Echocardiographic Evaluation of left Ventricular Function During Coronary Artery Angioplasty MOHSIN ALAM, MD, FAREED KHAJA, MD, JAMES BRYMER, MD, MARIO MARZELLI, MD, and SIDNEY GOLDSTEIN, MD
Balloon occlusion of a stenotic coronary artery during percutaneous coronary artery angioplasty provides a unique opportunity to study the effect of acute myocardial &hernia on left ventricular (LV) function. Simultaneous M-mode and 2-dimensional (2-D) echocardiograms and a 6-lead electrocardiogram were recorded during 20 eplsodes of coronary artery occlusion and release in 12 patients. No patient had prevjous myocardial infarction and all had normal LV function by angiography. All patients had isolated single coronary artery disease, with left anterior descending stenosis in 6 and right coronary stenosis in 4. In 18 of 20 episodes (go%), M-mode echocardkgraphy during balloon occlusion revealed a sfgnificant (p
artery occlusion. Two-dimensknal echocardlography revealed varyIn degrees of hypokinesla, akineda and dysklnesla during balloon occluskn in 18 lnstances. The echocardiographic changes were observed within 15 to 20 seconds of balloon occluslon and resolved 10 to 20 seconds after balloon deflatkn. All patients who had echocardkgraphk changes during balloon occlusion also had concomitant electrocardiographic (ECG) ST-segment elevation, whereas 2 patients wlth normal LV function had no ECG changes. Both of these patlents had profuse collateral blood supply to the stenotk coronary artery. The echocardiographic and ECG abnormalities Increased proportionately to the length of balloon occlusion. This study confirms previous animal and recent human studies of transient LV dysfunction during coronary occlusion. Echocardlography during balloon angloplasty provides a unique model to study the effects of myocardial ischemia in humans. (Am J Cardiol 1986; 57: 20-25)
1
eft ventricular (LV] function during acutely induced ischemia has been extensively studied in animal models.1-8 Reports indicate that there is a decrease in LV systolic and diastolic wall thickness, wall motion and endocardial velocities of the ischemic segment contractions. In humans, such studies are confined to patients during acute myocardial infarction. In this setting, baseline measurements before the onset of symptoms of infarction are not available. The only evidence of reproducible acute ischemia on LV function in man were those performed during stress-induced episodes of angina pectorisgJO or during spontaneous or ergonovine-induced coronary artery spasm.ll Hauser et all2 recently demonstrated transient LV dysfunction by %dimensional (2-D) echocardiography ,during coronary occlusion at time of coronary angio-
plasty. M-mode echocardiography, a more sensitive measurement of LV thickness and endocardial velocities, was not performed. Balloon occlusion of stenotic coronary arteries during percutaneous transluminal coronary angioplasty (PTCA) provides a unique opportunity to study the effects of prospectively induced regional ischemia on LV function in humans.
Methods M-mode and 2-D echocardiographic studies were performed in 12 patients immediately before, during and after balloon occlusion at the time of PTCA. All patients had isolated l-vessel coronary artery disease (>75% decrease in luminal diameter), 8 with left anterior descending and 4 with right coronary artery narrowing. Nine of the 12 patients showed no collaterals and 3 had well developed collateral blood supply to the stenotic coronary artery. The mean distal coronary artery pressure measured from dilatation catheter tip was 47 mm Hg before balloon, occlusion, and it decreased to a mean value of 27 mm Hg during balloon inflation. The distal pressures decreased in 2 of 3 patients with good collaterals and remained unchanged in 1 patient during balloon inflation.
From the Divisions of Cardiovascular Medicine, Henry Ford Hospital, Detroit, Michigan, and the University of Pisa, Pisa, Italy. Manuscript received April 8, 1985; revised manuscript received June 10.1985, accepted June 12,198s. Address for reprints: Mohsin Alam, MD, Echocardiography Laboratory, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202. 20
January
In 1 patient during PTCA of a proximal left anterior descending coronary artery, transient obstruction of the circumflex coronary artery occurred. No patient had previous myocardial infarction and LV function and wall motion at rest were normal by angiography in these patients. M-mode and 2-D echocardiographic studies were performed from the left parasternal approach. The Mline cursor was placed at the level of chordae tendineae of the mitral valve and simultaneous 2-D (longaxis) and M-mode tracings of LV wall motion were recorded on commercial videotape. Views of the left ventricle were obtained before coronary occlusion. and continuously through 30 to 75 seconds of balloon inflation and for 30 to 100 seconds after deflation. Twenty good-quality views of left ventricle were obtained during 29 balloon inflations for coronary dila tation in these 12 patients. The time of onset of LV impairment was determined from the continuously recorded videotape during and after balloon occlusion. The following variables of LV function were measured on M-mode tracings. Measurements were performed according to the criteria established by the American Society of Echocardiography13 and methods described previously? (1) LV wall thickness during systole and diastole; (21 percent changes in systolic wall thickness, calculated as [(systolic wall thickness diastolic wall thickness)/diastolic wall thickness] X 100; (3) systolic and diastolic excursion of the septum and posterior wall; (4) systolic and diastolic endocardial velocities of the septum and posterior wall: (5) LV internal diameter during systole and diastole; and (6) percent fractional shortening of the left ventricle, calculated as: [(LV diastolic dimension - LV systolic dimension)/LV diastolic dimension] X 100. In 6 patients LV function was determined at least twice. Each inflation was performed within 30 to 120 seconds of the preceding one. M-mode measurements of LV mechanics were performed immediately before balloon occlusion, and at 5 to 20, 30 to 45 and, when
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available, 60 to 75 seconds of balloon occlusion and deflation. Two-dimensional echocardiographic analysis: Two-dimensional long-axis views obtained before, during and immediately after balloon occlusion were analyzed in real-time, slow-motion and stop-frame format for the presence of normal, hypokinetic, akinetic or dyskinetic wall motion. The wall motion abnormalities were analyzed in the area of the septum, apex and posteroinferior wall. The observers analyzing the echocardiographic images were not blinded to the location of coronary disease or the time of inflation or deflation of balloon catheter. Electrocardiographic analysis: A 6-lead electrocardiogram using leads 1, 2, aVF, VI, V3 and VS was recorded during the echocardiographic studies. The presence or absence of ST-segment elevation during balloon occlusion and release and its relation to the echocardiographic findings were determined. LAD
ANGIOPLASTY
percent 90
r
80 70 Change
60
Systolic
50
Thickness
40 30 20
.
p 4.00
1
10 0’ Before Balloon
During Occlusion
FIGURE 1. Percent change in M-mode derived systolic left ventricular thickness before and during balloon occlusion of a coronary artery. Mean systolic thickness decreases significantly (p
FIGURE 2. M-mode echocardiograms of the left ventricle (LV) before, during and after balloon occlusion of a left anterior descending coronary artery (LAD). Septal (S) systolic and diastolic wall thickness, endocardial velocities and wall motion decrease markedly during occlusion phase. Lefl ventricular systolic chamber dimensions increase during balloon occlusion. These changes revert to baseline after balloon deflation. PW = posterfor wall; RV = right ventricle.
1
I
LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD + LC Right Right Right Right Right
Coronary Artery Dccluded
25 23 17 20 19 18 21 20 20 21 21 21 21 22 21 20 18 19 16 19 20 2
<0.001
12 12 10 11 11 12 20 15 16 13 12 16 12 15 15 15 11 11 IO 19 13 3
12 12 10 11 11 10 10 12 13 13 13 16 15 15 15 13 11 12 11 11 12 2
Pre
10 10 9 10 11 12 IO 10 14 10 12 10 IO 9 10 10 11 10 1
10 9 9
Before
20 33 11 10 10 33 100 36. 33 30 20 14 20 25 50 50 22 10 0 73 30 23
70 62 73 60 110 67 54 62 62 31 40 47 40 54 64 58 45 73 66 21
108 92
During
% Change Systolic Thickness Pre
Function
During
(mm)’
Diastolic Thickness
Lefl Ventricular
During
Systolic Thickness (mm)’
Pre
Echocardiographic
* Ventricular septum for LAD, posteroinferkx wall for rfgftt coronary A = akinesia; D = dyskinesia; H = hypokinesia; LAD = left anterior
11 12 Mean i SD p value
9 IO
8
7
4 5 6
2 3
Pt
TABLE
6 5 4 4 4 4 10 6 7 2 2 4 3 4 3 4 7 7 5 18 6 4
During
Coronary
60 58 44 40 42 54 46 46 46 42 40 61 55 52 55 58 43 45 66 72 51 9
Pre
14 16 16 18 19 20 45 32 34 22 16 23 30 23 20 40 30 31 49 74 29 15
During
Systolic Velocity (mm/s)’
Artery
artery and LC. descending; LC = left circumflex:
14 15 IO 8 9 10 10 10 10 9 10 12 10 10 10 13 11 12 10 18 11 2
Pre
Systolic Excursion (mm)’
and During
During
LV = left ventricular;
77 32 75 31 20 62 61 32 64 33 62 30 66 67. 53 35 51 35 70 32 60 24 51 40 46 34 56 38 52 41 84 38 50 31 51 34 49 36 110 112 63 39 15 19
Pre
Diastolic Velocity (mm/s)’
Angioplasty
<0.02
57 56 55 50 48 51 46 45 41 47 43 54 61 53 50 55 44 43 50 46 50 6
During
N = normal;
52 55 56 47 49 49 47 37 40 43 42 57 53 50 54 54 43 42 52 47 49 6
Pre
(mm)
Diastolic Dimension
36 40 50 35 34 38 33 30 29 36 34 40 50 38 51 41 33 32 36 27 30 7
53 60 19 36 39 34 36 30 41 49 47 40 32 40 33 33 35 28 42 42 39 9
Pre
N N N N N N N N N N N N N N N N N N N N
Pre
A A H A A H N H H D D D D D D A A A A N
During
2-D Wall Motion
2-D = Zdimenslonal.
33 26 9 30 29 25 36 33 29 23 21 26 18 28 10 25 25 25 28 42 26 a
During
% LV Fractional Shortening
deviation;
During
SD = standard
24 22 45 30 39 32 29 22 23 22 22 34 36 30 36 36 28 30 30 27 29 6
Pre
Systolic Dimension (mm)
January
Results M-mode and 2-D echocardiographic abnormalities of LV wall motion, wall thickness and endocardial velocities were observed in 16 of 20 instances (90%) of balloon occlusion. These changes were observed in the area of the ventricular septum for left anterior descending and posteroinferior wall for right coronary artery. The maximal changes observed in the area supplied by the instrumented coronary arteries are summarized in Table I. Wall thickness: Mean systolic, diastolic and percent change in systolic wall thickness of the left ventricle decreased significantly [Fig. 1) in the region of the ventricular septum during left anterior descending occlusion [Fig. 2) and posteroinferior wall during right coronary artery occlusion. No changes were observed in the contralateral segments of the left ventricle. The only patient who had inadvertent occlusion of both the left anterior descending and circumflex coronary arteries showed systolic and diastolic thinning in both the septum and posterior wall (Fig. 3). The decrease in wall thickness was observed at 15 to 20 seconds of the balloon inflation and was of greater magnitude after 60
LAD
- CX
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to 75 seconds of balloon occlusion than at 30 to 45 seconds (Fig. 4). Wall thickness always returned to preocclusion levels within 10 to 20 seconds of balloon deflation without an overshoot or rebound increase iFig. 21. Wall motion: During balloon occlusion systolic excursion decreased in the area of the ventricular septum for left anterior descending (Fig. 2) and posterior wall in right coronary occlusions (Fig. 5). Wall motion of the opposite or contralateral segment of the left ventricle, however, was not significantly altered. Owing to marked systolic wall thinning and increase in LV systolic dimension, mean fractional shortening of the left ventricle was also significantly (p
24 22
;
*-u
. ....... ...
...A
10 8
-
‘.., .‘...._ ‘... x,
6 4
00
- - -0’ S-15 IBefore
0
..* ,....’
‘L.... ...._...* ._......a-” o-
‘0
.’
\
. ‘0
30-45
60-75
5
During
Balloon
FIGURE 3. M-mode echocardiograms of the left ventricle (LV) before and during balloon occlusion of a left anterior descending coronary artery (LAD), during which occlusion of the circumflex coronary artery (CX) also occurred. Wall thickness, wall motion and endocardial velocities involving both septum (S) and posterior wall (PW) decrease. Left ventricular systolic and diastolic chamber dimensions increase during the occlusion phase. RV = right ventricle.
/
o---
2 -
6CCLUSlON
23
20-30
Seconds
After
Occlusion
M
Mean M-mode
systolic
thickness
(mm) of involved
LV segment.
&.......A o--o
Mean M-mode
systolic
excursion
(mm) of involved
LV segment.
Mean
EKG ST segment
elevation
(mm).
FIGURE 4. Decrease in M-mode mean left thickness, systolic excursion and increase (EKG) ST-segment elevation relative to the sion. These changes increase with longer occlusion and return to baseline afler deflation.
ventrlclular systolic wall in electrocardiographic length of balloon occluduratlons of coronary 20 seconds of balloon
24
ECHOCARDIOGRAPHIC
EVALUATION
DURING
ANGIOPLASTY
mm/second 90 -
mm
Systolic Excursion
16
r
14
-
12
-
10
-
8
-
6
-
4
‘-
2
-
80
t
p<.oo1 1
70
-
Systolic
60
-
Endocardial
5~
_
Velocity
4.
_
30
-
20
-
10
-
0 Balloon FIGURE 5. Change in M-mode ventricular segments during nary angioplasty.
motion in all segments before balloon occlusion. During balloon inflation, hypokinesia, akinesia and dyskinesia of the involved LV segments (Fig. 7] were noted in 18 of 20 instances (Table I]. These changes were most pronounced after 60 to 75 seconds of deflation. In 2 patients LV function was unchanged during PTCA. Neither patient had electrocardiographic (ECG) changes during coronary occlusion and both had profuse collateral blood supply to the stenotic artery. Electrocardiographic findings: The 6-lead electrocardiogram showed varying degrees of ST-segment elevation during balloon occlusion in 10 patients (Fig. 4). All 10 had echocardiographic LV dysfunction during balloon occlusion and 9 had no collateral blood supply to the stenotic coronary artery. The 2 patients who failed to show ECG and echocardiographic changes LAD
t
Before
Occlusion
systolic excursion of the Involved left the balloon occlusion phase of coro-
t
p-c.001
0
During
Before
-
Balloon FIGURE 8. Change In M-mode systolic involved left ventrlclular regions during nary angioplasty.
During Occlusion endocardial the occlusion
velocities of the phase of coro-
had abundant collateral blood supply. ECG changes were observed at the time as the echocardiographic abnormalities, and were most marked with longer durations of balloon occlusion (Fig. 4).
Discussion During balloon occlusion of a human coronary artery, we found a decrease in wall thickness, endocardial velocities and wall motion of the ischemic segments of the left ventricle. Our data confirm previous animal’-* and human studies.g-12 Although hyperdynamic wall motion of the involved segments of the left ventricle after reperfusion has been reported,*l it was not present in our study. Our 2-D data showing new areas of LV hypokinesia, akinesia and dyskinesia in 18 of 20 segments (90%)
ANGIOPLASTY
FIGURE 7. End-diastolic and end-systolic 2-dimensional parasternal long-axis view durlng balloon occlusion of a left anterlor descending coronary artery (LAD). Note akinetic motion of the ventricular septum (S) during balloon occlusion, with normal posterior wall (PW) motion. A = aorta, LA = RV = right left atrium; LV = left ventricle; ventricle.
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SYSTOLE
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DIASTOLE
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are similar to those reported by Hauser et all2 Furthermore, the time of onset and disappearance of LV impairment was remarkably similar in both studies. In contrast to their study, we did not observe that echocardiographic changes preceded ECG changes. Furthermore, our M-mode data revealed a direct relation between the duration of balloon occlusion and severity of LV impairment. In their study, simultaneous Mmode images were not recorded. As the endocardial echoes are better delineated on M-mode than stopframe 2-D images, the changes in measurements of LV wall thickness and endocardial velocities are more accurately determined by M-mode echocardiography. Two patients who showed no echocardiographic changes in LV function during coronary occlusion had abundant collateral blood supply to the stenotic artery, suggesting that the presence of collaterals may preserve ventricular function, at least during short periods of ischemia, in humans. In 1 instance, in which both the left anterior descending and circumflex coronary arteries were occluded, changes were noted in both septal and posteroinferior walls, indicating that global hypokinesia and abnormal LV function can occur in patients with the equivalent of left main coronary occlusion All changes observed were reproducible in patients who had more than 1 LV study performed during multiple balloon inflations. The lapse of 15 to 20 seconds before changes in LV wall thickness and function were observed is comparable to that in openchest animal models, in which 5 to 30 seconds of coronary occlusion were required before changes in LV function were observed.6-8 A similar time course was observed for resolution of abnormalities after balloon deflation and restoration of blood flow in these patients.
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References 1. Goldstein S. de Jong JW. Changes in left ventricuJar wall dimensions during regional myocordiol ischemia. Am J CardioJ 1974:34:56-62. 2. Theroux P. Franklin D. Ross J Jr, Kemper WS. Regional myocardiul Junetion during acute coronary artery occlusion ond its modification by pharmacologic agents in the dog. Circ Res 1974;35:896-908. 3. Kerber RE, Marcus ML, Ehrbhardt J. Wilson R. Abboud FM. Correlation between echocardiographicofly demonstrated segmental dyskinesis and regional myocordial perfusion. Circulation 1975;52:1097-1104. 4. Sasayama S, Franklin D, Ross J Jr, Kemper WS, McKown D. Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog. A study based on (I modified ultrasonic technique. Am J CordioJ 1976;38;870-879. 5. Ross J Jr, Franklin D. Analysis of regional myocordiol function, dimensions, and wall thickness in the characterization of myocardial &hernia ond infarction. Circulation 1976;53:suppJ 1:1-88-J-92. 6. Sabbah HN, Stein PD. Early segmental thinning of the left ventricular wall following regional ischemia. Cothet Cordiovosc Diagn 1983;9:473-482. 7. Pandian NC, Kerber RE. Two-dimensional echocordiogrophy in experimental coronary stenosis. I. Sensitivity and specificity in detecting transient mvocardiol dvskinesis: comparison with sonomicrometers. Circulation 1982;66:597-602.
8. Pandian NG, Kieso RA. Kerber RE. Two-dimensional echocordiography in experimental coronary stenosis. II. Relationship between systolic wall thinning and regional myocardiol perfusion in severe coronary stenosis. Circulotion 1982;66:603-611. 9. Crawford MH, Amon KW, Vance WS. Exercise &dimensional echocardiography. Quantitation of left ventricular performonce in patients with severe angina pectoris. Am J CordioJ 1983;51:1-6. 10. Visser CA, van der Wieken RL, Kan G, Lie KL, Sokele EB. Meltzer RS. Durrer D. Comparison of two-dimensional echocardiography with radionuelide angiography during dynamic exercise for the detection of coronary artery disease. Am Heart J 1963;106:526-534. 11. Distante A, Rovai D. Picano E, Moscarelli E, Palombo C, Morales MA, Michelassi C, L’Abbate A. Transient changes in left ventricular mechanics during attacks of Prinzmetol’s angina: on M-mode echocordiogrophic study. Am Heart J 1984:107:465-474. 12. Hauser AM, Gangadharan V, Ramos RG, Gordon S. Timmis GC, Dudlets P. Sequence of mechanicoJ, electrocardiographic and clinical effects of repeated coronary artery occlusion in humon beings; echocardiogrophic observotions during coronary angioplosty. IACC 1985:5:193-197. 13. Sahn DJ, DeMaria A, Kisslo J, Weyman A. The committee on M-mode stondardizntion of the American Society of Echocordiography. Recommendations regarding quantitation in M-mode echocardiogrophy: results of o survey of echocordiogrophic measurements. Circulation 1978:58: 1072-1083.