Pathogenesis and diagnosis of Q waves on the electrocardiogram

INTRODUCTION — By definition, a Q wave on the electrocardiogram (ECG) is an initially negative deflection of the QRS complex. Technically, a Q wave indicates that the net direction of early ventricular depolarization (QRS) electrical forces projects toward the negative pole of the lead axis in question. Although prominent Q waves are a characteristic finding in myocardial infarction (MI), they can also be seen in a number of noninfarct settings. Failure to appreciate the other causes of Q waves can lead to important diagnostic errors. (See "Basic principles of electrocardiographic interpretation".)

The presence of a Q wave does not indicate any specific electrophysiological mechanism. To the contrary, Q waves can be related to one or more of the following four factors (table 1) [1,2]:

●Physiologic and positional effects

●Myocardial injury or replacement

●Ventricular enlargement

●Altered ventricular conduction

Clinicians should be aware of three principles with respect to Q waves: not all Q waves are pathologic, not all pathologic Q waves are due to MI caused by fixed coronary artery occlusion, and there is no consensus on the precise criteria for the diagnosis of pathologic Q waves with respect to their width, extent, and location. Accordingly, Q waves should always be interpreted in the clinical context (eg, acute MI presentation, asymptomatic presentation) [3]. Furthermore, pathologic Q waves due to infarction may regress or disappear entirely following the event [1,2]. In one large prospective study (CIRCUS) including 780 patients with anterior ST-elevation MI treated with a percutaneous coronary intervention, persistent Q waves after reperfusion were associated with a fourfold increase in the risk of heart failure or death compared to non-Q-wave MI. In contrast, Q-wave regression was associated with significantly lower risk of major adverse cardiac events [4].

A broader discussion of the ECG in MI is provided elsewhere. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

PHYSIOLOGIC AND POSITIONAL FACTORS — Physiologic activation of the ventricles begins at the left side of the interventricular septum. These early septal depolarization forces are oriented anteriorly and to the right. As a result, small (<0.04 s in duration) "septal" Q waves typically occur in the lateral precordial leads (which have a left-right spatial orientation) and in one or more of the limb leads (except aVR). Depending upon the electrical axis, more prominent Q waves (as part of QS or QR-type complexes) can also appear in the limb leads: in aVL with a vertical axis; and in leads III and aVF with a horizontal axis. A QS complex in which the QRS is entirely negative can also occur in lead V1 as a normal variant and rarely in leads V1 and V2.

Prominent Q waves may be associated with a variety of other positional factors that alter the orientation of the heart in relation to the lead axis:

●Misplacement of chest lead electrodes is an important cause of anterior pseudo-infarction patterns. Slow R wave progression in the precordial leads, sometimes with actual QS waves, may be due solely to improper placement of chest electrodes above their usual position or on, rather than under, the left breast in women.

●In dextrocardia, normal R wave progression may be restored by recording right-sided precordial leads, assuming that there are no underlying structural abnormalities.

●A rightward mediastinal shift in left pneumothorax may contribute to the apparent loss of left precordial R waves.

●Other positional factors associated with slow or delayed (formerly referred to as "poor") R wave progression include pectus excavatum, chronic obstructive pulmonary disease (COPD) and, much more rarely, congenitally corrected transposition of the great vessels or congenital absence of the left pericardium.

MYOCARDIAL DAMAGE AND REPLACEMENT — The reason why Q waves do or do not develop following coronary occlusion is related to the duration of occlusion, the extent to which collateral vessels maintain myocardial viability during occlusion or hypoperfusion, and the location and size of the infarction. Loss of electromotive forces due to myocardial necrosis in MI leads to R wave loss. Delayed conduction through an ischemic area or conduction around it results in recording potentials from the opposite ventricular wall with Q wave formation in the appropriate leads. Furthermore, relatively tall and slightly broad R waves (usually 30 ms or wider) in V1 and V2 may be Q wave "equivalents" in patients with lateral or inferior-posterior-lateral wall infarctions. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Location of ischemia or infarction'.)

A common clinical misconception is the presumption that patients with heart failure and prominent Q waves necessarily have "ischemic" cardiomyopathy. Any process, acute or chronic, that causes sufficient loss of regional electromotive potentials or (bi)ventricular dilation can result in Q waves. Examples include dilated cardiomyopathy, myocarditis, replacement of myocardial tissue by electrically inert fibrous tissue or other electrically inert material such as amyloid fibrils or by metastatic tumor, scleroderma, sarcoidosis, and Duchenne muscular dystrophy (which may simulate a postero-lateral infarct). Transient Q waves can also occur with myocardial ischemia (without infarction) and with certain severe metabolic disturbances such as hyperkalemia. In addition, transient or persistent Q waves may occur with stress-induced (takotsubo) cardiomyopathy. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)

ALTERED CONDUCTION — An intrinsic change in the sequence of ventricular depolarization can lead to pathologic, noninfarct Q waves. The two most important conduction disturbances associated with pseudo-infarct Q waves are left bundle branch block (LBBB) patterns and Wolff-Parkinson-White (WPW) preexcitation patterns.

Left bundle branch block — With LBBB, the initial septal depolarization forces are oriented from right to left, opposite from the normal direction. As a result, QS complexes may appear in the right and mid-precordial leads and occasionally in one or more of leads II, III, and aVF. A similar pattern may appear with right ventricular pacing, where right-to-mid-precordial QS waves are initiated by an electronic "spike." Biventricular pacing (as part of cardiac resynchronization therapy) may produce prominent Q waves (eg, as part of QS waves in anterolateral leads) (see "Cardiac resynchronization therapy in heart failure: Indications and choice of system"). Diagnostic confusion with any form of ventricular pacing is most likely when the spikes escape visual recognition due to very low amplitude. (See "Basic approach to delayed intraventricular conduction".)

Wolff-Parkinson-White preexcitation patterns — With WPW pattern, an accessory (atrioventricular) conduction pathway bypasses the atrioventricular node and initiates ventricular depolarization in an anomalous fashion. (See "General principles of asynchronous activation and preexcitation".)

Depending upon the location of this bypass tract, initial negative QRS forces (and therefore Q waves) may be seen in the right precordial (V1 to V3), left precordial (V4 to V6), and/or limb leads. WPW can also produce a tall wide R wave in lead V1, simulating a "posterior" infarction.

The diagnosis of classic WPW is made by finding the triad of a relatively short PR interval (usually but not always less than 120 ms), a wide QRS complex, and a delta wave (slurred or notched segment on the upstroke or downstroke of the QRS complex in one or more leads).

Clinicians should be aware that in addition to producing pseudo-infarct patterns, both LBBB and WPW can mask the findings of a true infarction. As a result, both the sensitivity and specificity of the ECG in diagnosing infarction are reduced by these conduction disturbances. Furthermore, LBBB and WPW may occur as transient or intermittent findings, adding to diagnostic confusion.

Left anterior fascicular (hemi-)block — Considerable confusion surrounds the effect of left anterior fascicular block (LAFB) on the ECG and, in particular, on the question of whether this common conduction disturbance can actually cause an anterior pseudo-infarct pattern (eg, QS complexes V1 to V3). The ECG diagnosis of LAFB is supported by the presence of marked left axis deviation (usually more negative than -45°) with slight or no widening of the QRS complex. However, LAFB has only minor effects on the QRS complex in the horizontal plane (chest) leads. Probably the most common finding is a relatively prominent S wave in leads V5 and V6.

Slow R wave progression per se is not a routine feature of LAFB, although some authors have reported minuscule q waves in leads V1 to V3 in this setting. These micro-q waves (less than 0.1 mV in depth or less than one mm with standard calibration) may become more apparent if the leads are recorded one interspace above their usual position and may disappear in leads one interspace below their usual position. As a general rule, however, prominent Q waves (as part of QS or QRS complexes) in the right to-mid precordial leads should not be attributed to LAFB alone.

VENTRICULAR ENLARGEMENT — While pathologic Q waves are often incorrectly considered a specific marker of ventricular injury and loss of myocardial depolarization forces, an important cause of pseudo-infarct patterns, paradoxically, is left or right ventricular enlargement. Slow R wave progression is commonly observed with left ventricular hypertrophy or with right ventricular overload syndromes (acute and chronic). Q waves in these settings may reflect a variety of mechanisms, including a change in the balance of early ventricular depolarization forces, as well as altered cardiac geometry and position.

Chronic obstructive pulmonary disease — A marked loss of R wave voltage sometimes with frank Q waves from V1 to the lateral chest leads can be seen with advanced chronic obstructive pulmonary disease (COPD). The presence of low limb voltage and P pulmonale (increased height of the P wave in lead II) point toward the diagnosis of COPD rather than a myocardial infarction, although the two diagnoses can coexist.

This diminution or frank loss of precordial R wave progression in COPD may in part reflect right ventricular dilation. In addition, downward displacement of the heart in the emphysematous chest may play a major role in the genesis of slow R wave progression in some cases. Partial or complete normalization of R wave progression in this setting can sometimes be achieved simply by recording the chest leads an interspace lower than usual. In contrast, Q waves due to infarction are not altered by this change in lead position.

Acute pulmonary embolism — A variety of pseudoinfarct patterns can occur with acute cor pulmonale due to pulmonary embolism or other factors.

●Acute right ventricular overload can cause slow R wave progression and sometimes right to mid precordial T wave inversions (right ventricular "strain"), changes that mimic an anterior infarction.

●The classic S1Q3T3 pattern can occur, but is neither sensitive nor specific for pulmonary embolism. A prominent Q wave (usually as part of a QR complex) in lead aVF may also be seen with this pattern. However, acute right ventricular overload by itself does not cause a pathologic Q wave in lead II.

●Right heart overload, acute or chronic, may be associated with a QR complex in lead V1 and sometimes V2, simulating anterior infarction. The precise mechanism of this pattern has not been determined. This finding may occur with chronic pulmonary thromboembolic hypertension.

●Acute pulmonary embolism more rarely may cause actual ST-elevation in right-mid chest leads, probably related to right ventricular ischemia in the context of chamber dilation and hypoxemia.

Hypertrophic cardiomyopathy — Pseudoinfarct patterns are an important finding in patients with hypertrophic cardiomyopathy, with or without obstruction. The ECG in this disorder can simulate anterior, inferior, posterior, or lateral MI.

The pathogenesis of the depolarization abnormalities in hypertrophic cardiomyopathy is not fully understood. Prominent inferolateral Q waves (in leads II, III, aVF, and V4 to V6) and tall right precordial R waves are probably related to increased depolarization forces generated by the markedly hypertrophied septum. Abnormal septal depolarization may also contribute to the bizarre QRS complexes.

The polarity of the T waves may be useful in the differential diagnosis of Q waves due to hypertrophic cardiomyopathy versus infarction. When prominent Q waves (in leads showing a small terminal r wave or none at all) are due to hypertrophic cardiomyopathy, the T wave will be upright. With infarction, prominent Q waves may be associated with upright or inverted T waves. Thus, a prominent Q wave (as part of a QS or Qr-type complex) with T wave inversion argues against hypertrophic cardiomyopathy. On the other hand, upright T waves in this setting have no diagnostic value.

Heart failure with reduced or preserved left ventricular ejection fraction — A pseudoinfarction pattern can be seen in patients with left ventricular dysfunction (systolic and/or diastolic) in the absence of coronary disease and MI. This finding may be due in part to the presence of left ventricular conduction delays, left or biventricular enlargement, or to left ventricular scarring.

CLINICAL APPROACH TO DIFFERENTIAL DIAGNOSIS — The unexpected or unaccounted presence of Q waves on the ECG poses an important clinical problem. The Q waves may be the residua of a previously unsuspected "silent" MI; they may also represent a normal or positional variant, or an important noncoronary type of heart disease. The decision about how far to proceed in investigating unexpected Q waves must be individualized. The history and physical examination, as always, may provide essential information.

Unfortunately, given the multiple etiologies and variable amplitude/duration criteria proposed for different leads, no single, reliable algorithm exists to guide clinicians through the differential diagnosis of Q waves. The following general approach may provide some help to clinicians in assessing Q waves, particularly unexpected ones.

●Consider a repeat ECG, with particular attention to lead placement. A negative P wave in lead I with a Q wave in that lead strongly suggests left-right arm electrode reversal. Slow R wave progression in V1 to V3/V4 (and even frank QS waves) may be due to precordial lead placement above their standard positions.

●Compare with prior ECG(s), if available.

●Employ Bayesian principles. The prior probability of Q waves being pathologic in young, healthy subjects is relatively low compared with older individuals with risk factors for coronary artery disease. Furthermore, in young adults, prominent Q waves, when pathologic, are more likely to represent noncoronary causes, eg, hypertrophic cardiomyopathy.

●Check for associated ST-T changes suggesting evolving ischemia (eg, ST elevations and T-wave inversions).

●Check for increased QRS duration since noninfarction Q waves may be due to left bundle branch block, right ventricular pacing with very subtle pacemaker spikes, and WPW preexcitation syndromes (negative delta waves). The latter finding may only be evident at slower heart rates, with increased vagal tone slowing conduction through the atrioventricular node but not down the bypass tract.

●Consider echocardiography the most useful and accessible noninvasive test in the assessment of unexplained Q waves. Echocardiography may, for example, confirm the likelihood of underlying MI by showing regional wall motion abnormalities. Furthermore, a number of conditions associated with noninfarct Q waves may be diagnosed or suggested by echocardiography: hypertrophic cardiomyopathy, cardiac amyloidosis, left ventricular hypertrophy, right ventricular overload syndromes including pulmonary embolism, non-ischemic cardiomyopathies, and chronic constrictive pericarditis. Cardiovascular magnetic resonance imaging may also be useful in selected cases, such as cardiac sarcoid [5]. (See "Cardiac imaging with computed tomography and magnetic resonance in the adult", section on 'Cardiovascular magnetic resonance imaging'.)

SUMMARY

●Definition – A "Q" wave on the ECG is an initially negative deflection of the QRS complex, but its presence does not indicate any specific electrophysiological mechanism. (See 'Introduction' above.)

●Differential diagnosis – In addition to myocardial infarction (MI) due to coronary artery disease, any process, acute or chronic, that causes sufficient loss of regional electromotive potentials can result in pathologic Q waves (table 1). (See 'Myocardial damage and replacement' above and 'Clinical approach to differential diagnosis' above.)

•Altered conduction – Many changes in the sequence of ventricular depolarization with widening of the QRS can lead to pathologic, noninfarct Q waves. The two most important conduction disturbances associated with pseudoinfarct Q waves are left bundle branch block (LBBB) and Wolff-Parkinson-White (WPW) preexcitation patterns. (See 'Altered conduction' above.)

•Ventricular enlargement – Another important cause of pseudoinfarct patterns is left or right ventricular enlargement. (See 'Ventricular enlargement' above.)

●Further evaluation – The most useful noninvasive test in the assessment of Q-waves not explained by the presence of coronary artery disease is the echocardiogram. Cardiovascular magnetic resonance imaging may also be helpful in selected cases. (See 'Clinical approach to differential diagnosis' above.)