coexisting with pericardial effusion. idiopathic ...

Echocardiography in the diagnosis of idiopathic hypertrophic subaortic stenosis coexisting with pericardial effusion. B N Alimurung, J M Felner and R C Schlant Chest 1979;76;187-192 DOI 10.1378/chest.76.2.187 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/76/2/187

Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1979by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692

Downloaded from chestjournal.chestpubs.org by guest on July 10, 2011 © 1979 American College of Chest Physicians

Echocardiography in the Diagnosis of Idiopathic Hypertrophic Subaortic Stenosis Coexisting with Pericardial Effusion* Benjamin N. Alimurung, M.D.; Joel M. Felner, M.D.,°* Robert C. Schlant, M.D.

Of 89 patients with idiopathic hypertrophic subaortic stenosis who had M-mode echocardiagrams recorded, seven patients with coexisting moderate to large pericardial effusions were identified. The clinical profile, Mmode echocardiograms, and cardiac catheterization and angiocardiographic studies in two of the seven patients were analyzed. That the two entities were not associated

was suggested by the identification of an etiology for the pericardial effusion in four of the patients. Although the "swinging heart" phenomenon was exhibited in the echocardiograms of each patient, the presence of a significant pericardial effusion did not preclude the ability to establish a diagnosis of idiopathic hypertrophic subaortic stenosis by M-mode echocardiography.

~jl/|"-mode echocardiography is a reliable tool for the diagnosis of idiopathic hypertrophic subaortic stenosis ( I H S S ) or hypertrophic obstructive cardiomyopathy ( H O C M ) . The characteristic echocardiography markers that have been proposed by previous investigators include the following: ( 1 ) asymmetric septal hypertrophy (ASH) with a ratio of interventricular septal thickness to posterior left ventricular wall thickness equal to or greater than 1.3; ( 2 ) systolic anterior motion ( S A M ) of the mitral valve; ( 3 ) diminished diastolic E - F slope of the anterior mitral valve leaflet; " ( 4 ) decrease in the percentage of systolic thickening and the amplitude of excursion of the interventricular septum ( I V S ) ; ( 5 ) narrowed left ventricular outflow tract during both systole and diastole; ( 6 ) partial or total premature systolic closure of the aortic leaflets; and ( 7 ) reduced internal diameter of the left ventricle.

is postulated that these changes occur as a result of excessive abnormal movement of the heart within the expanded pericardial space—"the swinging heart" phenomenon, However, other echocardiographic features such as asymmetric septal hypertrophy and decreased septal excursion do not occur in patients with pericardial effusion alone. Although the simultaneous occurrence of IHSS and pericardial effusion has been reported, to our knowledge no critical analysis of the echocardiogram has been described.

Recent observations " have demonstrated that none of the above echocardiographic features are unique to IHSS. In addition, several of the echocardiographic features of IHSS can be mimicked by a moderate to large pericardial effusion. In particular, a large pericardial effusion even in the absence of hypertrophic cardiomyopathy may produce systolic anterior motion of the mitral valve resembling that seen with I H S S . Furthermore, early systolic closure of the aortic leaflets and altered motion of the interventricular septum " have been described in patients with large pericardial effusions. It

All patients were studied at Grady Memorial Hospital, Atlanta, between January, 1 9 7 5 and July, 1977. During this 19-month period, 8 9 patients had M-mode echocardiograms characteristic of IHSS. Of these 89 patients, seven (three men and four w o m e n ) had M-mode echocardiograms which showed the classic features of both IHSS and a significant pericardial effusion. Their ages ranged from 3 5 to 5 9 years ( m e a n 4 9 . 9 ) . The pertinent clinical data are summarized in Table 1. None of these seven patients presented with cardiac tamponade. All had echocardiograms performed in order to evaluate an enlarged cardiopericardial silhouette. Six of the seven patients had an apical or left parasternal systolic murmur. In the remaining patient no murmur was audible. The diagnoses of IHSS and pericardial effusion were confirmed at cardiac catheterization and angiocardiography in two patients (cases 1 and 4 ) .

1

2

3

4

B

6

9

20

The purpose of this study is to describe Pur experience with the diagnosis of IHSS coexisting with pericardial effusion and to evaluate the influence of a significant pericardial effusion on the echocardiographic features of IHSS.

7

MATERIALS AND METHODS

8

9

15

1 8 1 7

16

17

18

" F r o m the Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta. * "Teaching Scholar, American Heart Association. Manuscript received October 11; revision accepted January 8. Reprint requests: Dr. Schlant, Emory University, 69 Butler Street SE, Atlanta 30303

CHEST, 76: 2, AUGUST, 1979

All patients were examined in both supine and left lateral decubitus positions, utilizing commercially available equipment—series C - 1 0 0 unirad diagnostic echoscope; 2 . 2 5 megahertz /s inch ( 1 . 5 9 c m ) diameter transducer focused at 1 0 5

ECHOCARDIOGRAPHY IN DIAGNOSIS OF IHSS AND PERICARDIAL EFFUSION


187

T a b l e 1—Clinical Profile

Chest X - r a y Film

Etiology of Pericardial Effusion*

Case N o

Age, Sex

Presenting Problem

ECG

1

53, M

orthostatic dizziness, syncope, chest pain

P - R 0.12 see; LVH

enlarged cardiac silhouette

viral

2

55, M

dyspnea, systolic murmur left parasternal area

first degree A-V block; LVH


hydralazine

3

56, F

dyspnea

LVH


unknown

4

51, F

paroxysmal nocturnal dyspnea

LVH

enlarged cardiac silhouette; calcified mitral annulus

scleroderma

5

59, F

asymptomatic; apical .-ystolie murmur

LVH


unknown

6

40, F

dyspnea, systolic murmur left parasternal area

Inferior dead zone


systemic lupus erythematosus

7

35, M

asymptomatic; apical systolic murmur

LVH


unknown

*None had cardiac tamponade L V H -left ventricular hypertrophy cm. Recordings were made at 5 0 mm/second paper speed, on a model 1 7 4 Tektronix strip chart recorder or Honeywell 1856 visicorder, using either light or heat-sensitive paper. A standard M-mode heart scan was performed with the transducer in the left parasternal area at the third, fourth or fifth interspace. The transducer was then rotated in a partial arc, from the mitral valve to the cardiac apex and to the ascending aorta. Appropriate attenuation was done at various segments of the heart scan to allow the echocardiographcr to best discern the echo-free spaces anteriorly and posteriorly, representing the pericardial effusion. Echocardiographic

complex of the simultaneously recorded E C G . Normal values for septal and posterior wall thickness and for percentage of systolic thickening, and systolic excursion of the interventricular septum and left ventricular posterior wall were obtained from the author's own laboratory. Finally, the amount of pericardial effusion was estimated according to the criteria proposed by Felner and Schlant and F e i g e n b a u m . An echo-free space present both anteriorly and posteriorly signifies at least a moderate effusion ( a p proximately 1 0 0 ml of fluid); if the posterior echo-free space is greater than 1 cm, a large effusion is present (greater than 1 0 0 0 ml of fluid). 15

15

21

Measurements RESULTS

The analysis of the echocardiograms and the echocardiographic measurements (Table 2 ) were done according to previously established m e t h o d s . ' ' ' Furthermore, measurements at end-diastole were made at the onset of the QRS 1

4

5

Echocardiography

1 0

Pericardial

A significant anterior echo-

Effusion:

Table 2—Echocardiographic Data Interventricular Septum

Left Ventricle

Svstolic Mitral Valve Case

E - F Slope

Aortic

No

(mm/see)

SAM

1

29

Present

Valve

IVS'iy'PWT

M S M , P C 20/10 (2.0)

Svstolic

Thick-

Systolic

ening

Excursion

LVOT

(mm)

(mm)

(mm)

(mm)

(mm)

(mm)

26

9

22

46

12

10

23

130

\/o)

LVID

d

LVID,

PWT

d

rwT„

Thickening

110)

Pericardial Effusion Anterior

Posterior

Moderate Large

2

22

Present

MSM

21/15 (1.4)

9

3

20

37

20

15

22

47

Moderate Moderate

3

89

Present

PC

24/10 (2.4)

17

5

21

48

34

10

17

70

Moderate Large

4

19

Present

MSN, PC

19/14 (1.4)

0

7

20

33

20

14

23

64

Moderate Large

5

24

Present

PC

24/15 (1.6)

17

5

17

34

6

15

23

53

Moderate Moderate

6

79

Present

MSN, PC

18/10 (1.8)

11

3

19

42

28

10

18

80

Moderate Large

7

53

Present

PC

18/12 (1.5)

11

8

30

53

31

12

22

83

Moderate

Moderate

SAM—systolic anterior motion

PWT,j—posterior wall thickness end-diastole

MSN--midsystolic notch

PWT„—posterior wall thickness end-systole

L V I D — l e f t ventricular internal diameter, end-systole

PC—premature closure

IVSTd—interventricular septal thickness end-diastole

L V O T — l e f t ventricular outflow tract

188

ALIMURUNG, FELNER, SCHLANT

LVIDd—left ventricular internal diameter, end-diastole S



free space between the right ventricular free wall and chest wall and posterior echo-free space between the left ventricular epicardium and pericardium was present in six of the seven patients (Fig 1 ) . In the remaining patient, although no anterior echo free space was seen, a large posterior echo-free space was present throughout the cardiac cycle. It must be emphasized that Feiner and Schlant and Feigenbaum caution that the proposed guidelines for quantitating the amount of pericardial fluid provide only gross estimates. When the posterior echo-free space is greater than 10 mm, in association with an anterior echo-free space the amount of pericardial effusion is estimated to be 1000 ml or more. Due to the presenting problem of orthostatic dizziness, syncope and chest pain in case 1, approximately 1200 ml of pericardial fluid was withdrawn during cardiac catheterization. Figure 1 shows the echocardiogram obtained before and after pericardiocentesis. Interventricular Septal and Left Ventricular Echograms: A summary of echocardiography data is tabulated in Table 2. The mean interventricular septal thickness at end-diastole ( I V S T ) was 19.7 mm with a range of 18-24 mm and the mean posterior wall thickness at end-diastole ( P W T ) was 12.3 mm with a range of 10-15 mm. The IVST„/ PWT„ ratio exceeded 1.3 (range 1.4-2.40) in all seven patients. The mean end-systolic thickness of the interventricular septum ( I V S ) was 22.6 mm with a range of 18-28 mm. The degree of systolic thickening of the IVS, expressed as a percentage of the end-diastolic thickness, ranged from 5.29 percent with a mean of 14.1 percent. Maximum systolic 15

21

d

d


FIGURE 1. A series of echocardiograms from case 1. Echocardiograms A, B and C were o b tained prior to pericardiocentesis. A shows the left ventricle a t the level of the posterior papillary muscle on the left and the mitral valve on the right. T h e r e is a moderate anterior pericardial effusion, a large posterior pericardial effusion and asymmetric septal hypertrophy ( A S H ) ; B shows systolic anterior motion (arrow a) and the decreased E - F slope (arrow b) of the anterior mitral valve leaflet. C shows the aorta, aortic leaflets and the left atrium. Arrows c and d point to the midsystolic notching and gradual premature closure of the anterior and posterior aortic leaflets, respectively. Echograms D , E and F were recorded after removal of approximately 1 2 0 0 ml of pericardial fluid. D shows the markedly diminished anterior and posterior pericardial effusion, but the same degree of A S H . E shows systolic anterior motion (arrow e) of the mitral valve which is now b e t t e r visualized, b u t the height and width do not appear to b e different from the pre-pericardiocentesis e c h o in B . T h e diastolic E - F slope of the mitral valve has now increased and is no longer closely apposed to the interventricular septum; F shows the midsystolic notching on the anterior aortic leaflet (arrow f). A P E = anterior pericardial effusion; R V = right ventricle; I V S = interventricular septum; L V = left ventricle; P W = posterior wall; P P E = posterior pericardial effusion.

posterior excursion of the IVS ranged from 3-9 mm (mean 5 . 7 ) . Systolic anterior septal (paradoxic) motion was not observed. In contrast to the systolic thickening of the septum, the degree of left ventricular wall systolic thickening ranged from 47-130 percent (mean 65.3 percent). The mean left ventricular internal diameters at end-diastole and at end-systole were 41.8 mm (range 33-34 mm) and 21.6 mm (range 6-24 m m ) , respectively. The left ventricular outflow tract ( L V O T ) ranged from 17-30 mm with six of the seven patients 22 mm or less. Mitral and Aortic Valve Echograms: The E-F slope of the anterior mitral valve leaflet was 19-89 mm/sec (mean 45 mm/sec). Systolic anterior movement of the mitral valve was obvious in all seven patients (Table 2 ) . The posterior mitral valve leaflet moved normally in all patients. Midsystolic notching and/or premature closure of the aortic leaflets was apparent in all seven patients. The aortic leaflets were not thickened in any of the patients. Figure 2 is a series of echograms from case 6 demonstrating characteristic changes in the mitral and aortic valve. Cardiac

Catheterization

and

Angiocardiography

In the two patients (cases 1 and 4 ) who underwent left and right heart catheterization, there was no gradient at rest across the left ventricular outflow tract. During inhalation of amyl nitrite, a peak



189

IVS-J AO

}LCM

LA

PW-J PPE

FIGURE 2. A series of echocardiograms from case 6. A shows the left ventricle at the level of the posterior papillary muscle. T h e r e is a moderate anterior pericardial effusion between the chest wall and right ventricular wall and a moderate posterior effusion between the left ventricular epicardium and pericardium at the level just below the mitral valve. B at the level just below the mitral valve, demonstrates the asymmetric hypertrophy of the interventricular septum (large double-headed arrow) relative to the posterior left ventricular free wall (small doubleheaded arrow). C, at the level of the mitral valve, shows prominent systolic anterior motion (arrow a) and decreased diastolic E - F slope of the anterior mitral valve leaflet. D, at the level of the aortic valve, shows midsystolic notching ( a r r o w h) on the posterior leaflet of the aortic valve. A small echo-free space is present behind the left atrium representing pericardial fluid in the oblique pericardial sinus. A P E = anterior pericardial effusion; P P E = posterior pericardial effusion; I V S = interventricular septum; P W = posterior wall; L A = left atrium.

gradient of 60 mm Hg and 40 mm Hg, respectively, was present and catheter entrapment was ruled out. In both patients, there was a small left ventricular cavity at end-diastole with almost complete cavity obliteration at end-systole. Systolic anterior movement of the mitral valve was not seen, but a prominent bulge of the hypertrophied septum into the left ventricle was present. There was no evidence of pericardial constriction and the aortic valve was tricuspid without calcification or regurgitation. The mitral valve was normal in case 1, whereas a calcified annulus without evidence of mitral regurgitation was seen in case 4. Neither patient had a diastolic gradient across the mitral valve and both had normal coronary arteries. In addition, in case 1, no significant hemodynamic changes were detected after removal of approximately 1200 ml of pericardial fluid. No significant effects were seen on the systolic function of the left ventricle by removal of the pericardial fluid. DISCUSSION

Echocardiographic Abnormalities tral and Aortic Valves

involving

the Mi-

The systolic anterior movement of the mitral valve in patients with isolated large pericardial effusion and the "swinging heart" phenomenon generally occur simultaneously with excessive motion of the 190


other cardiac structures anterior and posterior to the mitral valve. When exaggerated anterior excursion of the whole heart occurs during systole, the resultant mitral valve echo may display anterior motion simulating the systolic anterior motion seen with idiopathic hypertrophic subaortic stenosis. Vignola et a l have suggested that the patterns of motion exhibited by the mitral valve of either a "pseudo" posterior prolapse or SAM may be a function of the extent and timing of posterior and anterior cardiac swinging respectively, and the heart rate. In eight patients reported "when the heart rate was 120 beats/minute or greater, the posterior cardiac swinging occurred during the beginning or end of systole. When the rate was less than 120 beats/minute, the swinging occurred in midsystole." In our seven patients, mild-to-moderate cardiac swinging was present in five, but the extent and timing of SAM did not demonstrate any consistent correlation with the heart rate. 22

Since a large pericardial effusion may conceivably affect the position of the heart in the pericardial sac, the systolic anterior motion of the mitral valve in such patients, without IHSS, is considered to be a motion artifact resulting from the exaggerated movement of all cardiac structures along the anterior-posterior axis relative to the transducer stationary on the subjects' chest In contrast, in hypertrophic cardiomyopathy, the precise mechanism of SAM is not 16



entirely established. Both a Venturi effect due to rapid early left ventricular ejection and excessive traction by a distorted and hypertrophied papillary muscle have been suggested as important factors responsible for the systolic hump on the mitral valve. Abnormally positioned mitral leaflets across the left ventricular outflow tract pushed forward by the ejecting current of blood may provide another explanation. 4

6

The abnormalities noted on the aortic leaflets during systole were more characteristic of those seen with IHSS. " It is well recognized, however, that as an isolated feature, changes on the aortic valve are not specific for IHSS. Any condition leading to severely decreased forward cardiac output may demonstrate various degrees of premature closure of the aortic leaflets. 7

15

15

Other studies have suggested that an inspiratory decrease of the E-F slope of the anterior mitral valve leaflet may occur in patients with cardiac tamponade. This has been postulated to be a reflection of the compromised left ventricular filling during inspiration in patients with cardiac tamponade. Though four of our patients had diminished mitral valve E - F slopes, none clinically had cardiac tamponade. This decrease in mitral valve diastolic slope is consistent with the reported restriction in diastolic filling of the poorly compliant left ventricular cavity of IHSS. 23,24

3

Interventricular Septal Echograms: A spectrum of changes involving the interventricular septum ( I V S ) including paradoxic motion or exaggerated systolic posterior motion have been described " in patients with large pericardial effusions. However, other echocardiographic features such as asymmetric septal hypertrophy and decreased septal excursion do not occur in patients with pericardial effusion alone. Our observations and measurements (Table 2 ) of the IVS confirmed that excessive cardiac motion had no significant influence on septal thickness and degree of systolic thickening in patients with hypertrophic cardiomyopathy. In IHSS, the septal-to-posterior wall ratio is reported to be in excess of 1.3 or 1.5. While the latter ratio improves the specificity of this calculation, it is uncertain what effect the higher ratio has upon its sensitivity. In the group examined in this report, this ratio ranged from 1.4 to 2.40 (Table 2 ) . 16

1

18

8

Other studies " have documented that an I V S T /PWT,i ratio greater than 1.3, originally considered as characteristic of IHSS, occurs in infants and young children without heart disease. In addition, patients with a wide variety of cardiac lesions not associated with IHSS, including ventricular septal defect, coarctation of the aorta, tetralogy of Fallot, 8

9

a


acromegaly, and pulmonary valve stenosis may demonstrate IVST i/PWT ratios in excess of 1.3. " None of our patients had any of these conditions (Table 1 ) . d

(

Clinical

8

9

14

Implications

It is apparent from our study that the presence of a large pericardial effusion does not preclude the ability to establish a diagnosis of IHSS by M-mode echocardiography. Although a "swinging heart" in patients with pericardial effusion may influence the motion of the heart valves, in the presence of ASH and/or decreased septal excursion, a diagnosis of IHSS may be made accurately in the presence of a large pericardial effusion. It must be stressed, however, that none of the characteristic features of IHSS should be assessed in isolation to avoid erroneous interpretation. Though the study was not designed to investigate an association between the two entities, our data would suggest that IHSS and pericardial effusion are not etiologically related entities. In four of our seven patients, an etiology for pericardial effusion was identified (Table 1 ) . In the other three patients, the cause of the effusion has not been established conclusively, although pericardial effusion occurring in IHSS might be expected to occur in patients with severe congestive heart failure related to cardiomyopathy or coronary artery disease. There is no evidence to indicate that the two conditions are related in any fashion other than the potential to coexist in a patient. It would be reasonable to postulate that when significant pericardial fluid is detected in a patient with IHSS, another cause must be searched for to explain the pericardial effusion. REFERENCES 1 Henry W L , Clark E C , Epstein S E : Asymmetric septal hypertrophy. Echocardiographic identification of the pathognomic anatomic abnormality of IHSS. Circulation 47:225-233, 1973 2 Shah PM, Gramiak R, Kramer D H : Ultrasound localization of left ventricular outflow obstructive cardiomyopathy. Circulation 4 0 : 3 - 1 1 , 1 9 6 9 3 Shabetai R, Davidson S: Asymmetric hypertrophic cardiomyopathy simulating mitral stenosis. Circulation 4 5 : 3 7 45, 1 9 7 2 4 Abbasi AS, MacAlpin R N , E b e r L M , et al: Echocardiographic diagnosis of idiopathic hypertrophic cardiomyopathy without outflow obstruction. Circulation 4 6 : 8 9 7 - 9 0 4 , 1972 5 Rossen RM, Goodman D J , Ingham R E : Ventricular systolic septal thickening and excursion in idiopathic hypertrophic subaortic stenosis. N E n g l J Med 2 9 1 : 1 3 1 7 - 1 3 1 9 , 1974 6 Henry W L , Clark C E , Griffith J M , et al: Mechanism of left ventricular outflow obstruction in patients with ob-



191

7

8

9 10

11

12

13

14

15

192

structive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). Am J Cardiol 3 5 : 3 3 7 345, 1975 Shah P M , Gramiak R, Adelman AG, et al: Role of echocardiography in diagnostic and hemodynamic assessment of hypertrophic subaortic stenosis. Circulation 4 4 : 8 9 1 - 8 9 8 , 1971 Freizi O, Emanuel R: Echocardiographic spectrum of hypertrophic cardiomyopathy. Br Heart J 3 7 : 1 2 8 6 - 1 3 0 2 , 1975 Maron BJ, Henry W L , Clark C E : Asymmetric septal hypertrophy in childhood. Circulation 5 3 : 9 - 1 8 , 1976 Goodman DJ, Rossen RM, Popp R L : Echocardiographic pseudo-idiopathic hypertrophic subaortic stenosis. Chest 6 6 : 5 7 3 - 5 7 4 , 1974 Child JS, Levisman JA, Abbasi A S : Echocardiographic manifestations of infiltrative cardiomyopathy. Chest 7 0 : 726-731, 1976 Gabor G E , Mohr B D , Gael P C : Echocardiographic and clinical spectrum of mitral annular calcification. Am J Cardiol 3 8 : 8 3 6 - 8 4 2 , 1 9 7 6 Cope G D , Kisslo JA, Johnson M L : A reassessment of the echocardiogram in mitral stenosis. Circulation 5 2 : 6 6 4 670, 1975 Carter W E , Allen H D , Salin DJ, et al: The asymmetrically hypertrophied septum. Further differentiation of its causes. Circulation 5 3 : 1 9 - 2 7 , 1976 Felner JM, Schlant R C : Echocardiography: A Teaching Atlas. New York, Crane & Stratton, 1976, pp 3 4 1 , 3 7 8 -


380,393,515-523 16 Nanda N C , Gramiak R, Gross C M : Echocardiography of cardiac valves in pericardial effusion. Circulation 5 4 : 5 0 0 5 0 4 , 1976 17 Feigenbaum H, Zaky A, Grabhorn L L : Cardiac motion in patients with pericardial effusion: A study using reflected ultrasound. Circulation 3 4 : 6 1 1 - 6 1 9 , 1966 18 Warren GH, Lynn RR, Allen F H : Echocardiographic observation of ventricular volume changes and swinging septal position in massive pericardial effusion. J Clin Ultrasound 3 : 2 8 3 - 2 8 6 , 1 9 7 5 19 Levisman JA, Abbasi AS: Abnormal motion of the mitral valve with pericardial effusion. Pseudo-prolapse of the mitral valve. Am Heart J 9 1 : 1 8 - 2 0 , 1976 2 0 Riba A L , Morganroth J : Unsuspected substantial pericardial effusions detected by echocardiography. JAMA 2 3 6 : 2 6 2 3 - 2 6 2 5 , 1976 2 1 Feigenbaum H: Echocardiography. Philadelphia, Lea and Febiger, 1972, pp 175 2 2 Vignola PA, Pohost GM, Curfman G E , et al: Correlation of echocardiographic and clinical findings in patients with pericardial effusion. Am J Cardiol 3 7 : 7 0 1 - 7 0 7 , 1976 2 3 Tajik A J : Echocardiography in pericardial effusion. Am J Med 6 3 : 2 9 - 4 0 , 1977 2 4 D'Cruz IA, Cohen HC, Prabhu R, et al: Diagnosis of cardiac tamponade by echocardiography. Changes in mitral valve motion and ventricular dimensions, with special reference to paradoxical pulse. Circulation 5 2 : 4 6 0 - 4 6 5 , 1975



Echocardiography in the diagnosis of idiopathic hypertrophic subaortic stenosis coexisting with pericardial effusion. B N Alimurung, J M Felner and R C Schlant Chest 1979;76; 187-192 DOI 10.1378/chest.76.2.187 This information is current as of July 10, 2011 Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/76/2/187 Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.chestpubs.org/site/misc/reprints.xhtml Reprints Information about ordering reprints can be found online: http://www.chestpubs.org/site/misc/reprints.xhtml Citation Alerts Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to the right of the online article. Images in PowerPoint format Figures that appear in CHEST articles can be downloaded for teaching purposes in PowerPoint slide format. See any online figure for directions.
