The collaborative expert consensus of the 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 the 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:
MI can further be classified based on presenting EKG findings and the location of ischemia. The 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 the obtuse marginal branch of the LCx or diagonal branch of LAD can cause isolated lateral myocardial infarction (LMI).
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-eluting 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). The prevalence of MINOCA is estimated at around 6% based on a meta-analysis done in 2015. Some of the causes of MINOCA include:
Recent trends suggest that the incidence of ST-elevation myocardial infarction (STEMI) has declined and incidence of non-ST-elevated MI (NSTEMI) has increased. 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 an overall LMI incidence of 13.4% amongst patients presenting with STEMI. 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.
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. 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.
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. The prevalence of silent MI is reported as high as 23%.
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. Physical findings such as diaphoresis, extra heart sounds, heart murmurs, and elevated jugular venous pressure can guide toward the diagnosis of LMI.
Patients suspected of having acute LMI should have a prompt evaluation with an electrocardiogram (ECG) and measurements of serial cardiac troponins. Recognizing distinct ST-T involvement patterns can aid in early diagnosis of MI.
In patients with normal troponin and non-diagnostic ECG, a quick evaluation with an echocardiogram can be done. Echocardiogram has high sensitivity and low specificity when diagnosing MI. 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. Coronary angiogram remains the most definitive and diagnostic test of choice.
LMI presenting as STEMI should be treated immediately. Early reperfusion has shown benefits with improved clinical outcomes. Percutaneous intervention (PCI) has demonstrated superior results when compared to fibrinolytic therapy. 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. Antiplatelet therapy with aspirin and either P2Y12 inhibitor (Clopidogrel, Ticagrelor, Prasugrel) or Glycoprotein IIb/IIIa inhibitor is recommended before and after PCI. Multiple studies have demonstrated mortality benefits with beta-blockers (Metoprolol, Carvedilol, Bisoprolol) and high-intensity high potency statins (Rosuvastatin). Patients presenting with cardiogenic shock or mitral valve rupture post-MI may need a mechanical supportive device such as an intra-aortic balloon pump (IABP) after PCI.
Additionally, symptomatic management includes the usage of Morphine, Oxygen (in patients with hypoxemia), and nitrates (nitroglycerin).
LMI patients presenting as NSTEMI should receive initial medical therapy with oxygen (if hypoxic, Saturation of oxygen <94%), beta-blockers (Carvedilol, Metoprolol, Bisoprolol), and a statin (Rosuvastatin or Atorvastatin). Antithrombotic therapy including antiplatelet medications (using aspirin and a P2Y12 inhibitor such as Ticagrelor, Clopidogrel or Prasugrel) and anticoagulants such as unfractionated heparin should be initiated as soon as possible. NSTEMI patients have also shown better outcomes with early reperfusion strategy. Contrary to STEMI fibrinolysis has no role in the management of NSTEMI.
All patients with LMI should be placed on life-long therapy with aspirin, beta-blockers, and high intensity-high potency statins.
Patients presenting with chest pain will have the following in the differential diagnosis:
LMI has overall favorable outcomes. Long-term outcomes in patients with STEMI and NSTEMI have improved over the last decade. Hreybe et al. reported marginally elevated risk of ventricular fibrillation in patients presenting with an anterior or lateral MI.
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. 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.
Patient education is the cornerstone of 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. 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.
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