Journal List > Korean Circ J > v.50(7) > 1144936

Kim and Chang: Author's Reply to Septal Bounce or Ventricle Interdependence in Constrictive Pericarditis: Same or Different
We appreciate the letter regarding our recently published article,1) which demonstrated that tuberculous pericarditis with constrictive physiology at initial diagnosis can be reversible with the appropriate steroid therapy.
Ventricular interdependence and septal bouncing are often confused, but, strictly speaking, they are different concepts. Septal bouncing is paradoxical abnormal septal motion caused by hypercontraction of the septal myocardium to compensate for lateral left ventricular wall motion. Longitudinal motion of the mitral annulus on tissue Doppler imaging is also increased in constrictive pericarditis despite high left ventricular filling pressure, because of compensatory hypercontraction due to limited lateral expansion of the entire heart.2) On the other hand, ventricular interdependence, so-called ventricular discordance, is a result of variation in intracardiac pressure under limited expansion of the pericardium during the respiratory cycle. Therefore, the presence of ventricular interdependence and septal bouncing are echocardiographic parameters for diagnosis of constrictive pericarditis; however, they do not always appear in combination because of their different mechanisms.3) Furthermore, septal bouncing can be present in other conditions such as left bundle branch block or right ventricular pacing.4)
Regarding the chronicity of the disease, we conducted chest computed tomography in all patients at initial diagnosis. There were no pericardial calcifications. The causes of transient constrictive pericarditis included various diseases such as postoperative pericarditis and idiopathic pericarditis as well as pericardial tuberculosis. If constrictive pericarditis is detected during the early stages of inflammation, the disease process can be reversed without scarring, so-called transient constrictive pericarditis.5) Diagnosis of transient constrictive pericarditis is based on clinical course of the disease, not from etiology. Tuberculous pericarditis can be a cause of transient constrictive pericarditis; however, reversal of the constrictive physiology is not always observed during treatment of tuberculous pericarditis, as shown in our study.1)

Notes

Conflict of Interest: The author has no financial conflicts of interest.

Author Contributions:

  • Writing - original draft: Kim MS, Chang SA.

  • Writing - review & editing: Chang SA.

References

1. Kim MS, Chang SA, Kim EK, et al. The clinical course of tuberculous pericarditis in immunocompetent hosts based on serial echocardiography. Korean Circ J. 2020; 50:599–609. PMID: 32096358.
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2. Ha JW, Oh JK, Ling LH, Nishimura RA, Seward JB, Tajik AJ. Annulus paradoxus: transmitral flow velocity to mitral annular velocity ratio is inversely proportional to pulmonary capillary wedge pressure in patients with constrictive pericarditis. Circulation. 2001; 104:976–978. PMID: 11524387.
3. Welch TD, Ling LH, Espinosa RE, et al. Echocardiographic diagnosis of constrictive pericarditis: Mayo Clinic criteria. Circ Cardiovasc Imaging. 2014; 7:526–534. PMID: 24633783.
4. Himelman RB, Lee E, Schiller NB. Septal bounce, vena cava plethora, and pericardial adhesion: informative two-dimensional echocardiographic signs in the diagnosis of pericardial constriction. J Am Soc Echocardiogr. 1988; 1:333–340. PMID: 3272782.
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5. Chang SA, Choi JY, Kim EK, et al. [18F]Fluorodeoxyglucose PET/CT predicts response to steroid therapy in constrictive pericarditis. J Am Coll Cardiol. 2017; 69:750–752. PMID: 28183513.
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