Med 1977; 297:1-6 9 Rossman CM, Forrest JB, Ruffin RE, Newhouse MT. Immotile cilia syndrome in persons with and without Kartageners syndrome. Am Rev Respir Dis 1980; 121:1011-15 10 Sturgess JM, Chao J, Wong J, Aspin N, Turner JAP. Cilia with defective radial spokes: a cause of human respiratory disease . N Eng) J Med 1979; 300 :53-6 11 Sturgess JM , Chao J, Turner JAP. Transposition of ciliary microtubules : another cause of impaired ciliary motility. N Eng) J Med 1980; 303:318-22 12 Chao J, Turner JAP, Sturgess JM. Genetic heterogeneity of dynein-deficiency in cilia from patients with respiratory disease. Am Rev Respir Dis 1982; 126:302-05 13 Van der Baan S, Veerman AJP, Weltevreden E, Feenstra L. Primaire ciliaire dyskenisie : trilhaaractiviteit en ultrastruetuur bij 11 patienten met het syndroom van Kartagener. Ned TIjdschr Geneeskd 1982; 126:2376-79 14 Levison L, Mindorff CM, Chao J, Turner JAP, Stringer DA. Pathophysiology of the ciliary motility syndromes . Eur J Respir Dis 1983; 64(suppI127) :I02-16 15 Rossman C, Forrest J, Newhouse M. Motile cilia in "immotile cilia" syndrome. Lancet 1980; 1:1360 16 Pederson M, Mygind N. Ciliary motility in the "Immotile cilia syndrome." Br J Dis Chest 1980; 74:239-44 17 Rossman CM, Forrest JB, Lee RMK\v, Newhouse MT. The dyskinetic cilia syndrome: ciliary motility in immotile cilia syndrome. Chest 1978; 4:580-82 18 Rutland J, De longh RU. Random ciliary orientation: a cause of respiratory tract disease . N Eng) J Med 1990; 13:1681-84 19 Pederson M, Stafanger G. Bronchopulmonary symptoms in primary ciliary dyskinesia: a clinical study of 27 patients. Eur J Respir Dis 1983; 64(suppI127) :118-28 20 Jonsson MS, McCormick JR, Gillies CG, Condos B. Kartageners syndrome with motile spermatozoa. N Eng) J Med 1982; 307:1131-33 21 Escudier E, Escalier D, Homasson JP, Pinchon MC, Bernaudin JF. Unexpectedly normal cilia and spermatozoa in an infertile man with Kartageners syndrome. Eur J Respir Dis 1987;70:18086 22 Herzon FS, Murphy S. Normal ciliary ultrastructure in children with Kartagener's syndrome. Ann Otol Rhinol Laryngol 1980; 89:81-3 23 Greenstone M, Rutman A, Pavia D, Lawrence D, Cole PJ. Normal axonemal structure and function in Kartageners syndrome : an explicable paradox. Thorax 1985; 40:956-57

Dynamic Left Ventricular Outflow Obstruction Related to Atrial Flbrillation*

authors'" have reported left ventricular outflow Several tract obstruction in 5 to 10 percent of patients under-

going mitral valve annuloplasty. Most commonly, these patients have had myxomatous degeneration with severe mitral regurgitation as the indication for surgery. Most series have reported a mix of patients, including those with sinus rhythm as well as patients in atrial fibrillation.I.. To our knowledge, there have been no reports in the literature to date differentiating the degree of outflow tract obstruction based on the patient's underlying rhythm. We report the case of a single patient with Carpentier mitral valvuloplasty who exhibited a marked difference in left ventricular outflow tract gradient depending on rhythm, and discuss the possible origins of this observation. CASE REPORT A 48-YeaMlld white male patient was admitted to Creighton St. Joseph Hospital, Omaha for mitral valve repair. The patient had a six-month history of congestive heart failure. Preoperative evaluation, including physical examination, echo Doppler studies, and cardiac catheterization confirmed the diagnosis of severe mitral regurgitation secondary to myxomatous degeneration of the valve with ruptured chordae . Intraoperatively, transesophagea! echocardiography was performed prior to opening the chest. Left atrial enlargement and left ventricular enlargement were noted and left ventricular systolic function was normal. Doppler interrogation confirmed severe mitral regurgitation with blleaflet prolapse. Additionally, a portion of the posterior leaflet was flail and associated with visualized ruptured chordae . No systolic anterior motion of the mitral valve or left ventricular outflow tract obstruction was noted . Carpentier valvuloplasty was performed, with partial resection of the posterior mitral valve leaflet, shortening and retethering of the ruptured chordae, and insertion of a size 34 Carpentier ring. Repeated intraoperative transesophageal echocardiography revealed mild mitral regurgitation and no evidence of left ventricular outflow tract obstruction. The patient developed postoperative atrial fibrillation and was digitalized. On the fourth postoperative day, the patient had an episode of syncope while ambulating. Orthostatic blood pressure measurements reHected volume depletion. Fluid intake was liberalized and diuretic therapy was discontinued. The morning of the seventh postoperative day, no orthostatic blood pressure drop was noted; rhythm continued to be atrial fibrillation with a mean heart rate of 80 beats/min and blood pressure of 108160 mm Hg. A transthoracic echo-Doppler study showed systolic

KeUy \bughn-Whitley, M .D.; and Arr.-m Mooss; M.D., F.C.C .P.

A 48-year-old male patient underwent mitral aoouloplasty for severe mitral regurgitation secondary to myxomatous degeneration of the mitral valve, with ruptured chordae. Intraoperative transesophageal echocardiography showed satisfactory repair. The patient developed postoperative atrial fibrillation and clinical and echocardiographic evidence of left ventricular outflow obstruction. Following conversion to sinus rhythm, the evidence for left ventricular outflow obstruction markedly improved. We suggest that postoperative atrial fibrillation may precipitate dynamic left ventricular outflow obstruction following mitral aoouloplasty. (Chen 1992; 102:1618-19) -From the Division of Cardiology, Creighton University School of Medicine, Omaha. 1618

FIGURE 1. Marked systolic anterior motion of the mitral valve in atrial fibrillation. Average heart rate, 80 beats/min; left ventricular diastolic dimension, 5.2 em; left ventricular outflow tract early systolic dimension, 2.3 em. DynamIc Left Ventricular OUtflow0bslruclI0n Related to Atrial FIbrillation (Whitley

et eI)

: l e

AM

17 -

-

obstruction. Because of the irregular rhythm, the redundant (and unresected) anterior mitral valve leaflet may be in a more open position at the time of ventricular systole, predisposing to an enhanced Venturi effect and hence greater obstruction. Since drug therapy, heart rate , blood pressure, body position (at the time of echocardiogram), and volume status were similar at the time of both studies, it is unlikely that these mechanisms can be invoked as the source of our observations.

1

REFERENCES

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FIGURE 2. Improvement in systolic anterior motion of the mitral valve in sinus rhythm. Average heart rate, 84 beats/min; left ventricular diastolic dimension, 5.2 em; left ventricular outflow tract early systolic dimension, 2.4 em . anterior motion of the mitral valve (Fig 1) and left ventricular outflow obstruction with peak gradient of74 mm Hg, mean gradient of 41 mm Hg, and trace mitral regurgitation. Systolic anterior motion and left ventricular outflow tract gradients were compared between varying RR intervals and no significant correlation was found . In the next 2 h, the rhythm converted spontaneously to sinus rhythm with a mean rate of 841m in. The patient's volume status and weight remained unchanged over the ensuing 24 h. A repeat echoDoppler study was performed 24 h after the initial identification of left ventricular outflow tract obstruction. Chamber sizes and function were comparable; mild systolic anterior motion was again present; however, it was much less prominent than on the previous study (Fig 2). The left ventricular outflow tract peak gradient was 12 mm Hg. Mild mitral regurgitation was noted . The medications were changed to disopyramide phosphate (Norpace) and atenolol; digoxin and quinidine therapy was discontinued. A six-week postdischarge echocardiogram done in sinus rhythm with heart rate of 70 beats/min revealed no evidence of outflow obstruction. DISCUSSION

Since the advent of mitral valvuloplasty using the Carpentier ring,' hundreds of patients have undergone repair with this technique. Left ventricular outflow obstruction complicating Carpentier ring mitral valvuloplasty has been reported by several investigators.I.' The proposed mechanisms for the finding of left ventricular outflow tract obstruction include inhibition of the normal posterior systolic motion of the mitral valve by the semirigid Carpentier ring, reduction in left ventricular volume following correction of the mitral regurgitation, decrease in left ventricular outflow dimensions,•.•.5 redundancy of the mitral leaflets, and inability of the mitral annulus to move posteriorly due to the rigid ring.1.O We report a single case of significant change in systolic anterior motion and left ventricular outflow tract obstruction apparently related to rhythm change from atrial fibrillation to normal sinus rhythm. Possible mechanisms for this difference remain obscure . It is possible that the atrial fibrillation rhythm itself may produce some unusual dynamic anterior motion of the mitral valve in systole, leading to outflow tract

1 Schiavone WA, Cosgrove DM, Lever HM, Stewart WJ, Calcedo EE. Long-term follow up of patients with left ventricular outflow tract obstruction after Carpentier ring mitral valvuloplasty. Circulation 1988; 78(suppll):fi0.65 2 Galler M, Kronzon I, Slater J, Lighty G\v, Politzer F, Colvin S, et al. Long-term follow up after mitral valve reconstruction: incidence of postoperative left ventricular outflow obstruction. Circulation 1986; 74(suppll):99-103 3 Carpentier A, Deloche A, Dauptain J, Sayer R, Blondeau P, Piwnica A, et al. A new reconstructive operation for correction of mitral and tricuspid insufficiency. J Thorac Cardiovasc Surg 1971; 61:1-13 4 Rahko PS, BerkolfHA. Echocardiographic comparison of cardiac size and function before and after surgery for isolated mitral regurgitation: superiority of mitral valve repair vs mitral valve replacement. Acta Cardioll990; 45:189-94 5 Fundaro P, Salati M, CiaHfi A, Santoli C. PolytetraRuorethylene posterior annuloplasty for mitral regurgitation. Ann Thome Surg 1990; 5O:161Hi6 6 Cohn LH, Disesa Vj, Couper GS, Peigh PS, Kowalker \Y, Collins 11. Mitral valve repair for myxomatous degeneration and prolapse of the mitral valve. J Thorac Cardiovasc Surg 1989; 98:987-93

Successful Medical Therapy of Rhodococcus equl Pneumonia In a Patient with HIV Infectlon* }amu D. Cury, M.D.; lbul T. HarringtOfl, M.D. ; and Ian K. Hosetn, M.D.

A 34-year-old HIV-infected man was successfully treated with antimicrobial therapy alone for RhodococcuI equi pneumonia and hassurvived longer than six months. In the current literature, only two of seven HIV-infected patients so treated have survived as long as six months. Based on our experience and the available literature, it seems reasonable to treat HIV-infected patients with R equi pneumonia who do not require surgical intervention with prolonged intravenous therapy followed by long-term oral therapy with at least two effective antibiotics. The optimal choice and duration of antibiotic therapy need to be detenninecl. (Chm 1992; 102:1619-21)

IIUV = human immunode8ciency virus I

R hodococcw

equi is a cause of pneumonia in individuals with cell-mediated immunodeficiency including those

*From the University of Florida Health Science CenterlJacksonville, University Medical Center, Jacksonville . Reprint requem: Dr. Cury, Deparlment ofMedicine , 655l\bt Sixth Strut, Jacksonville, FL 32209 CHEST I 102 I 5 I NOVEMBER, 1992

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