Anteroseptal Myocardial Infarction

Etiology

The etiology of anteroseptal myocardial infarction is like any other MI, but the culprit lesion usually involves the left anterior descending artery or a diagonal branch.[5]

1. Obstructive: Thrombus or embolus obstructing the coronary blood flow.

2. Non-obstructive: This is also called myocardial infarction with non-obstructive coronary arteries (MINCOA) which includes atheromatous lesion, coronary spasm, myocardial bridging or coronary artery dissection, etc.[7]

Epidemiology

Epidemiology of anteroseptal myocardial infarction as a separate entity has not been the topic of directed studies. In general, MI is one of the major public health problems as the rise in the risk factors for coronary heart disease continues to prevail in society. Studies show that the incidence of NSTEMI is increasing. However, the magnitude and proportion of STEMI and hospital mortality of MI are decreasing.[8]

Pathophysiology

The most common mechanism is the erosion or rupture of an unstable atherosclerotic plaque in the left anterior descending artery. Erosion or plaque rupture leads to exposure of underlying thrombogenic material in the vascular bed with the blood components leading to thrombus formation or emboli of the atheromas to the distal vessels that can cause occlusion of small caliber vasculature.

History and Physical

History cannot differentiate anteroseptal myocardial infarction from other forms of MI. Symptoms are thus similar to any other MI. The classic symptoms of MI are substernal chest tightness (with or without radiation to the jaw, neck, left shoulder, or inner aspect of the left arm) associated with shortness of breath, nausea, and diaphoresis. Patients may also less commonly have nausea, epigastric pain, unexplained generalized fatigue, or syncope. Unexplained new-onset or increased exertional dyspnea is the most common anginal equivalent. In women and elderly patients, MI may sometimes present with atypical symptoms, although the frequency of typical presentation is more common. Patients with diabetes may have a silent presentation, which means that the patients may not experience any significant symptoms of MI. When it comes to a patient with a known history of known coronary artery disease or previous angina, chest pain symptoms require careful evaluation with a high degree of suspicion as these patients represent a cohort with a high pretest probability. The clinician should perform a careful inquiry of symptoms including the location of the pain, onset, characteristics, radiation, timing, severity, and aggravating and relieving factors. Correlation of symptoms with prior MI presentation (if any present) is also beneficial.

 Any new onset of cardiovascular symptoms in patients with established coronary artery disease or coronary artery disease equivalent should require careful evaluation with high suspicion for possible MI.

A thorough physical examination should include the assessment of heart rate, rhythm, blood pressure in both arms, auscultation of the cardiac areas for heart sounds, gallop sounds, pericardial rubs, and murmurs. The physical examination in patients with MI can be normal or may have some abnormal findings as indicated below. 

• Inspection: Inspect the precordium for apical impulse, neck for any venous distension, and dependent areas for edema. The patient may have signs of heart failure such as edema. The presence of signs of heart failure should expedite the diagnostic assessment and treatment of this condition. 
• Palpation: Pulse rate and rhythm, blood pressure in both arms, heaves. An unequal pulse volume and palpable systolic BP difference of greater than or equal to 15 mmHg between both arms suggest aortic dissection.
• Auscultation: Precordium on four cardiac areas for acute onset gallops, murmurs, or rubs. Acute ischemia may cause an S4, a paradoxical S2 heart sound splitting, or a new systolic murmur at the mitral area which may occur due to mitral regurgitation resulting from papillary muscle dysfunction. S3 may be present when there is decompensated heart failure. These signs are however non-specific as they may occur without an MI. The presence of a precordial rub may help identify acute pericarditis and may help exclude acute MI. A pleural friction rub may be audible in pneumonitis and/or pleuritis and may support a non-MI cause of chest pain.

Evaluation

A 12 lead EKG should be obtained within 10 minutes of patient presentation, in those with clinical suspicion for the acute coronary syndrome. Changes in ECG in patients may include ST depression, transient ST-elevation, new T-wave inversions, or even Q-waves.

Anteroseptal MI on ECG usually is characterized by the presence of ST-elevations in V1-V3 leads acutely followed by the development of Q waves in V1-V3 precordial leads. The presence of Q-waves in these leads is classically referred to as an age-indeterminate anteroseptal infarct. Q-waves are considered significant if the Q wave duration (onset to its nadir) is more than 0.03 sec or the height of the Q wave is more than 25% of the height of the succeeding R wave. ST changes qualify as new ST-segment elevation at the J-point in two contiguous leads with the cut-points: greater than or equal to 1 mm in all leads other than leads V2-V3. For leads V2-V3: greater than or equal to 2 mm in men 40 years and older, greater than or equal to 2.5 mm in men under 40 years, or greater than or equal to 1.5 mm in women regardless of the age. These values assume the usual calibration of 1mV/10mm. 

Abnormal cardiac troponin above the 99th percentile of the upper reference limit is usually indicative of infarction. Cardiac troponins are the primary modality for the diagnosis of MI or acute coronary syndrome. They are the most sensitive and specific biomarkers for the acute coronary syndrome. They usually rise within a few hours of the symptom onset and may remain elevated for several days. In a large area of myocardial involvement, they may remain elevated for up to 2 weeks. A negative troponin value on admission offers greater than 95% negative predictive value for MI. They are also useful for risk stratification in patients with MI. The main diagnostic biomarkers indicating myocardial damage and necrosis are cardiac troponin I and cardiac troponin T.

Other tests: A chest X-ray is useful to identify other potential causes of chest pain. There may be a widened mediastinum in patients with aortic dissection. Computed tomography of the chest with contrast can exclude causes such as pulmonary embolism and aortic dissection. Point of care ultrasound (POCUS) of the heart can be used to evaluate for any new wall motion abnormalities of the left ventricle. One of the advantages of using POCUS is that the wall motion abnormality appears earlier in the ischemic cascade compared to the EKG changes or serum troponin elevation.

Treatment / Management

Management of ASMI is no different than any MI/acute coronary syndrome in general. The goals of treatment in MI are immediate relief of ischemia, prevention of MI progression, and death. The focus involves early diagnosis, pain relief, initiation of antiplatelet therapy, and intravenous anticoagulation along with restoring early reperfusion.  In the case of STEMI, early reperfusion is the key to prevent tissue death, life-threatening arrhythmias and improve prognosis and long-term mortality.

Supplemental oxygen administration is necessary for patients with ASMI with arterial oxygen saturation less than 90%, high-risk features of hypoxemia, and the presence of increased work of breathing or clinical respiratory distress. In patients with ongoing ischemic chest pain should, sublingual nitroglycerin (0.3 mg to 0.4 mg) should be administered every 5 minutes for up to 3 doses. After that, the use of intravenous nitroglycerin may be a consideration in the absence of any contraindication. Patients may be administered intravenous morphine sulfate if there are continued ischemic pain symptoms despite treatment with maximally tolerated nitrate therapy. Oral beta-blocker therapy should be given within the first 24 hours in all patients without any contraindication to their use such as low-output state, presence of cardiogenic shock, decompensated heart failure, or presence of an active heart block. In patients with contraindication to beta-blocker use and ongoing or recurrent ischemic discomfort, the use of a non-dihydropyridine calcium channel blocker such as diltiazem may be an option as initial therapy. All patients should receive high-intensity statin therapy. Intra-aortic balloon pump counterpulsation therapy may be used in patients with severe persistent or recurrent ischemia despite intensive medical therapy, while they are awaiting invasive angiography and revascularization. In the absence of a specific contraindication, ACE inhibitors should be started in all patients with LV systolic function less than 40% and in those with the presence of diabetes mellitus, hypertension, or stable chronic kidney disease. Aldosterone receptor blockers can be used instead of ACE inhibitors, in patients who are ACE-inhibitor intolerant. In patients with ASMI and LVEF less than 40% with or without HF,  selective aldosterone blockers such as eplerenone as an adjunct to ACE inhibitors and beta-blockers offer a long-term mortality benefit.

Prompt initiation of antiplatelet therapy is beneficial in patients with acute ASMI. Non–enteric-coated aspirin (162 mg to 325 mg) should be administered in all patients with acute coronary syndrome as early as possible after initial presentation. A maintenance dose of aspirin (81 mg/day to 325 mg/day) will then continue indefinitely. A P2Yinhibitor such as clopidogrel or ticagrelor or prasugrel should be given in addition to aspirin usually for up to 1 year to all patients after the MI. Contraindications to prasugrel include patients with prior stroke. In patients requiring an early invasive strategy with intermediate to high-risk features (such as positive cardiac biomarkers), the addition of GP IIb/IIIa inhibitor (such as eptifibatide or tirofiban) in addition to dual antiplatelet therapy may be considered as part of an initial antiplatelet regimen. 

Anticoagulation is the recommendation for all patients irrespective of the treatment strategy. Treatment options for anticoagulation include enoxaparin, unfractionated intravenous heparin, fondaparinux, or bivalirudin. Argatroban is a direct thrombin inhibitor that can be used in patients with a history of heparin-induced thrombocytopenia for either prophylaxis or the treatment of thrombosis, including those requiring PCI.

Enoxaparin is given as an initial intravenous dose of 30 mg in all patients followed by 1 mg/kg subcutaneously every 12 hours dosing (can be used as 1 mg/kg SC once daily dose if creatinine clearance is less than 30 mL/min). It is given for the duration of hospitalization or until PCI is completed. Unfractionated heparin is dosed at an initial loading dose of 60 IU/kg (maximum 4000 IU) followed by infusion of 12 IU/kg per hour (maximum 1000 IU/h) with close monitoring of the activated partial thromboplastin time, continued for 48 hours or until PCI is performed. Fondaparinux administration is a 2.5 mg SQ daily dose that is usually maintained for the duration of hospitalization or until PCI. Fondaparinux should always be used in addition to another anticoagulant such as intravenous heparin or bivalirudin to reduce the risk of catheter thrombosis. Bivalirudin is administered as 0.10 mg/kg initial loading dose, followed by 0.25 mg/kg per hour (only to be used in patients managed with an early invasive strategy) and is continued until diagnostic angiography or PCI. The anticoagulant effect of bivalirudin is monitored by measuring the activated clotting time.

Eventually, the focus is to restore myocardial perfusion by revascularization. An urgent invasive strategy (coronary angiography with revascularization intent based on coronary anatomy within 24 hrs) is indicated in all patients with acute coronary syndrome who have refractory angina or electrical or hemodynamic instability or in patients with increased risk for hard clinical events.  A delayed invasive approach (within 24 to 72 hrs) is reasonable for patients with low to intermediate clinical risk. The ischemia-guided strategy aims to avoid the routine use of early invasive procedures. Ischemia-guided therapy focuses on the optimization of medical therapy and treats based on risk stratification or ischemic burden as defined by the use of initial non-invasive strategies such as myocardial perfusion imaging. Ischemia-guided therapy is reasonable for low-risk patients such as those with a low-risk score ( TIMI score of 0 or 1, GRACE score<109) and low-risk Troponin-negative female patients.

The goals of therapy after MI are to restore the patient to normal activities with a focus on aggressive lifestyle and risk factor modification. The goal for long-term medical therapy relates to the potential prognostic benefits that studies have shown related to the use of antiplatelet agents, beta-blockers, statins, and renin-angiotensin-aldosterone system inhibitors, especially for patients with LVEF under 40%. Treatment of major risk factors such as smoking, hypertension, diabetes mellitus, hyperlipidemia, obesity, and lack of physical activity. Patients should also undergo a cardiac rehabilitation program after their discharge.

In summary:

• Early diagnosis - history, EKG, cardiac troponins
• Pain relief - nitroglycerin
• Hemodynamic stability - airway, breathing, circulation
• Reperfusion- PCI vs. fibrinolysis
• Prevention of rethrombosis: aspirin plus P2Y12 inhibitor - clopidogrel vs. ticagrelor depending upon the choice of reperfusion 
• Preventing life-threatening arrhythmias - beta-blocker therapy
• Improve prognosis and long term mortality - statins, aspirin, clopidogrel, beta-blockers, ACE inhibitors, revascularization, cardiac rehabilitation and aggressive lifestyle/behavioral modification

Differential Diagnosis

Differential diagnosis of anteroseptal myocardial infarction will include any differential of the acute coronary syndrome:

• Pulmonary embolism
• Pericarditis
• Aortic dissection
• Acid peptic disease
• Pleuritic chest pain due to pulmonary infection or infarction
• Musculoskeletal pain - costochondritis, rib pain

Prognosis

The prognosis of anteroseptal myocardial infection has not been the object of research as a separate entity. In general, survivors of a myocardial infarction face a substantial excess risk of further cardiovascular events, including an increase in mortality. However, the prognosis for an individual varies markedly according to the presence or absence of adverse risk factors and measures for secondary prevention. Short and long-term death rates following MI have fallen substantially in the past few decades with improvements in medical care, particularly the widespread use of reperfusion techniques and the adjunctive use of multiple medical therapies for primary and secondary prevention.

Complications

Complications of anteroseptal myocardial infection will include the complications of any myocardial infarction including:

1. Myocardial Dysfunction

2. Heart Failure

3. Mechanical Complication: Septal rupture, papillary muscle rupture, free wall rupture.

Septal rupture: Apical septum rupture is a rare complication but can occur with anteroseptal MI involving LAD lesion. Prompt diagnosis is necessary, and the treatment of choice is the definitive surgery.[9]

Papillary muscle rupture and free wall rupture are very uncommon with anteroseptal infarction. These complications are more related to the multivessel disease.[10]

4. Conduction Abnormalities

Conduction disturbances are associated with anteroseptal MI. One study showed that right bundle branch block was the most common conduction abnormality in anteroseptal MI and it progressed to complete AV block in one-third of the patients.[11]

5. Post-infarction Pericarditis