Lateral Wall Myocardial Infarction


Article Author:
Dipesh Ludhwani
Lovely Chhabra


Article Editor:
Nagendra Gupta


Editors In Chief:
Michael Firstenberg
Lawrence Greiten


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
6/30/2019 8:03:28 PM

Introduction

The collaborative expert consensus of European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA) and World Heart Federation (WHF) released the fourth universal definition of Myocardial Infarction (MI) in August 2018. Diagnosis of type I MI focuses on detection of a rise and/or fall of cardiac Troponin (cTn) with at least one value above the 99th percentile and with the presence of at least one of the following factors:

  1. Symptoms of acute MI
  2. New signs of ischemia on electrocardiogram (ECG)
  3. Occurrence of pathological Q waves
  4. New wall motion abnormality or loss of viable myocardium as evident on imaging
  5. Coronary thrombus identification on angiography[1] 

MI can further be classified based on presenting EKG findings and location of ischemia. Left ventricular lateral wall is supplied by branches of the left anterior descending artery (LAD) and Left circumflex artery (LCx). Lateral and posterior walls together form the left ventricular free wall which is a common site for free-wall rupture (FWR) post-MI. Isolated lateral wall involvement is sporadic and is usually seen as part of multi-territorial infarction such as anterolateral, posterolateral, and inferolateral MI. Occlusion of obtuse marginal branch of LCx or diagonal branch of LAD can cause isolated lateral myocardial infarction (LMI).

Etiology

Isolated LMI, similar to other acute MI, is caused by acute atherosclerotic plaque rupture with subsequent thrombus formation in LCx or one of its branches. More commonly, LAD is involved in the ensuing anterolateral MI. In patients with recent drug eluding stents, medication non-compliance can cause stent restenosis resulting in acute MI.  On rare occasions, patients can present with myocardial infarction with non-obstructive coronary arteries (MINOCA). Prevalence of MINOCA is estimated around 6% based on a meta-analysis done in 2015.[2] Some of the causes of MINOCA include:

  • Coronary artery spasm
  • Spontaneous coronary artery dissection (SCAD)
  • Coronary artery embolism (CAE): Atrial myxoma, atrial fibrillation, infective endocarditis, rheumatic valve disease, mitral stenosis
  • Autoimmune conditions such as Takayasu arteritis
  • Myocardial bridging

Epidemiology

Recent trends suggest that incidence of ST-elevation myocardial infarction (STEMI) have declined and incidence of non-ST-elevated MI (NSTEMI) have increased.[3] Around 25% to 40% of patients with MI present as STEMI and of those, 23% have diabetes mellitus. A study based on atherosclerosis risk in communities (ARIC), reported overall LMI incidence of 13.4% amongst patients presenting with STEMI.[4] Patients with traditional cardiovascular risk factors such as age, family history, obesity, smoking, hypertension, dyslipidemia, diabetes, and alcohol use are predisposed to suffer from LMI.

Pathophysiology

Atherosclerotic plaques with large lipid-rich core and covered by a thin, fibrous cap are extremely unstable and susceptible to rupture. Such plaques may not necessarily cause obstruction. Metalloproteases and cytokines released by T-lymphocytes and macrophages present at the site of plaque weaken the fibrous tissue rendering it vulnerable to erosion.[5] Sudden acute plaque rupture exposes sub-endothelial collagen which serves as a nidus for future platelet adhesion and activation. Thromboxane A2, 5-hydroxytryptamine, platelet-activating factor, and ADP released by platelets promote platelet aggregation and vessel vasoconstriction. Activation of coagulation cascade results in fibrin formation and stabilization of occlusive thrombus. Prolonged ischemia leads to necrosis and infarction. The sub-endocardial region of the ventricular wall is most prone to ischemia however with time it can involve the entire wall thickness. Such ischemic events spanning the entire myocardial wall thickness present as STEMI. Infarcted tissue undergoes a series of changes from necrosis to granulation tissue and subsequent scar formation. During this interval from the appearance of granulation tissue to scar formation (between 4 to 14 days), infarcted myocardium is extremely prone to rupture.

History and Physical

Most MI, regardless of location, present with a similar array of symptoms. Some of the common presenting symptoms include left-sided chest pain radiating to arm/neck, shortness of breath, nausea, vomiting, palpitation, diaphoresis, and fatigue. People with a history of previous MI can relate current symptoms to previous episodes and tend to seek care sooner. Silent MI refers to a group of patients presenting with no acute signs or symptoms. Prevalence of silent MI is reported as high as 23%.[6]

All patients suspected of having LMI should have a thorough history and physical exam performed. Details regarding the nature of chest pain including onset, aggravating/relieving factors and radiation can help make an important clinical decision. Patients should be examined for signs of excessive lipid accumulation such as xanthoma and xanthelasma.[7] Physical findings such as diaphoresis, extra heart sounds, heart murmurs, and elevated jugular venous pressure can guide toward the diagnosis of LMI.

Evaluation

Patients suspected of having acute LMI should have a prompt evaluation with an electrocardiogram (ECG) and measurements of serial cardiac troponins.[8] Recognizing distinct ST-T involvement pattern can aid in early diagnosis of MI.

ECG Findings

  • ST-Elevated LMI: ST elevation in lead I, aVL, V5, and V6; Reciprocal ST depression in inferior lead III and aVF
  • High lateral STEMI: High lateral STEMI can present as ST elevation involving lead I and aVL. Subtle ST elevation in V5, V6 and reciprocal changes in lead III and avF may be present. This is usually caused by occlusion of the first diagonal branch of LAD and is sometimes referred to as South African flag sign.
  • Old LMI presents with deep and broad Q waves I leads I and aVL
  • Inferolateral STEMI presents with ST-elevation involving lateral (I, aVL, V5, V6) and inferior leads (II, III, aVF): This is usually seen with occlusion of the proximal LCx artery.
  • Anterolateral STEMI presents with ST-elevation involving lateral (I, aVL, V5, V6) and anterior leads (V1, V2, V3): This is highly indicative of proximal LAD occlusion.

In patients with normal troponin and non-diagnostic ECG, a quick evaluation with echocardiogram can be done. Echocardiogram has high sensitivity and low specificity when diagnosing MI. [9]Severe ischemia produces regional wall motion abnormalities (RWMA) which can be visualized on echocardiogram. However, it is difficult to differentiate acute ischemia from old infarct based on RWMA. Patients with normal echocardiogram but having moderate pre-test probability should be evaluated with a stress test.[10] Coronary angiogram remains the most definitive and diagnostic test of choice.

Treatment / Management

LMI presenting as STEMI should be treated immediately. Early reperfusion has shown benefits with improved clinical outcomes.[11] Percutaneous intervention (PCI) has demonstrated superior results when compared to fibrinolytic therapy.[12] ACC/AHA guidelines for STEMI management recommend early PCI with preferable door to balloon time of fewer than 90 minutes at PCI capable facility and less than 120 minutes at non-PCI capable facility.[13] Antiplatelet therapy with aspirin and either P2Y12 inhibitor or Glycoprotein IIb/IIIa inhibitor is recommended before and after PCI. Multiple studies have demonstrated mortality benefits with beta-blockers and high-intensity high potency statins.[14] Patients presenting with cardiogenic shock or mitral valve rupture post-MI may need a mechanical supportive device such as intra-aortic balloon pump (IABP) after PCI.

LMI patients presenting as NSTEMI should receive initial medical therapy with oxygen (if hypoxic), beta-blocker, and a statin. Antithrombotic therapy including antiplatelet medications and anticoagulants such as unfractionated heparin should be initiated as soon as possible. NSTEMI patients have also shown better outcomes with early reperfusion strategy.[15] Contrary to STEMI fibrinolysis has no role in the management of NSTEMI.[16]

All patients with LMI should be placed on life-long therapy with aspirin, beta-blockers, and high intensity-high potency statins.

Differential Diagnosis

Patients presenting with chest pain should be ruled out for acute pericarditis, acute gastritis/peptic ulcer disease, aortic dissection, cardiac tamponade, costochondritis, pneumothorax, Prinzmetal’s angina, and pulmonary embolism.

Prognosis

LMI has overall favorable outcomes. Long-term outcomes in patients with STEMI and NSTEMI have improved over the last decade.[17] Hreybe et al. reported marginally elevated risk of ventricular fibrillation in patients presenting with an anterior or lateral MI.[18]

Prognosis tends to be worse in patients presenting with life-threatening complications such as arrhythmias, sudden cardiac arrest, free wall/papillary muscle rupture and cardiogenic shock. Risk stratification using TIMI scores can help identify patients with increased in-hospital mortality.[19] Thirty-day mortality rates for STEMI are 13% with medical therapy alone, 6-7% with optimal fibrinolytic therapy, and 3% to 5% with primary percutaneous coronary intervention when performed within 2 hours of hospital arrival. There is an even lower risk of death of only 2% in patients with NSTEMI after 30 days, as compared to STEMI.

Complications

  1. Left ventricular free wall rupture
  2. Pericarditis
  3. Ventricular aneurysm
  4. Acute mitral regurgitation
  5. Left ventricular thrombus
  6. Congestive heart failure
  7. Ventricular fibrillation
  8. Ventricular tachycardia
  9. Sudden cardiac arrest
  10. Cardiogenic shock
  11. PCI related complications

Deterrence and Patient Education

Patient education is the cornerstone in preventing future MI events. Interventions such as smoking cessation, weight reduction, medication adherence, and dietary modification have all been well established in improving overall cardiovascular mortality.[20][21] Targeting strict blood pressure, glycemic, and lipid goals can help decrease the risk of complications after MI. Patients should be encouraged to participate in cardiac rehabilitation programs to improve overall cardiac function and achieve better heart rate control.

Enhancing Healthcare Team Outcomes

A multidisciplinary approach has been shown to improve health care outcomes in patients admitted with MI.[22][23] Adherence to guideline-directed therapy is equally important. Establishing a cardiac alert response team for emergencies can help provide timely dedicated care.


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Lateral Wall Myocardial Infarction - Questions

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What are the EKG findings in a patient presenting with lateral wall ST-elevation myocardial infarction (STEMI)?



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A 65-year-old male presents to the emergency department with complaints of chest pain which started 30 minutes ago. On admission, his vitals are stable his EKG shows ST elevation in lead I and aVL. His troponins are mildly elevated, and rest of serum chemistry is normal. Which is the next step?



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High lateral myocardial infarction is most commonly causes by obstruction of which artery?



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Which condition is associated with South African flag sign on EKG?

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Which of the following arteries most commonly supplies the sinoatrial node?



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Lateral Wall Myocardial Infarction - References

References

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