Anteroseptal Myocardial Infarction

Article Author:
Sandeep Bhattarai
Lovely Chhabra
Muhammad Hashmi

Article Editor:
Christopher Willoughby

Editors In Chief:
Kranthi Sitammagari
Mayank Singhal

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Radia Jamil
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Saad Nazir
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Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
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James Hughes
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Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon

9/12/2019 3:56:07 PM


Anteroseptal myocardial infarction (ASMI) is a historical nomenclature based on electrocardiographic (EKG) findings. EKG findings of Q waves or ST changes in the precordial leads V1-V2 define the presentation of anteroseptal myocardial infarction. The patients who had an MI with EKG changes in V1-V2 or to V3 or V4, the autopsy report found out that the infarction involved the majority of the basal anterior septum.[1] This nomenclature was in use until recently. Based on more recent studies using echocardiography and cardiac magnetic resonance imaging in the MI patients with ECG changes on V1, V2, there is rarely involvement of the basal anterior septum, but rather apical and anteroapical myocardial segments are most likely involved.[2][3][4][5]

The term antero-septal is based on autopsy data. Multiple attempts have tried to differentiate the myocardial segments based on different imaging modalities. Echocardiogram segments myocardium into 16 segments while single photon emission computed tomography myocardial perfusion imaging (SPECT-MPI) uses a 17-segment model. The 17 segment model is based on the long-axis of heart from base to apex and short-axis through 360 degrees circumferential location dividing a circle into six 60 degrees segments into basal and mid locations, and 90 degrees segment in the apical location, dividing the heart into a total of 17 segments, a model which seems to be in more agreement to the autopsy studies.

The left ventricle divides into 17 segments:

  1. Basal anterior
  2. Basal anteroseptal
  3. Basal inferoseptal
  4. Basal inferior
  5. Basal inferolateral
  6. Basal anterolateral
  7. Mid anterior
  8. Mid anteroseptal
  9. Mid inferoseptal
  10. Mid inferior
  11. Mid inferolateral
  12. Mid anterolateral
  13. Apical anterior
  14. Apical septal
  15. Apical inferior
  16. Apical lateral
  17. Apex/apical cap

Anteroseptum includes basal anteroseptal, mid anteroseptal and apical septal segments. Isolated anteroseptal infarction is very uncommon.

The coronary artery supplying these segments is most commonly the left anterior descending artery and its septal branches, however, anatomical variation is sometimes a possibility.[6] 


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 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] 


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 MI 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, the 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 mm Hg 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. 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.


A 12 lead EKG should be obtained within 10 minutes of patient presentation, in those with clinical suspicion for acute coronary syndrome. Changes on 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. 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 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 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, 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, 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 of acute ASMI. Non–enteric coated aspirin (162 mg to 325 mg dose) should be administered in all patients with the 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 which 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 2.5 mg SQ daily dose which 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 the 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 which 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 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


The prognosis of anteroseptal MI 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 of anteroseptal MI 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 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 

Deterrence and Patient Education

Risk factor modification using behavioral and lifestyle changes such as dietary modification, increase in activity level, and smoking cessation are associated with better outcomes after acute coronary syndrome. Patient education is essential at the time of discharge and referral to a cardiac rehabilitation program should be made.

Patient education on a healthy diet, weight reduction, physical activity, and smoking cessation require emphasis.

A cardiac rehabilitation program is a comprehensive, long-term service involving medical evaluation, supervised exercise, cardiac risk factor modification, education, and counseling.

Enhancing Healthcare Team Outcomes

Anteroseptal MI is an electrocardiographic definition. The treatment of ASMI should be like any other acute coronary syndrome. An early invasive intervention strategy for patients with acute coronary syndrome is usually the most acceptable approach in whom significant coronary vascular obstruction is a known entity. Low-risk patients with ASMI benefit substantially from guideline-directed optimal medical therapy, although this is often suboptimally used. Role of noninvasive imaging modalities is important in patients with acute coronary syndrome at intermediate risk and helps guide the choice of therapies: invasive versus optimal medical therapy.

Newer and more potent antiplatelet therapies in addition to anticoagulant use are always indicated, irrespective of the choice of the treatment strategy. Evidence-based decisions often require a patient-specific tailored approach by comparing the effectiveness of available data from the controlled investigations. A multi-disciplinary 'heart-team' care approach, which includes physicians, specialists, specialty-trained nursing staff, and pharmacists, collaborating to optimize treatment is paramount to achieve the best long-term patient outcomes. [Level V]

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Anteroseptal Myocardial Infarction - Questions

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A 65-year-old male presents to the emergency department with a history of chest pain which is central in location and crushing in nature, for 1 hour. The pain is radiating to his jaw and left arm. It started suddenly and has been getting worse by the minute. He has been feeling nausea and is now starting to have shortness of breath. He has been suffering from chronic kidney disease stage IV for 2 years and is on medication for that. He's a chronic smoker and drinks nearly 10 units/week. On examination he is in pain, he is sweating, his blood pressure is 160/90, heart rate 110/min regular, and a saturation of 96% on room air. His heart sounds are normal but there are end-inspiratory fine crackles in the bases of both his lungs. A 12-lead electrocardiogram shows ST elevation of 6 mm in leads V1-V4. A portable chest radiograph shows evidence of left ventricular failure. In terms of prognosis, which one of the following management options is going to be the most beneficial in this patient?

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A 68-year-old male with a past medical history of hypertension, diabetes, hyperlipidemia, coronary artery disease presented to the emergency department for chest pain. At baseline, he has a history of chest pain on excursion relieved by rest or nitroglycerin. This time, he states the chest pain started while he was resting, and nitroglycerin did not help him. He describes chest pain as chest tightness. His vitals are heart rate 110 bpm, respiratory rate 25/min, temperature 38.1 C, blood pressure 140/95 mm Hg. His oxygen saturation is 94% on room air. He gets aspirin and nitroglycerin sublingual tablets. An immediate EKG reveals ST-segment elevation in V1-V4 precordial leads. A cardiologist is consulted. He is rushed to the cath lab for primary cutaneous intervention. He gets a stent placed in one of the arteries. What artery is most likely to be involved if ST elevation is in V1-V4 leads?

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A 64-year-old female is evaluated following a primary percutaneous coronary intervention with stent placement in the mid-left anterior descending artery. She presented 3 hours ago with findings of an anteroseptal myocardial infarction complicated by heart failure. Medical history is significant for hyperlipidemia, hypertension, and type 2 diabetes mellitus. Her medications include atorvastatin, aspirin, clopidogrel, metformin, and furosemide. On the physical examination, vital signs are within normal limits. Oxygen saturation is 96% on 3 L oxygen by nasal cannula. Auscultation of the chest reveals an S3 and bibasilar crackles. A chest radiograph shows pulmonary edema. An echocardiogram demonstrates a left ventricular ejection fraction of 40%. Which of the following would be the most appropriate treatment after diuretics?

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A 65-year-old male with a history of hypertension, dyslipidemia, and a stroke called 911 after experiencing 2 hours of worsening substernal chest pain and dyspnea. An ECG performed by emergency medical services (EMS) showed a 3 mm ST-elevation in V1-V3, consistent with acute myocardial infarction. He is a resident of a rural area and was taken to a local emergency room 20 minutes away, which is a non-percutaneous coronary intervention (PCI) capable facility. En route, the patient was given aspirin 325 mg. On arrival to the hospital, he is given morphine and sublingual nitroglycerin. Labs reveal a troponin level of 19 ng/ml and normal serum chemistry and hemogram. The nearest PCI-capable facility is 92 minutes away and time for arrangement of transfer would be 30 minutes. Which of the following is the most appropriate course of action in the management of this patient?

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A 68-year-old woman who was diagnosed with a non–ST-elevation myocardial infarction 5 days ago is being evaluated before discharge from the hospital. Nuclear stress testing revealed a small septal perfusion defect and normal left ventricular ejection fraction. She declined angiography during her stay. She has had no further discomfort since the day of admission. Medical history is significant for hyperlipidemia, hypertension, and transient ischemic attack. Current medications are low-dose aspirin, ramipril, metoprolol, and atorvastatin. Her physical examination and vital signs are unremarkable. In addition to her current medications, which of the following is indicated?

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Anteroseptal Myocardial Infarction - References


MYERS GB,KLEIN HA,STOFER BE, Correlation of electrocardiographic and pathologic findings in anteroseptal infarction. American heart journal. 1948 Oct;     [PubMed]
Allencherril J,Fakhri Y,Engblom H,Heiberg E,Carlsson M,Dubois-Rande JL,Halvorsen S,Hall TS,Larsen AI,Jensen SE,Arheden H,Atar D,Clemmensen P,Ripa MS,Birnbaum Y, Correlation of anteroseptal ST elevation with myocardial infarction territories through cardiovascular magnetic resonance imaging. Journal of electrocardiology. 2018 Jul - Aug;     [PubMed]
Porter A,Wyshelesky A,Strasberg B,Vaturi M,Solodky A,Imbar S,Sagie A,Battler A,Birnbaum Y, Correlation between the admission electrocardiogram and regional wall motion abnormalities as detected by echocardiography in anterior acute myocardial infarction. Cardiology. 2000;     [PubMed]
Allencherril J,Fakhri Y,Engblom H,Heiberg E,Carlsson M,Dubois-Rande JL,Halvorsen S,Hall TS,Larsen AI,Jensen SE,Arheden H,Atar D,Clemmensen P,Shah DJ,Cheong B,Sejersten M,Birnbaum Y, Appropriateness of anteroseptal myocardial infarction nomenclature evaluated by late gadolinium enhancement cardiovascular magnetic resonance imaging. Journal of electrocardiology. 2018 Mar - Apr;     [PubMed]
Cerqueira MD,Weissman NJ,Dilsizian V,Jacobs AK,Kaul S,Laskey WK,Pennell DJ,Rumberger JA,Ryan T,Verani MS, Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002 Jan 29;     [PubMed]
Lanz J,Wyss D,Räber L,Stortecky S,Hunziker L,Blöchlinger S,Reineke D,Englberger L,Zanchin T,Valgimigli M,Heg D,Windecker S,Pilgrim T, Mechanical complications in patients with ST-segment elevation myocardial infarction: A single centre experience. PloS one. 2019;     [PubMed]
Reeder GS, Identification and treatment of complications of myocardial infarction. Mayo Clinic proceedings. 1995 Sep;     [PubMed]
Shalev Y,Fogelman R,Oettinger M,Caspi A, Does the electrocardiographic pattern of     [PubMed]
McManus DD,Gore J,Yarzebski J,Spencer F,Lessard D,Goldberg RJ, Recent trends in the incidence, treatment, and outcomes of patients with STEMI and NSTEMI. The American journal of medicine. 2011 Jan;     [PubMed]
Norris RM,Mercer CJ,Croxson MS, Conduction disturbances due to anteroseptal myocardial infarction and their treatment by endocardial pacing. American heart journal. 1972 Oct;     [PubMed]
Akdemir R,Gunduz H,Emiroglu Y,Uyan C, Myocardial bridging as a cause of acute myocardial infarction: a case report. BMC cardiovascular disorders. 2002 Sep 21;     [PubMed]


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