CLINICAL STUDIES
Persistent ST segment depression in precordial leads V5–V6 after Q-wave anterior wall myocardial infarction is associated with restrictive physiology of the left ventricle
Abid Assali, MDa,
Samuel Sclarovsky, MDa,
Itzhak Herz, MDa,
Mordechai Vaturi, MDa,
Irit Gilad, PhDa,
Alejandro Solodky, MDa,
Nili Zafrir, MDa,
Yehuda Adler, MDa,
Alex Sagie, MDa,
Yochai Birnbaum, MDa and
David Hasdai, MDa
a Department of Cardiology, Rabin Medical Center, Beilinson Campus, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Manuscript received December 9, 1998;
revised manuscript received September 10, 1999,
accepted October 27, 1999.
Reprint requests and correspondence: Dr. David Hasdai, Department of Cardiology, Rabin Medical Center (Beilinson Campus), Petah Tiqva, 49100, Israel
dhasdai{at}post.tau.ac.il
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Abstract
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OBJECTIVES
To examine the relationship between the persistence of ST segment depression in leads V5–V6 after Q-wave anterior wall myocardial infarction (MI) and the filling pattern of the left ventricle (LV).
BACKGROUND
Precordial ST segment depression predominantly in leads V5–V6 is associated with increased in-hospital morbidity and mortality after acute myocardial ischemia, perhaps due to reduced diastolic distensibility of the LV.
METHODS
We prospectively studied 19 patients after Q-wave anterior wall MI (>6 months). All patients underwent 12-lead ECG recording, symptom-limited treadmill exercise testing with single photon emission computed tomography thallium-201 imaging, transthoracic Doppler echocardiography, cardiac catheterization and measurement of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels. Patients were classified based on the presence of ST segment depression in leads V5–V6: Group I = ST segment depression <0.1 mV (n = 10); Group II = ST segment depression  0.1 mV (n = 9).
RESULTS
Patients in Group II had greater LV end diastolic pressures (32.4 ± 6.5 mm Hg vs. 14.8 ± 6.1 mm Hg; p = 0.0001), higher plasma ANP (44.4 ± 47.1 pg/ml vs. 10.7 ± 14 pg/ml; p = 0.04) and BNP levels (89.4 ± 62.7 pg/ml vs. 23.6 ± 33.1 pg/ml; p = 0.01), greater left atrium area (20.6 ± 3.1 cm2 vs. 17.8 ± 2.4 cm2; p = 0.05), lower peak atrial (A), higher early (E) mitral inflow velocities, a higher E/A ratio and a lower deceleration time (167 ± 44 ms vs. 220 ± 40 ms; p = 0.05). Lung thallium uptake during exercise was more common in Group II (78% vs. 10%, p = 0.04).
CONCLUSIONS
Persistent ST segment depression in leads V5–V6 in survivors of Q-wave anterior wall MI is associated with increased LV filling pressure and a restrictive LV filling pattern.
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Abbreviations and Acronyms
| | A | = peak atrial velocity | | ACE | = angiotensin converting enzyme | | AMI | = acute myocardial infarction | | ANP | = atrial natriuretic peptide | | BNP | = brain natriuretic peptide | | DT | = decceleration time | | E | = peak inflow early velocity | | E/A | = ratio of E and A | | FS | = fractional shortening | | LV | = left ventricle or ventricular | | LVEDP | = left ventricular end diastolic pressure | | LVEF | = left ventricular ejection fraction | | MI | = myocardial infarction | | SPECT | = single photon emission computed tomography |
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Several studies have demonstrated that patients with precordial ST segment depression after acute myocardial infarction (AMI) have larger infarcts, greater incidence of recurrent ischemia, worse left ventricular ejection fraction (LVEF) and a higher rate of adverse clinical events, including greater mortality (1–3). Willems et al. (4) reported that precordial ST segment depression also portends important prognostic information during anterior wall AMI, reflecting both greater infarct size and higher in-hospital mortality. Persistent ST segment depression before discharge is also an independent risk factor for increased mortality and morbidity after AMI treated with thrombolytic therapy (5–7).
Most of these prior studies have not differentiated among the various patterns of precordial ST segment depression. The importance of the location of predominant precordial ST segment depression, however, has been emphasized by several recent studies. ST segment depression predominantly in left precordial leads (V4–V6) in patients after inferior wall AMI was associated with increased in-hospital mortality, presumably due to diffuse ischemia associated with concomitant coronary artery disease particularly involving the left anterior descending coronary artery (8–10). Sclarovsky et al. (11) also previously reported that patients with unstable angina pectoris and ST segment depression predominantly in leads V4–V6 (in the absence of tachycardia) had severe coronary artery disease, often with left main coronary artery involvement, and a poor prognosis when they developed AMI (12).
The pathophysiology behind these observations is not clear. Recently we postulated that ST segment depression predominantly in leads V4–V6 during acute inferior wall myocardial infarction (MI) is reflective of transient diffuse ischemia, causing reduced diastolic distensibility of the left ventricle (LV) (13) and increased secretion of atrial natriuretic peptide (ANP) (14). The primary objective of this study was to examine the hypothesis that there is a relationship between persistent ST segment depression in the precordial leads V5–V6 in patients with previous Q-wave anterior wall MI and the filling pattern of the LV.
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Methods
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Patients.
We prospectively studied 19 consecutive patients >6 months after Q-wave acute anterior MI (pathological Q-wave in leads V1 to V3 and abnormal wall motion in the anterior wall as detected by echocardiography) with functional class 1 or 2 and taking angiotensin enzyme converting (ACE) inhibitors. We excluded patients with another infarction other than the index infarction, chronic renal failure (serum creatinine level >1.5 mg%), valvular heart disease or cardiomyopathy, severe LV dysfunction (LVEF <25%), cor pulmonale, LV hypertrophy or interventricular conduction defects (left bundle branch block, left anterior fascicular block, left posterior fascicular block or right bundle branch block).
Study protocol.
The following protocol was approved by the local institutional review board. After informed consent was obtained, each patient underwent the following tests: 12-lead ECG recording, symptom-limited treadmill exercise testing using the Bruce or modified Bruce protocol with single photon emission computed tomographic (SPECT) thallium-201 imaging, transthoracic two-dimensional and Doppler echocardiography and left ventriculography and coronary angiography using the Judkin’s technique via the femoral artery. Blood samples were also drawn from the antecubital vein in the supine position after an overnight fast for the measurement of plasma ANP and brain natriuretic peptide (BNP) levels.
Electrocardiographic analysis.
The ECG recordings were analyzed by two independent investigators blinded to the results of other tests. All ECG recordings had abnormal Q-wave in leads V1 to V3. Patients were further classified into two groups based on the presence of ST segment depression in precordial leads V5–V6, as previously described (13,14). Briefly, the degree of ST segment depression was determined in all leads (measured manually to the nearest 0.05 mV, 0.06 s after the J point). For each patient the sum of the ST segment depression was calculated. Patients were classified as Group I if the sum of ST segment depression in leads V5–V6 was <0.1 mV and Group II if the sum of ST segment depression was 0.1 mV in leads V5–V6 (Fig. 1).
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Figure 1 Representative electrocardiograms of patient with previous anterior wall MI with (upper panel) and without (lower panel) significant precordial ST segment depression in leads V5–V6.
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Echocardiography.
M-mode and two-dimensional echocardiography, spectral pulsed-wave and color Doppler studies were obtained (by an experienced operator blinded to the results of other tests) using a Hewlett-Packard (Andover, Massachusetts) phased array sector scanner with a 2.5 MHz transducer (77020A). M-mode measurements were derived from imaging two-dimensional parasternal short-axis views and included end diastolic and end systolic LV cavity diameter at the mitral and midventricular level. Septal and posterior wall thickness were obtained from the short axis view at the mitral level. Left ventricular inflow velocities were obtained by pulsed-wave Doppler echocardiography, by placing the sample volume at the level of the mitral leaflet tips and at midventricle, 3 cm into the LV, from the apical four-chamber view. Measurements included the following parameters from the mitral flow velocity spectrum (average of five beats): peak inflow early (E) and peak atrial (A) velocities (cm/s), as well as their ratio E/A and the deceleration time (DT) of the early wave (ms).
SPECT thallium-201 imaging.
All patients underwent SPECT thallium-201 imaging during symptom-limited treadmill exercise testing using the Bruce or modified Bruce protocol (15). At peak exercise, a dose of 3 mCi of thallium-201 was injected intravenously, and SPECT imaging was performed. Rest SPECT images were obtained 4 h after exercise. If fixed defects were detected, reinjection was also performed at 24 h. The SPECT images were analyzed for fixed or reversible abnormalities, findings suggestive of multivessel abnormality and increased lung thallium uptake.
Hemodynamic assessment and coronary angiography.
Systemic blood pressure and LV end diastolic pressure (LVEDP) were measured during cardiac catheterization but before coronary angiography. Coronary angiography was performed using 5–6F catheters. The severity of coronary artery stenosis was visually assessed by two blinded investigators using orthogonal views. Single plane left ventriculography was performed in the right anterior oblique view. All procedures were performed using nonionic contrast media.
Measurement of plasma ANP and BNP levels.
Blood samples were taken from the antecubital vein in the supine position after an overnight fast. The sample was transferred immediately into chilled glass tubes containing disodium ethylenediamine tetraacetic acid (1 mg/ml) and aprotinin (500 units/ml) and centrifuged immediately at 4° C, and the plasma was frozen and stored at –80° C until assayed. Atrial natriuretic peptide and BNP were determined using direct immunoradiometric kits (Shionora & Co., Ltd., Osaka, Japan and purchased from Cis Bio International, France). The kits (16) are highly sensitive and employ two different monoclonal antibodies that recognize the C-terminal region and the ring structure of ANP and BNP, respectively. The first antibody is bound to the solidified bead, which is incubated with the hormone, and the second I(125) monoclonal antibody is added to form a sandwich complex. After incubation the beads are washed to remove unbound radioiodinated antibody. A direct positive correlation is obtained between hormone concentration (2.5–2,000 pg/ml for both hormones) and radioactivity measured by gamma counter.
Statistical analysis.
All continuous data are expressed as mean ± SD unless otherwise indicated. Comparisons of parameters between two groups were made by the Fisher exact test or the unpaired Student t test. Correlation coefficients between hemodynamic, Doppler and plasma ANP and BNP levels were calculated by Pearson linear regression analysis. P  0.05 was considered statistically significant.
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Results
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The clinical and demographic features of the patient population are presented in Table 1. No difference between groups was found in relation to age, medications, coronary artery risk factors and history of revascularization procedures. The mean ST segment depression (for leads V5 and V6 together) in Group II was 0.34 ± 0.14 mV, as compared with 0.013 ± 0.019 mV for Group I (p = 0.0001).
Systemic blood pressure, LVEDP and LVEF are presented in Table 2. Systemic blood pressure and LVEF were similar in both groups. The LVEDP was significantly higher in Group II compared with Group I (32.4 ± 6.5 mm Hg vs. 14.8 ± 6.1 mm Hg; p = 0.0001). There was a positive correlation between the sum of ST segment depression and the LVEDP (r = 0.65; p = 0.003).
The left anterior descending coronary artery was occluded without distal perfusion in 2 (22%) patients in Group II, as compared with none of the patients in Group I. In the remaining patients in Group II, the distal vessel received native collateral circulation in two patients, circulation via an arterial graft in two patients and antegrade flow in three patients. In Group I, the distal vessel received native collateral circulation in three patients, circulation via an arterial graft in two patients and antegrade flow in five patients. None of the patients in either group had mitral regurgitation grade >2, and four patients in each group had mitral regurgitation 2.
The plasma ANP and BNP levels of the two groups are also presented in Table 2. Patients in Group II had significantly higher plasma ANP (44.4 ± 47.1 pg/ml vs. 10.7 ± 14 pg/ml; p = 0.04) and BNP levels (89.4 ± 62.7 pg/ml vs. 23.6 ± 33.1 pg/ml; p = 0.01) than patients in Group I. We observed a positive correlation between the sum of ST depression in leads V5–V6 and plasma BNP levels (r = 0.63; p = 0.004) but not with ANP levels.
The two-dimensional echocardiographic data are presented in Table 3. The LV end diastolic and systolic diameters were similar in both groups. No significant difference was found in the thickness of the LV (interventricular septum and posterior wall). The LV systolic function as measured by two-dimensional echocardiographic [LV fractional shortening (FS)] was also not significantly different. The diameter of the left atrium, however, was significantly higher in Group II than in Group I (4.12 ± 0.38 cm vs. 3.66 ± 0.24 cm; p = 0.007). Similarly, the left atrium area was found to be bigger in Group II compared with Group I (20.6 ± 3.1 cm2 vs. 17.8 ± 2.4 cm2; p = 0.05). We found a significant correlation between the sum of ST depression in leads V5–V6 and the left atrium diameter (r = +0.51, p = 0.03).
The transmitral Doppler measurements are presented in Table 4. Patients in Group II had significantly lower A, higher E and a higher E/A ratio compared with patients in Group I. Decceleration time was lower in Group II (167 ± 44 ms vs. 220 ± 40 ms; p = 0.05). Five of the nine patients in Group II had a DT of less than 160 ms (as compared with 2 of 10 in Group I, p = 0.17) and five of nine patients had an E/A ratio greater than 1.1 (as compared with 1 of 10 in Group I, p = 0.06). We found a significant correlation between the sum of ST depression in leads V5–V6 and the transmitral Doppler flow parameter E (r = +0.53, p = 0.02) and borderline with A (r = –0.43, p = 0.07) and the E/A ratio (r = +0.43, p = 0.07). A correlation was found between ANP plasma levels and the transmitral Doppler flow parameters E (r = +0.62, p = 0.004), A (r = –0.43, p = 0.07) and E/A ratio (r = +0.62, p = 0.005).
Exercise testing.
The exercise data are shown in Table 5. There were no differences between the two groups in exercise duration, peak heart rate, peak systolic blood pressure and the rate-pressure product. Patients in Group II had more angina and dyspnea during exercise, but these differences were not significant. Seventy-eight percent of the patients in Group II had increased lung thallium uptake during exercise compared with 10% in Group I (p = 0.04).
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Discussion
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Acute MI causes complex alterations in LV structure and function. In this study several measures were used to assess LV function of patients with previous Q-wave anterior wall MI according to the pattern of ST segment depression in leads V5–V6. This study demonstrates that persistent ST segment depression in leads V5–V6 in patients with previous Q-wave anterior wall AMI is associated with 1) increased LVEDP, 2) restrictive diastolic mitral flow pattern, 3) larger left atrium diameter and area, 4) increased lung thallium uptake during symptom-limited treadmill exercise testing, and 5) and increased plasma levels of ANP and BNP.
Relation between ST segment depression and LVEDP.
Our data indicate that patients with persistent ST segment depression in leads V5–V6 had higher LVEDP compared with those without. We found that the LVEDP can be predicted by the magnitude of ST segment depression in these leads, with a significant direct correlation. The similar systolic function is suggestive of a predominantly diastolic abnormality. This is also supported by the finding of Doppler variables of the mitral diastolic flow and larger left atrium found by two-dimensional echocardiography, which are also suggestive of a restrictive filling pattern. Hasdai et al. (13) previously reported that ST segment depression predominantly in leads V4–V6 during the acute phase of inferior MI is reflective of diffuse ischemia due to extensive coronary artery disease with reduced diastolic distensibility and increased LVEDP. This can also be learned from the work of Grossman et al. (17) and of Dwyer (18), demonstrating that atrial pacing in ischemic patients results in significant ST segment depression in leads V4–V6 and an increase in LVEDP, as opposed to lack of ECG changes and a decline in LVEDP in nonischemic subjects.
Relation between ST segment depression and the filling pattern of the LV.
During the past decade, several studies have related the Doppler mitral flow velocity pattern to LV and pulmonary capillary wedge pressure recording. Three abnormal patterns have been described and correlated with hemodynamic findings (19,20). One of these patterns, the restrictive pattern, is characterized by increased early filling (E), reduced atrial filling (A), increased E/A ratio and short DT of early filling. Recently, the restrictive pattern was found to be the best predictor of cardiac death after AMI (21,22). In our study, we demonstrated that patients with previous Q-wave anterior wall MI with persistent ST segment depression in leads V5–V6 have a Doppler mitral flow velocity pattern that is consistent with restrictive physiology. They have increased early filling (E), reduced atrial filling (A), higher E/A ratio and shorter DT of early filling.
Both myocardial relaxation and compliance are affected by ischemia. Abnormal myocardial relaxation and decreased LV compliance have been described in the subacute phase of AMI (23). It appears that while all the infarctions in our cohort had evidence of diastolic dysfunction, patients in Group II demonstrated a more severe diastolic dysfunction characterized by restrictive physiology. The chronic diffuse subendocardial ischemia due to elevated LVEDP in patients with previous Q-wave anterior wall MI with persistent ST segment depression in leads V5–V6 may be the cause for this restrictive pattern of filling. Our study, as others (21,22), demonstrates that patients with restrictive filling physiology also have more functional impairment (more angina, dyspnea and lung thallium uptake during exercise).
Relation between ST segment depression and the natriuretic peptides.
Atrial natriuretic peptide and BNP are two of the major peptides in the natriuretic family with a similar ability to promote natriuresis and diueresis, inhibit the renin-angiotensin-aldosterone axis and cause vasodilation. Brain natriuretic peptide may be the superior prognosticator for risk stratification after AMI independent of LVEF (24). The mechanism for the release of ANP and BNP remain uncertain. Disease states associated with increased pulmonary capillary wedge pressure and increased atrial stretch are associated with increased secretion of ANP from the atrium (24). Unlike ANP, BNP is synthesized in and secreted primarily from the LV in response to increased myocardial stretch, suggesting that BNP may be a more specific indicator of ventricular pathology (25). Measurement of both these peptides may be a superior, noninvasive way to stratify risk in post-MI patients, because high levels of these peptide in the plasma are associated with higher risk to develop symptomatic heart failure and death (24,25).
In a previous study (14) we demonstrated that patients with acute inferior wall MI and precordial ST segment depression predominantly in leads V4–V6 had higher ANP levels than patients without ST segment depression or patients with ST segment depression predominantly in leads V1–V3. This finding was also associated with increased in-hospital mortality. In this study we found that patients with previous Q-wave anterior wall MI who had persistent ST segment depression in leads V5–V6 had higher levels of both ANP and BNP, which correlated with the sum of the ST segment depression in these leads and the magnitude of the LVEDP. Since this group of patients had similar LVEF as the group without persistent ST segment depression in the precordial leads V5–V6, we assume that these finding are best explained by the elevated LVEDP and the restrictive filling pattern of the LV.
Clinical implications.
Because a restrictive LV filling pattern is a useful indicator of function and prognosis, it is of great practical value to identify patients likely to have this filling pattern by a simple and noninvasive method. This study demonstrates that persistent ST segment depression in leads V5–V6 among patients who have survived Q-wave anterior wall AMI accurately identifies a subgroup of patients with high LV filling pressure and restrictive LV filling pattern. This ECG requires less expertise to obtain and interpret than other available techniques and, thus, may be more readily implemented.
Study limitations.
These results are affected by the selection criteria of the population. By including only survivors of Q-wave anterior wall AMI >6 months, patients with a worse prognosis who died before were not studied. Thus, our results cannot be generalized to the whole population immediately after AMI. Second, we did not measure the isovolumic relaxation time, which is probably the most sensitive of the Doppler indexes in detecting impaired relaxation (26) or the flow velocity pattern in the pulmonary veins that correlates with the LVEDP better than the mitral Doppler variables (27). In our study we analyzed only the mitral flow velocity profile, which is more standardized, easy to obtain in all patients and extensively used in the noninvasive assessment of LV filling abnormalities.
Conclusions.
This study demonstrates that persistence of ST segment depression in leads V5–V6 in a subgroup of patients who have survived Q-wave anterior wall AMI is associated with high LV filling pressure and a restrictive LV filling pattern.
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References
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Abstract
Methods