reversed carvallo's sign

16 Coumel P. Supraventricular tachycardias. In: Krikler DM, God- win JF, eds. Cardiac arrhythmias. London: WB Saunders, 1975:116-143

17 Marquez-Montes J, Rufilanchas JJ, Esteve-Alderete JJ, Mendez J, Ugarte J, Rodriguez E, et al. Tratamiento quirurgico en 24 pacientes con sindrome de Wolff-Parkinson-White y taquicar- dias: diagnostic0 topografico de 10s haces de Kent y evaluation de resultados. Rev Esp Cardiol 1981; 34:271-281

18 Josephson ME, Horowitz LN, Farshidi A, Spear JF, Kastor JA, Moore EN. Recurrent sustained ventricular tachycardia: 2. Endocardia mapping. Circulation 1978; 57:440447

19 Janse MJ, Van Capelle FJL, Anderson RH, Touboul P, Billette J. Electrophysiology and structure of the atrioventricular node of the isolated rabbit heart. In: Wellens HJJ, Lie KI, et al, eds. The conduction system ofthe heart. Leiden: Stenfert & Kroese, 1976: 296-315

Reversed Rivero-Carvallo's Sign in Right-Sided Hypertrophic Obstructive Cardiomyopathy* Kyozo Ishikawa, M. D . , E C . C . P ; Fukiyo Hirata, M . D . ; Shunkichi Hirata, M . D . ; and Masarnichi lshikawa, M.D

An 18-year-old patient had right-sided hypertrophic obstructive cardiomyopathy. His case was quite unique in that the intensity of the systolic murmur was apparently decreased during the inspiratory phase and increased during the expiratory phase (reversed Rivera-Carvalloi sign).

H ypertrophic cardiomyopathy is classically associated with predominant left-sided obstruction, but cases of

isolated and dominant right ventricular outflow obstruction (RVO) have been described.14 I t is usually expected that the

*From the Kyorin University School of Medicine, Second Depart- ment of Internal Medicine, Tokyo, Japan.

Reprint requests: D1: Ishikawa, Kyorin University, 6-20 Shinkawa, Mitaka City , Tokyo, lapan

systolic murmur resulting from subpulmonic stenosis in RVO may b e increased in intensity during the inspiratory phase and decreased during the expiratory phase (Rivero-Carvallo's sign). The present patient with RVO in hypertrophic cardio- rnyopathy was quite unique in that the intensity of the systolic murmur was apparently decreased during the inspiratory phase and increased during the expiratory phase (reversed Rivero-Carvallo's sign).

The patient, an 18-year-old man, was referred to us for cardiac evaluation because of cardiac murmur. He had been in good health and asymptomatic. He had never experienced chest pain or any kind of unconsciousness. Examination revealed a grade 316 systolic murmur with late systolic accentuation. This systolic murmur became louder on expiration and quieter on inspiration (Fig 1). Intracardiac phonocardiogram recorded in the right ventricular outflow portion apparently demonstrated that the systolic murmur became louder on expiration than on inspiration (Fig 2). Cardiac catheterization revealed no intracardiac shunts, and a systolic gradient of 7 mm Hg was recorded between the right ventricular inflow and outflow tracts (Fig3). The pulmonary artery pressure was 1718 mm Hg. No pressure gradient was recorded in the left ventricular cavity. Electrocardiograms showed right axis deviation and right ventricular hypertrophy (Fig 4).

A selective angiogram with right ventricular injection revealed protrusion of the interventricular septum into the right ventricular outflow tract. Left ventricular obstruction was not demonstrated by the left ventricular angiogram. Echocardiography demonstrated a thick interventricular septum (27 mm) but did not reveal systolic fluttering of the pulmonary valve, which was considered to be characteristic of RV0.3.4

The data from the cardiac catherization and angiography demonstrated the presence of isolated RVO. The systolic pressure gradient within the right ventricle was slight in degree (7 mm Hg) but apparently nonartifactual. Dur ing the cardiac catheterization, the pressure recordings within the right ventricle were carefully repeated several times, reveal-

Expiration Inspiration FIGURE 1. Respiratory change in the intensity of systolic murmur. During expiration the intensity of the systolic murmur was increased whereas its intensity was markedly decreased during inspiration.

Reversed Riveco-Carvallo's Sign (lshikawa eta/)

Downloaded From: http://journal.publications.chestnet.org/ on 12/12/2015

m a t i m Expiration FIGURE 2. Intracardiac phonocardiography recorded in the outflow tract ofthe right ventricle. ?he systolic murmur became louder on expiration than on inspiration.

ing the constant existence of a systolic pressure gradient within the right ventricle. It seems most likely that the systolic murmur in the present case originated from subpulmonic stenosis due to RVO. The question then arises as to why the systolic murmur became louder in expiration and not in inspiration. In cases where the systolic murmur is from a right-sided origin, its intensity would tend to be increased in inspiration, which is commonly understood as Rivero- Carvallo's sign. However, the systolic murmur in the present case apparent ly increased in expiration, which is diametrically opposite to Ftivero-Cwallo's sign. The precise mechanism responsible for such a "reversed Rivero-Car- vallo's sign" remains unclear. However, it is tempting to speculate that an increase in the venous return into the right ventricle in inspiration may dilate the dimensions of the right ventricle as well as the obstructed portion of the right

ventricular o u a o w tract. As a result, the systolic murmur originating from the RVO may be decreased. Such a reversed Rivero-Cwallo's sign has never been described previously in ~ubl i shed cases with RV0.14

The degree of the right intraventricular systolic pressure daerences in a number of RVO collected from published reports was found to vary from 7 to 118 mm Hg.' It would appear that the distensibility of the obstructed portion may be ereater in mild cases than in more severe cases. Conse- - quently, in mild cases such as the present case, an increase in the venous return in inspiration might dilate the obstructed portion with a resultant decrease in the intensity of the systolic murmur. On the other hand, in severe cases, the hstensibility and dilatation of the obstructed portion could not be expected to decrease the systolic murmur to such an extent.

P A R V R A FIGURE 3. Right heart catheterization. The pressure was continuously recorded while the catheter tip was being slowly drawn from the pulmonary artery to the right atrium. n e r e was a slight but clearly apparent pressure gradient between the right ventricular outflow portion and inflow portion.

CHEST 1 83 I 4 1 Aprfl, 1983 6QS


VI v2 v3 v4 v5 v6 FIGURE 4. Electrocardiogram showing right

1/2 112 112 axis deviation and right ventricular hypertrophy.

I t is possible but not certain that, with advancing severity of this disease, the intensity of the systolic murmur might vary from inspiratory decrease to inspiratory increase. How- ever, long-term follow-up observations will b e required to confirm the validity of such a hypothesis.

1 Lockhart A. Charpentier S, Bourdarias JP, Ismail MB, Ourbak P, Scebat L. Right ventricular involvement in obstructive car- diomyopathies; haemodynamic studies in 13 cases. Br Heart J 1966; 28:122

2 Momw AG, Fisher RD, Fogarty TJ. Isolated hypertrophic obstruction to right ventricular outflow: clinical, hemodynamic, and angiographic findings before and after operative treatment. Am Heart J 1969; 77:814

3 Cardiel EA, Alonso M, Delcan JL, Menarguez L: Echocardio- graphic sign of right-sided hypertrophic obstructive cardiomyopathy. Br Heart J 1978; 40:1321

4 Kishimoto C, Kaburagi T, Takayam S, Kanyu I, Yokoyama S, Ekatsu Y: A case of hypertrophic obstructive cardiomyopathy with isolated obstruction to the right ventricular outflow: the echocardiographic findings. J Cardiography 1980; 10:881

Azathioprine-Associated Pulmonary Dysfunction* Michael J. Krowka, M.D.t; Richard I . Breuer, M.D.S; and Thomas]. Kehoe, M.D.5

We present a case of azathioprine-associated alveolitis diagnosed by gallium-67 scanning and transbronchial bi- opsy. Ihe patient denied respiratory symptoms, exhibited spiking fevers, and had normal chest roentgenograms. Allopurinol inhibition of a z a t h i o p ~ e metabolism may have been a contributing factor.

P ulmonary toxicity of immunosuppressive and cytotoxic agents has been recently reviewed.'.' Respiratory dys-

function is usually characterized by dyspnea, cough, abnormal pulmonary function tests, and chest roentgenographic

- - -

*From the Department of Medicine, Evanston Hospital, North- western University Medical School, Evanston, Illinois.

tResident in Internal Medicine. $Associate Professor, Division of Gastroenterology. %Associate Attending. Division of Pulmonary Medicine.

changes in a febrile patient. Early detection of such toxicity, prior to chest roentgenographic abnormalities, has been described and may have a significant impact on morbidity and ~nor t a l i t y .~ We describe a patient with azathioprine- related pulmonary dysfunction characterized by normal findings o n ches t roentgenogram a n d abnormal gal- l i ~ m - 6 7 ( ~ ~ G a ) lung scan.

A 35-year-old man was admitted for evaluation of intermittent fever (39.4OC). Crohn's disease had been diagnosed when he was aged 17. Four bowel operations performed because of obstruction or fistulas resulted in an ileostomy in 1970. Subsequent medical therapy included a two-month trial of azulfidine because of radi- ologic demonstration ofileal recurrence two years prior to admission. Kidney stones were passed in 1971, 1972, and 1979. Stone analysis indicated 90 percent urate in each instance. Allopurinol therapy was begun two years prior to admission and continued at doses ranging from 100 to 200 mglday. Eight months prior to admission, ileal obstruction resolved with tube decompression and initiation of prednisone therapy, 60 mg/day. The prednisone was decreased to 20 mg/day, but four months later bleeding from the ileum recurred. Azathioprine, 50 mgtday, along with prednisone, 40 mg/day, success- fully controlled the bleeding. By one month prior to admission, prednisone had been reduced to 40 mg every other day and azathioprine had been increased to 125 mg/day. At no time did the patient complain of respiratory difficulties.

Physical examination indicated blood pressure of 120180 mm Hg without orthostatic changes. Temperature was 39.1°C orally, respira- tions 18 per minute, with a regular pulse rate of SO per minute. The chest was clear to auscultation and percussion. Cardiac examination was within normal limits. Abdominal examination was significant for mild, &se tenderness without rebound or hepatosplenomegaly. There was no adenopathy, and the neurologic examination was normal.

Fever workup included cultures of induced sputum, urine, blood, spinal fluid, and bone marrow. All were negative. Chest roentgenograms were normal. The WBC was elevated to 15,50O/cu mm, with 65 percent polymorphonuclear leukocytes and no eosinophils. Atypical lymphocytes were not seen on the peripheral smear. Antinuclear antibody and rheumatoid factor titers were less than 1:20. Lymphocyte stimulation, immune complex, and complement studies were not done. Hepatorenal function was normal, and the urinalysis was unremarkable. Forty-eight hours after admission, azathioprine and allopurinol therapy was stopped, and prednisone administration continued at 40 mg/day. AGCa scan obtained to locate a possible abdominal abscess was unremarkable. However, both lungs demonstrated spectacular uptake at 6, 24, and 48 hours after

696 A z a t h i i n e - W a t e d Pulmonary Dysfunction (Krowke et al)


reversed carvallo's sign

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