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).
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.
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).
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 cm 2 vs. 17.8 ± 2.4 cm 2 ; 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).
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.
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.
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).
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.
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).
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.
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.
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 ttest. 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.
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).
Clinical Characteristics of Patients According to ECG Patternlegend legend
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).
Hemodynamic, Left Ventricle Function, ANP and BNP Data of the Two Groups According to ECG Patternlegend
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 cm 2 vs. 17.8 ± 2.4 cm 2 ; 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).
Two-Dimensional Echocardiographic Data According to ECG Patternlegend
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).
Transmitral Doppler Variables in Patients Grouped According to ECG Patternlegend legend
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).
Exercise Treadmill Data During Symptom-Limited Treadmill Exercise Testing According to ECG Pattern
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.
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.
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.
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.
d o t o r e g . c o m
ST segment depression is the most common ECG sign of ischemia.
ECG 1. The ECG above belongs to a patient with stable angina pectoris. The patient complained of effort angina in the last 2
weeks. Coronary angiography was performed and then the patient was referred to coronary artery bypass graft operation
because of 3 vessel disease. ST segment flattening is one of the first signs of coronary ischemia and generally preceedes ST
ECG 2. ST segment depression.
ECG 3a. This ECG is from a different patient. The first stage of treadmill exercise test shows no ST segment depression.
ECG 3b. In the peak exercise, ST segment depression developes in leads II, III, aVF, V3-V6.
ECG 3c. Persistence of ST segment depression in the recovery period (after treadmill has been stopped) suggests severe
coronary ischemia. Lateron, coronary angiography was performed and 3 vessel disease (extensive coronary artery disease)
ECG 4. This 67 years old man complains of chest pain even during resting. He had undergone coronary artery bypass graft
operation. The ECG during the chest pain shows ST segment depression in leads V2-V6.
ECG 5. The ECG above belongs to a hypertensive patient with normal coronary arteries. His blood pressure was not under
control for a long time. ST segment depression is present in lateral leads. The deep S wave in lead C2 and the high R waves
in leads C4 and C5 suggest the presence of left ventricular hypertrophy. In patients with chronic hypertension, observation of
ST depression in lateral leads does not necessarily suggest coronay artery disease.
ECG 6a. This ECG belongs to a 70 years old patient who complained of chest pain for the last 2 months. Coronary angiography
revealed 99% stenosis in the bifurcation of left main coronary artery, and 70% stenosis in the right coronary artery. The distinct
ST segment depression in leads C3-C6 with mild ST sedpression in inferior leads suggest extensive coronary artery disease.
The presence of ST segment elevation in lead aVR also raises the suspicion of left main coronary artery disease.
ECG 6b. This ECG was recorded 6 hours later. Because of the effective medical therapy, ST depression is now confined only
ECG 6c. This ECG was recorded 12 hours later, just before the coronary bypass surgery. There is distinct ST depression in leads
C5 and C6. Diagnosis of left main coronary artery disease necessitates immediate coronary bypass operation.
Figure 1a. Coronary angiography of the same patient shows 99% stenosis at the
bifurcation of left main coronary artery LAD, Cx and
proximal part of left main coronary artery are normal.
of the proximal right coronary artery .
performed on the same day showed significant stenosis of the LAD and Cx coronary arteries. The patient was referred
to coronary artery bypass graft operation.
ECG 8a. In this patient with coronary artery disease, ST segment depression and U waves with increased amplitude (higher
than that of the T wave) is observed during ischemic chest pain.
The types of ST segment depression in the patient with acute coronary ischaemic syndrome and no evidence of infarction. (A) Horizontal. (B) Horizontal. (C) Downsloping. (D) Upsloping.
Acute posterior wall myocardial infarction
Most cases of posterior AMIs are attributable to lesions in a dominant right coronary or left circumflex coronary artery and thus mainly affect the dorsal—or posterior—area of the heart. Acute posterior wall myocardial infarction occurs in up to 20% of AMIs, with the vast majority occurring along with inferior or lateral AMI. 10, 11 Isolated posterior wall AMIs, however, do occur. 12 Electrocardiographic abnormalities suggestive of an posterior wall AMI include the following (in leads V1, V2, or V3) (fig 4A): (1) horizontal STD with tall, upright T waves; (2) a tall, wide R wave; and (3) an R/S wave ratio greater than 1.0 in lead V2. 3, 11 STD in the right precorial leads may therefore represent either reciprocal change secondary to an inferior or lateral AMI or may indicate a posterior AMI. Boden et al noted that in patients presenting with angina or an anginal equivalent and an ECG demonstrating STD in leads V1–V3, about one half of the patients were found to have had a posterior wall AMI. 13 Perhaps the best way to help the clinician determine the aetiology of right precordial horizontal STD is to use additional electrocardiographic leads that imagine the posterior wall of the left ventricular directly—namely, leads V8 and V9 (fig 4B). ST segment elevation greater than 1 mm in the posterior leads V8 and V9 confirms the presence of posterior wall AMI. 10, 11, 14
An additional lead ECG uses the standard 12 leads in addition to other leads, including the posterior leads V8 and V9, placed under the left mid-scapular line and the left paraspinal border. Refer to fig 4B for STE seen in the patient with posterior AMI. Numerous studies have shown using additional lead ECGs in selective cases (that is, suspected posterior AMI) increases the sensitivity without sacrificing the specificity of detecting acute posterior wall AMI. 10, 11, 14
Reciprocal ST segment depression
Reciprocal STD—also known as reciprocal change—is defined as horizontal or downsloping STD in leads that are separate and distinct from leads manifesting STE. The causes of reciprocal change are thought to be secondary to coexisting distant ischaemia, a manifestation of infarct extension, or an electrophysiological phenomenon caused by displacement of the injury current vector away from the non-infarcted myocardium. 3 Reciprocal change can be identified in about one third of patients with anterior wall AMIs and up to 80% of patients with inferior AMIs will demonstrate anterior ST segment depression in leads V1, V2, or V3. The presence of reciprocal change increases the positive predictive value for a diagnosis of AMI to greater than 90%. 8 Perhaps the greatest utility of reciprocal change is in patients with acute cardiac symptoms and ST segment elevation of uncertain aetiology; such is the case in approximately 5% to 10% of AMI patients in the ED. 8 Although an STE AMI may be obvious in many instances, the presence of reciprocal change identifies a subset of patients with more extensive disease, and thus may benefit from more aggressive treatments. In the setting of an inferior AMI without obvious changes indicative of acute transmural ischaemia (that is, no STE), the presence of reciprocal, significant STD in lead aVl—especially if disproportionate to the size of the QRS complex—may herald early cardiac ischaemia. This lead is perhaps not as closely scrutinised as other leads, but recognition of this STD in aVl may give the clinician an “early warning” of an impending inferior AMI. 9 Refer to figure 3 for an example of reciprocal change.
Non-ST segment elevation AMI
Patients with non-STE infarction—formerly known as the non-Q wave AMI—may have transient and non-specific findings, such as ST segment depression (figs 8 and 9) or T wave abnormalities (fig 10) in any of the anatomic leads of the 12-lead ECG. Symmetric convex downward ST segment depression or inverted or biphasic T waves are characteristically seen. Differentiating non-STE anterior myocardial infarction from posterior AMI can be difficult and can be done with the use of the additional lead ECG. 10, 11, 14
(A) The right precordial leads V1 to V3 in a chest pain patient ultimately diagnosed with AMI. (B) Additional posterior leads V8 and V9 reveal STE, confirming the diagnosis of isolated posterior wall AMI.
Non-acute coronary ischaemic syndrome causes of ST segment depression
Intraventricular conduction disorders
Intraventricular conduction delays such as LBBB and the associated ST segment-T wave abnormalities can mimic both acute and chronic ischaemic changes. Much has been written about the evaluation of the ST segment elevation in the presence of LBBB 1, 8 ; considering chest pain patients in the ED, LBBB is responsible for 15% of STE syndromes and is the second most frequently encountered electrocardiographic pattern responsible for non-ischaemic STE. 17, 18 LBBB, however, can also cause significant ST segment depression, and it is imperative that these electrocardiographic changes be distinguished from those that occur in the presence of ACS. 3 The “rule of appropriate discordance” states that in LBBB, ST segment-T wave configurations are directed opposite from the major, terminal portion of the QRS complex. As such, leads with either QS or rS complexes should have significantly elevated ST segments mimicking an AMI while leads with a large monophasic R wave demonstrate ST segment depression. T waves in leads with monophasic R waves are frequently inverted. Loss of this normal QRS complex-T wave discordance may imply acute ischaemia in patients with LBBB. 18 Refer to figure 5 for an example of LBBB.
Using data from the GUSTO-1 trial, Sgarbossa et al reported three specific electrocardiographic criteria that are independent predictors of infarction in the setting of LBBB. 19 These criteria were ranked by a scoring system based on the probability of AMI: (1) ST segment elevation >1 mm concordant with the QRS complex (score of 5); (2) ST segment depression >1 mm in leads V1, V2, or V3 (score of 3); and 3 ST segment elevation >5 mm discordant with the QRS complex—“too much” discordance (score of 2). A score of 3 or more suggests that the patient is having an AMI based on the electrocardiographic criteria. With a score less than three, the electrocardiographic diagnosis is less assured and further non-electrocardiographic studies are indicated. Several, more recent studies have questioned the usefulness of these criteria and found the sensitivity to detect an AMI as low as 10%. 20, 21 Despite this, many clinicians find these criteria useful and dispel the notion that it is not possible to diagnose AMI in the face of LBBB.
Left ventricular hypertrophy
There have been several electrocardiographic criteria and scoring systems proposed to diagnose LVH, with the Estes 22 and Scott 23 criteria being most widely used; however, despite adequate specificity, the sensitivity to detect LVH using a wide variety of electrocardiographic criteria has ranged from only 12% to 29%. 4, 24 This poor sensitivity and the inability to consistently appreciate the ST-segment—T wave changes created by LVH has confounded the ability to distinguish between ischaemic and LVH related STD. 4 The LVH related repolarisation abnormalities are referred to as a “strain pattern”, and can be encountered in approximately 70% of LVH cases. 1 This strain pattern by itself has a 52% sensitivity in the recognition of LVH with a specificity nearing 95%. 25 This strain pattern is characterised by downsloping STD with abnormal T waves in leads with prominent R waves (I, aVL, V5, and V6). The downsloping STD—usually without J point depression—is greater than 1 mm and is followed by an inverted T wave. This T wave inversion is asymmetrical, with gradual downsloping and a rapid return to baseline, often with the terminal portion of the T wave becoming positive (so called “overshoot”). 26 Additionally, T wave inversion is greater in lead V6 than in V4, with greater than 3 mm of depression in V6. 1 Identifying this strain pattern is consistent with LVH repolarisation changes and could easily be confused with acute ischaemia. The strain pattern, however, has a relative permanence and should not change over the short-term as compared with the dynamic changes seen in ACS. Refer to figure 6 for an example of LVH.
At therapeutic levels, digitalis produces characteristic electrocardiographic changes, including PR interval prolongation (vagal effect), STD, T wave inversion, and shortening of the QT interval. These changes are referred to as the digitalis effect, which must be distinguished from digitalis toxicity, which manifests primarily as cardiac arhythmia. The electrocardiographic manifestations of digitalis—the digoxin effect—are as follows: “scooped” ST segment depression, most prominent in the inferolateral precordial leads and usually absent in the rightward leads; flattened T waves; increased U wave; and shortening of th QT interval. 3, 4, 26 Occasionally, the J point is depressed, mimicking acute ischaemia. This extreme example of digitalis effect usually occurs only in those leads with tall R waves. 4 Patients with baseline STD or T wave inversion will have an accentuation of these repolarisation abnormalities when treated with digitalis, while patients with normally upright T waves will experience T wave inversion. 3 Often it may be impossible to differentiate the STD created by digitalis and those occurring with ischaemia. In general, however, digitalis will create a “sagging” ST segment while ischaemia creates the typical horizontal or downsloping depression. See figure 7 for an example of digoxin effect on the ECG.
There are several strategies to assist the clinician in differentiating among the various causes of electrocardiographic ST segment depression. The most time sensitive concern is determining whether the STD is attributable to an ACS or attributable to less acute causes such as LBBB, LVH or digitalis. With regard to ACS, determining if the STD represents reciprocal change or a posterior AMI also has significant implications. Using the rule of appropriate discordance, using additional ECG leads in select cases, and performing waveform shape analysis all can be of great benefit when faced with the patient with cardiopulmonary complaints and STD.
Obtaining serial ECGs is perhaps the most powerful tool available to helping distinguishing from among the causes of ST segment changes. The dynamic ECG changes seen with ACS are absent from the relative short-term permanence seen with LVH, LBBB, and the digitalis effect. A comparison with a prior ECG tracing is, of course, invaluable. However, with the often unavailability of old ECGs and without the luxury of time to obtain serial ECGs, a thorough knowledge of confounding electrocardiographic patterns in patients with STD wil assist the physician in making timely and important clinical decisions.
ST Depression Treatment Questions
What is ST depression?
A finding on an electrocardiogram (EKG) may often be referred to as a ST depression. The measurement of the vertical distance between the trace and isoelectric lines at a location of 2-3 millimeters from the QRS complex may often be used in order to determine ST depression. If the measurement is more than 1 millimeter in V5-V6 or 1.5 millimeters in AVF or III the ST depression may be significant. If the ST depression of at least 1 millimeter after adenosine has been administered a reversible ischemia may present itself on a cardiac stress test. However, a ST depression of at least 2 millimeters may present itself to be reversible on an exercise stress test. In the case of non-transmural ischemia, the cause of ST depression may be an elevated resting potential in the myocardial cells. However, the ST segment may less likely be affected as it shows in a depolarized state. ST depression may often cause many commonly asked questions regarding the causes and treatments. Read below where Experts have answered many commonly asked questions regarding ST depression.
What test should be done following a ST depression on a nuclear stress test?
Ischemia may often present itself as a ST depression during a nuclear stress test. However, false positive stress test may be as high as 40% in women and 10% in men. A myocardial perfusion imaging test may be the next test that a medical practitioner may decide to perform in order to confirm a diagnosis.
What are ST depression causes?
An ST depression may not be a classic heart attack. The ST depression causes may include: Myocardial ischemia Artifact Hypothermia IVCD (Interventricular Conduction Delay) Hypokalemia Hypocalcaemia Hypomagnesaemia Digoxin Left ventricular hypertrophy Stroke Sub arachnoids hemorrhage Sub-endrocardial MI in a few cases There may be a need for further testing such as a stress test to find the underlying cause of the ST depression.
What is the description of ST elevation and ST depression?
An ST elevation or ST depression may be an indicator of IHD (ischemic heart disease) is either situation of resting or while performing a stress test. In the case that ST elevation or ST depression is present, the stress test may need to be stopped and chest pain may become present with or without sweating. The chest pain may be present in the restrosternal area and may be relieved with rest and may be referred to as anginal pain. A myocardial infarction may often be present if the pain is present after rest and possibly continues for 15 minutes or more. The chest pain may go up both of the upper arms, neck, back or epigastrium. If a myocardial infarction is thought to be present further medical treatment may be necessary.
When taking a stress test or echocardiogram what is a st depression with the comments OM1, Om is small, OM3 is major branch of circumflex?
A myocardial inducible ischemia may be implied on a stress test by a ST depression. This could also mean that there could be some narrowing of the coronary arteries. In the case of narrowed arteries then the arteries may not be able to supply enough oxygenated blood during exercise related stress. A diffuse disease may be present in the right coronary artery. OMs (Obtuse Marginal arteries) could be smaller caliber arteries. A bypass surgery may be needed to graft the veins to RCA and OM arteries. Anytime that a ST depression is present on an ECG or stress test there may be cause for questions and concerns about what the results mean or possibly even which type of Expert to turn to for information. If you have these or similar questions you can and should ask an Expert.
Wanneer een stuk hartspier niet voldoende zuurstof en voedingsstoffen krijgt ontstaat er ischemie, in de praktijk vaak ‘zuurstofgebrek’ genoemd. Ischemie kan o.a. veroorzaakt worden door:
Kortdurende ischemie veroorzaakt reversibele effecten; de hartcellen kunnen weer herstellen. Als de myocardischemie langer aanhoudt, sterven er hartspiercellen: een hartinfarct. Daarom is het belangrijk om ischemie vroegtijdig te herkennen op het ecg.
Ernstige ischemie geeft vaak al binnen enkele minuten veranderingen op het ecg. Terwijl de ischemie aanhoudt, ontstaan en verdwijnen er ecg-veranderingen. Daardoor is het mogelijk een inschatting te geven van de duur van de ischemie, wat weer belangrijk is voor de behandeling.
De diagnose acuut hartinfarct wordt niet alleen gesteld op basis van het ecg. Er is sprake van een hartinfarct als:
- Hartenzymen (CK-MB of Troponine T) in verhoogde mate worden aangetroffen in het bloed en
- een van de volgende criteria aanwezig zijn:
- De patient klachten heeft van een infarct
- Het ecg toont ST-elevatie of -depressie
- Er ontstaan pathologische Q-golven op het ecg
- Er heeft een coronairen-interventie plaatsgevonden (bijvoorbeeld een stent-plaatsing)
- LAD-afsluiting proximaal van de eerste septale en diagonale tak
- Nieuw rechterbundeltakblok
- ST-elevatie in AVR
- ST-elevatie > 2 mm in afleiding V1
- ST-depressie in afleiding II, III en AVF
- LAD-afsluiting distaal van de eerste septale en proximaal van de eerste diagonale tak
- ST-depressie in afleiding III groter dan in afleiding II
- Pathologische Q in afleiding AVL
- LAD-afsluiting proximaal van de eerste septale en distaal van de eerste diagonale tak
- Tekenen van afsluiting van de septale tak
- ST-depressie in afleiding AVL
- Distale LAD-afsluiting:
- Pathologische Q in V4-V6
- Geen ST-depressie in afleiding II, III en AVF
Kenmerken van een RCA-afsluiting
- ST-elevatie in III groter dan in II (ezelsbruggetje: de afleiding met hoogste ST-elevatie wijst de culprit aan)
- ST-depressie in afleiding I
- Indien de rechterventrikel meedoet: ST-elevatie in V4R
- ST-elevatie in afleiding II groter dan in III
- ST-segment iso-elektrisch of geeleveerd in afleiding I
- ST-segment iso-elektrisch of gedeprimeerd in afleiding V4R
Kenmerken van een RCX-afsluiting
Met name de hartspiercellen in de subendocardiale lagen hebben het eerst last van de verminderde doorbloeding. Subendocardiale ischemie uit zich in ST-depressie en is meestal reversibel. Bij een myocardinfarct ontstaat transmurale ischemie, myocardcellen sterven daarbij definitief af.
In de minuten, uren en dagen na het begin van een myocardinfarct, zijn er verschillende veranderingen te zien op het ecg. Eerst ontstaan spitse T-toppen (ook wel hyperacute T-toppen genoemd), dan ST-elevatie, dan negatieve T-toppen en als laatste pathologische Q-golven. Na een groot doorgemaakt infarct kan een aneurysma cordis ontstaan.
Het vinden van verhoogde hartenzymen bij laboratoriumonderzoek is dus belangrijker dan ecg-afwijkingen. De hartenzymen zijn echter pas 5-7 uur na het begin van een hartinfarct in verhoogde mate in het bloed aan te tonen. Met name in de eerste uren van een hartinfarct is het ecg dus wel belangrijk.
Ischemie kan een breed scala aan ecg-veranderingen geven, waarvan een groot deel niet specifiek zijn en dus ook bij andere aandoeningen voorkomen. De volgende criteria zijn opgesteld voor tekenen van ischemie op het ecg (in afwezigheid van een LBTB of LVH):
ST-elevatie Nieuwe ST-elevatie op het J-punt in twee belendende afleidingen met als grens: minimaal 2 mm bij mannen en 1,5 mm bij vrouwen in afleiding V2-V3 en 1 mm in alle andere afleidingen ST-depressie en T-topveranderingen: Nieuwe horizontale of down-sloping ST-depressie van 0,5 mm in twee aanpalende afleidingen; en/of T-topinversie van 1 mm in twee aanpalende afleidingen met een prominente R-golf of R/S-ratio > 1.
Soms is er slechts in 1 afleiding uitgesproken ST-elevatie. Indien in zo’n geval de belendende afleidingen geen duidelijke R-golf hebben (en bijvoorbeeld een klein QRS-complex hebben), dan sluit de afwezigheid van ST-elevatie daar, ischemie niet uit.
De hartspier kan zelf nauwelijks zuurstof opnemen uit het bloed dat het rondpompt. Alleen de binnenste lagen (endocard) profiteren van dit zuurstofrijke bloed. De buitenste lagen van de hartspier (epicard) zijn afhankelijk van kransslagvaten voor de toevoer van zuurstof en voedingsstoffen. Met behulp van het ecg is te zien welk kransslagvat is afgesloten. Dit is van belang omdat de gevolgen van bijvoorbeeld een voorwandinfarct en een onderwandinfarct verschillen: de voorwand levert de belangrijkste bijdrage aan de pompfunctie en uitval zal dus lijden tot een bloeddrukdaling en hartslagversnelling en op de lange termijn tot hartfalen. Een onderwandinfarct gaat vaak gepaard met een polsvertraging doordat de sinusknooparterie te weinig doorbloed wordt; op de lange termijn is het effect op de conditie minder groot omdat de bijdrage van de onderwand aan de pompfunctie minder is.
Het hart wordt door de rechter- en linkercoronairvaten voorzien van zuurstof en nutrienten. Het linkercoronairvat (de hoofdstam of LM, left main) splits zich in de left anterior descending artery (LAD) en de ramus circumflexus (RCX). De rechtercoronair arterie (RCA) voedt de ramus descendens posterior (RDP). Bij 20% van de bevolking wordt de ramus descendens posterior door de ramus circumflexus gevoed. Dit noemt men een links-dominant hart.
Hieronder volgt een opsomming van de verschillende infarctvarianten. Veel voorkomend zijn het voorwandinfarct (LAD), het onderwandinfarct (meestal RCA) en het infero-postero-lateraalinfarct (vaak RCX).
Reciproke depressies zijn gedeprimeerde ST-segmenten in het ‘tegenoverliggende’ gebied. Bij een voorwandinfarct is er bijvoorbeeld ST-elevatie in de voorwandafleidingen, maar ST-depressie in de onderwandafleidingen. Reciproke depressie komt bij 60-70% van patienten met een bewezen infarct voor. Dit is visueel voor te stellen doordat de onderwandafleidingen ‘van de andere kant’ naar het hart kijken, namelijk vanaf de onderkant. Zij zien de ST-elevatie dus ook andersom, als ST-depressie. Reciproke depressies zijn een sterke aanwijzing van een myocardinfarct en helpen om dit te onderscheiden van bijvoorbeeld pericarditis waarbij ook ST-elevaties te zien zijn, maar geen reciproke depressies.
De locatie van de afsluiting kan goed in beeld worden gebracht door middel van een hartkatheterisatie. Op het verslag daarvan wordt de plaats van de afsluiting vaak aangeduid met een cijfer (bijvoorbeeld LAD(7) ) volgens de indeling van de American Heart Association.
Onderscheidende ecg-kenmerken tussen een proximale of distale LAD-afsluiting