Atrial myocardial infarction: A tale of the forgotten chamber

    Atrial myocardial infarction: A tale of the forgotten chamber Marvin Louis Roy Lu, Toni De Venecia, Soumya Patnaik, Vincent M. Figueredo PII: DOI: Reference:

S0167-5273(15)30634-3 doi: 10.1016/j.ijcard.2015.10.070 IJCA 21360

To appear in:

International Journal of Cardiology

Received date: Revised date: Accepted date:

4 August 2015 3 October 2015 5 October 2015

Please cite this article as: Lu Marvin Louis Roy, De Venecia Toni, Patnaik Soumya, Figueredo Vincent M., Atrial myocardial infarction: A tale of the forgotten chamber, International Journal of Cardiology (2015), doi: 10.1016/j.ijcard.2015.10.070

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ACCEPTED MANUSCRIPT Atrial Myocardial Infarction: A Tale of the Forgotten Chamber Marvin Louis Roy Lu1, MD; Toni De Venecia1, MD; Soumya Patnaik1, MD; Vincent M.

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Figueredo2,3, MD

Einstein Medical Center, Department of Medicine, Philadelphia, PA

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Einstein Institute for Heart and Vascular Health, Einstein Medical Center, Philadelphia,

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PA 3

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Sidney Kimmel College of Medicine at Thomas Jefferson University, Philadelphia, PA

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Conflict of Interest: The authors have no conflicts of interest to report

infarction,

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Keywords: atrial electrocardiogram

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Running Title: Atrial Myocardial Infarction

Corresponding Author:

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wave,

PR

displacement,

atrial

Vincent M. Figueredo, M.D. Einstein Institute for Heart and Vascular Health 5501 Old York Road, 3rd Floor Levy Building

Philadelphia, PA 19141 Phone: 215-456-8991 Fax: 215-456-3533 [email protected]

arrhythmia,

ACCEPTED MANUSCRIPT Abstract It has been almost a century since atrial infarction was first described, yet data

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describing its significance remain limited. To date, there are still no universally accepted

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criteria for the diagnosis of atrial infarction. Atherosclerosis is the leading cause of atrial

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infarction but it has also been described in cor pulmonale and pulmonary hypertension. Atrial infarction almost always occurs concomitantly with ventricular infarction. Its clinical

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presentation depends largely on the extent and site of ventricular involvement. Atrial

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infarction can present with supraventricular tachyarrhythmias. Electrocardiographic (ECG) criteria for diagnosing atrial infarction have been described but none have yet to

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be validated by prospective studies. Atrial ECG patterns include abnormal P-wave

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morphologies, PR-segment deviations, as well as transient rhythm abnormalities, including atrial fibrillation, atrial flutter, atrial tachycardia, wandering atrial pacemaker

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(WAP) and atrioventricular (AV) blocks. Complications of atrial infarction include thromboembolic events and cardiogenic shock. There are no specific additional recommendations in the management of myocardial infarction with suspected involvement of the atria. The primary goal remains coronary reperfusion and maintenance of, or conversion to, sinus rhythm.

ACCEPTED MANUSCRIPT Introduction: Myocardial infarction (MI), an entity referring to irreversible damage or death of cardiac

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muscle, is the leading causes of morbidity and mortality worldwide. As the bulk of

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myocardium is predominantly located in the ventricles, most MI present clinically due to

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symptoms of ventricular myocyte ischemia, or the consequences of ventricular myocardial dysfunction. Atrial infarction, usually concurrent with ventricular infarction, is

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poorly recognized and understudied.. Atrial infarction was first described in 1925 by

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Clerc and colleagues (1). The first case series was published in 1942 by Cushing and associates (2). Its incidence among patients with MI has been reported to range from

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0.7% to 42% (2-7), mostly based on autopsy findings. The overall incidence is likely

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higher if MI survivors are also taken into account. To date, there are still no universally accepted criteria for the diagnosis of atrial infarction. Little attention has been given to

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this chamber and its clinical implications.

In this article we will review the etiology, pathophysiology, clinical presentation, diagnosis, and management of this frequently overlooked disease entity.

ACCEPTED MANUSCRIPT Etiology, Pathophysiology and Anatomic Correlates of Atrial Infarction: The majority of atrial infarctions occur as a consequence of atherosclerotic heart

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disease. However, one case series found that chronic obstructive pulmonary disease

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with cor pulmonale can cause atrial infarction, likely secondary to a combination of

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hypoxia from the pulmonary disease and increased atrial pressure (8). Another case report found an isolated sinus node infarction in a 31 year-old otherwise healthy female

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with primary pulmonary hypertension presenting with syncope (9).

In contrast to ventricular infarction, the majority of atrial infarctions involve the right

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atrium versus the left (10,16). A review of case series showed that the right atrium is

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involved in 81% to 98% of cases, the left in only 2 to 19% (10). Biatrial infarction

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occurred in 19 to 24% (10). Interestingly, atrial infarction is more frequently found in the atrial appendages, rather than the lateral or posterior walls of the atria (10). The considerably higher oxygen content of left atrial blood may explain the difference in incidence between right and left atrial infarction. Of note, there is one case series that found a greater incidence of left atrial involvement, hypothesizing it to be secondary to the greater incidence of left ventricular infarction (11).

ACCEPTED MANUSCRIPT The blood supply of the atria arises mainly from the ramus ostii cava superioris (ROCS). The ROCS originates from the proximal right coronary artery (RCA) in 60% of the

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general population and from the proximal left circumflex artery (LCx) in 40% (12). Its

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course and termination however, remain constant regardless of its origin. The ROCS runs cephalad along the atria and posterior to the aorta. It then extends to the interatrial

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groove anteriorly and gives off interatrial branches, before encircling the base of the

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superior vena cava and terminating near its opening. The ROCS supplies the sinoatrial (SA) node. The right and left intermediate, and posterior atrial arteries arise from the

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RCA and LCx, respectively, and often anastomose with the ROCS over the body of the atria or in the interatrial groove. The artery to the atrioventricular (AV) node originates

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posteriorly from the RCA in 83% of cases, from the LCx in 7%, and from both in 10% (12). It courses through the crux cordis, deep into the coronary sinus to the base of the

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interatrial septum. There are other small atrial arteries that are inconsistently found and will not be mentioned in this review. Because the walls of the atria are so thin (2-3 mm), atrial infarction almost always results in transmural injury.

These variations in blood supply to atrial chambers, SA and AV node explain in part why the clinical presentation and electrocardiographic (ECG) abnormalities of atrial infarction are unpredictable and inconsistent. Manifestations of SA nodal abnormalities such as SA blocks and atrial fibrillation will depend on factors such as the location of the occlusion (proximal or distal to the ROCS origin) and the presence/absence of collateral vessels. Manifestations of AV nodal involvement such as AV nodal blocks are less

ACCEPTED MANUSCRIPT frequent in left coronary artery lesions as it supplies the AV node in only 7-10% of

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patients.

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Making the Diagnosis:

Atrial infarctions are almost always described concomitantly with ventricular infarction in

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the literature. Isolated atrial infarctions are rare (13, 26). Atrial infarction presentation depends largely on the extent and site of ventricular involvement. In addition, they may

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initially present with supraventricular tachyarrhythmias. These arrhythmias have been found to occur more frequently in combined atrial and ventricular infarction compared to

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ventricular infarction alone (61-74% vs 8%) (2). They may also present as cardiogenic shock secondary to atrial rupture or loss of atrial “kick”, as well as with stroke or other

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thromboembolic events (4,10). The diagnosis of atrial infarction should be strongly considered in the presence of ischemic symptoms of chest pain together with elevated cardiac biomarkers, the presence of atrial arrhythmias, and ECG abnormalities as detailed below.

ACCEPTED MANUSCRIPT Atrial ECG Patterns The sensitivity and specificity of the ECG in atrial infarction is limited by the variations in

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coronary anatomy as presented above. Consistent ECG patterns (Figure 1, 2a and 2b)

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are generally subtle because of the thinner atrial walls and their inability to generate a high enough voltage to be appreciated on the ECG. This atrial voltage is also often

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overshadowed by the depolarization of the larger ventricles. As a result, it can create

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inter-observer variations in interpretation. One study found considerable variations in interpreting PR-segment deviations among clinicians with different years of experience,

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although they had fair to moderate overall agreement rates (14). In addition, as with ventricular infarction, the PR-segment is also affected by the presence of a previous

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myocardial infarction, pre-existing arrhythmias, or previous interventions, such as

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placement of a pacemaker or coronary-artery bypass surgery.

The diagnosis of atrial infarction rests largely on ECG findings. Though, several atrial infarction ECG patterns have been described, none have been validated by prospective studies. The first ECG description of atrial infarction was in 1939 which reported deviations of the PQ segment from the isoelectric line in leads II and III (15). In 1942, experimental atrial infarction in 18 dogs, through ligation and cauterization of one or more atrial arteries, showed morphologic P wave changes such as notching, increase in amplitude and transient changes in contour; depression of the PR segment; or transient rhythm abnormalities, such as premature atrial contractions (PACs), atrial flutter, atrial tachycardia, wandering atrial pacemaker (WAP) and AV blocks (2). However, there was no constant ECG pattern noted (2) and supraventricular dysrhythmias were the most

ACCEPTED MANUSCRIPT consistent finding (2,5). In 1944, Young and colleagues associated PR segment deviation with atrial infarction where an elevation of >0.5mm or depression of >0.8mm

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was considered abnormal (16). Hellerstein described a case of biatrial posterior wall

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infarction that showed PR segment elevations in leads II and III with episodes of atrial

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fibrillation and high degree AV block (17).

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There are other mechanisms that have been shown to produce P wave morphologic abnormalities and PR-segment changes besides atrial ischemia/infarction. Sympathetic

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overstimulation, pericarditis, atrial dilatation or hypertrophy, and intra-atrial blocks have been described (11, 17-20). Hypersympathetic activity produces descending PR

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segment, depressed J point and ascending ST segment with the P-R and S-T segment

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having concordant deviations. Pericarditis can cause ECG changes if the inflammation

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involves the epicardium or the visceral pericardium as the parietal pericardium is electically inert. The most common ECG abnormality is a widespread saddle-shaped or upward concave ST elevation and PR depression with the reciprocal changes in aVR and V1 (21-22).

The most widely accepted ECG criteria of atrial infarction to date are those proposed by Liu et. al in 1961 (11). They proposed major criteria as follows: (a) PTa (PR) segment elevation of more than 0.5mm in leads V3 and V6 with reciprocal depression of PTa segments in leads V1 and V2; (b) PTa (PR) segment elevation of more than 0.5mm in lead I with reciprocal depressions in leads II and III; and (c) PTa (PR) segment depression of more than 1.5 mm in the precordial leads with 1.2 mm depressions in leads I, II and II, associated with any atrial arrhythmia. Morphologic changes in the P wave, such as an irregular or notched shape, either in a “M” or “W” pattern, were

ACCEPTED MANUSCRIPT considered minor criteria. They also suggested that atrial infarction should always be suspected in patients having an acute myocardial infarction with any form of

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supraventricular dysrhythmia.

However, two other studies do not completely agree with Liu and colleagues (18,23).

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Burch stated that a fraction of a millimeter of PR segment depression was associated

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with atrial infarction in all cases based on his 30-year autopsy study (23). A more recent study studied atrial ECG changes of 666 subjects patients with ST-elevation myocardial

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infarction did not find a single patient who fulfilled any of the Liu major criteria (18).

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Localizing an atrial infarction (right, left, or biatrial) using ECG patterns is equally challenging and the evidence is limited and often conflicting (2, 4, 13, 15, 17, 24).

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Theoretically, PR-segment displacements should correlate to the location of the infarct in the same manner as ST-segment displacements in ventricular infarction. Thus, involvement of the postero-basal wall which corresponds to the left atrium will result in PR (PTa) segment elevation in leads II and III with reciprocal depression in lead I (17). Likewise, involvement of the anterior or anterolateral wall which corresponds to the right atrium will produce PR (PTa) segment elevation in lead I with reciprocal depression in lead II, III and the anterior precordial leads V2-V4 (2, 11, 15). There remain no universally accepted criteria.

ACCEPTED MANUSCRIPT Echocardiogram The clinical utility of the echocardiogram in atrial infarction is limited, as it is difficult to

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observe atrial wall motion on routine transthoracic echocardiography. Published case

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reports using transesophageal echocardiography (TEE) have described right atrial infarction (7,8,25). Findings included (a) akinesis of the right atrial free wall (figure 3a),

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(b) dilatation of the right atrial cavity with spontaneous contrast suggesting impaired

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contractile function (figure 3b), and (c) absence of atrial contribution to right ventricular filling as evidenced by the lack of Doppler A waves across the tricuspid valves with

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normal mitral A waves (figure 3c). All these findings are in the setting of normal sinus rhythm. One retrospective study of 38 patients with acute left ventricular infarction with

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extension to the right chambers found six patients (16%) with right atrial wall motion abnormalities, four patients spontaneous right atrial contrast, and two had loss of

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Doppler A waves (8). However, only three out of the six patients described had ECG abnormalities suggesting atrial infarction.

ACCEPTED MANUSCRIPT Angiogram Angiographic descriptions of atrial infarction are limited to case reports and series. One

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case report described a 90% proximal stenosis of the sinus node artery in a patient with

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chest pain and PR segment shifts in inferior leads suggestive of atrial infarction (24). In

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a case series by Vargas-Baron, two out of three patients with atrial ECG abnormalities and five out of six patients with TEE findings of atrial infarction had significant

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obstructions of atrial circulation on angiogram (8).

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Other diagnostic studies

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One case report described akinesis and enlargement of the right atrium using a

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radionuclide gated cardiac blood pool study in a patient suffering from inferior wall myocardial infarction that developed episodes of atrial flutter, atrial fibrillation and complete heart block (27).

ACCEPTED MANUSCRIPT Complications

associated

ventricular

infarction.

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mentioned

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Complications of atrial infarction can occur either in isolation or in combination with previously,

atrial

infarction

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concommitant with ventricular infarction gives rise to supraventricular tachyarrhythmias

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approximately ten times more frequently than ventricular infarction alone (18). Arrhythmias include atrial fibrillation and flutter, premature atrial complexes, sinus arrest

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and WAP. In addition, abnormal P wave morphology (Liu minor criteria) have been

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shown to significantly predict ensuing new onset atrial fibrillation (18). A study by Jim et al, showed that PR-segment depression of ≥1.2 mm in the inferior leads was associated

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with increased frequencies of atrioventricular block, supraventricular arrhythmias, and

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cardiac free-wall rupture in patients with acute inferior MI (28). Atrial infarction could

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also in part explain the association of left atrial myocardial dysfunction as assessed by speckle tracking echocardiography and post-operative atrial fibrillation (29-31).

Thromboembolic complications such as pulmonary embolism and systemic embolism have been associated with atrial infarction (10). The most frequent, pulmonary embolism, is thought to occur as the majority of atrial infarction cases involve the right atrium (2).

ACCEPTED MANUSCRIPT Atrial rupture is a devastating complication of atrial infarction. Hemodynamic compromise and pericardial tamponade ensues, albeit more slowly in atrial than

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ventricular rupture. Fifteen percent of patients with atrial rupture survive longer than 24

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hours compared to just 2% of those with ventricular rupture (4), indicating that with early

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recognition, surgical correction can potentially be life-saving.

The loss of atrial „kick‟ with atrial infarction can lead do deceased ventricular filling causing

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hemodynamic

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consequences such as cardiogenic shock.

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pressures,

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Prognostic Significance of Atrial ECG Changes

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Abnormal P wave morphology that was described in Liu minor criteria 1 have been shown to predict new-onset atrial fibrillation and 90-day mortality in acute STEMI (18). We examined index ECG in 224 consecutive patients with acute STEMI. We found that length of stay was longer with abnormal P waves (such as notched, irregular, flattening in a M or W pattern) or PR displacement in any lead. Left main coronary disease was found to be more prevalent with abnormal P wave morphology. Abnormal P wave morphology in any ECG lead was associated with higher 30-day (OR 3.09) and 1-year mortality (OR 5.33). PR displacement in any lead was also associated with increased 30-day (OR 2.33) and 1-year mortality (OR 6.56). Abnormal P wave, PR depression in II III and AVF, and elevation in AVR or AVL were associated with increased 1-year mortality (OR 12.49) as was PR depression in the precordial leads (OR 21.65). After

ACCEPTED MANUSCRIPT adjusting for age, ejection fraction, peak troponin I, and left main disease, we found that PR displacement (present in 31% of STEMI in this series) in any lead was associated

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with increased 1-year mortality (adjusted OR 6.22) (32).

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Management:

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There are no specific recommendations in the management guidelines of myocardial

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infarction if concomitant atrial infarction is suspected (33-34). Restoration of perfusion to the ventricular myocardium remains the main objective. One case of a patient with an

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inferior ST elevation myocardial infarction (STEMI) complicated by atrial fibrillation

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observed that the ECG immediately converted to sinus rhythm after balloon dilatation

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and stenting of the large left atrial branch of the left circumflex artery (35).

The role of anti-arrhythmics in atrial infarction has yet to be explored. One large randomized control study found that the use of metoprolol in patients with acute myocardial

infarction

significantly

reduced

the

incidence

of

supraventricular

tachyarrhythmia, among its other benefits (33). If supraventricular tachyarrhythmias such as atrial fibrillation occur, initial treatment should include rate control with a beta blocker. Direct current cardioversion should be strongly considered if the patient is unstable, and can usually be done without the need for anticoagulation except when there is suspicion that the arrhythmia is not associated with the acute myocardial infarction.

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Conclusion: Though the entity “atrial infarction” has been reported for over a century, its recognition

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remains elusive. The diagnosis of atrial infarction should be suspected in any patient

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who presents with typical chest pain, elevated cardiac biomarkers and ECG changes

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consistent with atrial infarction; either the presence of abnormal P-wave morphologies, PR-segment deviations, or supraventricular tachyarrhythmias. Patients should be

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monitored for complications such as arrhythmias, thromboembolic events and heart failure. Management is focused on coronary reperfusion and maintenance of sinus

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rhythm. With ischemic heart disease being the most common cause of death worldwide,

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improved survival.

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adequate knowledge and further investigation of this disease entity may be one key to

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Hop Paris 1925;41:1603-7.

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2. Cushing EH, Feil HS, Stanton EJ, et al. Infarction of the cardiac auricles (atria):

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clinical, pathological and experimental studies. Br Heart J 1942;4:17. 3. Bean WB. Infarction of the heart. Ann Intern Med 1938;12:71-94.

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4. Lazar EJ, Goldberger J, Peled H, et al. Atrial infarction: diagnosis and management.

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AM Heart J 1988;116:1058-63.

5. Wartman WB, Sanders JC. Localization of myocardial infarcts with respect to the

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muscle bundles of the heart. Arch Path01 Lab Med 1950;50:321-64.

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6. Chida K, Ohkawa S, Maeda S, Kuboki K, Imai T, Watanabe C, Ueda K, Shimada H, Sugiura M. A clinicopathologic study of atrial infarction complicating left ventricular

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posterior myocardial infarction. J Cardiol. 1992;22(1):1-10. 7. Hilton TC MD, Pearson AC MD, Serota H MD, Dressler FA MD, Kem MJ MD. Right atrial infarction and cardiogenic shock complicating acute myocardial infarction: Diagnosis

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(1990)120:2 427-430 8. Vargas-Barron J MD, Espinola-Zavaleta N MD, Romero-Chdenas A MD, Simon-Ruiz S MD, Keirns C MD, Pena-Duque MD, Rijlaarsdam M MD, Lupi-Herrera E MD. Clinical-Electrocardiographic correlation of myocardial infarction with extension to right chambers. Echocardiography: A Jrnl. of CV Ultrasound & Allied Tech. 1988;15:2 171-180

ACCEPTED MANUSCRIPT 9. Howard JF, Leach JK, Weitzner S, et al. Atrial infarction with chronic obstructive lung disease. Rocky Mt Med J 1970:67:47-51

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10. Gardin JM, Singer DH. Atrial infarction: importance, diagnosis and localization. Arch

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infarction patterns predict new onset atrial fibrillation after ST-elevation myocardial

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infarction? Insights from the Assessment of Pexelizumab in Acute Myocardial Infarction Trial (APEX AMI). Journal of Electrocardiology 43 2010:351-358.

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ACCEPTED MANUSCRIPT Figures: Figure 1. Various ECG abnormalities of atrial infarction (31)

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A – Normal P wave and PR segment. B - Notched P wave and PR segment elevation. C

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– Notched P wave and PR segment elevation.

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Figure 2a. Abnormal P waves (29)

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Abnormal P wave in II, III, V2-V6

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Figure 2B. PR Segment Displacements (29)

Abnormal P wave in V5, PR segment depression in II, III, AVF, V3-V6 with PR segment

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elevation in V1, AVR

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akinetic right atrial wall (8)

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Figure 3a. Transesophageal echocardiogram showing an adhering thrombus to the

Figure 3b. Transesophageal echocardiogram with M-mode showing dilated hypokinetic right atrium with spontaneous echo contrast (8) Figure 3c. Doppler echocardiogram showing the absence of doppler A waves in the tricuspid doppler velocity tracings found in right atrial infarction (7) Mitral inflow (left panel) showing preserved E and A wave and Tricuspid inflow (right panel) with only an E wave

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ACCEPTED MANUSCRIPT Highlights

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We reviewed the etiology and pathophysiology of atrial infarction We described the various ECG and echocardiographic findings in atrial infarction Atrial infarction is associated with increased mortality and morbidity in STEMI

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