Increasing precordial QRS voltage correlates with improvement in left ventricular function following anterior myocardial infarction

JOURNAL OF ELECTROCARDIOLOGY,

21 (4), 1988, 303-312

Increasing Precordial QRS Voltage Correlates With Improvement in Left Ventricular Function Following Anterior Myocardial Infarction BY DAVID M. SALERNO,

M.D., PH.D., RICHARD W. ASINGER,M.D., JOSEPHELSPERGER, CCPT,

DARRYL ERLIEN, M.S., AND MORRISON HODGES, M.D.

SUMMARY To evaluate whether changes in QRS voltage reflect changes in left ventricular function after myocardial infarction, 28 patients were studied following anterior myocardial infarction. Two-dimensional echocardiograms and la-lead electrocardiograms were obtained during the acute phase of the infarction and again after at least 30 days of recovery (mean, 8 1 8 months). At follow-up, 11 patients (group A) showed improvement in left ventricular systolic function; 9 had increased net QRS voltage in VI-6 and 8 in V1--4. No improvement in ventricular function was found in 17 patients (group B); 7 had increased QRS voltage in VI_ 6 (p < 0.05 vs group A) and only 5 in VI-4 (p < 0.05 vs group A). For detection of improved left ventricular function, the sensitivity, specificity, and predictive value of the change in net QRS voltage for leads VI_6 was 82%, 59%, and 56% respectively, and for leads VI-4 was 73%, 71%, and 62% respectively. Neither R wave voltage, Q wave voltage, nor the total number of Q waves was reliable for identifying patients with improving left ventricular function. Thus, increasing net QRS voltage in the precordial electrocardiographic leads during long-term follow-up after anterior myocardial infarction correlates with and has a reasonable sensitivity for detection of improvement in left ventricular systolic performance.

It has been reported that left ventricular function may improve after acute myocardial infarction.lp7 Although this may occur as early as the first week after infarction, in some studies improvement has required follow-up of 1 month or more.lb7 This increase in left ventricular systolic performance can occur without any pharmacologic or surgical intervention. Various therapeutic modalities, such as emergency reperfusion of the infarct-related coronary artery with either streptokinase or bypass grafting, have been reported to improve left ventricular function following myocardial infarction8-I4 although other re-

ports have failed to confirm this improvement.15 However, documentation of the efficacy of these therapeutic modalities has been complicated by spontaneous changes in systolic performance of the left ventricle. Although the electrocardiographic Q wave is generally considered a permanent marker of prior myocardial infarction, there is evidence that Q waves may resolve in up to 6.7% of cases following myocardial infarction. l6 This resolution usually occurs after 1 month but has been observed to occur more rapidly.16-17 The mechanism for this resolution is unknown. Furthermore, the relationship between resolution of the electrocardiographic abnormality and improvement in mechanical systolic performance of the ventricle following myocardial infarction has not been clarified. We assessed this relationship by comparing these parameters in a consecutive series of patients with anterior myocardial infarction who did

From the Division of Cardiology, Department of Medicine, Hennepin County Medical Center and University of Minnesota, Minneapolis, Minnesota. Reprint requests to: David M. Salerno, M.D., Division of Cardiology, Hennepin County Medical Center, 701 Park Avenue South, Minneapolis, MN 55415.

303

SALERNO

304

not undergo likely to these paduring long-term study. Our was that precordial voltage predict improved ventricular function anterior myocardial

METHODS Patient Population The study population represents a consecutive series of patients admitted to the coronary care unit of Hennepin County Medical Center with a diagnosis of first acute anterior myocardial infarction confirmed by a typical enzyme pattern as well as the development of new electrocardiographic Q waves in at least two precordial leads. Patients were excluded if they had a previous myocardial infarction, if they received thrombolytic therapy or emergency coronary artery bypass grafting therapy for acute myocardial infarction, or if, during follow-up, they had a second acute myocardial infarction, percutaneous transluminal coronary angioplasty, or bypass surgery. Patients were also excluded if the follow-up period was less than 30 days from the onset of myocardial infarction. Patients with bundle branch block were excluded. Patients were required to have both a 12-lead electrocardiogram and two-dimensional echocardiogram a minimum of 30 days following the onset of myocardial infarction. Two-dimensional Echocardiography Two-dimensional echocardiography was performed as soon as possible following admission to the hospital, daily for 3 consecutive days, after 1 week, at hospital discharge, and sequentially during outpatient followup study. The apical four-chamber view was used for analysis. Consistent tomographic image location was maintained by positioning the transducer simultaneously to produce the greatest left ventricular size, to demonstrate all four cardiac chambers, and to visualize both AV valves.l* This view was used because it images those areas of the left ventricle that are usually supplied by the left anterior descending coronary artery” and are typically involved in anterior myocardial infarction.” Quantitative analysis of this view gives the best correlation with left ventricular ejection fractionzl The apical two-dimensional echocardiograms were quantitatively analyzed, as previously describedF2 to obtain left ventricular end-diastolic area (LVEDA) (normal, 18-38 cm2), end-systolic area (LVESA) (normal, 9-23 cm2), and left ventricular systolic area change as a percentage of LVEDA (lOO[LVEDALVESAYLVEDA) (normal, 33-56%). Based on data from our laboratory of interobserver and intraobserver variability, a 5% or greater increase in area change of the left ventricle was defined as improvement in left ventricular systolic performance, since smaller changes may be within the range of error for this measurement (*2 SD). Group A patients had at least a 5% increase

ET AL in left ventricular area change from initial to final echocardiogram and group B patients had less than a 5% increase or any amount of decrease in left ventricular area change. The investigator performing the echocardiographic analysis was blinded to the results of the electrocardiographic measurements. Electrocardiography Twelve-lead electrocardiograms, recorded at 25 mm/ set, were obtained upon admission, daily for 3 days, at discharge, and during routine long-term outpatient follow-up. Using visual reference to the 40-msec lines and the O.l-mV lines on the electrocardiographic paper, each electrocardiographic lead except aVR was analyzed for measurement of the duration of the Q wave and the amplitude of the Q wave, R wave, and S wave. The investigator performing these measurements was blinded to the results of the echocardiographic measurements. Pathologic Q waves were defined as at least 0.1 mV deep and 20 msec in duration.23 Initial R waves were defined as at least 0.025 mV in amplitude and terminal R waves at least 0.1 mV to be included as an R wave.23 The total voltage for each lead was calculated by the formula: QRS voltage = [R - (Q + S)] Pertinent lead groups were then summed. For example, the net total precordial voltage = zVr_&R - (Q + S)). Figures 1 and 2 illustrate the electrocardiograms and echocardiograms from a patient in each group. Selection of Initial and Follow-up Data The echocardiogram obtained on the first day of the acute infarct was used for the initial analysis of left ventricular function, as left ventricular dysfunction was found in a preliminary study in our laboratory of daily echocardiograms during acute infarction to be greatest on day 1. However, the third electrocardiogram was selected because this electrocardiogram usually represented the maximum development of Q wave abnormality during the first week after infarction, as demonstrated in a preliminary study in which all the electrocardiograms of several patients with acute anterior infarction were analyzed and the changes in electrocardiographic voltage plotted over time. Because increasing electrocardiographic voltage always occurred within 30 days, follow-up electrocardiograms were obtained at least 30 days after infarction for each of the 28 patients in this report. The last available electrocardiogramechocardiogram pair was used for the follow-up data. Data Analysis For comparison of the electrocardiograms with echocardiograms, the following definitions were used: truepositive (TP), patients with improvement in both tests; false-positive (FP), patients with improvement in electrocardiogram but not in echocardiogram; true-negative (TN), patients with no improvement in either test;

305

QRS VOLTAGE AFTER MYOCARDIAL INFARCTION

vl

v2

v3

v4

‘f5

v6

~Vl-6

hChmn&p30% I-

xv1-4

Day2

(mv) -1.5 -1.5 -0.3 0.3

0.8

0.5 -1.7 -3.0 Ama Change35%

Day34 1 cm.

(mV) -1.3 -1.3

0

1.0

1.1

0.7

0.2 -1.6

Fig. 1. Initial and follow-up electrocardiograms and apical two-dimensional echocardiograms (end-systolic and enddiastolic outlines) for one group A patient.

vl

VP

v3

v4

VS

v6

-3.0 -3.2

1

(mV) -0.8 -1.9 -1.7 -0.9

0

0.6

cm. ~

-4.7 -5.3

Fig. 2. Initial and follow-up electrocardiograms and apical two-dimensional echocardiograms (end-systolic and enddiastolic outlines) for a group B patient.

SALERNO

306

and false-negative(FN), patientswith improvementin echocardiogrambut not in electrocardiogram.The following equationswere then used:

ET AL TABLE I Clinical Characteristics of the Patients Group

Sensitivity(%) = TP T+PFNx 100 Specificity(%) = TNTSJFPx 100 Predictivevalues (%) = TP ‘,’ FP x

100

Comparisonswithin groups were made using Student’s t-test for paired data and between groups using Student’st-testfor unpaireddata. Chi-squareanalysis was used to compare nonnumericalpatient characteristics and to compare the number within each group with improvementin the electrocardiographicfindings. A p value co.05 was required to reject the null hypothesis.

RESULTS Patient Characteristics The clinical characteristics of group A (echocardiogram improved during follow-up) and group B (echocardiogram unimproved during follow-up) patients were compared (Table I). There was no difference between the groups for age or gender. Clinical evaluation of cardiac function was comparable both in the hospital and during follow-up study, as compared by Killip class, congestive heart failure, and requirements for treatment for heart failure. Comparable numbers of patients had angina pectoris and were treated with beta blockers. However, ventricular fibrillation was more frequent in group A (p < 0.05) when prehospital and inpatient events were combined. Two-dimensional Echocardiography (Table II) Eleven of the 28 patients (39%) had an improvement in left ventricular systolic area change during long-term follow-up and were assigned to group A; 17 patients (61%) had no change or a worsening in left ventricular systolic area change and were assigned to group B (Fig. 3). Both groups had comparable left ventricular systolic area change on initial study and both were below the normal range for this value (see Methods). At follow-up echocardiogram, group A patients had significantly better left ventricular systolic area change than group B patients. Group A patients had some decrease in end-systolic area, although this was of only borderline statistical significance (p < 0.1). Group B patients had a decrease in left

A

(n = 11) Age (years) Men (n) Peak CK (units) Peak CK MB (units) Peak CK MB (%) Killip class initial Worst During hospitalization CHF Angina Digoxin Diuretics Vasodilators Beta blockers After hospitalization CHF Angina Digoxin Diuretics Vasodilators Beta blockers Ventricular fibrillation Prehospital In-hospital Combined

53 I 9 1,769 ? 195 f 13 2

14 1,400 133 6

1.5 I? 0.5 1.9 2 1.0

Group B (n=17) 55 lr 9 2,363 i: 404 2 17 4

p

17

NS

2,280 406 5

NS NS NS

1.7 * 0.7 1.9 i 0.6

NS NS

(27) (91)

4 (24) 13 (76)

4 (36) 8 (73) 11 (100)

7 (41) 13 (76) 16 (94)

6

(55)

4 (24)

NS NS NS NS NS NS

3 7 2 3 8 3

(27) (64) (18) (27) (73) (27)

6 a 6 7 9 4

(38)* (50)* (38)* (44)* (56)’ (25)’

NS NS NS NS NS NS

0 (0) 1 (6) 1 (6)

NS NS 0.05

3 10

2 (18) 3 5

(27) (45)

Patient characteristics for patients with improvement in echocardiographic left ventricular percent area change (group A) are compared with patients who did not have improvement (group B). Unless otherwise indicated, data represent the number of patients, with percentage shown in parentheses. P values derived by unpaired f-test for alphanumeric data and chi-square analysis for other data. CK, creatinine kinase; CHF, congestive heart failure; NS, not significant. * Follow-up clinical information was available for 16 of the original 17 patients.

ventricular systolic area change and had a significant increase in both left ventricular end-diastolic area and left ventricular end-systolic area. Electrocardiographic Voltage (Table II) The net total precordial voltage [xV1_6(R - (Q + S))] was greater on the initial electrocardiogram for group A then for group B patients. This was also true for the follow-up electrocardiogram. The mean voltage improved from the initial to the follow-up electrocardiographic examination in group A patients but not in group B patients (p < 0.05). Overall, 9 of 11 group A patients had increased net voltage in V1--6, compared with 7 of 17 group B patients (p < 0.05). The total voltage of the Q waves was equal between the groups at initial electrocardiogram but was less negative at

QRS VOLTAGE AFTER MYOCARDIAL INFARCTION

307

TABLE II Echocardiographic and Electrocardiographic Measurements at First and Second Study Group A

Days post-M I Echo (no.) ECG (no.) Echo A area (%) EDA (cm*) ESA (cm2) ECG (XV,-Vs) R-QS (mV x 10-l) R (mV x 10-l) Q (mV x 10-l) Q (no.) ECG (XV,-V4) R-QS (mV x 10-l) R (mV x 10-l) Q (mV x 10-l) Q (no.) ECG (ZIi,iII,F) R-QS (mV x 10-l) Q (no.) ECG (Xl,L,Vs-V,) R-QS (mV x 10-l) Q (no.)

Group B

First Study

Second Study

Change

First Study

Second Study

1.4 k 0.5 3.4 * 0.7

247 c 236 272 2 273

-

1.5 k 0.9 3.4 2 1.2

213 rt 221 215 ? 216

13 ir 5’ -0.3 k 59 -3 k 5’

24 t 8 29 + 6 22 ” 6

20 + 7t 35 t 811 28 + 7//

-4

-2

23 2 7 30 2 6 24 k 6

35 + 11*t 30 k 4* 21 t 75

-32 k 25$ 15 + 13 -38 k 19 4t2

-23 20 -25 3

-40

-33

k 17 5*6 -37 2 18 3kl

2 4 6?7 7k7

t ” 2 *

28!j# 13# 1611 l#

8 -+ 8$ 5t6 13 -I- 12 -1 * 1

-48 _t 15 10 c 12 -37 k 22 321

-49 2 19 13 ? 11 -31 +- 24 2 2 211

IfI 13 3*8 6 t 12 -1 -+ 1

k 8 2 -25 2 2 ?

229 7# 1611 l#

7 + 12$ 3*4 13 * 12 -1 2 1

-48

-52

-5

k 16 2t3 -34 * 22 3-r-l

214 5 -c 511 -29 ? 25 2 ? 211

3 2 11 0.4 -t- 0.7

459 0.3 * 0.7

-0.1

1 * 12* k 0.5

3 * 10 0.2 * 0.4

-3 ? 1211 0.5 ? 1.0

14 t 13 0.6 k 1.0

15 t 13 0.5 * 0.7

-0.2

2*6 -+ 0.4

5 t 16 1.4 k 1.5

10 i 19# 0.7 2 0.9#

Data represent mean r standard 2 5% from the first to the second obtained 2 30 days after infarction. * p < 0.001 versus group B. t p < 0.005 versus first study. $ p < 0.05 versus group B. 0 p < 0.01 versus group B. I/ p < 0.01 versus first study. # p < 0.05 versus first study.

Change

2 14 3a3 6 k 12 -1 k 1 -5 + 7 0.4 ? 0.9 4 5 10 - 0.6 ? 1

deviation. Group A includes patients with an improvement in area change of echocardiogram. Group 6 includes all other patients. Second studies were “Change” data represent the change from first to second study.

follow-up examination only for group A patients. Furthermore, group A patients had a significant increase in total R wave voltage in leads VI-V6 at follow-up examination versus initial examination, whereas this was not true for group B patients. However, only the net precordial voltage signalled a difference between the two groups. Examination of leads VI-V4 revealed a similar pattern (Figs. 4,5). Again, the net voltage in each lead (R - (Q + S)) increased in group A but not in group B patients. Eight of 11 group A patients showed increased net voltage in VI-V+ compared with 5 of 17 group B patients (p < 0.05). The net QRS voltage CR - (Q + S)) was analyzed for the lateral leads (I, aVL, and V5-V6). The net voltage increased slightly during followup in group B patients. No significant differences between the groups were detected. The net QRS

voltage in the inferior leads (II, III, and aVF) decreased slightly at follow-up for group B patients but not for group A patients (Table II). Q Wave Analysis (Table II) The number of pathologic Q waves decreased slightly but significantly in both group A and group B patients during follow-up examination. This was seen not only in leads VI--Vs but also in v1-v‘$, Sensitivity, Specificity, and Predictive Value of Electrocardiography

The sensitivity, specificity, and predictive value for improvement in left ventricular function for each electrocardiographic parameter are shown in Table III. Total net precordial voltage in either

SALERNO

308 GROUP A

ET AL

GROUP B

I

50

40

30

20

0 -2

10

03 0

-I

Fig. 3. Left ventricular systolic change in area (%) for group A and B patients on initial and final follow-up echocardiograms.P values representthe differencebetween the initial and follow-up echocardiograms,by paired t-test.

leads VI-V4 or VI-Vs were comparable in their ability to predict improvement in left ventricular function. Other electrocardiographic criteria were less useful in distinguishing between the echocardiographic groups.

DISCUSSION This study confirms previous reports that demonstrated spontaneous changes in left ventricular function in some patients during long-term follow-up after myocardial infarction.3-7 We selected

Group A

27

Group B 2

O-

Fig. 4. Net precordial voltage (R - (Q + S)) in leads VI-VI for group A and B patients on initial and followup electrocardiograms. P values compare initial and follow-up electrocardiograms by paired t-test.

-3

p<.o5

Group A

0

Group B

Fig. 5. Change in net precordial voltage (R - (Q + 3) in leads VI-V4 for group A and B patients from initial to final follow-up electrocardiograms. These changes are compared by unpaired t-tests. Patients with increasing voltage are indicated by solid circles and patients with decreasing voltage by circles.

our patients carefully, to exclude those who received interventions that might alter left ventricular function, such as thrombolytic therapy, percutaneous transluminal coronary angioplasty, or coronary artery bypass surgery. Patients who had other events that might alter left ventricular function, such as a second myocardial infarction during the follow-up period, were also excluded. We cannot exclude silent myocardial infarction during follow-up, although it seems unlikely that it would occur since all patients had clinically apparent symptoms during their first infarction. Medical therapies that might alter left ventricular performance were comparable between the patients who showed improvement in left ventricular function and those who did not. Although our study was retrospective, all sequential patients who met the entrance criteria were included in the study, to exclude selection bias. Although the follow-up electrocardiograms and echocardiograms were not always performed on the same day, these time discrepancies were small. In a preliminary study of the analysis of sequential electrocardiograms and echocardiograms from several patients (unpublished data) we found that the initial echocardiogram showed maximal abnormality, as previously reported in other studies.24,25We used the third electrocardiogram (36-72 hours following the onset of infarction) as the first, since it appeared from our

QRS VOLTAGE

AFTER

MYOCARDIAL

INFARCTION

309

TABLE III Sensitivity, Specificity, and Predictive Value of Electrocardiographic Measurements for Improvement in Left Ventricular Function

Sensitivity

Predictive Value

WI

Specificity W)

73 73 91 64

71 41 35 65

62 44 48 54

82 82

59 29

56 43

82

41

47

73

47

47

45

18

26

55

29

33

WI

vi-v4 R

-

(Q

+

S) (mV)

R (mV) Q (mV) Q 0-d VrVs R - (Cl + S) (mV) R (mV)

Q b-W Q (4

II, III, aVF R - (Q + S) (mV) I, aVL, Vs-Vs R - (Q + S) (mV)

preliminary study as well as from clinical observation that usually this electrocardiogram had the lowest net precordial voltage. Although variability in precordial electrode placement might cause changes in net precordial voltage, this seems unlikely, since in our preliminary study with multiple serial electrocardiograms on the same patients the trend of changes in voltage was steady. It is possible that the ventricular fibrillation that occurred more commonly in group A might have caused left ventricular dysfunction of a global nature that later improved. However, ventricular fibrillation occurred outside the hospital in only two of these patients and was treated promptly in the three inpatients. This spontaneous gradual improvement in systolic performance following myocardial infarction has important clinical implications for the management of individual patients, and research implications with regard to the study of interventions that might alter left ventricular function following myocardial infarction. Studies must be carefully controlled to avoid erroneously concluding that the intervention in question produced improvement, since improvement can be seen in more than a third of patients spontaneously (39% in our study). The mechanism for this delayed improvement in left ventricular function is uncertain; it has been speculated that part of the initial myocardial systolic dysfunction may be due to “stunned myocardium” due to ischemia that in-

jures but does not destroy myocardial cells.‘(j Presumably these cells require a period of time to recover their contractile function. The initial echocardiographic wall motion abnormality demonstrates the area “at risk,” whereas the final echocardiogram may indicate the area of actual infarction. Stunned myocardium may improve by spontaneous lysis of clot in the perfusing coronary artery, by recruitment of collateral blood vessels, or by medical interventions that improve blood flow or reduce cardiac work. Other possible mechanisms for the improvement in cardiac function include compensatory hypertrophy and dissipation of toxic metabolites. It has previously been reported that electrocardiographic Q wave abnormalities may change in a significant portion of patients following myocardial infarction.16 It has been suggested that this may occur by a second infarction that “cancels” the negative forces (contracoupe effect).27 Our study demonstrates that electrocardiographic improvement can also occur during longterm follow-up in patients who sustain only one myocardial infarction. Others have noted transient Q waves after prolonged ischemia without infarction in animal studies28 and in humans 2s-33 adding further support to the concept of “stunned” but viable myocardium. While the presence of left ventricular hypertrophy was not addressed in this study, equal numbers of patients were receiving therapy directed

310

SALERNO ET AL

toward hypertension in both groups, so it seems unlikely that hypertension would have caused the differences in precordial voltage between the two groups. Neither the Q wave amplitude nor R wave amplitude in the precordial leads was as reliable as the net QRS voltage across the precordium for prediction of changes in left ventricular performance. Similarly, the total number of Q waves was an insensitive guide to improvement in left ventricular function. Thus, changes in the net precordial voltage (R - (Q + S)) voltage in VI-V6 appear to be the most reliable electrocardiographic sign of change in left ventricular function after anterior myocardial infarction in an individual patient. It should be noted that measurements from VI-V6 correlate with 35lead precordial electrocardiographic maps.34 The mechanism for this electrocardiographic recovery is unknown. Perhaps recovery of electrical function in a muscle cell predicts recovery of mechanical function in the “stunned” myocardial cell following myocardial infarction. This has potential implications for evaluating spontaneous reperfusion of the coronary artery following myocardial infarction, as improvement in electrocardiographic parameters may be indicative of coronary patency or adequate collateralization, whereas failure of the electrocardiogram to improve may suggest persistent occlusion without recanalization or reperfusion. Our data do not provide an answer to this question, since acute and follow-up coronary angiography was not done, although it has been reported recently that precordial electrocardiographic changes may correlate with coronary patency following myocardial infarction.35,36 Also, anterior electrocardiographic forces have been reported to return after coronary bypass surgery.37*38 An alternative explanation for these electrocardiographic changes during long-term follow-up after myocardial infarction is that changes in left ventricular volume or left ventricular intracavitary pressure might result in changes in electrocardiographic voltage. A decrease in QRS amplitude has been shown in dogs undergoing acute volume expansion. 3g However, in comparisons of rest and exercise changes in left ventricular volume in humans, increases in R wave voltage have been thought to reflect enlargement of the left ventricular chamber.40*41Thus, it is uncertain whether the larger net precordial voltage in the patients with smaller left ventricular chambers

during follow-up in our study were caused by the smaller volumes or represented increased myocardial mass with electrical function. We conclude that there are spontaneous changes in left ventricular systolic function following anterior myocardial infarction. There are also gradual changes in the total precordial electrocardiographic QRS voltage in some patients following anterior myocardial infarction. Improvement in the electrocardiographic QRS voltage may predict improvement in left ventricular function. Acknowledgments: The authors acknowledge Frank L. Mikell, M.D., who participated in the data collection, and Belinda Anderson and Rosemary Van Schooten, for their assistance in the preparation of the manuscript.

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