Acute Myocardial Infarction – Causes, Symptoms, Treatment

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Acute myocardial infarction is one of the leading causes of death in the developed world. The prevalence of the disease approaches three million people worldwide, with more than one million deaths in the United States annually. Acute myocardial infarction can be divided into two categories, non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Unstable angina is similar to NSTEMI. However, cardiac markers are not elevated.

Acute coronary syndrome (ACS) can be divided into subgroups of ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. ACS carries significant morbidity and mortality and the prompt diagnosis, and appropriate treatment is essential. STEMI diagnosis and management are discussed elsewhere. NSTEMI and Unstable angina are very similar, with NSTEMI having positive cardiac biomarkers. The presentation, diagnosis, and management of NSTEMI are discussed below.

An acute ST-elevation myocardial infarction (STEMI) is an event in which transmural myocardial ischemia results in myocardial injury or necrosis. The current 2018 clinical definition of myocardial infarction (MI) requires the confirmation of the myocardial ischemic injury with abnormal cardiac biomarkers.[rx] It is a clinical syndrome involving myocardial ischemia, EKG changes and chest pain.

Inferior wall myocardial infarction (MI) occurs from a coronary artery occlusion with resultant decreased perfusion to that region of the myocardium. Unless there is timely treatment, this results in myocardial ischemia followed by infarction. In most patients, the inferior myocardium is supplied by the right coronary artery. In about 6-10% of the population, because of left dominance, the left circumflex will supply the posterior descending coronary artery. Approximately 40% of all MIs involve the inferior wall. Traditionally, inferior MIs have a better prognosis than those in other regions, such as the anterior wall of the heart. The mortality rate of an inferior wall MI is less than 10%. However, several complicating factors that increase mortality, including right ventricular infarction, hypotension, bradycardia heart block, and cardiogenic shock.

Acute myocardial infarction

Types of Myocardial Infarction

I: Ischemic

  • Reinfarction
  • Extension of infarction
  • Angina

II: Arrhythmias

  • Supraventricular or ventricular arrhythmia
  • Sinus bradycardia and atrioventricular block

III: Mechanical

  • Myocardial dysfunction
  • Cardiac failure
  • Cardiogenic shock
  • Cardiac rupture (Free wall rupture, ventricular septal rupture, papillary muscle rupture)

IV: Embolic

  • Left ventricular mural thrombus,
  • Peripheral embolus

V: Inflammatory

  • Pericarditis (infarct associated pericarditis, late pericarditis, or post-cardiac injury pericarditis).
  • Pericardial effusion

Myocardial infarction in general can be classified  from Type 1 to Type 5 MI based on the etiology and pathogenesis.

  • Type 1 MI – is due to acute coronary atherothrombotic myocardial injury with plaque rupture. Most patients with ST-segment elevation MI (STEMI) and many with non-ST-segment elevation MI (NSTEMI) comprise this category.
  • Type 2 MI – is the most common type of MI encountered in clinical settings in which is there is a demand-supply mismatch resulting in myocardial ischemia. This demand-supply mismatch can be due to multiple reasons including but not limited to the presence of a fixed stable coronary obstruction, tachycardia, hypoxia or stress. However, the presence of fixed coronary obstruction is not necessary. Other potential etiologies include coronary vasospasm, coronary embolus, and spontaneous coronary artery dissection ( SCAD). Sudden cardiac death patients who succumb before any troponin elevation comprise
  • Type 3 MI – are related to coronary revascularization procedures like Percutaneous Coronary Intervention (PCI) or Coronary artery Bypass Grafting ( CABG).
  • Types 4 and – are related to coronary revascularization procedures like Percutaneous Coronary Intervention (PCI) or Coronary artery Bypass Grafting ( CABG).
  • Types 5 MIs –  are related to coronary revascularization procedures like Percutaneous Coronary Intervention (PCI) or Coronary artery Bypass Grafting ( CABG).

Causes of Acute Myocardial Infarction

Myocardial infarction is closely associated with coronary artery disease. INTERHEART is an international multi-center case-control study which delineated the following modifiable risk factors for coronary artery disease: 

  • Smoking
  • Abnormal lipid profile/blood apolipoprotein (raised ApoB/ApoA1)
  • Hypertension
  • Diabetes mellitus
  • Abdominal obesity (waist/hip ratio) (greater than 0.90 for males and greater than 0.85 for females)
  • Psychosocial factors such as depression, loss of the locus of control, global stress, financial stress, and life events including marital separation, job loss, and family conflicts
  • Lack of daily consumption of fruits or vegetables
  • Lack of physical activity
  • Alcohol consumption (weaker association, protective)

Symptoms of Acute Myocardial Infarction

Common heart attack signs and symptoms include:

  • Chest pain or discomfort in the center of the chest; also described as a heaviness, tightness, pressure, aching, burning, numbness, fullness or squeezing feeling that lasts for more than a few minutes or goes away and comes back. It is sometimes mistakenly thought to be indigestion or heartburn.
  • Pain or discomfort in other areas of the upper body including the arms, left shoulder, back, neck, jaw, or stomach
  • Difficulty breathing or shortness of breath
  • Sweating or “cold sweat”
  • Fullness, indigestion, or choking feeling (may feel like “heartburn”)
  • Nausea or vomiting
  • Light-headedness, dizziness, extreme weakness or anxiety
  • Rapid or irregular heartbeats
  • Pressure, tightness, pain, or a squeezing or aching sensation in your chest or arms that may spread to your neck, jaw or back
  • Nausea, indigestion, heartburn or abdominal pain
  • Shortness of breath
  • Fatigue
  • Lightheadedness or sudden dizziness

Diagnosis of Acute Myocardial Infarction

Physical Examination

  • The presentation of myocardial infarction is variable. The patient may present fairly well-appearing or might be obviously in extremis. In every patient with chest pain, it is important to perform a focused physical exam.

 Obtain vital signs, including blood pressures in both arms.

Heart rate

  • Tachycardia is common, but bradycardia with or without heart block may ensue if the RCA is involved as it typically supplies the SA and AV nodes
  • Arrhythmia is possible at any time in the course of myocardial infarction

Blood pressure

  • Hypertension is common and may be significant, but hypotension is possible and raises mortality risk.

    • Isolated posterior infarction is less common than posterior infarct associated with inferior/inferolateral infarction. As such, the infarcted area may be preload dependent, and the administration of nitroglycerin may lead to significant hypotension.
  • A significant discrepancy between blood pressure in each arm should raise concern for aortic dissection.

General appearance

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  • Patients may be ill-appearing, diaphoretic, or in obvious distress.
  • Levine’s sign: holding a clenched fist to the chest

Neck

  • Look for jugular venous distention, a sign of heart failure.

Heart exam

  • Murmurs

    • Acute mitral regurgitation due to ischemia of the papillary muscles may be silent or produce a murmur. The regurgitation is better appreciated by echocardiography with Doppler.
    • Concomitant aortic stenosis may result in significant hypotension if the patient receives nitroglycerin.
  • Distant heart sounds may be a result of pericardial effusion, which should raise suspicion of other etiologies like dissection and subsequent hemopericardium.

Lung exam

  • Bilateral rales on auscultation are likely secondary to heart failure
  • Unequal breath sounds should raise concern for pneumothorax

Chest exam

  • Tenderness to palpation of the chest wall may be musculoskeletal
  • “Hamman’s crunch” or Crepitus is evidence of subcutaneous emphysema, which may be from rib fractures, pneumothorax or pneumomediastinum

Abdominal exam

  • Tenderness in the abdomen should prompt concern for intra-abdominal etiology (cholecystitis, pancreatitis, GERD), which may lead to radiation of pain into the chest or difficulty differentiating visceral abdominal pain from chest pain.

Neurological exam

  • Neurologic deficits should also raise the suspicion for aortic dissection

Extremities

  • Edema: bilateral edema can be evidence of heart failure whereas unilateral edema should prompt further evaluation for DVT and PE
  • Pulse deficits, mottling, or cool extremities are evidence of decreased perfusion. If unilateral, consider aortic dissection
  • Patients may present in cardiac arrest. If the presenting rhythm is ventricular fibrillation or ventricular tachycardia, the recommendation that the patient goes for coronary angiography after achieving the return of spontaneous circulation (ROSC), and the patient is stable for transfer.

For any patient presenting with chest pain concerning ACS, cardiac workup should be initiated, including history and exam as above, electrocardiogram (EKG), and cardiac biomarkers.

Evaluation of patients with acute onset of chest pain should begin with an electrocardiogram (ECG) and troponin level. The American College of Cardiology, American Heart Association, European Society of Cardiology, and the World Heart Federation committee established the following ECG criteria for ST-elevation myocardial infarction (STEMI):

EKG

In a typical 12-lead EKG, posterior infarction is an indirect observation due to the placement of the leads. Limb leads placement is on each of the four extremities.

Precordial leads are placed on the anterior chest

  • V1 – 4th intercostal space on the right margin of the sternum
  • V2 – 4th intercostal space on the left margin of the sternum
  • V4 – 5th intercostal space at the midclavicular line
  • V3  – midway between V2 and V4
  • V5 – 5th intercostal space on the anterior axillary line at the level of V4
  • V6 – 5th intercostal space on the midaxillary line at the level of V4

Areas of infarction

  • Inferior – II, III, aVF (RCA or LCx)
  • Lateral – I, aVL, V5, V6 (LCx or diagonal branch of LAD)
  • Septal – V1, V2 (LAD)
  • Anterior – V2, V3, V4 (LAD)

ST-elevation is visible if there is inferior, lateral, or inferolateral involvement associated with a posterior extension. However, ST-elevation will not show on the typical EKG in isolated posterior MI, and other EKG changes may be observable. However, for further clarification, posterior leads (V7-V9) may be placed to evaluate further. 

Posterior leads V7-V9 get placed on the posterior chest wall in the same horizontal plane as V6

  • V7 – left posterior axillary line
  • V8- the tip of the left scapula
  • V9 – left paraspinal region

ST-elevation may be more subtle, and ST-elevation greater than 0.5 mm in one lead indicates posterior ischemia and is diagnostic for posterior ST-elevation MI (STEMI). When possible, compare to old EKGs.

Other changes that may present in posterior STEMI include

  • ST-depression in the anterior leads, which may be deep (over 2 mm) and flat
  • Large R-wave in V2-V3, which are larger than the S-wave

    • R-waves in V2-V3 that are greater than those in V4-V6 is an abnormal R-wave progression
  • Large and upright anterior T waves
  • Signs of ischemia in inferior and/or lateral territories, including possible ST elevation
  • Mirror image effect of EKG regarding posterior wall ischemia

    • If turned upside down, tall anterior R-waves become deep posterior Q-waves, ST-depression becomes ST-elevation, and upright T-waves become inverted T-waves
    • If these changes are not present, it does not rule out posterior STEMI

If there is an obvious posterior STEMI, and there is low suspicion of other pathology, the goal is to get the patient the lab for percutaneous intervention (PCI). There is no need to wait for lab results. IV access should be obtained, and labs sent. If there are more subtle EKG changes, but not definitive STEMI, consider serial EKGs. Sometimes on repeat EKGs, subtle ischemia evolves into STEMI.

ECG

The resting 12 lead ECG is the first-line diagnostic tool for the diagnosis of the acute coronary syndrome (ACS). It should be obtained within 10 minutes of the patient’s arrival in the emergency department. Acute MI is often associated with dynamic changes in the ECG waveform. Serial ECG monitoring can provide important clues to the diagnosis if the initial EKG is non-diagnostic at the initial presentation. Serial or continuous ECG recordings may help determine reperfusion or re-occlusion status. A large and prompt reduction in ST-segment elevation is usually seen in reperfusion.

ECG findings suggestive of ongoing coronary artery occlusion (in the absence of left ventricular hypertrophy and bundle branch block):

ST-segment elevation in two contiguous lead (measured at J-point) of

  • Greater than 5 mm in men younger than 40 years, greater than 2 mm in men older than 40 years, or greater than 1.5 mm in women in leads V2-V3 and/or
  • Greater than 1 mm in all other leads

ST-segment depression and T-wave changes

  • New horizontal or down-sloping ST-segment depression greater than 5 mm in 2 contiguous leads and/or T inversion greater than 1 mm in two contiguous leads with prominent R waves or R/S ratio of greater than 1

The hyperacute T-wave amplitude, with prominent symmetrical T waves in two contiguous leads, maybe an early sign of acute MI that may precede the ST-segment elevation. Other ECG findings associated with myocardial ischemia include cardiac arrhythmias, intraventricular blocks, atrioventricular conduction delays, and loss of precordial R-wave amplitude (less specific finding).

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ECG findings alone are not sufficient to diagnose acute myocardial ischemia or acute MI as other conditions such as acute pericarditis, left ventricular hypertrophy (LVH), left bundle branch block (LBBB), Brugada syndrome, Takatsubo syndrome (TTS), and early repolarization patterns also present with ST deviation.

ECG changes associated with prior MI (in the absence of left ventricular hypertrophy and left bundle branch block)

  • Any Q wave in lead V2-V3 greater than 0.02 s or QS complex in leads V2-V3
  • Q wave > 03 s and greater than 1 mm deep or QS complex in leads I, II, aVL, aVF or V4-V6 in any two leads of contiguous lead grouping (I, aVL; V1-V6; II, III, aVF)
  • R wave > 0.04 s in V1-V2 and R/S greater than 1 with a concordant positive T wave in the absence of conduction defect

Lab Studies

  • CBC
  • Metabolic profile
  • Troponin
  • Coagulation studies
  • Consider  B-type natriuretic peptide (BNP) / NT pro-BNP

Imaging Studies

  • Obtain bedside chest x-ray  – (CXR) or two-view CXR
  • Consider bedside echocardiography – this is an operator-dependent skill but can be of significant value. Bedside echocardiography can evaluate for pericardial effusion, gross wall motion abnormalities, size of the ventricles, valvular abnormalities, and ejection fraction estimation. A suprasternal notch view is useful to visualize the aorta and evaluate for possible dissection. The proximal aorta is usually dilated with or without a visible intimal flap.
  • Echocardiogram – Sound waves (ultrasound) create images of the moving heart. Your doctor can use this test to see how your heart’s chambers and valves are pumping blood through your heart. An echocardiogram can help identify whether an area of your heart has been damaged.
  • Coronary catheterization (angiogram) – A liquid dye is injected into the arteries of your heart through a long, thin tube (catheter) that’s fed through an artery, usually in your leg or groin, to the arteries in your heart. The dye makes the arteries visible on X-ray, revealing areas of blockage.
  • Cardiac CT or MRI – These tests create images of your heart and chest. Cardiac CT scans use X-rays. Cardiac MRI uses a magnetic field and radio waves to create images of your heart. For both tests, you lie on a table that slides inside a long tubelike machine. Each can be used to diagnose heart problems, including the extent of damage from heart attacks.
  • Biomarker Detection of MI – Cardiac troponins (I and T) are components of the contractile apparatus of myocardial cells and expressed almost exclusively in the heart. Elevated serum levels of cardiac troponin are not specific to the underlying model of injury (ischemic vs. tension) . The rising and/or falling pattern of cardiac troponins (cTn) values with at least one value above the 99 percentile of upper reference limit (URL) associated with symptoms of myocardial ischemia would indicate an acute MI. Serial testing of cTn values at 0 hours, 3 hours, and 6 hours would give a better perspective on the severity and time course of the myocardial injury. Depending on the baseline cTn value, the rising/falling pattern is interpreted. If the cTn baseline value is markedly elevated, a minimum change of greater than 20% in follow up testing is significant for myocardial ischemia. Creatine kinase MB isoform can also be used in the diagnosis of MI, but it is less sensitive and specific than cTn level.

Myocardial infarctions are generally clinically classified into ST-elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to an ECG.[rx] STEMIs make up about 25 – 40% of myocardial infarctions.[rx] A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:[rx]

  • Spontaneous MI related to plaque erosion and/or rupture fissuring, or dissection
  • MI related to ischemia, such as from increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood pressure or low blood pressure
  • Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a blood clot is found in a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood
  • Associated with coronary angioplasty or stents
    • Associated with the percutaneous coronary intervention (PCI)
    • Associated with stent thrombosis as documented by angiography or at autopsy
  • Associated with CABG
  • Associated with spontaneous coronary artery dissection in young, fit women

Treatment of Acute Myocardial Infarction

In summary,

  • Early diagnosis – history, EKG, cardiac troponins
  • Pain relief – nitroglycerin
  • Hemodynamic stability – airway, breathing, circulation
  • Reperfusion – PCI vs. fibrinolysis
  • Prevention of thrombosis – 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

Reperfusion

  • The definitive management of acute posterior STEMI is reperfusion therapy. Optimally this is done via percutaneous coronary intervention (PCI), though the next option would be fibrinolytic therapy. PCI is the preferred option if it can be initiated within 120 minutes, though within 90 minutes is the goal. If PCI is not available within 120 minutes, then fibrinolytic therapy should be given within 30 minutes.

Adjunctive Therapies

Aspirin 162 to 325 mg chewable or 600 mg per rectum

  • Aspirin should be given as soon as STEMI is suspected. Aspirin reduced mortality.

Nitroglycerin (NTG)

  • Should be given sublingually for rapid absorption and onset of action. It aides coronary vasodilatation and helps with symptomatic relief of angina. It does not reduce mortality. The most common side effect is a throbbing headache. NTG should not be given in inferior myocardial infarction due to the risk of hypotension. The right ventricle is preload dependent, and the vasodilation decreased blood return. 
  • It is imperative to ask male patients if they have used phosphodiesterase inhibitors such as sildenafil, vardenafil, or tadalafil, within 24 hours as the combination can cause life-threatening hypotension.

Oxygen

  • To only be used if SpO2 less than 90%. The AVOID trial SHOWED that in patients with STEMI who are not hypoxic, supplemental oxygen therapy might increase early myocardial injury and was associated with larger infarct size at six months.

Antiplatelet agents

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  • Clopidogrel: 600 mg loading dose for STEMI or 300 mg for NSTEMI followed by 75 mg daily
  • Ticagrelor: 180 mg loading dose followed by 90 mg twice daily.

GPIIB/IIIa inhibitors – not routinely used

  • Abciximab, eptifibatide
  • These are now much less commonly used since the advent of other agents and stents due to increased risk of bleeding.

Beta-blockers

  • Oral beta-blockers should be initiated within 24 hours.

ACE inhibitor or angiotensin receptor blocker (ARB)

  • Therapy should start within 24 hours in stable patients.

Statin 

  • High-intensity statin therapy should begin as soon as possible.

Anticoagulation

  • Heparin is required after thrombolysis to prevent re-thrombosis. Patients undergoing PCI should undergo heparinization to prevent thrombosis during the procedure
  • Other agents like low molecular weight heparin, fondaparinux, and bivalirudin may be alternatives.

Platelet inhibition

  • Aspirin is recommended in both STEMI and NSTEMI in an oral loading dose of 150 to 300 mg (non-enteric coated formulation) and a maintenance dose of 75 to 100 mg per day long-term regardless of treatment strategy (class I). Aspirin inhibits thromboxane A2 production throughout the lifespan of the platelet.

Enoxaparin

  • It 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

  • 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.

Monotherapy with calcium channel blockers

  • It should primarily be used in patients with a specific identified pathogenic mechanism which is expected to respond better to calcium channel blockers (e.g., vasospastic angina), or if a patient is intolerant of beta blockers. Aspirin (antiplatelet therapy) and statin (lipid-lowering therapy) are also used.

Psychotherapy 

  • Mental stress can provoke silent ischemia; especially in patients with underlying coronary artery disease. Data suggests a possible benefit from behavioral stress reduction in such patients.

Revascularization

  • The decision regarding the need for coronary artery revascularization are rarely if ever, based exclusively on the finding of silent myocardial ischemia. There are limited data evaluating the efficacy of coronary revascularization in the treatment of silent ischemia. The study showed no significant difference in mortality between the groups who underwent revascularization and those who continued medical therapy (19.1 and 18.3 percent, respectively).
  • Most P2Y12 inhibitors are inactive prodrugs (except for ticagrelor, which is an orally active drug that does not require activation) that require oxidation by hepatic cytochrome P450 system to generate an active metabolite which selectively inhibits P2Y12 receptors irreversibly. Inhibition of P2Y12 receptors leads to inhibition of ATP induced platelet aggregation. The commonly used P2Y12 inhibitors are clopidogrel, prasugrel, and ticagrelor. The loading dose for clopidogrel is 300 to 600 mg loading dose followed by 75 mg per day. Prasugrel, 60 mg loading dose, and 10 mg per day of a maintenance dose have a faster onset when compared to clopidogrel.

Long-Term Management

Lipid-lowering treatment  It is recommended to start high-intensity statins that reduce low-density lipoproteins (LDLs) and stabilize atherosclerotic plaques. High-density lipoproteins are found to be protective.

Antithrombotic therapy Aspirin is recommended lifelong, and the addition of another agent depends on the therapeutic procedure done, such as PCI with stent placement.

ACE inhibitors – are recommended in patients with systolic left ventricular dysfunction, or heart failure, hypertension, or diabetes.

  • Beta-blockers are recommended in patients with LVEF less than 40% if no other contraindications are present.
  • Antihypertensive therapy can maintain a blood pressure goal of less than 140/90 mm Hg.
  • Mineralocorticoid receptor antagonist therapy is recommended in a patient with left ventricular dysfunction (LVEF less than 40%).
  • Glucose lowering therapy in people with diabetes to achieve current blood sugar goals.

LifeStyle

  • Smoking cessation  is the most cost-effective secondary measure to prevent MI. Smoking has a pro-thrombotic effect, which has a strong association with atherosclerosis and myocardial infarction.
  • Diet, alcohol, and weight control A diet low in saturated fat with a focus on whole grain products, vegetables, fruits, and the fish is considered cardioprotective. The target level for bodyweight is body mass index of 20 to 25 kg/m2  and waist circumference of <94 cm for the men and <80 cm for the female.

Complications

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

  • Myocardial dysfunction
  • Heart failure
  • 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.
  • Papillary muscle rupture and free wall rupture are very uncommon with anteroseptal infarction. These complications are more related to multivessel disease.
  • Conduction abnormalities – Conduction disturbances are associated with anteroseptal MI. One study showed that the 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.
  • Post-infarction pericarditis

References

Acute myocardial infarction

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