over the posterior aspect of the ventricle close to the A-V groove. There was a distinct absence of normal ‘pericardial slide’ (see Supplementary data online, Figures 5 and 6) (free movement of the LV within the pericardium).
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Pulsed wave Doppler identified a restrictive transmitral inflow pattern. Mitral valve E and A velocity measured 0.74 and 0.36 m/s, respectively (Figure 3). Tissue Doppler imaging (TDI) of early diastolic myocardial velocity (E') and systolic myocardial velocity (S') measured 19 and 7 cm/s, respectively (Figure 4). The E/E' ratio was 3. Significant respiratory variation in Doppler inflow velocities was noted.
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Fluid intake was restricted to 1.2 L daily and arrangement was made for yearly review. Although no other intervention was required at present, it is likely that as the disease progresses, surgical intervention may become necessary.
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Discussion |
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Constrictive pericarditis is a well-known sequela of tuberculosis in which the pericardium becomes thickened and fibrotic. As a result, LV relaxation is reduced because the heart is limited by the constricting pericardium,1 and the resulting loss of function may eventually lead to congestive heart failure.
However, restrictive cardiomyopathy may also present with very similar clinical findings. As such, making the distinction between the two is a diagnostic challenge. Angiography, CT, MRI, and traditional Doppler echocardiographic methods do not provide robust diagnostic criteria and remain an unreliable means of distinction.2,3
The advent of tissue Doppler imaging (TDI) has changed this diagnostic challenge. TDI is a contemporary echocardiographic tool that allows the measurement of intrinsic myocardial velocities. In restrictive cardiomyopathy, there is a reduction in LV relaxation as a result of primary myocardial disease with a resultant decrease in E' velocity. In contrast, in constrictive pericarditis, there is no significant myocardial dysfunction;1 therefore, the TDI E' velocity is not reduced.2
The E' velocity, which reflects early diastolic LV relaxation in the longitudinal plane, is relatively easy to obtain. In one study, an E' value 
8 cm/s was shown to differentiate patients with constriction from those with restriction with 89% sensitivity and 100% specificity.2 In our patient, we obtained a considerably increased TDI E' velocity of 19 cm/s, as would be expected in a patient free of myocardial disease.
Moreover, recently published data4 reveal that the addition of systolic contraction velocity (S'), obtained by TDI provides incremental value to the E' velocity measurement. An S' value of 6 cm/s or more increases the sensitivity of an E' of 8 cm/s or more from 70 to 88%.4 In our case, the diagnosis was further confirmed by the addition of the S' velocity that was measured at 7 cm/s.
In conclusion, this study highlights the benefit of the TDI derived E' and S' velocities as a means of making the distinction between restriction and constriction. These measurements are of particular value because they can be obtained easily, are robust and reproducible, and when used in combination may significantly improve sensitivity and specificity in the identification of cases of constriction.
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Supplementary data |
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Supplementary data are available at European Journal of Echocardiography online.
Conflict of interest: none declared.
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References |
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- Rajagopalan N, Garcia MJ, Rodriguez L, Murray RD, Apperson-Hansen C, Stugaard M, et al. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial disease and restrictive cardiomyopathy. Am J Cardiol (2001) 87:86–94.[CrossRef][Web of Science][Medline]
- Ha JW, Ommen SR, Tajik AJ, Barnes ME, Ammash NM, Gertz MA, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy using mitral annular velocity by tissue Doppler echocardiography. Am J Cardiol (2004) 94:316–319.[CrossRef][Web of Science][Medline]
- Garcia MJ, Rodriguez L, Ares M, Griffin BP, Thomas JD, Klein AL. Differentiation of constrictive pericarditis from restrictive cardiomyopathy: assessment of left ventricular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol (1996) 27:108–14.[Abstract]
- Choi EY, Ha JW, Kim JM, Ahn JA, Seo HS, Lee JH, et al. Incremental value of combining systolic mitral annular velocity and time difference between mitral inflow and diastolic mitral annular velocity to early diastolic annular velocity for differentiating constrictive pericarditis from restrictive cardiomyopathy. J Am Soc Echocardiogr (2007) 20:738–43.[CrossRef][Web of Science][Medline]
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