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Correspondence

Case 2-1994: Tricuspid Regurgitation

N Engl J Med 1994; 330:1688-1689June 9, 1994

Article

To the Editor:

We were intrigued by Case 2-1994 (Jan. 13 issue),1 which describes constrictive pericarditis and mitral regurgitation associated with a myxomatous mitral valve. Tricuspid annuloplasty was required when severe tricuspid regurgitation was detected by transesophageal echocardiography after the patient was weaned from cardiopulmonary bypass.

We have recently described the same phenomenon in two patients who had severe tricuspid regurgitation after surgery for relief of constrictive pericarditis2. We believe that right ventricular dilatation after relief of the pericardial constraint is the underlying mechanism. Interoperative transesophageal echocardiography allows prompt detection and repair of the tricuspid regurgitation.

Todd L. Johnson, M.D., Ph.D.
William B. Bauman, M.D.
Richard A. Josephson, M.S., M.D.
Akron City Hospital, Akron, OH 44304

2 References
  1. 1

    Case Records of the Massachusetts General Hospital (Case 2-1994). N Engl J Med 1994;330:126-134
    Full Text | Web of Science | Medline

  2. 2

    Johnson TL, Bauman WB, Josephson RA. Worsening tricuspid regurgitation following pericardiectomy for constrictive pericarditis. Chest 1993;104:79-81
    CrossRef | Web of Science | Medline

To the Editor:

In the discussion of Case 2-1994, diagnostic importance is attached to the form of the venous pulse. We are told that prominent V waves and a marked Y descent were present, and that these features were consistent with constriction. The postoperative changes are attributed to pericardiectomy. Many clinicians will find the description of the venous-pulse recordings in this case confusing. The case participants appear to have neglected the influence of marked tricuspid regurgitation that, it seems, was present before operation, as evidenced by the enlarged, pulsatile liver and the need for tricuspid annuloplasty. In tricuspid regurgitation the venous pulse takes on the form of a right-ventricular-pressure tracing with a prominent systolic V wave. By necessity, the diastolic, or Y, descent will be prominent in such circumstances, independently of any pericardial effect.

In contrast, our experience suggests that a prominent systolic, or X, descent is the more common finding in pure constrictive disease. The X descent is a remarkable physiologic phenomenon. During ventricular systole, the right atrial pressure falls despite continuing venous return. This can occur only if the volume of the atria increases beyond that required to accommodate systemic venous return. This expansion occurs as a consequence of an increase in transverse dimension and descent of the tricuspid annulus toward the ventricular apex. In pericardial constriction, transverse expansion of the atrium is physically limited but systolic excursion of the tricuspid annulus is particularly marked, and this leads to the prominent X descent.

In this case, the X descent would have been obscured by the tricuspid regurgitation until this was corrected at surgery with annuloplasty.

R.H. Stables, M.A., M.R.C.P.
S.J. Brecker, M.D., M.R.C.P.
Royal Brompton National Heart and Lung Hospital, London SW3 6NP, United Kingdom

Author/Editor Response

Dr. Nash, the discussant of Case 2-1994, replies:

To the Editor: The conclusion by Drs. Stables and Brecker that severe tricuspid regurgitation was present before operation is not supported by the evidence. Examination of the tracing for right atrial pressure (Figure 4 of Case 2-1994) does not reveal a “prominent systolic V wave” or a contour suggestive of right ventricular pressure. Rather, the predominant feature is clearly a negative deflection -- the Y descent. Its prominence is a consequence of elevated mean right atrial pressure and rapid early ventricular filling. Note the distinction between the right atrial tracing and the pulmonary-capillary wedge tracing, which does display a prominent V wave. Pulsatile hepatomegaly is likewise not diagnostic of tricuspid regurgitation and is a well-described feature of “pure” constrictive pericarditis1,2. The X descent, which is not as prominent as the Y descent in this instance, was probably attenuated by atrial fibrillation, not tricuspid regurgitation. Without organized atrial contraction (i.e., in the absence of an A wave), there could be no contribution of atrial relaxation to the normal decline in atrial pressure during the early phase of ventricular systole.

What I believe to be the correct explanation of the tricuspid regurgitation in the patient is put forth by Johnson et al. Relief of the pericardial constraint led to right ventricular dilatation and new functional incompetence of the tricuspid valve. As they suggest, this became apparent only when an elevated central venous pressure was recorded while the patient was being weaned from cardiopulmonary bypass after the pericardiectomy and mitral-valve replacement. The tricuspid regurgitation was confirmed by intraoperative transesophageal echocardiography and corrected by tricuspid annuloplasty.

Ira S. Nash, M.D.
Massachusetts General Hospital, Boston, MA 02114

2 References
  1. 1

    Manga P, Vythilingum S, Mitha AS. Pulsatile hepatomegaly in constrictive pericarditis. Br Heart J 1984;52:465-467
    CrossRef | Web of Science | Medline

  2. 2

    Coralli RJ, Crawley IS. Hepatic pulsations in constrictive pericarditis. Am J Cardiol 1986;58:370-373
    CrossRef | Web of Science | Medline

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