Right ventricular infarction: Two-dimensional echocardiographic evaluation

Volume 107

Number 3 2DE visualization of coronary enlargement in children

nary artery by cross-sectional echocardiography. Circulation 54:169, 1976.

2. Hiraishi S, Yashiro K, Kusano S: Noninvasive visualization of coronary arterial aneurysm in infants and young children with mucocutaneous lymph node syndrome with two dimensional echocardiography. Am J Cardiol 43:1225, 1979.

3. Yoshikawa J, Yanagihara K, Owaki T, Kato H, Takagi Y, Okumachi F, Fukuya T, Tomita Y, Baba K: Cross-sectional echocardiographic diagnosis of coronary aneurysms in patients with the mucocutaneous lymph node syndrome. Circulation 59:133, 1979.

6. Yoshida H, Funabashi T, Nakaya S, Taniguchi N: Mucocuta- neous lymph node syndrome. A cross-sectional echocardiographic diagnosis of coronary aneurysm. Am J Dis Child 133:1244, 1979.

7. Fisher EA, Sepehri B, Lendrum B, Luken J, Levitsky S: Two-dimensional echocardiographic visualization of left coronary artery in anomalous origin of left coronary artery from the pulmonary artery. Circulation 63:698, 1981.

8. Reeder GS, Tajik AJ, Smith HC: Visualization of coronary artery fistula by two-dimensional echocardiography. Mayo Clin Proc 55:195, 1980.

4. Kawakubo K, Kuwako K, Umeda T, Machii K: Echocardio- 9. Satomi G, Iwasa M, Nakamura K, Minami Y, Adachi F, graphic assessment of the left main coronary artery and its Takao A: Subxiphoid frontal approach of two-dimensional correlation with coronary angiography. J Cardiography (in echocardiography. J Cardiography (in Japanese with English Japanese with English summarv) 10:821. 1980. summary) 10:213, 1980.

5. Rogers EW, Feigenbaum H, Weirnan AE; Godley RW, Vakili ST: Evaluation of left coronary artery in vitro by cross- sectional echocardiography. Circulation 62:782, 1980.

10. Satomi G, Endo M, Takao A, Nakamura K: A case of right coronary artery to left ventricle fistula: Two-dimensional echocardiographic study. Pediatr Cardiol 4:229, 1983.

Right ventricular infarction: Two-dimensional echocardiographic evaluation

Seventeen patients with predominant right ventricular infarction (RVMI) were studied with

two-dimensional echocardiography (2DE). On initial 2DE all had abnormal wall motion (AWM), defined as akinesis plus dyskinesis, in the inferior right ventricle (RV), inferior interventricular

septum, and inferior left ventricle (LV). The extent of RV vs LV AWM in short-axis sections at mitral, chordal, and papillary levels was 58%.vs 29%, 56% vs 38%, and 59% vs 38%,

respectively. The calculated topographic extent of AWM was greater in the RV than in the LV (58% vs 36%, p < 0.05), and the RV/LV ratio (1.65) exceeded (p < 0.001) unity. Peak creatine phosphokinase levels correlated significantly (p < 0.001) with the topographic extent of LV AWM

(r = 0.79) or RV + LV AWM (f = 0.75). Although all patients had RV dilatation, eight also had LV

dilatation. Serial studies detected the cause of mechanical complications (n = 13), mural echo densities suggesting thrombi (LV in six and RV in seven), and persistent AWM in survivors. Thus,

2DE provided diagnostic data, and assessment of RV and LV AWM confirmed predominant RV

involvement. (AM HEART J 107:505, 1984.)

Bodh I. Jugdutt, M.B.Ch.B., Bruce A. Sussex, M.B.B.S., Chittur A. Sivaram, M.B.B.S., and Richard E. Rossall, M.D. Edmonton, Alberta, Canada

From the Division of Cardiology, Department of Medicine, University of Right ventricular infarction (RVMI) is a potentially Alberta.

Supported in part by grants from the Special Services of the University of Alberta Hospital and the Canadian Heart Foundation by a Clinical Investigatorship (Dr. Jugdutt) of the Canadian Heart Foundation, and by a Clinical Fellowship (Dr. Sussex) of the Alberta Heritage Foundation for

reversible cause of cardiogenic shock,‘e3 so that aggressive diagnosis and therapy have been advo- cated.‘s2 Until Cohn et al.’ described its clinical and hemodynamic features.in 1974, RVMI was mainly a

Medical Research.

Received for publication Oct. 4, 1982; revision received March 24, 1983; accepted April 11, 1983.

Reprint requests: Dr. B. Jugdutt, 6-112, Clinical Sciences Building,

postmortem diagnosis.4p5 Although ECG evidence of inferior myocardial infarction (IMI) associated with ST segment elevation in the precordial lead VI6 or

University of Alberta, Edmonton, Alberta, Canada, T6G 2G3. the right precordial lead V4R7 has been suggested as

505

506 Jugdutt et al. March. 1984

American Heart Journal

Fig. 1. Echocardiograms of the short-axis sections at mitral (A), chordal (B), papillary (C), and apical (or, low papillary, D) levels. Rightward transducer angulation was often needed to visualize the RV wall.

a sign of predominant RVMI, this diagnosis still depends on demonstration of a disproportionate reduction in RV function by right heart catheterization.‘, 2. a Other noninvasive methods have therefore been used to detect RV involvement in IMI, such as gated scintigraphy,s dual thallium-201 and technetium-99m pyrophosphate imaging,‘O and M-mode echocardiography.lz l1 Theseg-” and other studies1-3’ 12-14 now suggest that RVMI is commonly associated with inferior left ventricular (LV) infarction and its clinical presentations form a spectrum.

Although two-dimensional echocardiography (2DE) has been used to estimate the extent of LV asynergy in myocardial infarctiorF7 and can detect RV asynergy in RVMI, l8 it has not been used to estimate the extent of RV asynergy. In this study, we used 2DE to evaluate 17 patients with clinical and hemodynamic evidence of predominant RVMI. We also applied 2DE methodology, used for assessing LV asynergy, to estimate the topographic extent of LV and RV asynergy.

METHODS

Patients. As part of ongoing 2DE studies in the coronary care unit, 228 consecutive patients admitted with a first acute myocardial infarction between 1980 and 1981 were carefully screened for clinical features of RVMI.‘-“,H Ninety-one patients had IMI and 31 of these had RVMI. Written informed consent for both 2DE19 and hemodynamic recordings was obtained from 20 of the patients with RVMI; 17 of these 20 patients (85%) had adequate visualization of RV and LV endocardium for detailed analysis and form the basis of this report.

The diagnosis of infarction was based on a typical history of chest pain accompanied by evolutionary ECG changes and a typical pattern of elevated serum enzymes. All of the following criteria were used for the clinical diagnosis of RVMP on admission: (1) ECG evidence of IML2” (2) evidence of systemic venous congestion, (3) absence of pulmonary congestion (on auscultation and portable chest radiograph), and (4) hypotension (systolic blood pressure ~100 mm Hg). We excluded patients with a past history or ECG evidence of previous infarction, and those with a past history of pulmonary hypertension, constrictive pericarditis, cardiomyopathy, or congenital or valvular heart disease.

Volume 107

Number 3 2DE evaluation of RV infarction 507

2DE recordings. Portable 2DE (Varian 3400R) was done on the first 2 days after admission and on day 10, prior to discharge. In all cases, complete 2DE examination&Y were made by two of us (B. J. and B. S.). Paraster- nal long-axis, serial parasternal short-axis, apical (four- and two-chamber), and subxiphoid views were recorded systematically to visualize both LV and RV walls. The position of the patient (degree of lateral body rotation and upper body elevation) and transducer (distance from midsternal line and the intercostal space) were recorded at the first study for use in subsequent examinations. Images were recorded on 0.5 inch videotapes (Sony) for subsequent review in real-time, slow-motion, and single-frame format. Images were gated on the ECG, by means of the R wave for end diastole and T wave for end systole.

For analysis of motion of endocardial surfaces,2’ special emphasis was placed on obtaining good endocardial deli- nition, avoiding oblique sections,2? and recording over several cardiac cycles at end expiration. Internal anatomic landmarks (junctions of the RV with the LV, and location of mitral valve leaflets, chordae tendineae, and papillary muscles) were used to facilitate orientation of the views. Rightward transducer angulation was often necessary to visualize the RV walls in short-axis views (Fig. 1). A previous review of 2DE data in 49 patients with IMI in our laboratory revealed that at least 50% of the endocardium must be visualized in any one segment throughout the cardiac cycle for reliable prediction of presence or absence of LV and RV asynergy. In those patients, adequate target visualization over five or more consecutive cardiac cycles in short-axis views for LV vs RV was: mitral 92 % vs 86 % , chordal 94 % vs 88%) papillary 86 % vs 88% and apical 69 % (LV only). Corresponding values in other views were: parasternal long-axis 88% vs 82%, apical four-chamber 90 % vs 87 % , and subxiphoid 78 % vs 82 % . The apical two-chamber view visualized the posterior LV wall in 88%. Review of images in real time improved target visualization and allowed filling in of missing endocardial segments.

Emphasis was also placed on identifying complications,2:r tricuspid regurgitation,24.2” and ventricular mural thrombi.Z”-2R Contrast 2DE was performed by means of 5 to 8 ml bolus injections of 5% dextrose in water into a peripheral vein (n = 13) or a Swan-Ganz catheter with- drawn from the right atrium (n = 4) and subcostal right atrial and inferior vena caval (IVC) imaging during quiet respiration, deep inspiration, and Valsalva maneuver. Tricuspid regurgitation was diagnosed if persistent contrast echoes were seen in the IVC and hepatic veins,24 the IVC dimension was greater than 24 mm, and systolic pulsation of the IVC was absent.2”

Blood pressure was recorded via an arterial line (Sta- tham P23Db). Right heart catheterization (Swan-Ganz) was used to measure right heart and pulmonary capillary wedge pressures. Cardiac outputs were measured by the thermodilution method. Blood samples for creatine phosphokinase (CPK) activity were taken every 4 hours for the first 12 hours and every 8 hours thereafter for 3

B.SHORT AXIS VIEWS

A. THE MODEL 1. MITRAL

c. SURFACE AREA AND “OLLIME

CALCULATION

RV LV

2. CHORDAL

3 PAPILLARY

1. APICAL

Fig. 2. A, Right ventricle (RV) is a crescent-shaped appendage attached to more conical left ventricle (LV). B, Extents of AWM in four short-axis sections (thick lines) were expressed as ratios of circumferences for LV (S/C, to S/C,) and as ratios of the arc lengths for RV (S/L, to S/L,); LV diameters (D, to D,) and RV septal chord lengths (I, to I,) were measured. C, Surface area of AWM (stippled) in endocardial shells was computed from AWM in four serial short-axis views at mitral, chordal, papillary, and apical levels. Long-axis lengths (h,, h2) of RV and LV were measured in apical four-chamber views and slices assumed to be of equal thickness. Total LV AWM area was computed for conical shapes. RV was opened out into two trapezoids and a triangle to compute total RV AWM area. Volumes were computed from areas and thicknesses of sections.

days or until baseline levels were reached. All complications during hospitalization were recorded. Follow-up data were collected at 6 weeks, 3 months, and every 6 months until March, 1982. Results of cardiovascular phys- ical examination, ECG, additional investigations (coronary angiography, radionuclide studies, 2DE), New York Heart Association functional class,*” and complications were recorded. All data were coded.

2DE analysis. Coded 2DE recordings (tape and log numbers) were analyzed separately by two of us (B. J. and B. S.). Images were viewed on a 14-inch television screen (Varian). Endocardial outlines of RV and LV cavities were traced on plastic overlays from frozen images at end diastole and end systole and modified on multiple play- backs. Careful visual assessment of wall motion was made as described by Gibson et alI7 Wall motion was classified

SO8 Jugdutt et al. March. 1984


100- NORMAL AUTOPSIED HU,W HEARTS

Y = 0.25 Y-1.65

N = 15. r = 0.74

SEE = lo.'30

P C c.001

LV MflSSCG)

Fig. 3. Direct relation between masses of RV and LV in 15 autopsied human hearts from patients dying of noncardiac disease. Ratio of RV to LV mass (0.24) was used to compute (RV + LV) AWM.

as normal, hypokinetic, akinetic, or dyskinetic by means of a modification of terminology described by Herman and Gorlin.29 The location of abnormal wall motion (AWM) in myocardial segments was identified by means of the standard nomenclature described by Edwards et al.“” The extent of AWM, defined as akinesis plus dyskinesis was marked on the end-diastolic endocardial outlines of the LV and RV. To gain insight into the severity of AWM, markings of relative extents of hypokinetic, akinetic, and dyskinetic regions were made by visual assessment of wall thickening and endocardial movement during systole.” Outer boundaries between hypokinetic and akinetic regions were modified by verifying that systolic thickening in the akinetic zone was absent (zero). Markings of dyskinetic segments (no systolic thickening or systolic thinning) were also modified by comparing diastolic and systolic outlines.

To calculate extents of AWM for the RV and LV, end-diastolic outlines of the four serial short-axis sections were digitized electronically (Hewlett-Packard (9874A) and the following measurements made (Fig. 2). LV circumferences (C, to C,), extent of LV AWM (S, to S,), LV internal diameters (D, to DJ, arc lengths of RV wall (L, to L,), extent of RV AMW (S, to S,), and septal chord lengths between junctions of the RV wall with the interventricular septum (I, to 13). The long-axis lengths (h,, hz) of the RV and LV (Fig. 2, C), as well as vertical lengths of the AWM defects were measured on apical four-chamber views. The ventricular septum was considered part of the

LV. Diameters of the LV short-axis sections were measured along an axis constructed from a point on the posterior endocardial surface near the ventricular septum (and at mitral, chordal, or papillary muscle attachments) to the anterolateral LV wall so as to divide the diastolic images into equal areas.31

To calculate the topographic extent of AWM, the surface area of AWM in endocardial shells for the RV and LV were calculated by using extents of AWM along the LV circumferences and RV arcs in the serial sections and depths of the sections derived from long-axis lengths (h,/4 for LV; hJ3 for RV). The surface area of AWM was expressed as a ratio of the total surface area (Fig. 2, C). Four conical shapes were assumed for the LV and two trapezoids with an apical triangle for the RV. Four main assumptions were made for each ventricle. The assumptions for the LV were: (1) muscle mass of a section was proportional to its circumference, or diameter; (2) the contribution of each section to LV mass was proportional to its circumference, or diameter; (3) sections were equally spaced and were not oblique; and (4) diastolic shape was not distorted. Similar assumptions were made for the RV but RV wall length and septal chord length were used instead of circumference and diameter in (1) and (2).

In order to relate AWM to CPK released from infarction of both ventricles, the total extent of AWM for (RV + LV) was computed: Total AWM (%) = (mass of LV AWM + mass of RV AWM) x lOO/(LV mass + RV mass) = (LV AWM as %

Volume 107


LV + P X RV AWM as % RV) X lOO/(l + P) = where P RV mass/LV mass. The ratio P was derived from autopsy data on RV and LV muscle mass in hearts from 15 patients dying of noncardiac diseases. Hearts were fixed in formalin after packing with gauze swabs to maintain diastolic dimensions. The RV wall and LV were carefully dissected, freed of fatty and valvular tissue, and weighed separately. The interventricular septum was included in the LV. The linear regression between RV and LV mass is shown in Fig. 3. The ratio of RV to LV mass averaged 0.24 * 0.01 (SE). Volumes at end diastole (EDV) and end systole (ESV) were estimated for the LV and RV by summating the volumes of the four LV and three RV sections. Volumes of the sections were calculated by multiplying the averaged digitized areas of serial sections by the vertical heights of each section (h,/4 for LV; h,l3 for RV). In an attempt to relate AWM to global function, ejection fraction (EF) was estimated from these volumes, thus: EF = [(EDV-ESV)/EDV] x 100.

Data analysis. The markings of AWM made by the two observers were compared and the consensus, after further review, was used to compute final data. For the 17 patients, the two observers showed 100% concordance in assessing the site of AWM but differed by 3.6 + 0.5 (SE) mm in marking the extent of AWM in short-axis sections (n = 64). For one observer (B. J.), the variability was 1.9 -+ 0.3 mm and outer boundaries of AWM had to be shifted by 1.8 + 0.3 mm (176 boundaries in 48 RV and 64 LV short-axis sections). Precomparison interobserver variation for AWM was minimal (F = 0.96). Numeric data were expressed as mean f SEM. Significance of differences within a group and between two groups was assessed by paired and unpaired t tests, respectively. Correlation coefficients were determined by linear regression analysis. Serial measurements were compared by means of multiple-measures analysis of variance.

RESULTS

Clinical and hemodynamic data. The data at the time of the initial 2DE on the 17 patients with RVMI are summarized in Table I. Initial 2DE was recorded 31.3 + 2.6 (SE) hours after admission. The interval between onset of chest pain and hospitalization for these patients was 6.8 + 1.2 (range 1 to 19) hours. There were eight men and nine women. Their ages averaged 64 & 3 years. Twelve patients had isolated IMI, three had inferolateral, and two had inferoposterior infarction. All patients had elevated jugular venous pressures (>lO cm HzO, with the zero reference being 5 cm below the second costochondral junction), positive Kussmaul’s signs with further jugular venous distension during inspiration, hypotension, and clear lung fields on auscultation with no evidence of pulmonary congestion on initial portable radiographs. 32 None had audible murmurs. Cardio- megaly (cardiothoracic ratio X0%) was found in

CASE 17 ( A.G. I

l --

0 1 2 3 4 5 6 7 a DAYS

r”, 1 -- I,, ,

4 5 6 7 8 DAYS

XQ (mvl 0 9 lo 12 15 15 15

XR (mV) 6 6 4 4 4 4 3 3

t t

Thinning of infero-basal

septum

Fig. 4. Clinical and echocardiographic findings in patient No. 17. Secondary rise in ST segments (top panel) on sixth day was associated with clinical syndrome of chest pain, LV failure, further hypotension, and minor rise in CPK (second panel). Q and R wave amplitudes did not change significantly (third panel). Bottom panel, 2DE sections at papillary level on admission (left) and day 6 (right) are diagrammed. Akinetic zone developed thinning in inferior regions of LV and septum, as well as dilatation of RV and LV chambers. B = sum of ST segment, or R, or Q amplitude in leads II, III, and aV,.

three patients (Nos. 3, 8, and 13). On right heart catheterization, the mean right atria1 (15.1 + 0.6 mm Hg) and RV end-diastolic (15.5 + 0.6 mm Hg) pressures exceeded (p < 0.05) the mean pulmonary capillary wedge pressures (14.0 it 0.6 mm Hg). The cardiac index averaged 2.1 f 0.1 L/min/m” (range 1.3 to 2.7). Therapy in all patients consisted of volume expansion and pressor agents.ls2

Clinical course and outcome. Five patients died (29%) at 3, 5,7, 20, and 33 days, respectively, after infarction (Table I). The remaining 12 patients (71%) survived the follow-up period of 13.5 + 2.0 (range 6 to 28) months and their mean functional class (New York Heart Association) was 1.8 +- 0.2. Two patients (Nos. 2 and 11) underwent coronary artery bypass surgery for recurrent angina at 13 and 15 months, respectively.

During hospitalization, 15 patients (88%) developed electrical complications (atria1 fibrillation in

510 Jugdutt et al. March, 1994


Table 1. Clinical features at the time of the initial echocardiogram and follow-up data in RV infarction

Heart Rlood Kuss- Peak CPK Pressures (mm Hg) Patient Age rate pressure JVP maul’s levels ECG

No. Ivr) Sex @pm) (mm Me) (cm H,O) sign IIl!lL) site RA RV PA PCW Cl

1 74 M 52 100/70 18 + 1835 I (18) 28118 30/16 14 2.0

2 72 F 46 80160 16 + 983 I (16) 25116 23/15 13 2.1

3 76 F 50 60/O 16 + 2250 I (16) 32/16 32,‘16 14 2.3

4 39 F 60 95/m 17 + 2300 I (17) 29117 29/15 14 2.1

5 64 F 55 88l56 16 + 1000 LP (1.5) 31/16 30/16 16 2.7

6 61 F 75 80/O 16 + 1899 I (16) 25117 24116 15 2.7

7 78 M 40 75/65 20 + 915 1.L (20) 29/20 28115 19 1.3

8 78 F 82 80/O 13 + 5780 W (13) 33/14 33/16 13 1.8

9 68 M 68 lW60 11 + 1063 I (11) 25111 24/11 11 1.9

10 39 M 60 65/50 1’ + 4990 I (12) 28/E “B/13 12 1.6

11 60 M 48 90/60 13 + 1926 I (13) 30/14 30114 14 2.0

12 66 F 84 1 ooi50 17 + 520 I (17) 32117 31/12 12 2.2

13 74 M 92 90/60 16 + 2094 I (16) 29116 33/16 15 2.0

14 79 F 60 80/60 15 + 1064 IL (15) 34/18 34/18 18 2.2

1 .ri 61 M 86 90/60 16 + 2585 IL (16) 34/15 %/I:3 13 2.3

16 47 M 80 90170 13 + 2277 I (13) 28114 27114 14 2.2

I7 59 F 50 60/30 13 + 3285 I (13) 25112 26/11 11 1.6 -~-- __--

Ahhreviations: AF = atria1 fibrillation: AVB = atrioventricular block: CA = cardiac arrest; CI = cardiac index (L/min/m’); I = inferior; JVP = jugular venous pressure (zero reference level = 5 cm below the second costochondral junction); L = lateral; P = posterior; PA = pulmonary artery; PCW = p&no- nary capillary wedge; PE = pulmonary embolism; PMD = papillary muscle dysfunction; PMR = papillary muscle rupture; RA = right atrium; RV = right ventricle; SE = systemic embolism; VT = ventricular tachycardia.

six; atrioventricular block in five, ventricular tachycardia in seven, and cardiac arrest in five). Four of the five patients who developed cardiac arrest were successfully resuscitated. A pacemaker was required in three patients (temporary in Nos. 3 and 15; permanent in No. 5). Four patients developed pericarditis but none developed cardiac temponade. Seven patients had marked precordial ST segment changes (>l mV) in the first 24 hours, with ST depression in six and elevation in one (No. 8). Prior to death, the latter patient developed ECG evidence of subendocardial anterior infarction. Thirteen patients (76% ) developed additional mechanical complications. Seven patients had cardiogenic shock with hypoperfusion and oliguria32; three of them did not respond to therapy and died (Nos. 3,8, and 14) but four survived follow-up (range 3 to 16 months). Nine patients developed an apical systolic murmur, diagnosed as mitral papillary muscle dysfunction in six (Nos. 1,4,5, 10,14, and 15) and papillary muscle rupture in three (Nos. 3,8, and 13). The latter three patients and one with severe papillary muscle dysfunction (No. 15) developed pulmonary congestion32 with marked cardiomegaly on days 6 to 7 and died. Cardiomegaly and pulmonary congestion developed abruptly in six other patients (Nos. 4, 6, 7, 11, 12, and 17) on days 5 to 7 but they survived follow-up (Table I). Deterioration in these patients was associ-

ated with further chest pain and hypotension. The data for patient No. 17 are summarized in Fig. 4. Five patients (Nos. 7, 9, 10, 13, and 14) developed pulmonary embolism with infarction proved by pulmonary scan and angiography. Three patients developed systemic embolism with stroke (Nos. 1, 7, and 8) proved by cerebral angiograms and scans.

Autopsy. Autopsy was performed on three of the four patients who died in the hospital (Nos. 3,8, and 13). Posterior papillary muscle rupture was confirmed in patients Nos. 3 and 8, but patient No. 13 had posterior papillary muscle infarction without rupture. In all three hearts, transmural infarction (with histologic confirmation) of the RV lateral wall, inferior RV wall, inferior ventricular septum, and inferior LV wall were found, together with occlusion of the right coronary (100% ), left circumflex (90% to 100% ), and left anterior descending (70% to 95% ) coronary arteries. The autopsied heart of patient No. 8 is shown in Fig. 5.

Other tests. Diagnostic coronary and LV angiography were performed in four late survivors (patients Nos. 5, 6, 10, and 17) and two patients who died (Nos. 8 and 13). Coronary arteriography revealed occlusions in the right coronary (100% ), left circumflex (50% to 100% ), and left anterior descending (50% to 90 % ) arteries. All six patients had akinesis of the inferoposterior LV wall. Radionuclide studies

Volume 107

Number 3

Chest

x-ray Major complications

Follow-up

Status (mo)

Clear PMD, VT, AF, SE Alive (16) Clear Shock, AF Alive (16) Clear PMR, shock, third-degree AVB Dead (0.25)

Clear PMD, VT Alive m3) Clear PMD, CA, third-degree AVB Alive (10) Clear Shock, AF, CA Alive (7)

Clear Shock, AF, PE, SE Alive (6) Clear PMR, shock, VT, SE, CA Dead (0.1)

Clear Second-degree AVB, PE Alive (6) Clear PMD, shock, PE, CA Alive (6) Clear VT Alive (23) Clear None Alive (161 Clear PMR, AF, PE Dead (1.3)

Clear VT, AF, shock, PMD, PE Dead (0.1) Clear PMD, third-degree AVB, VT Dead (0.75)

Clear First-degree AVB, VT Alive (14) Clear Shock, CA Alive (14)

were done in four patients (Nos. 2, 13, 15, and 17) prior to discharge from the hospital. Gated blood pool scans using in vivo labeling of red blood cells with stannous pyrophosphate followed by technetium-99m pertechnetate revealed dyskinesis in inferior and lateral walls of the right ventricle, and the inferior, inferoseptal, and lateral LV walls. Resting thallium-201 perfusion imaging in the same four patients revealed perfusion defects in inferior and inferolateral LV regions. Technetium-99m stannous pyrophosphate imaging in these patients revealed abnormal uptake (hot spots) in the inferior RV wall, the septum, and inferior LV wall.

Echocardiographic data. The 2DE features of RVMI from the 17 patients are summarized in Table II. All patients had akinesis or dyskinesis in the RV and LV, the involved segments being inferior RV, inferior interventricular septum, and inferior LV. There were variable extensions of AWM along the lateral walls of both the RV and LV (Figs. 4 and 6). The RV/LV end-diastolic internal diameter ratios in short-axis (mitral 0.67 + 0.05, chordal 0.63 + 0.05, and papillary 0.58 f 0.03), apical four-chamber (papillary muscle level 0.85 + 0.05), and longitudi- nal parasternal (mitral level 0.63 + 0.04) views were greater than 0.5, suggesting RV chamber dilatation. The LV end-diastolic internal diameters were greater than 60 mm in eight hearts in short-axis (mitral, chordal, papillary, and apical) and parasternal long- axis planes, with a mean value of 72 ? 3 (range 60 to 81) mm in the parasternal long-axis view, suggesting LV chamber dilatation. None of the patients had

2DE evaluation of RV infarction 511

Table II. The main 2DE findings in 17 patients with RV infarction

Observation

Right ventricle

Frequency

(4 70

Lateral segment akinesis or dyskinesis

Inferior (posterior) segment akinesis Anterior segment akinesis

Chamber enlargement Left ventricle

Inferoseptal segment akinesis Inferior (posterior) segment akinesis

Inferior (posterior) segment dyskinesis Inferolateral segment akinesis

Anterior segment akinesis

Anterolateral segment akinesis Anteroseptal segment akinesis Midseptal segment akinesis

Chamber enlargement Mural thrombus

Other Tricuspid regurgitation Abnormal ventricular septal motion

17117 100 17117 100

4/17 24 17/17 100

17117 100

17117 100

17117 100 6117 35

o/17 0 O/11 0 2117 13 6117 35

7/17 41

6117 35

4117 24 17/17 100

evidence of pericardial effusion on initial 2DE. Echocardiographic evidence of tricuspid regurgitation was found in four patients with positive contrast IVC studies and IVC diameters of 24 to 27 mm but no systolic pulsation.25 In the remaining patients, contrast studies were negative and IVC diameters ranged between 16 and 22 mm.

Echocardiographic densities suggestive of LV mural thrombi26-28 were found in the inferior LV akinetic region in six patients: two of them (Nos. 1 and 7) developed transient stroke and survived, but one patient died a day after the stroke (No. 8), and she was found to have a LV mural thrombus at autopsy. Echo densities (Fig. 7), similar in appear- ance to LV thrombi,26-28 were present on the akinetic RV lateral walls in seven patients, suggesting RV thrombi. Five patients with these RV echo densities developed pulmonary embolism (Nos. 7, 9, 10, 13, and 14) but although patient No. 14 died, autopsy was not done. In these patients, no extracardiac source of the pulmonary embolus was found clinically or on venography and radiolabeled fibrinogen studies. Patient No. 8 had a RV echo density prior to death but no clinically evident pulmonary embolism, and she was found to have a RV mural thrombus overlying the RV inferolateral wall infarct at autopsy. In that patient (No. 8), nearly the entire RV lateral wall was akinetic on 2DE.

The inital 2DE data on AWM in the 17 patients are summarized for survivors and nonsurvivors in



ANTERIOR

POSTERIOR m

Fig. 5. Cross-sectional slice of autopsied heart at chordal level in patient No. 8 showing transmural infarction (contoured in black) in inferolateral LV wall, inferior septum, and inferolateral RV wall. Endocardial extent of inferior infarction (40% of LV circumference; 68% of RV wall) was not significantly different from extent of AWM on initial 2DE (45% LV, 85% RV). Patient subsequently developed subendocardial anterolateral infarction (also contoured) and its extent agreed with extent of anterior LV AWM on 2DE 20 hours prior to death (39% vs 30%). Histology confirmed myocardial necrosis in contoured areas.

EXTENTS OF SEVERE ENDOCARDIAL ABNORMAL WALL

MOTION ON TWO-DIMENSIONAL ECHOCARDIOGRAMS AT THE CHORDAL LEVEL IN 16 PATIENTS

Fig. 6. Endocardial outlines of echocardiographic parasternal short-axis sections of heart at chordal level in 16 patients. Extents of abnormal endocardial wall motion (akinesis or dyskinesis) are shown as thick segments in RV and LV. All patients had abnormal motion in inferior RV, inferoseptal, and inferior LV segments with variable extensions into LV inferolateral and RV lateral walls.

Table III. For the whole group, the mean extent of AWM in the four serial LV short-axis sections were: mitral 29 % , chordal 38 % , papillary 38 % , and apical 35%. The topographic extent of AWM for the LV averaged 36% (range 19% to 48% ). Similarly, the

mean extent of AWM in the three serial RV sections, from base to apex, were 58%) 56%) and 59%) respectively. The topographic extent of RV AWM averaged 58% (range 34 to 77) and was greater (p < 0.05) than the extent of LV AWM. The ratio of RV to LV AWM averaged 1.65 (range 1.11 to 2.75), significantly greater than unity (p < 0.001). The estimated diastolic volumes averaged 83 cm3 for the RV and 104 cm3 for the LV, the ratio being 0.76 (Table III). The ratio of RV to LV systolic volumes averaged 1.00 & 0.12. The EFs were significantly less for the RV than the LV (27 vs 37%) p < 0.05). The RV/LV AWM and EDV ratios and EFs were not significantly different for survivors and nonsurvivors (Table III).

The correlation between peak serum CPK levels and the topographic extent of LV AWM (r = 0.79, p < 0.001) or total ventricular (RV + LV) AWM (r = 0.75, p < 0.001) are shown in Fig. 8. The linear regressions between peak CPK levels and extent of LV AWM or total ventricular (RV + LV) AWM for the serial short-axis sections (Fig. 9) revealed satisfactory correlation coefficients for chordal (r = 0.71 and 0.72, respectively) and papillary (r = 0.84 and 0.83, respectively) levels, but the correlations for mitral (r = 0.52 and 0.62, respectively) and apical (r = 0.45) levels were less satisfactory. There was no significant correlation between peak CPK and RV AWM (r = 0.32). Inverse but nonsignificant correlations were found between: (1) LV AWM and LV EF (r = -0.44); (2) RV AWM and RV EF (r = -0.35);

Volume 107


Fig. 7. Actual stop-frame Polaroid photographs showing mural echo densities (arrows) overlying akinetic regions of RV and LV in patients Nos. 8 (A) and 17 (B) at mitral and chordal levels, respectively. Patient No. 8 developed stroke and had both RV and LV thrombi at autopsy.

-

I -

, -

I_ 0

6000

Y=147.69x- 3762.94 l

n= 17 .r= 0.75 .

SEE= 964.74

PO.00 1

.

i

l .

.

. : f

4000

2000

20 40 6

TOTAL AWM LV AWM

Y=151.58x- 329408 ’

nr 17 .I= 0.79 .

SEE I 905.98

P<0.001

ABNORMAL WALL MOTION AS PERCENT AREA BY 2D ECHO

Fig. 8. Peak serum CPK level correlated with topographic extent of AWM on 2DE for both ventricles (left) or LV alone (right). Two highest CPK values (patients Nos. 8 and 10) were measured following successful resuscitation after cardiac arrest (Table I).

(3) peak serum CPK and LV EF (r = -0.34); and (4) peak serum CPK and RV EF (r = -0.28).

Serial studies. The 2DE studies done at 10 days and 6 months in survivors revealed persistent regional LV and RV AWM at the previous locations on 2-day studies. The extents of LV and RV AWM data are summarized in Table IV. There was no significant difference among the serial 2DE measurements. The 2DE densities in the LV and RV, suggestive of thrombi, were present on studies at 2 days and 10 days, but these were considerably smaller in those surviving 6 months. In the six survivors and four nonsurvivors who developed car-

diomegaly with pulmonary congestion abruptly, 2DE revealed systolic thinning in the inferior LV and inferior ventricular septum together with regional LV dilatation,33 but there was no significant increase in LV or RV AWM.

Validations. The locations of the 2DE AWM in the LV and/or RV were in agreement with those found by another method in eight patients: autopsy in three (Nos. 3, 8, and 13), LV angiography in six (Nos. 5,6,8,10,13, and 17), and radionuclide (gated blood pool scan, thallium-201 imaging, and technetium-99m pyrophosphate imaging) studies in four (Nos. 2, 13, 15 and 17).

514 Jugdutt et al. March. 1984


Table III. 2DE data in the 17 patients .- -

LVAWM RVAWM AWM (as 5;: circumference) (as % arc) Surface area (cm3 (as “; surface area)

Patient - - No. 1 2 3 4 1 2 3 LV LVAWM RV RVAWM LV RV RVILV

Survivors (n = 12) 1 25 41 49 37 64 58 71 76 29 42 26 38 63 1.66

2 16 27 35 26 39 45 39 67 18 41 17 27 41 1.52

4 25 33 37 25 35 46 53 58 18 34 15 31 43 1.39

5 25 36 32 32 48 53 56 97 30 43 22 39 52 1.33

6 31 36 33 37 61 63 53 99 34 82 50 34 60 1.76

7 27 27 28 29 79 82 60 164 45 83 64 28 17 2.75

9 27 35 36 43 72 81 77 115 37 84 64 34 77 2.26

10 35 57 56 33 64 66 68 126 61 99 65 48 65 1.35

11 12 47 39 50 69 49 68 76 27 64 39 36 60 1.67

12 16 26 18 16 39 28 38 68 13 35 12 19 34 1.79

16 36 42 43 40 60 58 63 63 25 58 35 40 60 1.50

I7 49 37 51 54 65 :x? 51 83 38 50 2 5 46 51 1.11

Nonsuruiuors In = 5) 3 33 41 36 42 53 .i.‘i 60 l”‘2 u 46 67 36 38 54 1.42

8 33 45 53 47 99 85 86 115 52 83 64 45 77 1.71

13 40 37 34 31 44 51 53 83 30 59 30 36 51 1.42 14 28 35 31 29 61 67 66 148 47 79 51 32 65 2.03

15 35 52 44 26 39 41 47 109 44 47 27 41 57 1.39

Total 29 38 38 3.5 58 56 59 98 35 62 38 :36 58 1.65

(mean +- SE) i2 t2 &2 ,2 i4 t4 +3 i7 +3 *5 k.5 +2 +3 k 0.10 ____ _____---

Abbreviations: AWM = abnormal wall motion; HSA = body surface area: LV = left ventricle; RV = right ventricle; 1.2J.4 refer to short-axis views at mitral, chordal, papillary muscle. and apical levels. respectively; EF = ejection fraction.

Table IV. Serial 2DE data in RV infarction in survivors (n = 12)

LV A WM C”;.) R V A WM C”;, ) __-

Patient No. 2 da73 10 days 6 mo 2 days 10 davs 6 mo

1 38 29 29 63 39 35

2 27 15 23 41 37 3 1

4 31 35 26 43 40 25

:, 39 31 27 52 44 59

6 34 37 30 60 59 65

I 28 42 30 17 67 25

9 34 40 32 77 63 60

10 48 53 26 65 67 56

11 36 35 27 60 50 45

12 19 15 12 34 25 15

16 40 27 23 60 39 18

17 46 50 41 51 47 47

Mean + SE 35 + 2 34 + 3 27 + 2 51 zk 4* 48 +_ 4* 39 + 5t

Abbreviations: AWM = abnormal wall motion (akinesis + dyskinesis); LV = left ventricle; RV = right ventricle.

*p < 0.001; tp < 0.02; significance compared to LV AWM at corresponding time interval.

DISCUSSION inferior LV wall, and inferior ventricular seDtum, There were three major findings in our study. with variable degrees of involvement of thk RG

First, our 2DE data indicate that the clinical syn- lateral wall, midventricular septum, and inferolater- drome of RVMI’ is associated with extensive regional LV wall. Second, the RV regional dysfunction was al biventricular dysfunction. Thus, all 17 patients associated with RV enlargement in all, confirming with initial clinical and hemodynamic features of 2DE observations made by D’Arcy and Nanda16 and dominant RVMI had AWM in the inferior RV wall, conclusions from autopsied hearts.12 However, eight

Volume 107

Number 3

Estimated volumes (cm’) Estimated

Diastole Systole EF f%)

LV RV RV/LV LV RV LV RV

68 42 0.62 41 24 40 43

58 44 0.76 34 35 42 20

46 29 0.63 28 19 40 35

96 40 0.42 59 25 39 38

93 127 0.29 71 93 24 27

236 146 0.62 163 124 31 15

117 140 1.20 53 101 55 28

136 128 0.94 95 93 30 27

62 90 1.45 29 64 54 29

57 39 0.68 27 28 53 27

62 65 1.05 42 48 33 26

80 42 0.53 58 27 27 35

145 98 0.68 96 82 34 16

129 124 0.96 80 114 38 8

77 80 1.04 59 54 24 32

202 123 0.61 131 90 35 27

106 55 0.52 76 40 28 28

104 83 0.76 67 62 37 27

*13 f10 r 0.07 29 k9 k2 +2

of our patients also had evidence of LV enlargement. Third, measurement of the topographic extent of AWM revealed that RV AWM exceeded LV AWM, and the ratio of RV to LV AWM averaged 1.65 and exceeded unity in all patients, confirming predominant RV involvement.

Correlation with other studies. We found close agreement between the site of AWM by 2DE and the site of abnormality assessed by another method in eight of our patients (autopsy in three, radionuclides in four, and LV angiography in six). In addition, the regional distribution of AWM in all 17 patients is in agreement with the distribution of infarction reported in autopsy studies in RVMI.5r l2 Thus, in 33 autopsied hearts with RVMI, Isner and Roberts12 found infarction (greater than 50% transmural extent) distributed in the posterior LV wall and ventricular septum in all (100% ), limited to the posterior RV free (lateral) wall in 27 (82%), and extending to the anterolateral RV free wall in six (18%). In our patients, values for the prevalence of AWM in corresponding regions were similar (100%) 75 % , and 25 % , respectively).

In order to study the correlation between our measure of AWM and peak CPK, we expressed AWM, measured along the LV circumference and RV wall in short-axis sections, as a percentage of the surface area of the ventricles. Because CPK is

2DE evaluation of RV infarction 515

released from areas of myocardial infarction in both ventricles, we combined the extents of AWM in the RV and LV to estimate biventricular AWM using a constant ratio (0.24), derived from autopsy data, to correct for the discrepancy between RV and LV mass. We found a significant correlation between peak CPK and the topographic extent of LV AWM (r = 0.79). Visser et a1.34 also reported a close correlation (r = 0.87) between the LV asynergic area and peak CPK-MB in a mixed group of 60 patients with inferior and anterior infarctions. However, the?* calculated LV asynergy as a percentage of the total number of involved segments in five short-axis sections, dividing each serial section into an equal number of segments (10, 8, 8, 6, and 4, respectively, from base to apex) dependent on the LV internal diameter. Thus, their approach34 differs from ours and arbitrarily assumes that each short-axis section makes constant contributions of 28, 22, 22, 17, and 11% , respectively, to LV mass.

No attempts have been made previously to measure RV AWM. However, the correlation between peak CPK and (RV + LV) AWM was not better than that between peak CPK and LV AWM alone (T = 0.75 vs 0.79). This lack of improvement in r value might be partly related to (1) our methodolog- ic assumptions, (2) possible underestimation of the extent of RV AWM because the aortic short-axis view was not used, which visualizes the RV infun- dibular region and part of the RV lateral wall, (3) possible differences in the kinetics of CPK release for RV and LV infarcts, (4) our use of a constant to correct for the difference between RV and LV mass in calculating the topographic extent of RV + LV AWM, and (5) the possibility that the relation between AWM and chamber dynamics might differ in the two ventricles. Nevertheless, we found significant correlations between peak CPK and LV AWM in individual sections at the mitral, chordal, and papillary levels (r = 0.52, 0.71, and 0.84, respectively) as well as corresponding (RV + LV) AWM at those levels (r = 0.78, 0.75, and 0.65, respectively). These data suggest that chordal and papillary sections might be useful in serial 2DE studies of RV and LV asynergy in RVMI. Serial studies of LV asynergy with the use of papillary sections have been reported by Eaton et a1.33

Other findings. Death and abrupt clinical deterioration in our patients were related mainly to mechanical complications. Portable 2DE revealed the cause of the mechanical complications in 13 patients and five died as a result. However, the extent of AWM between nonsurvivors and survivors was not significantly different in the RV (38% vs



. r-0.52 . rd.62

n317 nr17

A w 05 / . PC001

d 0 25 50 75 100 0 25 50 75 100

iTi LV CHORDAL A 6000-

RV+ LV . .

ii . . r.0.7 1 rs0.72

25 50 75 100

PAPILLARY RV+LV .

.

J

rd.83

nr17

. . D<O.OO 1

0 25 50 75 25 50 75

LV APICAL

r.0.45

0 25 50 75 100

ABNORMAL WALL MOTION BY 2D ECHO AS PERCENT AREA

Fig. 9. Peak serum CPK level correlated with 2DE estimates of AWM in individual short-axis sections, for LV on the left and for both ventricles (total) on the right.

35%) or LV (61% vs 57 % ). Serial studies in six survivors and four nonsurvivors, who developed abrupt cardiomegaly with pulmonary congestion on the sixth day, revealed regional LV dilatation without significant increase in the extent of AWM. Similar findings were observed by Eaton et al.33 in patients after acute myocardial infarction. The development of pulmonary congestion in our 10 patients emphasizes the importance of coexisting LV dysfunction in RVMI. In addition, serial 2DE studies showed persistent RV and LV AWM in survivors followed for an average period of 13.5

months, corroborating findings of Marmor et al.‘” with the use of radionuclide methods.

Portable 2DE also revealed unsuspected mural echo densities suggestive of thrombi in both ventricles. Six patients (35%) had LV thrombi and three of them developed cerebral embolism and stroke. Seven patients (41%) had RV thrombi and four of them developed pulmonary embolism but had no detectable extracardiac source for the embolus. These thrombi were also present on serial 2DE evaluations, and postmortem confirmation of both RV and LV thrombi was obtained in one patient.

Volume 107


Although the 2D diagnosis of LV thrombi has been validated previously,26s 27 this has not been done for RV thrombi. In 1959, Wade’s5 postmortem data suggested that RV thrombi and pulmonary embolism might be common in RVMI. Wade5 reported incidence values, per 100 cases of recent RVMI, to be as follows: 125 for right-sided mural thrombi (right atrium and RV), 27 for left-sided mural thrombi (left atrium and LV), 73 for pulmonary embolism (extracardiac source found in three cases), and 23 for systemic embolism. In contrast, in 1978, Isner and RobertsI reported a lower frequency of RV thrombus (9 % ) in their 33 autopsied hearts. The explanation for the discrepancy between these two studies might relate to such factors as the time of death after infarction and the use of anticoagulants, but these data were not given.5* l2 In our patients, initial 2DE studies were done about 31 hours after admission or about 38 hours after the onset of pain and before anticoagulant therapy was instituted.

Triple-vessel coronary artery disease with 100% occlusion of the right coronary artery was found in seven of our patients (at autopsy alone in one, autopsy and coronary arteriography in two, and coronary arteriography alone in four). Triple-vessel disease in RVMI has also been reported in other autopsy53 I2 and angiographic studies.17 Thus, in autopsied hearts with RVMI, Wade5 found that the majority had occlusion of a dominant right coronary artery associated with disease in the other two coronary vessels, while Isner and Roberts12 found .greater than 75 % occlusion of the right (93%), left anterior descending (74%), and left circumflex (74 % ) coronary arteries.

Limitations in quantifying asynergy by 2DE. The echocardiographic studies in our acutely ill patients with infarction were technically difficult. However, systematic and complete 2DE examinations were performed within 10 to 20 minutes. We obtained adequate 2DE images for analysis of RV and LV wall motion and thickening in 85 % of the original 20 patients. Visualization of RV and LV walls in parasternal short-axis views was most satisfactory at the papillary and chordal levels. Because of difficulties in detecting isolated hypokinesis by relying on endocardial motion aloneiS we restricted measurements of AWM to akinesis and dyskinesis. Since still frames degraded images (Fig. 7) and caused loss of integrative data,15* 35 we viewed images in motion and made a visual assessment of systolic thickening.17 In a correlative study of LV endocardial motion and systolic thickening by 2DE and pathologic infarction in dog hearts, Lieberman et a13’j showed that (1) systolic thickening provides better separation of

normal from infarcted myocardium than endocardi- urn motion alone, (2) systolic thickening decreased abruptly in segments with more than 20% transmural extent of infarction, (3) systolic thinning did not increase significantly as the transmural extent of infarction increased from 21% to 100%) and (4) evidence of any systolic thickening indicates less than 20% transmural extent of infarction. In this study, we defined akinesis as no endocardial motion and no systolic thickening in an attempt to restrict AWM to infarcted regions. We might still have overestimated pathologic infarct size, since nonin- farcted myocardium adjacent to infarcted myocardi- urn has been shown to contract abnormally.37 Thus, our measure of AWM might represent an index of AWM associated with infarction rather than a measure of infarcted myocardium.15x l7

Limitation of ventricular volume calculations. We estimated LV and RV volumes arbitrarily in an attempt to compare RV and LV diastolic and systolic volumes and derive an index of global function, that is, ejection fractions. These volume estimates need to be validated in future studies. Although 2DE has been used to estimate LV vo1ume21~31 and RV volume,3s it has not been used to estimate volumes in patients with RVMI. Nevertheless, the range of values for RV diastolic volumes by 2DE in our study is similar to that (57 to 146 ml) reported by Watanabe et al. 38 for normal subjects and patients with RV volume overload. The derived EFs in our patients were less for the RV than the LV, indicating dominant RV dysfunction and corroborating findings on radionuclide angiocardiography

‘by Marmor et all4 Conclusions. 2DE can be used to confirm the

diagnosis of RVMI in patients with IMI. It can detect akinesis and/or dyskinesis in inferior regions of both ventricles as well as RV dilatation. Domi- nant RVMI was characterized by a greater extent of RV vs LV regional dysfunction, with a ratio of RV to LV AWM greater than unity.

We thank Cheryl Trudell for technical assistance, Robert Cahn for computer programming and statistics, and Dr. P. Markesteyn

for assistance with autopsy studies. We also thank Joanne Dutchak, Christine Wortman, and Catherine Jugdutt for secre- tarial assistance.

REFERENCES

1. Cohn JN, Guiha NH, Broder MI, Limas CJ: Right ventricular infarction. Am J Cardiol 38:209, 1974.

2. Lloyd Ek, Gersh BJ, Kennelly BM: Hemodynamic spectrum of “dominant” right ventricular infarction in 19 patients. Am J Cardiol 48:1016, 1981.

3. Rackley CE, Russell RO, Mantle JA, Rogers WJ, Papapietro SE, Schwartz KM: Right ventricular infarction and function. AM HEART J 101:215, 1981.



7.

8.

9.

10.

11.

1”.

13.

14.

1.5.

16.

17.

18.

19.

20.

21.

Zaus EA, Kearn WM: Massive infarction of the right ventricle and atrium: Report of a case. Circulation 6:593, 1952. Wade WG: The pathogenesis of infarction of the right ventricle. Br Heart J 21:545, 1959. Chou T, Van Der Bel-Kahn J, Allen J, Brockmeier L, Fowler NO: Electrocardiographic diagnosis of right ventricular infarction. Am J Mkd ~0:1175,~981. Candell-Riera J. Fieueras J. Valle V. Alvarez A. Gutierrez L. Cortadellas J, C&a J, Salas A, Rms J: Right ventricular infarction: Relationships between ST segment elevation in V,R and hemodynamic, scintigraphic, and echocardiographic findings in patients with acute inferior myocardial infarction. AM HEART J 101:281, 1981. Rotman M, Raliff NB, Hawley J: Right ventricular infarction: A hemodynamic diagnosis. Br Heart J 36:941, 1974. Rigo P, Murray M, Taylor DR, Weisfeldt ML, Kelly DT, Strauss HW, Pitt B: Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction. Circulation 52:268, 1975. Wackers FJ, Lie KI, Sokole EB, Van Der Schoot JB, Durrer D: Prevalence of right ventricular involvement in inferior wall infarction assessed with myocardial imaging with thallium- 201 and technetium-99m pyrophosphate. Am J Cardiol 42:358, 1978. Sharpe DN, Botvinick EH, Shames DM, Schiller NB, Massie BM, Chatterjee K, Parmley WW: The non-invasive diagnosis of right ventricular infarction. Circulation 57:483, 1978. Isner JM, Roberts WC: Right ventricular infarction compli- cating left ventricular infarction secondary to coronary heart disease: Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction. Am J Cardiol 42:885, 1978. Cintron GB. Hernandez E. Linares E. Aranda JM: Bedside recognition, incidence and clinical course of right ventricular infarction. Am J Cardiol 47:224, 1981. Marmor A, Geltman EM, Biello DR, Sobel BE, Siegel BA, Roberts R: Functional response of the right ventricle to myocardial infarction: Dependence on the site of left ventricular infarction. Circulation 64:1005, 1981. Heger dJ, Weyman AE, Wann LS, Dillon JC, Feigenbaum H: Cross-sectional echocardiography in acute myocardial infarction: Detection and localization of regional left ventricular asynergy. Circulation 60:531, 1979. Parisi AF, Moynihan PF, Folland ED, Strauss WE, Sharma GVRK, Sasahara AA: Echocardiography in acute and remote mvocardial infarction. Am J Cardiol 46:1205, 1980. Gibson RS, Bishop HL, Stamm RB, Crampton RS, Beller GA, Martin RP: Value of early two dimensional echocardiography in patients with acute myocardial infarction. Am J Cardiol49:1110, 1982. D’Arcy B, Nanda NC: Two-dimensional echocardiographic features of right ventricular infarction. Circulation 67:167, 1982. Tajik AL. Seward JB, Hagler DJ, Mair DD, Lie JT: Two- dimensional real-time ultrasonic imaging of the heart and great vessels: Technique, image orientation, structure identification, and validation. Mayo Clin Proc 53:271, 1978. Criteria Committee of the New York Heart Association: Nomenclature and criteria for diagnosis of diseases of the heart and great vessels, ed 7, Boston, 1978, Little, Brown & Company, pp 95, 286. Gueret P, Meerbaum S, Wyatt HL, Uchiyama T, Lang TW, Corday E: Two-dimensional echocardiographic quantitation of left ventricular volumes and ejection fraction. Importance of accounting for dyssynergy in short-axis reconstruction models. Circulation 62:1308, 1980.

22.

23.

24.

25.

26.

“7.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

Kisslo JA, Robertson D, Gilbert BW, von Ramm 0, Behar VS: A comparison of real-time, two-dimensional echocardiography and cineangiography in detecting left ventricular asynergy. Circulation 56134, 1977. Mintz GS, Victor MF, Kotler MN, Parry WR, Segal BL: Two-dimensional echocardiographic identification of surgi- cally correctable complications of acute myocardial infarction. Circulation 64:91, 1981. Chen CC, Morganroth J, Mardelli TJ, Naito M: Tricuspid regurgitation in tricuspid valve prolapse demonstrated with contrast cross-sectional echocardiography. Am J Cardiol 46:983, 1980. Meltzer RS, Hoogenhuyze DV, Serruys PW, Haalebos MMP, Hugenholtz PG, Roelandt J: Diagnosis of tricuspid regurgitation by contrast echocardiography. Circulation 63:1093, 1981. Asinger RW, Mike11 FL, Sharma B, Hodges M: Observations on detecting left ventricular thrombus with two dimensional echocardiography: Emphasis on avoidance of false positive diagnosis. Am J Cardiol 47:145, 1981. Reeder GS, Tajik AJ, Seward JB: Left ventricular mural thrombus. Two-dimensional echocardiographic diagnosis. Mayo Clin Proc 56:82, 1981. Mike11 FL, Asinger RW, Elsperger KJ, Anderson WR, Hodg- es M: Tissue acoustic properties of fresh left ventricular thrombi and visualization by two-dimensional echocardiography: Experimental observations. Circulation 49:1157, 1982. Herman MV, Gorlin R: Implications of left ventricular asynergy. Am J Cardiol 23:538, 1969. Edwards WD, Tajik AJ, Seward JB: Standardized nomenclature and anatomic basis for regional tomographic analysis of the heart. Mayo Clin Proc 56:479, 1981. Folland ED, Parisi AF, Moynihan PF, Jones DR, Feldman CL, Tow DE: Assessment of left ventricular ejection fraction and volumes by real-time, two-dimensional echocardiography. A comparison of cineangiographic and radionuclide techniques. Circulation 60:760, 1979. Killip T, Kimball JT: Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol 20:457, 1967. Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Weisfeldt ML: Regional cardiac dilatation after acute myocardial infarction. Recognition by two-dimensional echocardiography. N Engl J Med 300:57. 1979. Visser CA. Lie KI. Kan G. Meltzer R. Durrer D: Detection and quantification of acute, isolated myocardial infarction by two-dimensional echocardiography. Am J Cardiol 47:1020, 1981. Falsetti HL, Marcus ML, Kerber RE, Skorton DJ: Editorial: Quantification of myocardial ischemia and infarction by left ventricular imaging. Circulation 63:747, 1981. Lieberman AN, Weiss JL, Jugdutt BI, Becker LC, Bulkley BH. Garrison JG. Hutchins GM. Kallman CA. Weisfeldt ML: Two dimensional echocardiography and infarct size: Rela- tionship of regional wall motion and thickening to the extent of myocardial infarction in the dog. Circulation 63:739, 1981. Kerber RE, Marcus ML, Ehrhardt J, Wilson R, Abboud FM: Correlation between echocardiographically demonstrated segmental dyskinesis and regional myocardial perfusion. Cir- culation 52:1097, 1975.

38. Watanabe T, Katsume H, Matsukubo H, Furukawa K, Ijichi H: Estimation of right ventricular volume with two dimensional echocardiography. Am J Cardiol 49:1946, 1982.

Date post:	30-Nov-2023
Category:	Documents
Upload:	independent
View:	0 times
Download:	0 times

Right ventricular infarction: Two-dimensional echocardiographic evaluation

Documents