- Email: [email protected]
Electrocardiographic associations of right precordial Q waves help to distinguish anterior myocardial infarction from aortic stenosis
International Journal of Cardiology 82 (2002) 159–166 www.elsevier.com / locate / ijcard
Electrocardiographic associations of right precordial Q waves help to distinguish anterior myocardial infarction from aortic stenosis Han B. Xiao*, Ihab S. Ramzy, Timothy J. Bowker, Mark Dancy Cardiology Unit, Central Middlesex Hospital, Acton Lane, London NW10 7 NS, UK Received 3 April 2001; accepted 31 October 2001
Abstract Right precordial Q waves are ECG evidence of anterior myocardial infarction and can be present in patients with pathological left ventricular hypertrophy particularly caused by aortic stenosis. The aim of this study was to investigate the ECG features associated with Q waves in aortic stenosis and those in anterior myocardial infarction. We studied 16 patients with anterior myocardial infarction and 19 patients with aortic stenosis by means of ECG, echocardiography and clinical history. On the ECG, heart rate (70620 beats / min vs. 83620) and QT interval (380665 ms vs. 390650) did not differ between the two conditions. PR interval (160615 ms vs. 185630, P,0.05) and QRS duration (8067.0 ms vs. 95615, P,0.01) were both longer in patients with aortic stenosis than in those with myocardial infarction. The Q wave voltage in V1 (1.060.55 mV vs. 1.560.60) or V2 (1.360.5 mV vs. 1.860.85) and R wave voltage in V5 (0.760.7 mV vs. 2.160.9) or V6 (0.760.4 mV vs. 1.560.7, all P,0.01) were significantly less in patients with anterior myocardial infarction than in those with aortic stenosis. Q wave voltage over 1.3 mV in V1 or R wave voltage over 1.5 mV in V5 can differentiate aortic stenosis from anterior myocardial infarction with a sensitivity of 79% for each and specificities of 81 and 93.8%, respectively. Though the frontal QRS axis was similar in the two groups (286458 vs. 14635, P.0.05), the horizontal QRS axis pointed laterally (2306208) in aortic stenosis and posteriorly (2606208, P,0.01) in anterior myocardial infarction. A horizontal QRS axis between zero and 2458 detected the presence of aortic stenosis with a sensitivity of 94.7% and a specificity of 81.3%. On echocardiography, left ventricular hypertrophy was found in most patients (94.7%) with aortic stenosis but not in those (0%) with anterior myocardial infarction. Left ventricular end diastolic dimensions (5.160.7 cm vs. 5.160.9, P.0.05) were similar in the two groups but the end systolic dimension was increased in patients with aortic stenosis (4.060.9 cm vs. 3.460.6, P,0.05). The systolic left ventricular function (shortening fraction: 2368.0% vs. 3467.0; Vcf: 0.860.26 circ / s vs. 1.360.26, both P,0.01) was significantly impaired in patients with aortic stenosis compared to those with myocardial infarction. In conclusion, in the presence of right precordial Q waves, the simple 12-lead ECG can provide important information on distinguishing anterior myocardial infarction from aortic stenosis. In particular, the QRS voltage in the chest leads and horizontal QRS axis can differentiate anterior myocardial infarction from aortic stenosis with high sensitivity and specificity. 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Anterior myocardial infarction; Aortic stenosis; Electrocardiographic associations; Right precordial Q waves
1. Introduction Right precordial Q waves (i.e. in V1 and V2 of a conventional 12-lead ECG) are usually considered as *Corresponding author. Tel.: 144-208-967-5000; fax: 144-208-9675007. E-mail address: [email protected] (H.B. Xiao).
ECG evidence of anterior myocardial infarction [1,2]. However they can be present in patients with no apparent history of anterior myocardial infarction (Fig. 1) [3–7]. Among the non-coronary diseases, aortic stenosis is one of the commonest conditions which produce right precordial Q waves as seen in myocardial infarction [4–6]. Although attempts have been made to differentiate Q waves in aortic stenosis
0167-5273 / 02 / $ – see front matter 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 01 )00603-9
160
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
Fig. 1. Precordial ECGs recorded in a patient with anterior myocardial infarction (A) and a patient with aortic stenosis (B) showing right precordial Q waves.
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
from those in anterior infarction by orthogonal electrocardiography [8], it is still not clear whether right precordial Q waves on standard 12-lead ECG in aortic stenosis differ from those in anterior myocardial infarction, either in their morphology or their genesis. In this study, we aim to investigate ECG features associated with Q waves in the two conditions by means of ECG, echocardiography and clinical history.
2. Material and method
2.1. Subjects
161
• QT interval: from the onset of the QRS complex to the end of the T wave. • Voltage of Q waves in leads V1 and V2. • Voltage of both R and S waves in V5 and V6. • Mean QRS voltage of chest leads: total voltage of Q waves in leads V1, V2 and of both R and S waves in V5 and V6 divided by 4. • Frontal QRS axis: the combined vector of the QRS complexes in leads I and III. • Horizontal QRS axis: by the same algorithm for calculating the frontal QRS axis, we used the combined vector of the QRS complexes in chest leads V6 and V1 to assess the horizontal QRS axis [9] (Fig. 2).
2.3. Echocardiography We investigated 16 patients with anterior myocardial infarction and 19 patients with aortic stenosis. All patients had Q waves in V1 and V2 of their 12-lead ECG. Anterior myocardial infarction was diagnosed by a typical history of acute chest pain and ECG evolution from anterior ST elevation to Q waves. All patients with anterior myocardial infarction were admitted to hospital and reviewed after discharge. They were enroled in this study 1–4 weeks after the myocardial infarction. Aortic stenosis was confirmed by continuous wave Doppler recording the peak velocity equivalent to a pressure drop of over 55 mmHg across the aortic valve. Patients with pulmonary hypertension and any organic valvular disease other than aortic stenosis were excluded. Patients with ECG patterns of bundle branch block or with a permanent pacemaker implanted were also excluded.
A Hewlett-Packard Sonos-1000 or Sonos-5500 Echocardiograph was used. Cross-sectional images of the left ventricular cavity were recorded on video tape and examined for regional wall motion abnormalities. Cross-sectional image guided M-mode echocardiograms of the left ventricle were recorded at the mitral valve tip level in the parasternal long axis
2.2. Electrocardiography A standard 12-lead ECG was recorded with Fukuda Denshi equipment (FCP4101). The time intervals, heart rate and frontal QRS axis were measured by built-in computer soft-ware. QRS voltage and horizontal QRS axis were determined manually. • Heart rate: calculated as 60 / RR interval (s). • PR interval: from P wave onset to QRS complex onset. • QRS duration: from the onset to the end of the QRS complex.
Fig. 2. Measurement of horizontal QRS axis: by the same algorithm for calculating frontal QRS axis, chest leads V6 and V1 (in the places of limb leads I and III, respectively) form a 1208 angle and are divided into two halves, positive and negative from the centre. The algebraic sums of the QRS amplitudes in leads V6 and V1 are plotted on the corresponding axes. From the plotted point, perpendicular lines are dropped to a point of intersection. The line between this intersection and the centre represents the mean horizontal QRS axis (a).
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
162
view. Recordings were made on photographic paper simultaneously with a lead II ECG, at a paper speed of 50 mm / s. From the M-mode echocardiograms the following measurements were made: • Left ventricular end diastolic dimension (LVEDD) at the onset of the QRS complex on the ECG. • Left ventricular end systolic dimension (LVESD) at the maximal excursion of the left ventricular posterior wall. • The thickness of the interventricular septum (TH IVS ) and the left ventricular posterior wall (TH LVPW ) at the onset of the QRS complex on the ECG, using leading edge methodology. • Left ventricular shortening fraction (LVSF) was calculated as (LVEDD2LVESD) / LVEDD (%). • The left ventricular mass was calculated according to the Penn convention [10]: LV Mass (g) 5 1.04ssTH IVS 1 TH LVPW 1 LVEDDd 3 2sLVEDDd 3d 2 14
2.4. Doppler Transmitral and transtricuspid flows were recorded by pulsed wave Doppler, and aortic flow was recorded by both pulsed and continuous wave Doppler. All records were made with simultaneous lead II ECG and at a paper speed of 50 mm / s. Peak velocities of mitral and tricuspid E and A waves were measured: • Left ventricular ejection time (LVET) was measured from the onset to the end of the aortic flow on pulsed wave Doppler. • Mean velocity of left ventricular circumferential fibre shortening (Vcf) was calculated as: Vcf 5 LVSF / LVET (circ / s) • Pressure difference between the left ventricle and the aorta (DP) was assessed from the continuous wave Doppler signals of the aortic flow velocity (V ) by the modified Bernoulli equation as: DP 5 4V 2
2.5. Data analysis All measurements were made for three cardiac cycles and the average taken. Data are expressed as
mean6standard deviation. Differences were evaluated by the unpaired Student’s t-test, Chi-square or Fisher’s exact test. A P value of less than 0.05 was considered to be statistically significant. Sensitivity and specificity for detecting aortic stenosis were calculated as follows: • The sensitivity was expressed as the proportion of true AS (aortic stenosis) cases (as confirmed by echo) relative to cases which were classified as AS by the given ECG measurements (%). • The specificity was expressed as the proportion of true MI (anterior myocardial infarction) cases (as confirmed by history and ECG evolution) relative to cases which were classified as MI by the given ECG measurements (%).
3. Results
3.1. General ( Table 1) The mean age of the total patient population was 73 (612) years. Patients with aortic stenosis were predominantly female and patients with anterior myocardial infarction were all male. Patients with anterior myocardial infarction were younger than those with aortic stenosis (63.5612 years vs. 79.569.0, P,0.01). Systolic (131620 mmHg vs. 129615) and diastolic (7469.0 mmHg vs. 76612, all P.0.05) blood pressures did not differ between the two patient groups.
3.2. Electrocardiography 3.2.1. Time measurements Electrocardiographically, the heart rate (70620 beats / min vs. 83620) and QT interval (380665 ms vs. 390650) were similar in the two groups. PR interval (160615 ms vs. 185630, P,0.05) and QRS duration (8067.0 ms vs. 95615, P,0.01) were significantly longer in patients with aortic stenosis than in those with myocardial infarction (Table 1). QRS duration over 85 ms was found in 17 of 19 patients with aortic stenosis and only in three of 16 patients with anterior myocardial infarction (P,0.01) (Table 2).
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
163
Table 1 Clinical and ECG data
Age (years) Sex (female:male) Systolic BP (mmHg) Diastolic BP (mmHg) Heart rate (bpm) PR interval (ms) QRS duration (ms) QT interval (ms) Frontal QRS axis (8) Horizontal QRS axis (8) Q wave voltage in V1 (mV) Q wave voltage in V2 (mV) R wave voltage in V5 (mV) R wave voltage in V6 (mV) Mean voltage of chest leads (mV) LVH according to Sokolow–Lyon criteria
Anterior infarction (n516)
Aortic stenosis (n519)
P value
60612 0:16 131620 7669.0 70620 160615 8067.0 390665 28645 260620 1.060.55 1.360.50 0.760.6 0.760.4 1.060.5 1 / 16 (6.25%)
7969.0 11:8 129615 76612 83620 185630 95615 390650 14635 230620 1.560.60 1.860.85 2.160.9 1.560.7 2.060.8 13 / 19 (68.4%)
,0.01 ,0.01 NS NS NS ,0.05 ,0.01 NS NS ,0.01 ,0.05 ,0.05 ,0.01 ,0.01 ,0.01 ,0.02
Note: P value was calculated by t-test, Chi-squared or Fisher exact test. NS, not significant; LVH, left ventricular hypertrophy.
Table 2 Critical ECG values between anterior myocardial infarction and aortic stenosis ECG criteria QRS duration $85 ms ,85 ms Sensitivity (%) Specificity (%) Q wave voltage in V1 $1.3 mV ,1.3 mV Sensitivity (%) Specificity (%) R wave voltage in V5 $1.5 mV ,1.5 mV Sensitivity (%) Specificity (%) Mean QRS voltage of chest leads $1.5 mV ,1.5 mV Sensitivity (%) Specificity (%) Horizontal QRS axis 0 to 2458 245 to 2908 Sensitivity (%) Specificity (%)
Anterior infarction (n516)
Aortic stenosis (n519)
P value
3 13
17 2 89.5
,0.001
15 4 78.9
,0.001
15 4 78.9
,0.001
16 3 84.2
,0.001
18 1 94.7
,0.001
81.2 3 13 81.2 1 15 93.8 2 14 87.5 3 13 81.2
Note: P value was calculated by Chi-squared or Fisher exact test.
164
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
3.2.2. QRS voltage The Q wave voltages in V1 (1.060.55 mV vs. 1.560.60) and in V2 (1.360.5 mV vs. 1.860.85) and the R wave voltages in V5 (0.760.7 mV vs. 2.160.9) and in V6 (0.760.4 mV vs. 1.560.7, all P,0.01) were significantly less in patients with anterior myocardial infarction than in those with aortic stenosis (Fig. 1). Left ventricular hypertrophy by Sokolow–Lyon criteria [11] was present in 13 / 19 (68.4%) patients with aortic stenosis and in only 1 / 16 (6.3%) patients with anterior myocardial infarction (P,0.01) (Table 1). Using the median as a critical value, a Q wave voltage over 1.3 mV in V1 or an R wave voltage over 1.5 mV in V5 can differentiate aortic stenosis from anterior myocardial infarction with a sensitivity of 79% for each and specificities of 81 and 93.8%, respectively (Table 2). The mean QRS voltage of chest leads over 1.5 mV could detect aortic stenosis with a sensitivity of 84.2% and a specificity of 87.5%. 3.2.3. QRS axis Though the frontal QRS axis was similar in the two groups (286458 vs. 14635, P.0.05), the horizontal QRS axis differed significantly, pointing laterally (2306208) in aortic stenosis and posterially (2606208, P,0.01) in anterior myocardial infarction (Fig. 3). A horizontal QRS axis from zero to
Fig. 3. The distribution of horizontal QRS axis in patients with anterior myocardial infarction (solid dots) and those with aortic stenosis (open circles).
2458 detected the presence of aortic stenosis with a sensitivity of 94.7% and a specificity of 81.3%.
3.3. Echocardiography Echocardiographically, left ventricular hypertrophy was found in most patients (18 / 19, 94.7%) with aortic stenosis but not in those with anterior myocardial infarction. As expected, anterior hypokinesis was only found in patients with anterior infarction. Left ventricular end diastolic dimensions (5.160.7 cm vs. 5.160.9, P.0.05) were similar in the two groups but the end systolic dimension was greater in patients with aortic stenosis (4.060.9 cm vs. 3.460.6, P, 0.05). The systolic left ventricular function (shortening fraction: 2368.0% vs. 3467.0; Vcf: 0.860.26 circ / s vs. 1.360.26, both P,0.01)was significantly impaired in patients with aortic stenosis compared to those with myocardial infarction. Both E (0.6060.20 M / s vs. 0.9060.39) and A (0.6360.23 M / s vs. 0.8860.24, both P,0.05) wave velocities of transmitral flow were significantly higher in aortic stenosis than in myocardial infarction (Table 3).
4. Discussion Pathological Q waves are a common ECG feature of myocardial infarction, though they are also present in patients with other conditions particularly aortic stenosis [3,4,6]. The other conditions are usually identified on autopsy [3,4] or by imaging techniques such as echocardiography [12]. The distinction cannot be made convincingly by Q wave morphology alone. However, the combination of clinical history, ECG and echocardiogram enables us to establish the association of Q waves with the underlying cardiac pathology. In this study we sought to describe the characteristic ECG features which distinguish anterior myocardial infarction from significant aortic stenosis in patients with right precordial Q waves. As one would expect, we found that the absolute values of QRS voltage in the precordial leads were significantly greater in aortic stenosis than in myocardial infarction. Horizontal QRS axis, a less frequently studied measurement, differentiated aortic stenosis from anterior myocardial infarction with a higher sensitivity than QRS voltage. This finding suggests
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
165
Table 3 Echocardiographic data
LV end diastolic dimension (cm) LV end systolic dimension (cm) LV shortening fraction (%) Vcf (circ / s) Ventricular septal thickness (cm) LV posterior wall thickness (cm) LV mass (g) Mitral E wave (M / s) Mitral A wave (M / s) Tricuspid E wave (M / s) Tricuspid A wave (M / s)
Anterior infarction (n516)
Aortic stenosis (n519)
P value
5.160.7 3.460.6 3467.0 1.360.26 1.160.20 0.9560.18 245695 0.6060.20 0.6360.23 0.4060.12 0.3660.12
5.160.9 4.060.9 2368.0 0.860.26 1.560.26 1.260.14 3506110 0.9060.39 0.8860.24 0.4760.09 0.4660.12
NS ,0.05 ,0.01 ,0.01 ,0.01 ,0.01 ,0.05 ,0.05 ,0.05 NS NS
Note: P value was calculated by t-test. LV, left ventricular; NS, not significant.
that the mechanisms for pathological Q waves in the two conditions are different. In anterior myocardial infarction, depolarisation in the posterior wall where presumably normal myocardium still exists dominates the entire QRS vector. This results in definite right precordial, or anterior negativity, thus true Q waves. In aortic stenosis, the hypertrophied myocardium in both anterior and posterior walls generates greater electrical potentials leading to a much larger QRS loop than normal. Thus the subsequent Q waves in aortic stenosis are probably the result of relative anterior negativity, hence pseudo-Q waves. However, right precordial Q waves are present in only 1 / 3 patients with significant aortic stenosis, where they are associated with impaired left ventricular systolic function and adverse prognosis [12]. It is therefore suggestive that right precordial Q waves in aortic stenosis probably are the result of myocardial fibrosis in the anterior wall [7] which is usually thicker than the posterior wall. Both the PR interval and the QRS duration were prolonged in aortic stenosis compared to those in myocardial infarction. It would appear that the prolongation of PR interval represents a conduction delay in the AV junction that does not seem to be of clinical significance. But, the prolongation of QRS duration found in most aortic stenosis patients is likely to be the consequence of left ventricular hypertrophy [13]. This study has limitations. Concomitant coronary artery disease could not be definitely excluded in patients with aortic stenosis as we did not carry out
coronary angiography. However, there was no clinical history of co-existing coronary artery disease in the patients with aortic stenosis. In addition, the ventricular septum was invariably hypertrophied on echo in 18 of 19 patients with aortic stenosis and there were no regional wall motion abnormalities, making co-existing old myocardial infarction unlikely. The other limitation is that the age and gender distribution are different between the two groups. As a retrospective clinical survey in a highly selected population, we were not able to match the age and gender, but we have no reason to suspect that the differences between the two groups were due to age or gender differences. In fact, QRS voltage is usually higher in males than in females and in younger than in older subjects [14], which is contrary to our finding that the younger and predominantly male myocardial infarction group had lower QRS voltages than the older and predominantly female aortic stenosis group. The presence of right precordial Q waves is suggestive of an old myocardial infarction or significant aortic stenosis. The differential diagnosis would normally depend upon echocardiography and cardiac catheterization, in addition to history and examination. We would conclude that the simple 12-lead ECG provides important information on distinguishing the two conditions even in the absence of echocardiography or angiography. The QRS voltage in the chest leads and particularly the horizontal QRS axis can help to differentiate aortic stenosis from myocardial infarction with high sensitivity and specificity.
166
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
Acknowledgements We are grateful to Dr Derek Gibson, Consultant Cardiologist at the Royal Brompton Hospital, for his assistance in preparing this manuscript.
References [1] Horan LG, Flowers NC. Diagnostic power of the Q wave: Critical assay of its significance in both detection and location of myocardial deficit. In: Schlant RC, Hurst JW, editors, Advances in electrocardiography, New York: Grune & Stratton, 1972, pp. 321–30. [2] Fisch C. Electrocardiography. In: Braunwald E, editor, Heart disease. A textbook of cardiovascular medicine, Philadelphia: W.B. Saunders, 1997, pp. 108–52. [3] Pardee HEB, Master AM. Electrocardiograms and heart muscle disease. J Am Med Assoc 1923;80:98–101. [4] Myers GB. QRS-T patterns in multiple precordial leads that may be mistaken for myocardial infarction. I. Left ventricular hypertrophy and dilatation. Circulation 1950;1:844–59. [5] Benchimol AB, Schlesinger P. Electrocardiographic changes in a case of left ventricular and septal hypertrophy resembling anterior myocardial infarction. Circulation 1950;1:970–4. [6] Master AM, Silverblatt ML, Rosenfeld I, Donoso E. Electrocardiographic patterns simulating coronary occlusion in patients with chronic rheumatic cardiovalvular disease. Am Heart J 1957;54:50– 8.
[7] Bayes de Luna A, Serra-Genis C, Guix M et al. Septal fibrosis as determinant of ‘Q’ waves in patients with aortic valve disease. Eur Heart J 1983;4(Suppl E):86. [8] Kini PM, Eddleman Jr. EE, Pipberger HV. Electrocardiographic differentiation between left ventricular hypertrophy and anterior myocardial infarction. Circulation 1970;42:875–81. [9] Goldman MJ. The cardiac vector. In: Goldman MJ, editor, Principles of clinical electrocardiography, Los Altos: Lange Medical, 1986. [10] Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation 1977;55:613–8. [11] Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J 1949;37:161. [12] Xiao HB, James D, Kaufman B, McCrea D, Dancy M. Absent right precordial R waves are associated with reduced left ventricular function and poor prognosis in patients with aortic stenosis. Int J Cardiol 2000;76:181–6. [13] Xiao HB, Brecker SJD, Gibson DG. Relative effects of left ventricular mass and conduction disturbance on activation in patients with pathological left ventricular hypertrophy. Br Heart J 1994;71:548–53. [14] Ostrander Jr. LD, Brandt RL, Kjelsberg MO, Epstein FH. Electrocardiographic findings among the adult population of a total natural community, Tecumseh, Michigan. Circulation 1965;31:888–98.
Electrocardiographic associations of right precordial Q waves help to distinguish anterior myocardial infarction from aortic stenosis Han B. Xiao*, Ihab S. Ramzy, Timothy J. Bowker, Mark Dancy Cardiology Unit, Central Middlesex Hospital, Acton Lane, London NW10 7 NS, UK Received 3 April 2001; accepted 31 October 2001
Abstract Right precordial Q waves are ECG evidence of anterior myocardial infarction and can be present in patients with pathological left ventricular hypertrophy particularly caused by aortic stenosis. The aim of this study was to investigate the ECG features associated with Q waves in aortic stenosis and those in anterior myocardial infarction. We studied 16 patients with anterior myocardial infarction and 19 patients with aortic stenosis by means of ECG, echocardiography and clinical history. On the ECG, heart rate (70620 beats / min vs. 83620) and QT interval (380665 ms vs. 390650) did not differ between the two conditions. PR interval (160615 ms vs. 185630, P,0.05) and QRS duration (8067.0 ms vs. 95615, P,0.01) were both longer in patients with aortic stenosis than in those with myocardial infarction. The Q wave voltage in V1 (1.060.55 mV vs. 1.560.60) or V2 (1.360.5 mV vs. 1.860.85) and R wave voltage in V5 (0.760.7 mV vs. 2.160.9) or V6 (0.760.4 mV vs. 1.560.7, all P,0.01) were significantly less in patients with anterior myocardial infarction than in those with aortic stenosis. Q wave voltage over 1.3 mV in V1 or R wave voltage over 1.5 mV in V5 can differentiate aortic stenosis from anterior myocardial infarction with a sensitivity of 79% for each and specificities of 81 and 93.8%, respectively. Though the frontal QRS axis was similar in the two groups (286458 vs. 14635, P.0.05), the horizontal QRS axis pointed laterally (2306208) in aortic stenosis and posteriorly (2606208, P,0.01) in anterior myocardial infarction. A horizontal QRS axis between zero and 2458 detected the presence of aortic stenosis with a sensitivity of 94.7% and a specificity of 81.3%. On echocardiography, left ventricular hypertrophy was found in most patients (94.7%) with aortic stenosis but not in those (0%) with anterior myocardial infarction. Left ventricular end diastolic dimensions (5.160.7 cm vs. 5.160.9, P.0.05) were similar in the two groups but the end systolic dimension was increased in patients with aortic stenosis (4.060.9 cm vs. 3.460.6, P,0.05). The systolic left ventricular function (shortening fraction: 2368.0% vs. 3467.0; Vcf: 0.860.26 circ / s vs. 1.360.26, both P,0.01) was significantly impaired in patients with aortic stenosis compared to those with myocardial infarction. In conclusion, in the presence of right precordial Q waves, the simple 12-lead ECG can provide important information on distinguishing anterior myocardial infarction from aortic stenosis. In particular, the QRS voltage in the chest leads and horizontal QRS axis can differentiate anterior myocardial infarction from aortic stenosis with high sensitivity and specificity. 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Anterior myocardial infarction; Aortic stenosis; Electrocardiographic associations; Right precordial Q waves
1. Introduction Right precordial Q waves (i.e. in V1 and V2 of a conventional 12-lead ECG) are usually considered as *Corresponding author. Tel.: 144-208-967-5000; fax: 144-208-9675007. E-mail address: [email protected] (H.B. Xiao).
ECG evidence of anterior myocardial infarction [1,2]. However they can be present in patients with no apparent history of anterior myocardial infarction (Fig. 1) [3–7]. Among the non-coronary diseases, aortic stenosis is one of the commonest conditions which produce right precordial Q waves as seen in myocardial infarction [4–6]. Although attempts have been made to differentiate Q waves in aortic stenosis
0167-5273 / 02 / $ – see front matter 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 01 )00603-9
160
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
Fig. 1. Precordial ECGs recorded in a patient with anterior myocardial infarction (A) and a patient with aortic stenosis (B) showing right precordial Q waves.
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
from those in anterior infarction by orthogonal electrocardiography [8], it is still not clear whether right precordial Q waves on standard 12-lead ECG in aortic stenosis differ from those in anterior myocardial infarction, either in their morphology or their genesis. In this study, we aim to investigate ECG features associated with Q waves in the two conditions by means of ECG, echocardiography and clinical history.
2. Material and method
2.1. Subjects
161
• QT interval: from the onset of the QRS complex to the end of the T wave. • Voltage of Q waves in leads V1 and V2. • Voltage of both R and S waves in V5 and V6. • Mean QRS voltage of chest leads: total voltage of Q waves in leads V1, V2 and of both R and S waves in V5 and V6 divided by 4. • Frontal QRS axis: the combined vector of the QRS complexes in leads I and III. • Horizontal QRS axis: by the same algorithm for calculating the frontal QRS axis, we used the combined vector of the QRS complexes in chest leads V6 and V1 to assess the horizontal QRS axis [9] (Fig. 2).
2.3. Echocardiography We investigated 16 patients with anterior myocardial infarction and 19 patients with aortic stenosis. All patients had Q waves in V1 and V2 of their 12-lead ECG. Anterior myocardial infarction was diagnosed by a typical history of acute chest pain and ECG evolution from anterior ST elevation to Q waves. All patients with anterior myocardial infarction were admitted to hospital and reviewed after discharge. They were enroled in this study 1–4 weeks after the myocardial infarction. Aortic stenosis was confirmed by continuous wave Doppler recording the peak velocity equivalent to a pressure drop of over 55 mmHg across the aortic valve. Patients with pulmonary hypertension and any organic valvular disease other than aortic stenosis were excluded. Patients with ECG patterns of bundle branch block or with a permanent pacemaker implanted were also excluded.
A Hewlett-Packard Sonos-1000 or Sonos-5500 Echocardiograph was used. Cross-sectional images of the left ventricular cavity were recorded on video tape and examined for regional wall motion abnormalities. Cross-sectional image guided M-mode echocardiograms of the left ventricle were recorded at the mitral valve tip level in the parasternal long axis
2.2. Electrocardiography A standard 12-lead ECG was recorded with Fukuda Denshi equipment (FCP4101). The time intervals, heart rate and frontal QRS axis were measured by built-in computer soft-ware. QRS voltage and horizontal QRS axis were determined manually. • Heart rate: calculated as 60 / RR interval (s). • PR interval: from P wave onset to QRS complex onset. • QRS duration: from the onset to the end of the QRS complex.
Fig. 2. Measurement of horizontal QRS axis: by the same algorithm for calculating frontal QRS axis, chest leads V6 and V1 (in the places of limb leads I and III, respectively) form a 1208 angle and are divided into two halves, positive and negative from the centre. The algebraic sums of the QRS amplitudes in leads V6 and V1 are plotted on the corresponding axes. From the plotted point, perpendicular lines are dropped to a point of intersection. The line between this intersection and the centre represents the mean horizontal QRS axis (a).
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
162
view. Recordings were made on photographic paper simultaneously with a lead II ECG, at a paper speed of 50 mm / s. From the M-mode echocardiograms the following measurements were made: • Left ventricular end diastolic dimension (LVEDD) at the onset of the QRS complex on the ECG. • Left ventricular end systolic dimension (LVESD) at the maximal excursion of the left ventricular posterior wall. • The thickness of the interventricular septum (TH IVS ) and the left ventricular posterior wall (TH LVPW ) at the onset of the QRS complex on the ECG, using leading edge methodology. • Left ventricular shortening fraction (LVSF) was calculated as (LVEDD2LVESD) / LVEDD (%). • The left ventricular mass was calculated according to the Penn convention [10]: LV Mass (g) 5 1.04ssTH IVS 1 TH LVPW 1 LVEDDd 3 2sLVEDDd 3d 2 14
2.4. Doppler Transmitral and transtricuspid flows were recorded by pulsed wave Doppler, and aortic flow was recorded by both pulsed and continuous wave Doppler. All records were made with simultaneous lead II ECG and at a paper speed of 50 mm / s. Peak velocities of mitral and tricuspid E and A waves were measured: • Left ventricular ejection time (LVET) was measured from the onset to the end of the aortic flow on pulsed wave Doppler. • Mean velocity of left ventricular circumferential fibre shortening (Vcf) was calculated as: Vcf 5 LVSF / LVET (circ / s) • Pressure difference between the left ventricle and the aorta (DP) was assessed from the continuous wave Doppler signals of the aortic flow velocity (V ) by the modified Bernoulli equation as: DP 5 4V 2
2.5. Data analysis All measurements were made for three cardiac cycles and the average taken. Data are expressed as
mean6standard deviation. Differences were evaluated by the unpaired Student’s t-test, Chi-square or Fisher’s exact test. A P value of less than 0.05 was considered to be statistically significant. Sensitivity and specificity for detecting aortic stenosis were calculated as follows: • The sensitivity was expressed as the proportion of true AS (aortic stenosis) cases (as confirmed by echo) relative to cases which were classified as AS by the given ECG measurements (%). • The specificity was expressed as the proportion of true MI (anterior myocardial infarction) cases (as confirmed by history and ECG evolution) relative to cases which were classified as MI by the given ECG measurements (%).
3. Results
3.1. General ( Table 1) The mean age of the total patient population was 73 (612) years. Patients with aortic stenosis were predominantly female and patients with anterior myocardial infarction were all male. Patients with anterior myocardial infarction were younger than those with aortic stenosis (63.5612 years vs. 79.569.0, P,0.01). Systolic (131620 mmHg vs. 129615) and diastolic (7469.0 mmHg vs. 76612, all P.0.05) blood pressures did not differ between the two patient groups.
3.2. Electrocardiography 3.2.1. Time measurements Electrocardiographically, the heart rate (70620 beats / min vs. 83620) and QT interval (380665 ms vs. 390650) were similar in the two groups. PR interval (160615 ms vs. 185630, P,0.05) and QRS duration (8067.0 ms vs. 95615, P,0.01) were significantly longer in patients with aortic stenosis than in those with myocardial infarction (Table 1). QRS duration over 85 ms was found in 17 of 19 patients with aortic stenosis and only in three of 16 patients with anterior myocardial infarction (P,0.01) (Table 2).
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
163
Table 1 Clinical and ECG data
Age (years) Sex (female:male) Systolic BP (mmHg) Diastolic BP (mmHg) Heart rate (bpm) PR interval (ms) QRS duration (ms) QT interval (ms) Frontal QRS axis (8) Horizontal QRS axis (8) Q wave voltage in V1 (mV) Q wave voltage in V2 (mV) R wave voltage in V5 (mV) R wave voltage in V6 (mV) Mean voltage of chest leads (mV) LVH according to Sokolow–Lyon criteria
Anterior infarction (n516)
Aortic stenosis (n519)
P value
60612 0:16 131620 7669.0 70620 160615 8067.0 390665 28645 260620 1.060.55 1.360.50 0.760.6 0.760.4 1.060.5 1 / 16 (6.25%)
7969.0 11:8 129615 76612 83620 185630 95615 390650 14635 230620 1.560.60 1.860.85 2.160.9 1.560.7 2.060.8 13 / 19 (68.4%)
,0.01 ,0.01 NS NS NS ,0.05 ,0.01 NS NS ,0.01 ,0.05 ,0.05 ,0.01 ,0.01 ,0.01 ,0.02
Note: P value was calculated by t-test, Chi-squared or Fisher exact test. NS, not significant; LVH, left ventricular hypertrophy.
Table 2 Critical ECG values between anterior myocardial infarction and aortic stenosis ECG criteria QRS duration $85 ms ,85 ms Sensitivity (%) Specificity (%) Q wave voltage in V1 $1.3 mV ,1.3 mV Sensitivity (%) Specificity (%) R wave voltage in V5 $1.5 mV ,1.5 mV Sensitivity (%) Specificity (%) Mean QRS voltage of chest leads $1.5 mV ,1.5 mV Sensitivity (%) Specificity (%) Horizontal QRS axis 0 to 2458 245 to 2908 Sensitivity (%) Specificity (%)
Anterior infarction (n516)
Aortic stenosis (n519)
P value
3 13
17 2 89.5
,0.001
15 4 78.9
,0.001
15 4 78.9
,0.001
16 3 84.2
,0.001
18 1 94.7
,0.001
81.2 3 13 81.2 1 15 93.8 2 14 87.5 3 13 81.2
Note: P value was calculated by Chi-squared or Fisher exact test.
164
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
3.2.2. QRS voltage The Q wave voltages in V1 (1.060.55 mV vs. 1.560.60) and in V2 (1.360.5 mV vs. 1.860.85) and the R wave voltages in V5 (0.760.7 mV vs. 2.160.9) and in V6 (0.760.4 mV vs. 1.560.7, all P,0.01) were significantly less in patients with anterior myocardial infarction than in those with aortic stenosis (Fig. 1). Left ventricular hypertrophy by Sokolow–Lyon criteria [11] was present in 13 / 19 (68.4%) patients with aortic stenosis and in only 1 / 16 (6.3%) patients with anterior myocardial infarction (P,0.01) (Table 1). Using the median as a critical value, a Q wave voltage over 1.3 mV in V1 or an R wave voltage over 1.5 mV in V5 can differentiate aortic stenosis from anterior myocardial infarction with a sensitivity of 79% for each and specificities of 81 and 93.8%, respectively (Table 2). The mean QRS voltage of chest leads over 1.5 mV could detect aortic stenosis with a sensitivity of 84.2% and a specificity of 87.5%. 3.2.3. QRS axis Though the frontal QRS axis was similar in the two groups (286458 vs. 14635, P.0.05), the horizontal QRS axis differed significantly, pointing laterally (2306208) in aortic stenosis and posterially (2606208, P,0.01) in anterior myocardial infarction (Fig. 3). A horizontal QRS axis from zero to
Fig. 3. The distribution of horizontal QRS axis in patients with anterior myocardial infarction (solid dots) and those with aortic stenosis (open circles).
2458 detected the presence of aortic stenosis with a sensitivity of 94.7% and a specificity of 81.3%.
3.3. Echocardiography Echocardiographically, left ventricular hypertrophy was found in most patients (18 / 19, 94.7%) with aortic stenosis but not in those with anterior myocardial infarction. As expected, anterior hypokinesis was only found in patients with anterior infarction. Left ventricular end diastolic dimensions (5.160.7 cm vs. 5.160.9, P.0.05) were similar in the two groups but the end systolic dimension was greater in patients with aortic stenosis (4.060.9 cm vs. 3.460.6, P, 0.05). The systolic left ventricular function (shortening fraction: 2368.0% vs. 3467.0; Vcf: 0.860.26 circ / s vs. 1.360.26, both P,0.01)was significantly impaired in patients with aortic stenosis compared to those with myocardial infarction. Both E (0.6060.20 M / s vs. 0.9060.39) and A (0.6360.23 M / s vs. 0.8860.24, both P,0.05) wave velocities of transmitral flow were significantly higher in aortic stenosis than in myocardial infarction (Table 3).
4. Discussion Pathological Q waves are a common ECG feature of myocardial infarction, though they are also present in patients with other conditions particularly aortic stenosis [3,4,6]. The other conditions are usually identified on autopsy [3,4] or by imaging techniques such as echocardiography [12]. The distinction cannot be made convincingly by Q wave morphology alone. However, the combination of clinical history, ECG and echocardiogram enables us to establish the association of Q waves with the underlying cardiac pathology. In this study we sought to describe the characteristic ECG features which distinguish anterior myocardial infarction from significant aortic stenosis in patients with right precordial Q waves. As one would expect, we found that the absolute values of QRS voltage in the precordial leads were significantly greater in aortic stenosis than in myocardial infarction. Horizontal QRS axis, a less frequently studied measurement, differentiated aortic stenosis from anterior myocardial infarction with a higher sensitivity than QRS voltage. This finding suggests
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
165
Table 3 Echocardiographic data
LV end diastolic dimension (cm) LV end systolic dimension (cm) LV shortening fraction (%) Vcf (circ / s) Ventricular septal thickness (cm) LV posterior wall thickness (cm) LV mass (g) Mitral E wave (M / s) Mitral A wave (M / s) Tricuspid E wave (M / s) Tricuspid A wave (M / s)
Anterior infarction (n516)
Aortic stenosis (n519)
P value
5.160.7 3.460.6 3467.0 1.360.26 1.160.20 0.9560.18 245695 0.6060.20 0.6360.23 0.4060.12 0.3660.12
5.160.9 4.060.9 2368.0 0.860.26 1.560.26 1.260.14 3506110 0.9060.39 0.8860.24 0.4760.09 0.4660.12
NS ,0.05 ,0.01 ,0.01 ,0.01 ,0.01 ,0.05 ,0.05 ,0.05 NS NS
Note: P value was calculated by t-test. LV, left ventricular; NS, not significant.
that the mechanisms for pathological Q waves in the two conditions are different. In anterior myocardial infarction, depolarisation in the posterior wall where presumably normal myocardium still exists dominates the entire QRS vector. This results in definite right precordial, or anterior negativity, thus true Q waves. In aortic stenosis, the hypertrophied myocardium in both anterior and posterior walls generates greater electrical potentials leading to a much larger QRS loop than normal. Thus the subsequent Q waves in aortic stenosis are probably the result of relative anterior negativity, hence pseudo-Q waves. However, right precordial Q waves are present in only 1 / 3 patients with significant aortic stenosis, where they are associated with impaired left ventricular systolic function and adverse prognosis [12]. It is therefore suggestive that right precordial Q waves in aortic stenosis probably are the result of myocardial fibrosis in the anterior wall [7] which is usually thicker than the posterior wall. Both the PR interval and the QRS duration were prolonged in aortic stenosis compared to those in myocardial infarction. It would appear that the prolongation of PR interval represents a conduction delay in the AV junction that does not seem to be of clinical significance. But, the prolongation of QRS duration found in most aortic stenosis patients is likely to be the consequence of left ventricular hypertrophy [13]. This study has limitations. Concomitant coronary artery disease could not be definitely excluded in patients with aortic stenosis as we did not carry out
coronary angiography. However, there was no clinical history of co-existing coronary artery disease in the patients with aortic stenosis. In addition, the ventricular septum was invariably hypertrophied on echo in 18 of 19 patients with aortic stenosis and there were no regional wall motion abnormalities, making co-existing old myocardial infarction unlikely. The other limitation is that the age and gender distribution are different between the two groups. As a retrospective clinical survey in a highly selected population, we were not able to match the age and gender, but we have no reason to suspect that the differences between the two groups were due to age or gender differences. In fact, QRS voltage is usually higher in males than in females and in younger than in older subjects [14], which is contrary to our finding that the younger and predominantly male myocardial infarction group had lower QRS voltages than the older and predominantly female aortic stenosis group. The presence of right precordial Q waves is suggestive of an old myocardial infarction or significant aortic stenosis. The differential diagnosis would normally depend upon echocardiography and cardiac catheterization, in addition to history and examination. We would conclude that the simple 12-lead ECG provides important information on distinguishing the two conditions even in the absence of echocardiography or angiography. The QRS voltage in the chest leads and particularly the horizontal QRS axis can help to differentiate aortic stenosis from myocardial infarction with high sensitivity and specificity.
166
H.B. Xiao et al. / International Journal of Cardiology 82 (2002) 159 – 166
Acknowledgements We are grateful to Dr Derek Gibson, Consultant Cardiologist at the Royal Brompton Hospital, for his assistance in preparing this manuscript.
References [1] Horan LG, Flowers NC. Diagnostic power of the Q wave: Critical assay of its significance in both detection and location of myocardial deficit. In: Schlant RC, Hurst JW, editors, Advances in electrocardiography, New York: Grune & Stratton, 1972, pp. 321–30. [2] Fisch C. Electrocardiography. In: Braunwald E, editor, Heart disease. A textbook of cardiovascular medicine, Philadelphia: W.B. Saunders, 1997, pp. 108–52. [3] Pardee HEB, Master AM. Electrocardiograms and heart muscle disease. J Am Med Assoc 1923;80:98–101. [4] Myers GB. QRS-T patterns in multiple precordial leads that may be mistaken for myocardial infarction. I. Left ventricular hypertrophy and dilatation. Circulation 1950;1:844–59. [5] Benchimol AB, Schlesinger P. Electrocardiographic changes in a case of left ventricular and septal hypertrophy resembling anterior myocardial infarction. Circulation 1950;1:970–4. [6] Master AM, Silverblatt ML, Rosenfeld I, Donoso E. Electrocardiographic patterns simulating coronary occlusion in patients with chronic rheumatic cardiovalvular disease. Am Heart J 1957;54:50– 8.
[7] Bayes de Luna A, Serra-Genis C, Guix M et al. Septal fibrosis as determinant of ‘Q’ waves in patients with aortic valve disease. Eur Heart J 1983;4(Suppl E):86. [8] Kini PM, Eddleman Jr. EE, Pipberger HV. Electrocardiographic differentiation between left ventricular hypertrophy and anterior myocardial infarction. Circulation 1970;42:875–81. [9] Goldman MJ. The cardiac vector. In: Goldman MJ, editor, Principles of clinical electrocardiography, Los Altos: Lange Medical, 1986. [10] Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation 1977;55:613–8. [11] Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J 1949;37:161. [12] Xiao HB, James D, Kaufman B, McCrea D, Dancy M. Absent right precordial R waves are associated with reduced left ventricular function and poor prognosis in patients with aortic stenosis. Int J Cardiol 2000;76:181–6. [13] Xiao HB, Brecker SJD, Gibson DG. Relative effects of left ventricular mass and conduction disturbance on activation in patients with pathological left ventricular hypertrophy. Br Heart J 1994;71:548–53. [14] Ostrander Jr. LD, Brandt RL, Kjelsberg MO, Epstein FH. Electrocardiographic findings among the adult population of a total natural community, Tecumseh, Michigan. Circulation 1965;31:888–98.