St elevation in v2 v3 v4 v5

Electrocardiographic Differential Diagnosis of ST Segment Elevation

ST segment elevation on the ECG in the context of a presentation compatible with ACS is considered to represent STEMI until proven otherwise. Several other conditions, particularly LBBB and LVH, also feature ST segment elevation that mimics infarction (seeTable 68.3). ST segment elevation resulting from STEMI is not the most common cause of ST segment deviation in adults with chest pain who are suspected of AMI. Caution is required when interpreting ST segment elevation in regard to the decision to initiate reperfusion treatment, whether it be PCI or fibrinolytic therapy.

Benign early repolarization is a normal electrocardiographic variant that does not imply, nor exclude, ACS or CAD. BER includes the following electrocardiographic characteristics: (1) ST segment elevation; (2) upward concavity of the initial portion of the ST segment; (3) notching of the terminal portion of the QRS complex at the J point (ie, junction of the QRS complex with the ST segment); (4) symmetric concordant T waves of large amplitude; (5) diffuse ST segment elevation on the ECG; and (6) relative temporal stability over the short term, although these changes may regress with advancing age. J point elevation is usually less than 3.5 mm, and the concave ST segment is usually elevated less than 2 mm in the precordial leads (although it may be elevated as much as 5 mm in some cases) and 0.5 mm in the limb leads. Maximal ST segment elevation in BER is typically seen in leads V2 to V5. Isolated BER in the limb leads is rare and should prompt reconsideration of STEMI (Fig. 68.11A and68.12).

Pericarditis, in the acute phase, also features diffuse ST segment elevation. In pericarditis, the ST segments are concave, with an initial upsloping contour, and are usually less than 5 mm in height. Occasionally, the initial contour is obliquely flat, but convex or domed ST segment morphology is strongly suggestive of STEMI. The ST segment elevation is usually seen in all leads with the exception of aVR (where it is depressed); V1 is variable. Focal pericardial inflammation manifests as a more accentuated change in the leads reflecting the affected region. PR segment depression is an insensitive yet specific associated electrocardiographic finding in pericarditis, which is typically best seen in the inferior leads and lead V6; correspondingly, PR segment elevation may be evident in lead aVR (Fig. 68.13; seeFig. 68.11B). In that ST segment changes are encountered in these patients, the most appropriate term applied is myopericarditis, rather thanpericarditis. Recall that the pericardium is electrically silent; thus, electrocardiographic changes result from epicardial irritation and ST segment elevation—hence, the termmyopericarditis.

Left ventricular aneurysm (LVA), wherein a focal area of myocardium paradoxically bulges outward during systole, has characteristic electrocardiographic changes that can be difficult to differentiate from those of STEMI. Considerable overlap exists between populations of patients with potential for STEMI and LVA, and the electrocardiographic changes of LVA tend to be regional rather than diffuse. Anatomically, LVA is usually found anteriorly, and changes are most often seen in leads V1 to V6 and leads I and aVL. ST segment elevation may be of any morphology (eg, convex or concave), and Q waves may be present (Fig. 68.14). The calculation of the ratio of the amplitude of the T wave to the QRS complex may help distinguish acute anterior MI from LVA. It has been shown that if the ratio of the amplitude of the T wave to the QRS complex exceeds 0.36 in any single lead, the ECG probably reflects STEMI. If the ratio is less than 0.36 in all leads, however, the findings are probably the result of a ventricular aneurysm.

ECG manifestations and the possible mechanisms in acute pulmonary embolism

ST-segment elevations or depressions have been previously described as a common but non-specific ECG manifestation in acute pulmonary embolism [12,13]. However, the majority of the studies suggest that the ST-segment elevations or depressions have its regularity and intrinsic mechanisms [14–19]. The typical and common ST-segment elevations are often founded in leads V1, V2, III, aVR while ST-segment depressions are often founded in leads I and V4/V5–V6 [14,15,17,19]. We have proposed that ischemic ECG changes in APE are mainly attributed to hypotension, hypoxemia, right ventricular stretches, and outpouring of catecholamines [14,15]. Increased right ventricular wall-stress could result in transmural right ventricular ischemia in addition to right ventricular strain. The typical manifestation of transmural right ventricular ischemia includes ST-segment elevations in right precordial leads with or without STE in the inferior leads [14]. We speculate that ST-segment elevation in the right precordial leads is an important ECG characteristic of high or intermediate risk in acute pulmonary embolism. However, ST-segment elevation may be short-lasting and, thereby, missed during the diagnostic workup. Meanwhile hypotension, hypoxemia, and outpouring of catecholamines can also result in left ventricular subendocardial ischemia. We have proposed three specific ischemic patterns suggestive of different types of myocardial ischemia in acute pulmonary embolism [15]: (1) left ventricle subendocardial ischemic ECG pattern presenting with STE in lead aVR with concomitant ST-segment depressions in leads I and V4–V6; (2) right ventricle transmural ischemic ECG pattern presenting with ST-segment elevations in leads V1 to V3/V4/V5, and (3) left ventricle subendocardial with concomitant right ventricle transmural ischemic ECG pattern presenting with ST-segment elevations in leads V1/V2 and/or III with concomitant ST-segment depressions in leads V4/V5 to V6. In our 131 acute pulmonary embolism patients with ST-segment depressions or elevations ≥0.1 mV with concomitant negative T-waves, there were 24 (18%) patients presenting left ventricle subendocardial ischemic pattern, 41 (31%) patients presenting right ventricle transmural ischemic pattern and 52 (40%) patients presenting left ventricle subendocardial and right ventricle transmural ischemia pattern [19]. These results indicate that the majority (89%) patients with negative T-waves presented with one of the three typical ischemic patterns. The ischemic ST-segment deviation patterns are affected by the following factors: the degree and the ratio of the right ventricle transmural ischemia and the left ventricle subendocardial ischemia, the changing ratio of the right/left ventricle diameter, the clockwise rotation around the longitudinal axis, the enlargement of the right ventricle, the acute coronary artery insufficiency secondary to a fall in cardiac output and increase of heart rate, the coexistence of cardiopulmonary disease. Probably, also other factors are involved such as paradoxical coronary embolism and coexistence of coronary artery disease. If the right ventricle transmural ischemia is dominant, the ECG will present ST-segment elevations in right precordial leads (such as Fig. 9.2A). If the left ventricle subendocardial ischemia is dominant, the ECG will present ST-segment elevation in leads aVR and ST-segment depression in leads I and V4–V6 (such as Fig. 9.1B). If right ventricle transmural ischemia and left ventricle subendocardial ischemia are codominant, the ECG will present ST-segment elevations in leads aVR, V1 or V1–V2/V3, and/or III, and ST-segment depressions in leads I and V4/V5 to V6 (such as Fig. 9.1A). Paradoxical coronary embolism via proven atrial septal defect and right to left shunt is another mechanism for ST-segment elevation. In this condition, the distribution of the ST-segment elevations may vary and depend on the embolismic coronary artery [14].

Grand et al. [20] found that ST-segment elevation in the right precordial leads is a transient ECG manifestation of moderate to severe acute pulmonary embolism. This phenomenon indicates transmural ischemia in the right ventricle due to hypotension, hypoxemia, right ventricular strain, and catecholamine surge [14,15]. Although ST-segment elevation in the right precordial leads (<2 mm) is not a rare phenomenon, prominent ST-segment elevation (≥0.2 mV) and confined to leads V1–V3 are not seen so frequently. The majority of the patients presenting prominent ST-segment elevation in the right precordial presented with hypotension or cardiogenic shock [6,21–23]. Negative T-waves in the right precordial leads are a frequent ECG manifestation of acute pulmonary embolism and may represent an evolutionary “post-ischemic” stage following ST-segment elevation [14,15]. In case of a new episode of transmural right ventricular ischemia, usually in the context of hypotension or cardiogenic shock, the deep negative T-waves will reduce or disappear or even pseudonormalize and the ST-segment elevation may reappear. Mohsen [21] and Wilson [22] respectively reported similar ECG findings to ours. The “coved” ST-segment elevations in leads V1–V4 [21,22] were identical to type-1 Brugada ECG pattern during cardiogenic shock. At baseline during hemodynamic stability before the Brugada ECG pattern, both cases presented with deep negative T-waves in leads V1–V4.

Electrocardiographic Findings in ST-Segment Elevation Myocardial Infarction

The initial ECG abnormality that occurs in patients with epicardial coronary artery occlusion is peaked hyperacute T waves in the distribution supplied by the IRA. T waves become tall and sharply peaked within minutes of occlusion of the IRA (Fig. 55.1,A). Peaked T waves may also be seen in patients with hyperkalemia, pericarditis, early repolarization, and LBBB. In the next several minutes, ST-segment elevation becomes evident on the ECG (seeFig. 55.1,B). To be diagnostic, the ST-segment elevation must be at least 1 mm above the baseline; this is generally considered the TP segment. Most typically, this ST elevation is convex or domed, though less commonly it may be straight or, rarely, concave. Concave ST-segment elevations are more characteristic of other conditions associated with ST-segment elevation (Box 55.1).

In addition to the clinical situation, a factor distinguishing STEMI from other conditions is the dynamic nature of the ST-segment changes with STEMI; serial ECGs commonly show waxing and waning ST-segment elevation. Hours to days later, the ST segments return toward baseline, the T waves invert, and pathologic Q waves develop in areas of the ECG that correspond to the IRA. The location of the ST elevations and other findings on the ECG generally correspond to the anatomic location of the myocardium and the associated IRA. Anterior infarctions exhibit ST elevation in leads V1 through V4 (Fig. 55.2). Findings in leads V1 and V2 indicate involvement of the septum. MIs with these findings are caused by occlusion of the left anterior descending (LAD) coronary artery. When additional ST elevations are seen in leads V5, V6, I, and aVL, the location of the LAD occlusion is probably proximal to the first diagonal branch, which causes an anterolateral infarction (seeFig. 55.1,B). Inferior infarctions are characterized by ST elevations in leads II, III, and aVF (Fig. 55.3,A) and are due most commonly to right coronary artery (RCA) occlusion. Reciprocal ST depressions may be present in leads I and aVL.

Inferior MIs are associated with concomitant right ventricular infarction, which can be evident on right-sided ECG leads, particularly in RV4 and RV5 (seeFig. 55.3,B). Inferior MIs are also frequently associated with posterior wall involvement, which is seen on the ECG as ST depressions in leads V1 through V3 and, on occasion, early R-wave progression with tall R waves in leads V1 through V3 (Fig. 55.4).

ST and T Abnormalities

ST segment elevation of greater than 0.2 mV in several leads may be seen in myocarditis46 and pericarditis.47 Myocardial infarction is rare in pediatric patients but, if present, produces the same ST segment changes as in adults. Wide Q waves (longer than 35 ms) and prolonged QT interval corrected for heart rate (>440 ms) are reported to be highly specific for myocardial infarction when combined with ST segment elevation >2 mm.46 ST segment depression has been reported in children with severe head injury.48

A “coved type” ST segment elevation has been reported in Brugada syndrome49 (see Chapter 7). Presentation with arrhythmic syncope and cardiac arrest is rare in the pediatric age group,50,51 and ECG changes are absent in most individuals with this sodium channel mutation before the age of 5 years.52

T wave inversion combined with ST segment depression in the left lateral precordial leads suggests LVH and is described as a “strain pattern” (see Figure 29-6). As previously mentioned, upright T waves in the right precordial leads between the ages of 7 days and 7 years suggest RVH.

Laboratory Tests

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Electrocardiogram (Fig. 1): A 12-lead ECG should be performed and shown to an experienced emergency physician within 10 min of emergency department (ED) arrival for all patients with chest discomfort (or anginal equivalent) or other symptoms suggestive of MI.Table 1 andTable 2 describe ECGfindings in myocardial infarction. If the initial ECG is not diagnostic for MI but the patient remains symptomatic and there is a high clinical suspicion for MI, serial ECGs at 5- to 10-min intervals or continuous 12-lead ST-segment monitoring should be performed to detect the potential development of ST deviation. In patients with inferior STEMI, right-sided ECG leads should be obtained to look for ST elevation suggestive of right ventricular (RV) infarction. The joint ESC/ACCF/AHA committee for the definition of MI established the definition for the diagnosis of ST-elevation MI, which is considered to be present when there is an ST-segment elevation in two contiguous leads, ≥2 mm for men and ≥1.5 mm for women in precordial leads and/or ≥1 mm in limb leads. ST-segment elevation is measured at 0.08 sec after the J point (the junction between the end of the QRS and the beginning of the ST segment). In addition, ST depression in >2 precordial leads (V1 to V4) may indicate transmural posterior injury; multilead ST depression with coexistent ST elevation in lead aVR has been described in patients with left main or proximal left anterior descending artery involvement.

New or presumably new LBBB at presentation occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation.

Diagnosing new STEMI in patients with old left bundle branch block could be challenging. Sgarbossa and colleagues emphasized that concordant 1 mm ST-segment elevation in any lead with a positive QRS deflection or discordant ST-segment elevation >5 mm in any lead with negative QRS deflection suggest STEMI.

New ST-segment depression ≥0.5 mV (0.5 mm) and T-wave abnormalities suggest NSTEMI. ECG findings alone, without laboratory results, are sufficient to diagnose STEMI; therefore, treatment should not be delayed until biomarkers are available.

Cardiac troponin levels: Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) are generally indicative of myocardial injury with increases in serum levels of >99th percentile of a normal reference population. Detection of a rise and fall pattern of the measurements is essential to the diagnosis of AMI. The rise may occur relatively early after muscle damage (3-6 hr), peak at 12 to 16 hr, and may be present for several days after MI (up to 7 days for cTnI and more than 14 days for cTnT). Earlier peaking and rapid decline of cardiac enzymes may present in light of successful revascularization (Fig. 2). cTnT or cTnI tests can be falsely positive for myocardial infarction in patients with renal failure, heart failure, myocarditis, aortic dissection, and pulmonary embolism. Recently, highly sensitive troponin assays (hs-cTnI, hs-cTnT) have also been developed to facilitate an early diagnosis of AMI. Most patients can be diagnosed with AMI within the first 2 to 3 hr of presentation. However, an initial negative high-sensitivity troponin at the time of presentation is not sensitive enough to completely rule out AMI. MI can be excluded in most patients by 6 hr of presentation, and guidelines suggest serial samples be obtained every 3 to 6 hr after an initial sample if there is a high degree of suspicion for AMI.

Troponin is the preferred marker for the diagnosis of myocardial necrosis. A single high-sensitivity assay for cardiac troponin (hs-cTnT) concentration below the limit of detection in combination with a nonischemic ECG may successfully rule out an MI in patients presenting to EDs with possible emergency acute coronary syndrome.1 Because troponins need 7 to 14 days to be cleared by the kidneys, they are not sensitive enough to detect a recurrent MI within days from the initial MI. CK-MB isoenzyme can be useful in such circumstances (Fig. 2).

CK-MB isoenzyme is also a useful marker for MI if troponin levels are not available. It is released in the circulation in amounts that correlate with the size of the infarct. An increased CK-MB value for the diagnosis of MI is defined as a measurement above the 99th percentile of the upper reference limit. CK-MB can be detected within 3 to 8 hr of the onset of chest pain, peak at 12 to 24 hr, and return to baseline levels within 24 to 48 hr.

Resting ST-Segment Displacement

ST-segment elevation on a resting ECG is a common and usually a healthy phenomenon. Although it is called “early repolarization,” it most likely is late depolarization. It is usually most prominent with bradycardia and normally sinks to the isoelectric line with tachycardia. Figure 4-7 is an illustration of exercise-induced ST depression and elevation on a baseline ECG with early repolarization. Abnormal elevation is measured from the upward shift from the baseline level (normally the ST segment sinks with increasing heart rate). Abnormal depression is measured only from where it crosses the isoelectric line. The drop from baseline elevation is not counted as abnormal. Figure 4-8 illustrates how ST shifts are measured when the baseline ECG shows depression. The additional depression is measured from the baseline level of the ST segment and not from the isoelectric line. Elevation is measured from the baseline depression and can actually result in “normalization” of the ST segment.

Abstract

ST-segment elevation acute myocardial infarction (STEMI) is a major health problem. The implementation of reperfusion strategies has resulted in a very significant reduction of shortterm mortality. However, STEMI survivors with large infarctions are at high risk of chronic heart failure and associated comorbidities. The possibility of reducing infarct size might help alleviating the epidemics of heart failure. In many cases, despite optimal opening of the occluded epicardial coronary artery, tissue perfusion is inadequate due to microvascular obstruction (MVO). Given the central role of MVO in final infarct size, it is the target of different interventions. In the past decades, many strategies (pharmacological and mechanical) have been tested with the aim of reducing MVO and in turn lessen infarct size. Many interventions have failed in the translation from positive experimental studies into clinical trials, while some others have passed the initial checkpoint of pilot trials and are being tested in properly sized endpoints-oriented clinical trials. In this chapter we will describe the state of the art of the different strategies that are actively being tested in this field.

Establishing a Working Diagnosis of Acute Coronary Syndrome

Patients with acute coronary syndromes are classified into two groups on the basis of ST-segment changes on their admission electrocardiograms (ECGs) (Fig. 18-3). This classification provides an initial working diagnosis so that appropriate therapy can be initiated.

Normal Variant

Diffuse ST segment elevation often is seen in healthy young individuals in the normal male pattern, often called “early repolarization” (see Chapter 1). Unlike that seen with pericarditis, this is a stable pattern, unchanged on serial observations. Similar to acute pericarditis, the ST segment changes are most marked in the precordial leads, but ST depression in lead V1, if present, favors a diagnosis of acute pericarditis.21 The normal variant is usually associated with tall T waves in the same leads in which the ST segment is elevated, and the ratio of the amplitude of ST elevation to the amplitude of the T waves (ST/ T ratio) in lead V6 is <0.25.22 It has been reported22 that with pericarditis the PR segment depression is seen in the limb leads and the precordial leads, whereas in normal subjects with ST elevation the PR segment depression is confined to either the limb leads or the precordial leads.

Chronic Phase

Resolution of ST segment elevation is quite variable. It is usually complete within 2 weeks of inferior MI, but it can be delayed further after anterior MI. Persistent ST segment elevation, often seen with a large anterior MI, is indicative of a large area of akinesis, dyskinesis, or ventricular aneurysm. Symmetrical T wave inversions can resolve over weeks to months or can persist for an indefinite period; hence, the age of an MI in the presence of T wave inversions is often termed indeterminate. Q waves usually do not resolve after anterior MI but often disappear after inferior wall MI.

Early recanalization therapy accelerates the time course of ECG changes so that, on coronary recanalization, the pattern can evolve from acute to chronic over minutes to hours instead of days to weeks. ST segments recede rapidly, T wave inversions and losses of R wave occur earlier, and Q waves may not develop or progress and occasionally may regress. Indeed, failure of ST segment elevation to resolve by more than 50 to 70% within 1 to 2 hours suggests failure of fibrinolysis and should prompt urgent angiography for “rescue angioplasty.”