Imaging/Diagnostic Testing l

Right ventricular function in patients with first inferio-r myocardial infarction: Assessment by tricuspid annular motion and tricuspid annular velocity Mahbubul Alam, MD, PhD, Johan Wardell, BMA, Eva Andersson, BhlA, Bassem A. Samad, MD, PhD, and RoIf Nordlander, MD, PbD Stockholm, Sweden

Background u I’k I ft n I e e ventricular function, right ventricular (RV) function has not been widely studied after a myocardial

infarction (Ml). The current study describes RV function determined by tricuspid annular motion ond tricuspid annular velocity

after Ml.

Methods and Results Thirty-eight patients with a first acute inferior MI were prospectively compared with 33

patients with a first anterior Ml and 24 age-matched healthy individuals. Association of RV infarction in inferior MI was

defined as the presence of 21-mm ST-segment elevation at the right precordial lead, V,R, of the electrocardiograms. From

the echocardiographic apical 4chamber views, the systolic motion of the tricuspid annulus was recorded at the RV free wall

with the use of 2-dimensional guided M-mode recordings. Peak systolic and peak early and late diastolic velocities of the

tricuspid annulus at the RV free wall also were recorded with the use of pulsed-wave Doppler tissue imaging. The tricuspid

annular motion was reduced in inferior Ml compared with that in healthy individuals (20.5 and 25 mm, P < .OOl ). The peak

systolic velocity of the tricuspid annulus was significantly reduced in inferior MI compared with that in healthy individuals (12

vs 14.5 cm/s, P < .OOl ) and patients with anterior MI (12 and 14.5 cm/s, P c .OO 1). Patients with inferior Ml were divided

into 2 subgroups: those with and those without electrocardiographic signs of RV infarction. The tricuspid annular motion was

significantly lower in patients with RV infarction than in patients without RV infarction (17 and 22.7 mm, P < .OO 1). In addition,

compared with patients without electrocardiographic signs of RV infarction, patients with RV infarction also had a significantly

decreased peak systolic tricuspid annular velocity (13.3 and 10.3 cm/s, P < .OO 1) and peak early diastolic velocity (13 and

8.2 cm/s, P < .OO 1).

Conclusions These results suggest that tricuspid annular motion and tricuspid annular velocity can be used to assess

RV function in association with inferior Ml. (Am Heart J 2000; 139:71 O-l 5.)

Right ventricular (RV) infarction may occur alone or in association with left ventricular inferior wall infarction. ST-segment elevation in the right precordial lead, V4R, is one of the most reliable electrocardiographic signs of acute RV infarction. l-3 It is well understood that electro- cardiographic evidence of RV infarction is associated with a poor prognosis.1g2 A hypokinetic or akinetic seg-

From the Division of Co&logy, Karolinsko Institute at South Hospital (Qdersjukhuset). Submitted March 29, 1999; accepted September 4, 1999. Reprint requests: Mohbubul Alom, MD, Division of Cardiology, Sijdersjukhuret, S 1 I8 83 Stockholm, Sweden. Emoil: mahbvbvl.olam~mmedkf~n.sos.rll.se Copyright 0 2000 by Mosby, Inc. 0002-8703/2000/$12.00 + 0 4/I/10291 I doi: IO. 1067/mhi.2000.10291 I

ment of the right ventricle observed by echocardiogra- phy also could be used to detect RV dysfunction after RV infarction.46 However, because of the complex shape, evaluation of RV function by echocardiography has been considered difficult.7vs However, a previous study has used tricuspid annular motion to assess RV function.9 Myocardial velocity determined by Doppler tissue imag- ing (DTI) is a new technique that has been used recently to analyze left ventricular function.10-12 The develop- ment of DTI opens up the possibility of also assessing RV function. However, this technique has not been used to assess RV function after myocardial infarction (MI). With the use of both the tricuspid annular motion and tricus- pid annular velocity determined by pulsed-wave DTI, the purpose of the current work was to study RV function in association with an acute first MI.

Figure 1

Alam et 01 711

Figure 2

Recording of tricuspid annular motion. M-mode cursor is placed

at tricuspid annulus of RV free wall in apical I-chamber view.

Tricuspid annular motion is expressed in millimeters and mea-

sured from lowest point to peak of contraction, as shown in

lower part of the figure.

Recording of tricuspid annular velocity. In 2-dimensional apical

I-chamber view, sample volume of pulsed-wave Doppler

myocardial velocity was placed at RV free wall (above).

Systolic and early and late diastolic velocities are shown in

lower part of the figure.

Methods The study protocol was approved by rhe local ethics com-

mittee.

Patients We selected 71 consecutive patients with a first acute MI

who were sent to our echocartliograph~ Iaborato~. None had lefr bundle branch block or atria1 fibrillation. A standard 124ead electrocardiogram and a right l~recordial electrocar-

diogram (lead V,R) were recorded immediately after arrival at the coronary care unit. The diagnosis of MI was based on characteristic chest pain, electrocardiographic changes. and diagnostic serial changes in cardiac enzymes. According fo the electrocardiograms, 33 patients had signs of anterior MI and 38 of inferior IMI. The infarction sites ;11so were con- firmed by echocardiographic determination of akinetic and/or hypokinetic areas on the left ventricle. The electro- cardiographic recording of the ST segment in lead V ,R ~3s available for 27 of the patients with inferior MI. The pres- ence of RV infarction in association with an inferior IMI was defined by an ST-segment elevation X.1 mV in lead V.,R.’ According to this definition. 9 had electrocardiographic signs of RV infarction and 18 had no signs of RV infarction. Blood pressure was recorded during the same day as close as possible fo the time of echocardiography. Hypotension was

defined as a systolic blood pressure ~100 mm Hg. Twenty- four age-matched healthy individuals without n histoy of

heart disease or systemic hypertension and having normal findings at rest electrocardiography and echocardiograph! served as control patients.

Standard echocardiography Echocardiography was performed with the patients in the

left lateral decubitus position 2 to 4 days after the IMI. The

equipment used was a Hewlett-Packard sonos 5500 phased- array system equipped with DTI technology. All echocardio- graphic measurements including DTI parameters were blinded from the elecrrocardiographic findings. Measure- ments were performed according to the recommendations of the American Society of Echocardiography.’ With the use of the apical 4 and 2-chamber views. the left ventricular ejection fraction was calculated as percentage of changes in left ventricular chamber volumes between diastole and sys tale by Simpson‘s method. The tricuspid annular motion was recorded af the RV free wall from the apical 4-chamber view. In the real-time 2-dimensional apical 4-chamber view. the M-mode cursor was placed through the tricuspid annu- lus in such a way that the annulus moved along the M-mode cursor. The displacement of the tricuspid annulus was recorded in M-mode. The total displacement was measured by using the leading edge of the echoes (Figure I). In a simi- lar way, the motion of the interventricular septum was also recorded by placing the cursor af the septal site of the annu- lus. The presence or absence of RV wall motion abnormalit) was assessed qualitatively from the parasternal long-axis view, parasternal short-axis view at the level of mid-ventri- cle (including the anterior and posterior sites near the inter- venrricular septum and excluding the free wall because of difficulties in visualization), and apical 4chamber view for the free wall. The wall motion was judged to be normal (0) or mildly (l+). moderately (2+>, or severely (3+) hypoki- n&c” at any of the RV sites. With the use of the apical 4 chamber view, pulsed-wave Doppler transtricuspid flow velocities were recorded by placing the sample volume between the leaflet tips in the center of the flow stream. The transtricuspid peak rapid filling velocity (E), peak atria1 filling velocity (A), E-wave deceleration time, and E/A ratio were measured. The presence of tricuspid regurgitation was assessed qualitatively by color flow (size of the jet) and con- rinuous-wave Doppler and was classified as absent (0), phys

712 Alam et al American Heart Journal

April 2000

~~~l.~bsol-dlinicol and echocardiogmphic poroheters in ‘$$j@&$$~~e!J yyj y!ap@ 9th mymordial infarction . .= .I

Healthy Anterior Inferior individuals MI MI

MCdf3/fe~Ol~ Age (~1 - Heort rote (beats/min) Left otrium (mm) Left ventricle (mm) Right ventricle (mm) LVEF (%) AST (bkat/L)

14/10 27/6 .63f7 63+9 67f 10 71 f12 34*3 39*4* 46f4 51 f5* 24+3 25 f 3 65f5 44+ lo*

7.2 f 6.6

26/l 2 65f12 67fll 3t3f4’ 50f6*

27.5 i 4’t 50 f 6.4*t

5.3 + 4.2

AST, Serum osportote ominotronsferose; LVEF, left ventricular ejection fraction. Resutk ore me& + SD. l P <. ,001 compared with healthy individuals. tP c .OOl comparing anterior and inferior Ml.

iologic (l+), mild (2+), moderate (3+>, and severe (4+>, according to the method described previously.** In the presence of tricuspid regurgitation, the RV systolic pressure was calculated from the sum of estimated mean right atrial pressure and maximum pressure difference between the right ventricle and right atrium.‘5 To obtain the maximum tricuspid regurgitation velocity, recording of continuous- wave Doppler flow velocity.was guided by color-flow sig- nal. Depending on the degree of tricuspid regurgitation, the value of right atria1 pressure was assigned as 4 mm Hg if the tricuspid regurgitation was l+, 8 mm Hg if 2+, 12 mm Hg if 3+, and 16 mm Hg if 4+. l4 Maximum pressure difference between the right ventricle and right atrium was calculated by applying the simplified Bernoulli equation$ AP = 4.V.V, where V is the maximum velocity of the tricuspid regurgita- tion Doppler signal.

Annular velocity by pulsed-wave DTI The pulsed-wave DTI was performed by activating the DTI

function of the same apparatus. A variable-frequency, phased- array transducer (2.0 to 4.0 MHz) was used, and bestquality recordings were performed with the use of low wall Nter set- tings (50 Hz). The gain was set to a minimal optimal level to

. . . mmmuze noise. A 3.5-mm sample volume was used. From the apical 4-chamber view, the DTI cursor was placed at the tri- cuspid annulus of the RV free wall in such a way that the anmhs moved along the sample volume line. During systole, a major positive velocity was recorded when the annulus moved toward the cardiac apex. During diastole, when the annulus moved toward the base away from the apex, 2 major negative velocities were recorded: one during the early phase of diastole and another during the late phase of diastole (Fig- ure 2). A Doppler velocity range of -20 to +20 cm/s was selected, and the velocities were measured on-line at a sweep speed of 50 nun/s. The velocities of the interventricular sep tum along the long axis also were assessed by placing the DTI sample volume at the septal site of the annulus. A mean of 5 consecutive cycles was used for the calculations of all echocardiographic Doppler parameters. All DTI parameters were taped on a CD-ROM, and calculations were performed later, independently, without knowledge of the clinical or other echocardiographic parameters.

Table II. Doppler transtricuspid flows in heolthy individuals and patients with either anterior or inferior myocordial infarction

Healthy Anterior Inferior individuals MI MI

Early wave (m/s) (E) 0.47f:O.l 0.46fO.l 0.52+0.1*t Late wave (m/s) (A) 0.39fO.l 0.45+0.1* 0.42fO.l* E/A 1.23kO.2 1.03f0.22’ 1.28f0.2t Deceleration time (ms) 193f57 226 f 66* 230f52+

Results ore mean f SD. l P c ,001 compared with healthy individuals. tP c ,001 comparing anterior ond inferior MI

Statistics Baseline hemodynamics and echocardiographic Doppler

variables are expressed as the mean value and 1 SD. The KruskaI-Wallis test was used to compare different parameters between groups. When intergroup differences were found, the Mann-Whitney U test was performed to determine which groups were SignScantly different. Categoric variables were analyzed with the &i-square test. A value of P < .05 was con- sidered statistically significant. To assess intraobserver vari- ability in calculating tricuspid annular velocity by DTI, mea- surement of peak systolic velocity was made in 18 randomly selected patients on 2 different occasions by 1 investigator. To test interobserver variability, measurements were made independently at the above sites after the first examination. The variability was assessed as the difference between the 2 sets of observations divided by the mean of the observations and expressed as a percentage.

Results Table I shows the basal clinical and echocardio-

graphic parameters for anterior and inferior MI, com- pared with healthy individuals. The left ventricular and left atria1 dimensions were significantly higher in patients compared with those in healthy individuals. Transtricuspid Doppler velocities are shown in Table II. The hemodynamic parameters, incidence and severity of tricuspid regurgitation, RV systolic pres- sure, and presence and severity of RV wall motion abnormality in patients with anterior MI, patients with inferior MI, and subgroups of patients with or without electrocardiographic signs of RV infarction are provided in Table III. Compared with patients without RV infarction, patients with electrocardio- graphic signs of RV infarction more frequently had tricuspid regurgitation, hypotension, and RV wall motion abnormality. None of the patients without RV infarction showed any sign of RV wall motion abnor- mality or tricuspid regurgitation of grade 22.

Tricuspid annular motion The systolic tricuspid annular motion was signi&

cantly lower in patients with inferior as well as ante- rior MI compared with healthy individuals (Table IV).

American Heart Journal Volume 139, Number 4 Alam et al 713

Table 111. RV hemodynamics and conventional echocardiographic fipdings in+ientswitft mnter@!&it#&& patients with inferior MI with or without electrocardiographic signs of RV infarction

Presence of Anterior MI Inferior MI RV infarction

(n = 33) (n - 38) (n - 91

Absence of RV infarction

(n = 18)

SBP (mm Hg) DBP (mm Hg) Percentage of patients with hypotension Percentage of patients with RV WMA Percentage of potients with RV WMA grade b2 Percentage of patients with TR Percentage of patients with TR grode 22 RVSP (mm Hg)

122f22 118f22 76f 14 70* 10

12 16 6 18 3 13

69 76 3 10

25+7 26+5

103k 18 128f23* 70+ 12 74+ 10

44 6t 55 0 44 0 89 731 33 0

29f7 24f4

DBP, Diastolic blood pressure; RVSP, right ventricular systolic pressure; SBP, systolic blood pressure; TR, tricuspid regurgitation; WM4 wall motion abnormality l P < .05, fP c .Ol, *P < ,001 compared with patients with RV infarction.

The decreased value was more pronounced in the patients with inferior MI. Compared with patients without electrocardiographic signs of RV infarction, the tricuspid annular motion was significantly lower in patients with RV infarction. The tricuspid annular motion was similar in magnitude in patients with anterior MI and inferior MI without electrocardio- graphic signs of RV infarction.

Tricuspid annular velocity by DTI The intraobserver and interobserver variabilities

were low (4.2% f 4% and 4.8% f 6.4%, respectively). The peak systolic tricuspid annular velocity in ante- rior MI was similar to that of the healthy individuals. On the other hand, the systolic velocity in inferior MI was significantly decreased compared with that ln both healthy individuals and patients with anterior MI (Table IV). The peak early diastolic velocity also was decreased in patients with inferior MI compared with that in healthy individuals. The late diastolic velocity was similar in patients with inferior MI compared with that in healthy individuals.

When patients with electrocardiographic signs of RV infarction were compared with patients without electrocardiographic signs of RV infarction, a signifi- cantly decreased peak systolic tricuspid annular velocity as well as peak early and late diastolic tricus- pid annular velocity were found in the patient popu- lation with RV infarction (Table IV). Patients with RV infarction also showed greater myocardial damage as determined from higher cardiac enzymes (serum aspartate aminotransferase 9.5 + 5.9 ukat/L compared with 3.7 f 2.1 pkat/L in patients without RV lnfarc- tion, P c ,001). The right ventricle was enlarged in patients with RV infarction compared with those without RV infarction (29 and 26 mm, respectively, P < .OOl>. The peak systolic, peak early, and late diastolic tricuspid annular velocities were similar

(P > .05) both in patients with anterior MI and patients with inferior MI without electrocardiographic signs of RV infarction.

Function of the septum The peak systolic and peak early diastolic velocities of

the interventrlcular septum in the infarction groups were significantly lower compared with that in healthy individuals (Table V). The decreased systolic velocity was more pronounced in patients with RV infarction.

Discussion Although RV infarction is not an uncommon condl-

tlon,t.*J7Js hemodynamically important RV infarction is an infrequent consequence of inferlor MI. l9 Occlusion of the proximal rlght coronary artery might produce infer0 posterior left ventricular infarction in association with RV infarction and depressed RV function.20~21 Assessment of RV function by echocardiography ls complicated because of the complex geometry.22 Contraction of both the septum and the RV free wall contrlbutes to the RV ejection fraction.23 Motion of the tricuspid anrmlus toward the cardiac apex in systole is an expression of RV contraction along the long axis. Previously, RV function has been evaluated by use of the amplitude of the trlcu~ pid annular motion determined by M-mode echocardiog- raphy.9 The advantage of recording the tricuspid armular motion is that it is devoid of myocardial dropout. Recently, myocardlal velocity recorded by either color- coded or pulsed-wave DTI has been used to assess left ventricular function.t@ta However, the effect of MI on RV velocities estimated by DTI Is not known.

In the current study, the M-mode echocardiographic tricuspid annular motion was sign&antly decreased in patients with inferior MI compared with healthy lndlvld- uals and patients with anterior MI. This ls probably an expression of decreased RV function along the long axis in inferior MI. Moreover, unlike anterior MI, the peak sy~

714 Alam et al Amer~con Heart Journal

April 2000

:+&-IV. Tricuspid annular motion determined by Mhode echocardiography and tricuspid annular velocity determined by Doppler tissue .iiaging .

Healthy Inferior MI with Inferior MI without individuals Anterior MI Inferior MI RV infarction RV infarction

Tricuspid annular motion (mm) Tricuspid annular velocity (cm/s) Systolic

Early diastolic (E) Late diastolic (1)

E/L ratio

25f4 22f4* 20.5 f 5’7 17 + 2.8 22.7 Z!I 4.91

14.5+2 14.5 f 3 12f2’T 10.3 + 1.8 13.3+2*

14f3 12.5 zk 4’ 11+3* 8.2 f 1 13 f 2.7* 16.5 + 3 18.5 + 4* 16f5t 13.6 f 3.5 17.7 * 4.7* 0.86 f 0.3 0.67_+0.1 l 0.74 k 0.1 l 0.69 zk 0.1 0.76 f 0.2

Retdk ore meon f SD. l P < .OOl compared with healthy individuals. TP c .OOl comparing anterior and inferior Ml. tP < ,001 comparing potienk with and those without signs of RV infarction.

, Table V. Myocardial velocities of the interventricular septum determined by Doppler tissue imoging

Healthy Inferior Ml without Inferior Ml with individuals Anterior Ml Inferior Ml RV infarction RV infarction

Systolic 8.8f 1.3 7.2 + 1.6* 7.2 AI 1.2* 7.9 It 1.4* 6.4f l.l*t Early diastolic (E) 10.7 f 2.3 7.0f 1.5’ 7.6 f 1.5’ 7.8+ 1.5’ 7.3 f 1 .O’ Late diastolic (L) 1 1.8 f 2.5 10.8 f 2.3 9.6 f 2.2 10.6 f 2.1 9.4 f 2.0 E/L ratio 0.95 SC 0.4 0.66 + 0.1 0.81 f 0.2 0.76 + 0.2 0.81 f 0.2

l P < ,001 compared with healthy individuals. tP < .O 1 compared with patienk with no elevation of ST segment in lead V,R

tolic tricuspid annular velocity determined by DTI was also reduced in patients with inferior MI compared with healthy individuals. In addition to a decreased peak sys- tolic velocity, the peak early diastolic tricuspid annular velocity was also reduced in patients with inferior MI compared with healthy individuals and patients with anterior MI. The reduced peak systolic and peak early diastolic velocities of the tricuspid annulus in inferior MI in the current study might be an expression of decreased RV function, which is probably due to the presence of a subset of patients with RV infarction.l@12

The presence of ST-segment elevation in the right precordial lead, V,R, has a high diagnostic accuracy for RV infarction and is usually associated with depressed RV function.1.2~4~24 In the current study, patients with electrocardiographic signs of RV infarc- tion had enlarged right ventricle, higher incidence of hypotension, and tricuspid regurgitation compared with patients without RV infarction. The RV wall motion abnormality was common in patients with electrocardiographic signs of RV infarction. None of the patients without electrocardiographic signs of RV infarction had RV wall motion abnormality. In addi- tion, both the tricuspid annular motion and the peak systolic tricuspid annular velocity were significantly decreased in patients with electrocardiographic signs of RV infarction compared with those without RV

infarction. The results imply greater RV damage in patients with ST-segment elevation in lead V,R. Simi- lar to the systolic velocity, the peak early diastolic velocity of the tricuspid annulus was also significantly reduced in patients with electrocardiographic signs of RV infarction compared with patients without RV infarction. This probably reflects a decreased regional diastolic function of the right ventricle caused by greater damage. With the use of DTI, some previous studies conducted to assess left ventricular regional diastolic function showed a similar decreased early diastolic velocity of the mitral annulus at the ischemic or infarction sites.12,25

The interventricular septum has traditionally been considered to be a part of the left ventricle. However, contraction of the septum also contributes to the RV ejection.23 In the current study, we found an equally depressed peak systolic velocity of the septum in both anterior MI and inferior MI compared with healthy individuals. However, patients with electrocardio- graphic signs of RV infarction revealed a more signitl- cantly reduced velocity at the septum compared with other groups.

Limitations The study evaluates changes only at the annulus along

the long axis. Changes at other RV sites were not

American Heor1 Journal Volume 139. Number 4 Alam et a) 715

considered. However, evaluation of the other RV sites might not be feasible in clinical practice because of technical difficulties of visualization by echocardiogra- phy. Echocardiographic examinations were performed 2 to 4 days after the development of MI. It is possible that some of the patients had already recovered from the damage in the right ventricle, because RV recovery generally occurs quickly after MI.26.27 Another limita- tion is that no coronary angiography was performed during the acute phase of the infarction for analysis of the state of right coronary artery.

Conclusions Patients with electrocardiographic signs of RV infarc-

tion have a decreased tricuspid annular motion and tri- cuspid annular velocity compared with patients with- out RV infarction. This probably reflects a reduced RV function after RV infarction. The method of recording the motion and velocity of the tricuspid annulus is sim- ple and can be used to assess RV function in patients with MI.

References 1. Erhardt 1, SiGgren A, Wahlberg I. Single right-sided precordial lead

in the diagnosis of right ventricular involvement in inferior myocardial

infarction. Am Heart J 1976;95:571-6.

2. Yoshino H, Udagawo H, Shim& H, et al. Inferior myocordial

infarction. Am Heart J 1998;135:689-95.

3. Braat SH, Brugoda P, DeZwar,n C, et al. Value of electrocardiogram

in detecting right ventricular involvement in patients with acute inferior

wall myocordial infarction. 8r Heart J 1983;49:368-77.

4. Zehender M, Kasper W, Kauder E, et al. Right ventricular infarction

OS an independent predictor of prognosis after acute inferior myocardiol

infarction. N Engl J Med 1993;328:981-8.

5. Lopez-Sendon J, Garcia-Fernandez MA, Coma-Canello I, et al.

Segmental right ventricular function after acute myocardial infarc-

tion: 2dimensionol echocardiographic study in 63 patients. Am J

Cardiol 1983;5 1:390-6.

6. Lopez-Sendon J, Lopez de Sa E, Roldan I, et al. Inversion of normal

interatrial septum convexity in acute myocardiol infarction: inci-

dence, clinical relevance and prognostic significance. J Am Coll

Cardiol 1990; 15:80 15.

7. Dell’ltalia U, Starling MR, Walsh RA, et al. Validation of ottenuotion-

corrected equilibrium radionuclide angiographic determinations of

right ventricular volume: comparison with cast-validated biplane

cineventriculography. Circulation 1985;72:3 17-26.

8. Fisher E, Dubrow RA, Hastreiter AR. Right ventricular volumes in

congenital heart disease. Am J Cardiol 1975;36:67-75.

9. HammorstrGm E, Wranne 8, Pinto FJ, et al. Tricuspid annular motion.

J Am Sot Echocardiogr 1991;4: 13 l-9.

10. Donovan Cl, Armstrong WF, Bach DS. Quantitative Doppler tissue

imaging of the left ventricular myocardium: validation in normal

subiects. Am Heart J 1995; 130: 100-4.

1 1. Miyotake K, Yamogishi M, Tanaka N, et al. New method for

evaluating left ventricular wall motion by color-coded tissue

Doppler imaging (TDI): in vitro and in viva studies. J Am Coll

Cardiol 1995;25:717-24.

12. Gorcsan J, Gulati VK, Mandarino WA, et al. Color-coded measures

of myocordiol velocity throughout the cardiac cycle by tissue

Doppler imaging to quantify regional left ventricular function. Am

Heart J 1996; 13 1: 1203-l 3.

13. Schiller N8, Shah PM, Crawford M, et al. Recommendations for

quantitotion of the left ventricle by 2dimensional echocardiogrophy.

J Am Sot Echocardiogr 1989;2:358-67.

14. Ribeiro A, Lindmorker P, Juhlin-Dannfelt A, et al. Echocardiography-

Doppler in pulmonary embolism: right ventricular dysfunction as a

predictor of mortality rate. Am Heart J 1997;134;479-87.

15. Currie PJ, Seward JB, Chon KL, et al. Continuous wave Doppler

determination of right venhiculor pressure: a simultaneous Doppler-

catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750-6.

16. Hatle 1, Angelsen 8. Doppler ultrasound in cardiology: physical

principles and clinical application. Philadelphia: Leo 8, Feibiger;

1982. p. 23.

17. Bowers TR, 0 ‘Neil1 WW, Grines C, e1 al. Effects of reperfusion on

biventriculor function and survival after right ventricular infarction.

N Engl J Med 1998;338:93340.

18. Shiraki H, Yoshikawo T, Anzai T, et al. Association between prein-

farction angina and o lower risk of right ventricular infarction. N

Engl J Med 1998;338:941-7.

19. Dell’ltalia LJ, Starling MR. Right ventricular infarction: an important

clinical entity. Curr Probl Cardiol 1984;9:1-72.

20. Cohn JN, Guiha NH, Broder Ml, et al. Right ventricular infarction:

clinical and hemodynamic features. Am J Cordial 1974;33:209-14.

21. Goldstein JA, Barzilai 8, Rosamond TL, et 01. Determinants of

hemodynamic compromise with severe right ventricular infarction.

Circulation 1990;82:359-68.

22. Dell’ltalia U. Reperfusion for right ventricular infarction. N Engl J

Med 1998;338;978-80.

23. Santamore WP, Dell’ltalia LJ. Ventricular interdependence: signifi-

cant let? ventricular contributions to right ventricular systolic function.

Prog Cardiovasc Dis 1998;40:289-308.

24. Kinch J, Ryan T. Right ventricular infarction. N Engl J Med 1994;

330:121 1-7.

25. Bach DS, Armstrong WF, Donovan Cl, et al. Quantitative Doppler

tissue imaging for assessment of regional myocardiol velocities during

transient ischemio and reperfusion. Am HeartJ 1996;132:721-5.

26. Dell’ltalio U, Lembo NJ, Starling MR. et al. Hemodynamically important

right ventricular infarction: followup evaluation of right ventricular sy*

tolic function at rest and during exercise with radionuclide ventriculcgr*

phy and respiratory gas exchange. Circulation 1987;75:9961003.

27. Steele P, Kirch D, Ellis J, et al. Prompt return to normal of

depressed right ventricular ejection fraction in acute inferior infarction.

BrHeortJ 1977;39:1319-23.