I. Problem/Condition.

Overview, pathophysiology and revised universal definition

Acute myocardial infarction (AMI), colloquially known as a “heart attack”, is death of myocardial tissue due to protracted ischemia. It is a leading cause of morbidity and mortality in the United States (US) and increasingly even in developing countries. Globally, it accounts for 12 million deaths annually.

Classic symptoms of AMI includes heaviness or pressure-like sub-sternal chest discomfort with radiation to the left arm, shoulder, neck or jaw, dyspnea, nausea, vomiting, light-headedness, dizziness and diaphoresis. However, in certain subgroups – females, diabetics and the elderly – atypical symptoms are encountered more frequently and hence diagnosis may not be obvious in certain situation. The electrocardiogram (EKG) is an essential tool in the evaluation and should be done as soon as possible but there are many conditions – cardiac and non-cardiac – that can cause similar EKG changes.

In terms of pathophysiology, there is an imbalance between oxygen supply and demand for prolonged period leads to myocardial cell necrosis. Atherosclerosis is the usual underlying culprit lesion in the genesis of an acute myocardial infarction.

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Atherosclerotic plaque formation with subsequent rupture of the lesion attracts platelets, which aggregate and form a thrombus. The thrombus occludes the coronary artery and decreases the flow of blood and oxygen to the myocardial tissue. Recently, endothelial glycocalyx damage (syndecan-1 release) has been attributed to atherosclerotic plaque vulnerability to increase platelet and leukocyte adhesion and sheer stress in the vessel. Alternative mechanisms that can cause this mismatch in oxygen supply and demand include coronary vasospasm, severe aortic stenosis, extreme exertion, and hemodynamic changes such as hypotension and hypertension.

In the past, there have been a number of ways to classify a myocardial infarction including anatomy (transmural versus non-transmural), pathology (acute, healing or healed) and by electrocardiography (ST elevation myocardial infarction (STEMI) versus non-ST elevation myocardial infarction (NSTEMI)), Q wave versus non-Q wave, anterior, inferior, right ventricular, etc.

To improve the accuracy of diagnosis and to provide a universal definition, a clinical classification system was published in 2000. In 2007, an international task force consisting of the European Society of Cardiology, the American College of Cardiology, the American Heart Association, and the World Heart Federation further refined the diagnostic criteria to reflect the advancements in biomarker knowledge.

The resulting classification system helps guide the therapeutic management of patients with an acute myocardial infarction and incorporates a more holistic viewpoint that synthesizes epidemiological, biochemical, electrocardiographic, pathological, imaging, societal, and clinical research perspectives.

The task force revised the universal definition of an acute myocardial infarction. They defined it as a consequence of myocardial ischemia that occurs in the clinical context of any one of the following:

  • The increase and/or decrease of cardiac biomarkers with at least one value above the 99th percentile of the upper range limit plus at least one of the items below:

    Ischemic symptoms

    EKG changes consistent with ischemia

    Pathological Q waves on EKG

    Imaging tests with new loss of viable myocardium or new regional wall motion abnormalities

  • Sudden cardiac death with symptoms consistent with ischemia plus one of the following:

    EKG with new ST elevation changes or new left bundle branch block (LBBB)

    Documented thrombus by angiography or autopsy

  • Percutaneous coronary intervention (PCI) with biomarker increase greater than three times the upper range limit

  • Coronary artery bypass graft (CABG) surgery with biomarker increase five times the upper range limit plus one of the following:

    EKG with new Q waves or LBBB

    Documented occlusion

  • Pathology proven findings of an acute myocardial infarction

II. Diagnostic Approach

A. What is the Differential Diagnosis for this problem?

There are a number of differential diagnoses to be considered when a clinician is evaluating a patient with a suspected AMI. These can be classified by organ systems such as cardiac, gastrointestinal, pulmonary, musculoskeletal, neurologic, and psychogenic diseases.

Cardiac differential diagnosis

With respect to other cardiac disease diagnoses, aortic dissection, pericarditis, left ventricular aneurysm, and early repolarization are all diagnoses that should be considered.

Gastrointestinal differential diagnosis

Gastrointestinal diseases often present with symptoms that can mimic an AMI. Disorders involving the esophagus, stomach, biliary system, and pancreas such as esophageal spasm, esophageal rupture, penetrating peptic ulcer, gastrointestinal reflux disease, cholecystitis, cholelithiasis, and pancreatitis can manifest as pain suggestive of a myocardial infarction.

Pulmonary differential diagnosis

Pulmonary diseases such as a pulmonary embolism or pneumothorax can present with symptoms that can be mistaken for a myocardial infarction. In particular, it is critical not to overlook these two diseases early in the diagnostic process given the potential for life- threatening consequences.

Musculoskeletal differential diagnosis

While musculoskeletal disorders generally have reproducible characteristics that allow for some differentiation from ischemic pain, it is important to still consider acute coronary syndrome (ACS) even if the initial assumption is a musculoskeletal etiology. Common musculoskeletal disorders include costochondritis, rib fracture, toothache, and muscle strain.

Neurologic differential diagnosis

Neuropathic pain, cervical disc diseases and herpetic neuralgia related to zoster are neurologic etiologies to consider in the differential diagnosis of AMI.

Psychogenic differential diagnosis

Once a myocardial infarction and the other differential diagnoses have been considered, psychogenic etiologies, such as depression and anxiety, should be considered among the diagnostic possibilities.

B. Describe a diagnostic approach/method to the patient with this problem

The key elements in the diagnosis of an AMI are a careful history, urgent EKG, biomarkers, and a high degree of suspicion in all patients with chest discomfort.

1. Historical Information Important in the Diagnosis of this problem

When evaluating a patient with suspected AMI, there are a number of questions that should be asked as part of the evaluation. These questions can be categorized as follows: general symptom characteristics, risk factor, contraindications to thrombolysis, thrombolysis in myocardial infarction (TIMI), and other miscellaneous but relevant questions. Listed below are the specific questions by category.

  • General symptom characteristics questions:

    When did the pain/discomfort/symptoms begin?

    How does it feel like?

    Where is it located/does the pain radiates to neck jaw or arms?

    Are there any exacerbating or relieving factors?

    Are there any other associated symptoms?

    Have you had similar pain in past and is the current pain similar to prior myocardial infraction episode?

  • Risk factor questions:

    Do you currently smoke?

    Do you have any history of high blood pressure?

    Do you have any history of elevated cholesterol?

    Do you have any family history of early heart disease such as myocardial infarction or sudden death before age 55 in males or 65 in females in first-degree relatives?

    Do you have any history of diabetes?

    Do you have a history of peripheral vessel disease or do you have symptoms of claudication?

  • Absolute contraindications to thrombolysis questions:

    Do you have any history of intracranial bleeding?

    Have you had an ischemic stroke within the past 3 months?

    Do you have any structural brain abnormality such as an aneurysm, mass or arteriovenous malformation?

    Have you had any closed head injury within the past 3 months?

    Have you had any tearing chest pain?

    Do you have any active bleeding or bleeding disorder?

  • Thrombolysis in myocardial infarction questions:

    Do you have known coronary artery disease?

    Have you used aspirin in the last 7 days?

    Have you had any severe angina in the last 24 hours?

  • Miscellaneous questions:

    Have you used any erectile dysfunction medications?

    Have you used cocaine?

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

With respect to the physical exam, there are no signs that are pathognomonic of a myocardial infarction. However, there are a number of physical findings that may be present and suggestive of conditions associated with a myocardial infarction.

  • A S4 may be heard if there is ventricular non-compliance.

  • Rales may be audible if pulmonary edema is present and the patient is experiencing heart failure. In this situation, there may be concurrent jugular venous distension peripheral edema and a S3 gallop.

  • Diaphoresis can be common in AMI.

  • Hypotension can signal ventricular dysfunction or failure, especially in the setting of a right ventricular infarction.

  • Hypertension can occur due to catecholamine released from activation of the sympathetic nervous system.

  • A low-grade fever can be a reflection of the inflammatory process associated with ischemia and cell death.

A neurological examination should be performed and documented in the event thrombolytic therapy is given.

3. Laboratory, Radiographic and Other Tests Useful in Diagnosing the cause of this problem.

All patients with suspected acute myocardial infarction should undergo evaluation with an EKG, cardiac biomarkers such as troponin I/T and/or creatinine kinase, muscle, brain (CKMB), a chest radiograph, as well as routine labs such as a complete blood count (CBC), chemistry panel, coagulation studies (partial thromboplastin time (PTT), prothrombin time (PT), international normalized ratio (INR)), and urine drug screen if appropriate.


An EKG should be obtained within 10 minutes of symptom presentation. With AMI the EKG can have a variety of presentations ranging from normal to dramatic ST segment elevation. If the initial EKG is unrevealing, serial repeat EKGs should be obtained until patient’s chest pain resolves or a definitive diagnosis is made. The diagnostic criteria for a STEMI are gender specific and listed below.

  • New ST segment elevation at the J point in 2 contiguous leads:

    >0.1mV in all leads other than V2-V3.

    For V2-V3 leads, ≥ 0.2mV in men≥ 40 years old and ≥ 0.25mV in men <40 years, or ≥0.15mV in women.


Troponin I or T are the preferred biomarkers in the diagnosis of myocardial infarction due to their high specificity and sensitivity. Improved sensitivity cardiac troponin (cTn) are increasingly being utilized for assessment which has resulted in early identification and treatment of patients with AMI. Serial measurements of these proteins should be done after the first sample is obtained. The International Joint Task Force recommends a repeat draw within 6-9 hours with a third draw between 12 and 24 hours, if suspicion remains high. However, if an AMI is occurring, most troponins will turn positive in the first 2-3 hours.

The biomarkers should demonstrate the typical rise and fall pattern and at least one value should be above the 99th percentile of the upper range limit. It should be noted that troponin values could remain elevated for 1-2 weeks after a myocardial infarction.

The other biomarker option is the CKMB. Like the troponins, serial measurements, along with a rise and fall pattern plus a value above the 99th percentile of the upper range limit are necessary for the diagnosis. However, CKMB may be unnecessary and provide no additional information in the initial diagnosis of an acute myocardial infarction when cardiac troponin is ready available.

Chest radiograph

A chest radiograph should also be performed to look for pulmonary edema accompanying a myocardial infarction. The chest x-ray is also valuable in evaluating other differential diagnoses such as aortic dissection, which may show a widened mediastinum or a pneumothorax.


While the history, EKG and biomarkers are the cornerstones in the diagnosis of an AMI, echocardiography may play a role in select situations. If there is a high suspicion for AMI but the EKG is without acute changes, and biomarkers are still pending, an echocardiogram performed at this juncture can be used to look for new wall motion abnormalities (RWMAs) as ischemic RWMAs develops quite early. Recently, In a recent German study, use of TTE was found to be useful in supporting or refuting further invasive management in patients with suspected AMI.

However, if biomarkers return normal, they take precedence over the imaging findings. The American College of Cardiology has given a class I recommendation for the use of echocardiogram to diagnose AMI when not obvious by standard tests but it does NOT recommend echocardiography for diagnosis when diagnosis is clear by usual tests.

C. Criteria for Diagnosing each diagnosis in the Method Above.

In 2007, an International Task Force revised a universal definition of an AMI. This change was in reflection of the advancements in knowledge of cardiac biomarkers – namely troponins I and T. The extreme sensitivity of these biomarkers led to the identification of infarcts not previously captured by traditional CKMB tests and this had implications both prognostically and therapeutically.

Criteria for acute myocardial infarction

Myocardial infarction can be defined as myocardial necrosis that occurs in the characteristic clinical context of ischemia plus any one of the following:

  • Typical increase and decrease of biomarkers – either troponin or CKMB – with at least one value above the 99th percentile of the upper range limit plus at least one of the following:

    Symptoms of ischemia

    EKG changes consistent with ischemia such as ST segment elevation, depression, or new LBBB

    Pathological Q waves on EKG

    Imaging tests reveal changes consistent with new loss of viable myocardium or new regional wall motion abnormalities

  • Sudden cardiac arrest with suggestive symptoms and new ST segment elevation or new LBBB

  • In PCI setting, increases of biomarkers greater than three times the upper range limit

  • In CABG setting, increases of biomarkers greater than five times the upper range limit plus one of the following:

    EKG with new Q waves or LBBB

    Documented occlusion

  • Pathology results consistent with a myocardial infarction

Clinical classification, causation, and criteria for types of myocardial infarction

The International Task Force further refined the definition to incorporate the cause and context of the AMI by classifying it into five types.

Type 1

  • AMI associated with a primary coronary occlusion involving acute plaque instability (e.g., plaque erosion/ rupture, fissuring or dissection) resulting in intracoronary thrombus.

Type 2

  • AMI associated with an imbalance of oxygen supply and demand to the myocardium. Examples include coronary vasospasm. coronary artery embolus, anemia, arrhythmias, respiratory failure and hemodynamic instability.

Type 3

  • AMI associated with sudden cardiac death plus one of the following:

    Ischemic symptoms

    EKG changes of ST segment elevation of new LBBB

    Documented intracoronary thrombus

Type 4a

  • AMI associated with PCI and greater than three times the 99th percentile of the upper range limit of the biomarker.

Type 4b

  • AMI associated with documented stent occlusion.

Type 5

  • AMI associated with CABG and five times the 99th percentile of the upper range of the biomarker plus one of the following:

    EKG with new Q waves/new LBBB

    Documented intracoronary thrombus

    Imaging tests with new loss of viable myocardium

Criteria for diagnosis of re-infarction

After a diagnosis has been made of a myocardial infarction, a recurrent infarction may occur. In this situation, the diagnosis of recurrent infarction is made when there are recurrent symptoms and/or EKG changes plus a greater than or equal to 20% increase of biomarkers with at least one value above the 99th percentile of the reference range.

Criteria for prior myocardial infarction

A diagnosis of a prior myocardial infarction can be made based on any one of the following:

  • EKG evidence of new pathological Q waves +/- symptoms

  • Imaging tests reveal area(s) of myocardial thinning or decreased contractility with no other explanation except a myocardial infarction

  • Autopsy findings confirm healed or healing myocardial infarction tissue

D. Over-utilized or "wasted" diagnostic tests associated with the evaluation of this problem.

With the new troponin assays, serum markers such as myoglobin and lactate dehydrogenase (LDH), previously used in the diagnosis of an AMI, are usually unnecessary. They are neither specific nor sensitive compared to the troponins. However, because myoglobin rises very rapidly and returns to normal rapidly, it could be useful in evaluating recurrent chest pain after an AMI when troponin and CKMB levels are still elevated.

Other markers such as C-reactive protein (CRP), lipoprotein A and homocysteine have a relationship to coronary artery disease but are not part of the standard set of tests recommended in clinical guidelines.

III. Management while the Diagnostic Process is Proceeding

A. Management of acute myocardial infarction

In evaluating a patient with a suspected myocardial infarction, there are a number of steps that should be undertaken immediately and simultaneously.

  • Obtain a focused history to gain key and relevant information. Use the questions listed in section II. B to query the patient on general symptoms, risk factors, contraindications to thrombolysis, TIMI, and other miscellaneous but relevant questions.

  • Complete an urgent EKG within 10 minutes of symptoms and while you are eliciting responses to the above questions.

  • Do a brief physical exam and obtain blood pressure in both arms to screen for a dissecting aortic aneurysm.

  • Obtain or ensure adequate intravenous (IV) access is available.

  • Order labs including troponin I or T, CKMB, a lipid profile, CBC, chemistry panel, coagulation profile, and a chest x-ray.

  • Do a TIMI risk score assessment.

  • HEART Score (History, ECG, Age, Risk factor and Troponin) or modified heart score could be used in patients with non-ST elevation acute myocardial infarction in ED.

  • Repeat the EKG in 10 minutes if the first EKG is non-diagnostic and suspicion is still high for a myocardial infarction.

  • Do a right-sided EKG to look for a right ventricular infarction: indicated by ST elevation in V1 and ST elevation in lead III> Lead II – suggesting inferior myocardial wall infarction.

  • If the EKG shows ST segment elevation and suspicion for a myocardial infarction is still high:

    Give aspirin 162-325mg per os (PO) or rectally, oxygen and nitroglycerin (NTG) – if no contraindication exists for NTG (e.g., aortic dissection, right ventricular infarction or recent use of phosphodiesterase inhibitors such as sildenafil).

    Give high dose statin therapy.

    Give morphine as needed for pain.

    Consider PCI within 90 minutes or thrombolytic therapy within 30 minutes.

    Consult cardiology immediately.

    If the troponins are elevated, this is a STEMI.

  • If there is no ST segment elevation on EKG and suspicion is still high for a myocardial infarction:

    Give aspirin 162-325mg PO or rectally, oxygen and NTG – if no contraindication exists for NTG (e.g. aortic dissection, right ventricular infarction or recent use of phosphodiesterase inhibitors such as sildenafil).

    Give high dose statin therapy.

    Give morphine as needed for pain.

    If the troponins are elevated, this is a NSTEMI

    Consult cardiology for possible early invasive strategy for moderate to high risk patients.

    If the troponins are NOT elevated, this is possibly unstable angina (UA)

    Consider cardiology consult for possible early invasive strategy for moderate to high risk patients.

See “ST elevation myocardial infarction” and “non-ST elevation myocardial infarction” chapters for further management.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

Pitfalls in the diagnosis of an AMI can occur anywhere in the process but often occur in several key places – namely the clinical context or presentation, the EKG interpretation and the troponin interpretation.


An AMI can present in a variety of ways, which can lead to uncertainty and delay in appropriate care. The classic symptoms of pressure-like chest discomfort with radiation down the left arm along with nausea, diaphoresis and dyspnea may not be present. Some patients may have no chest pain at all. Others may have symptoms that suggest a gastrointestinal or musculoskeletal etiology.

Therefore a high degree of suspicion should be maintained in all patients with chest pain or potential anginal equivalents. Additionally, certain subgroups – females, the elderly, diabetics, and even the young – can present in an atypical manner leading to mistriage and misdiagnosis.


The EKG may be misinterpreted especially when there is ST segment elevation. The misread can be either a false positive or false negative EKG for AMI.

Clinical conditions that can lead to either misinterpretation are listed below.

False positive reading of electrocardiogram
  • Acute pericarditis or myocarditis

  • Left ventricular hypertrophy (LVH)

  • Early repolarization

  • Hyperkalemia

  • LBBB

  • Wolf Parkinson White (WPW) syndrome

  • Brugada syndrome

  • Subarachnoid hemorrhage

  • Cholecystitis

  • Transposition of leads

  • Misinterpretation of the J point displacement

False negative reading of electrocardiogram
  • LBBB

  • Paced rhythm

  • Chronic ST elevation

  • Old myocardial infarction with Q waves


Troponins are easily misinterpreted as they can occur in other cardiac and non-cardiac conditions.

Troponin elevation in other cardiac conditions (i.e., non-acute myocardial infarction)
  • Congestive heart failure

  • Aortic dissection

  • Ventricular aneurysm

  • Pericarditis/myocarditis

  • LVH

  • Cardiac trauma

  • Cardioversion and defibrillation

  • Hypertrophic cardiomyopathy (HCMP)

  • Arrhythmias (tachycardic and bradycardic)

  • Heart block

  • Takotsubo

  • Infiltrative diseases

  • Inflammatory diseases

  • Drugs and toxins

Troponin elevation in non-cardiac conditions
  • Pulmonary diseases

    Pulmonary embolism

    Pulmonary hypertension (HTN)

    Respiratory failure

  • Renal failure

  • Sepsis

  • Neurological diseases:

    Cerebrovascular accident

    Subarachnoid hemorrhage

  • Burns

  • Extreme exertion

Drugs and dosages used in the management of myocardial infarction

The purposes of the medications used in the initial treatment of an AMI are to relieve pain and to restore blood flow to the coronary artery. By halting thrombus formation via inhibition of platelet activation and aggregation, the hope is that as much myocardium as possible can be salvaged.

Table I outlines medication classes and drugs commonly used in AMI and are listed to provide an overview of options. Other medication classes/drugs may be available and all options and contraindications must be taken into consideration before prescribing medications in AMI.

Table I.
Drug Name Class Route Dose Comments
Aspirin (ASA) Antiplatelet PO or rectal 162-325mg Reduces mortality
Clopidogrel Antiplatelet PO 75mg Use if ASA allergy
Oxygen Oxygen NC or face mask 2-4 L NC Keep pulse oximetry ≥90%
NTG Nitrates SL, topical, or IV 0.4mg SL every 5 minutes x 3 as needed PRN chest pain; 0.5-2 inch topical; start 5mcg/min IV and titrate to pain relief Contraindicated in systolic BP <90, right ventricular infarction or use of phosphodiesterase inhibitor in past 24-48 hours.
Morphine Pain medication IV 1-4mg IV
Metoprolol Beta-blocker PO or IV 5mg IV25mg PO Reduces mortality;avoid in cocaine-related ACS, hypotension
Heparin Anticoagulant;unfractionated heparin IV STEMI: 12 units/kg/hour IV; start 60 units/kg IV x1; max: 4000 units/bolus; 1000 units/hourNSTEMI: 12-15 units/kg/hour IV: 60-70 units/kg IV x1; max: 5000 units/bolus;1000 units/hour Goal partial PTT 50-70 seconds
Enoxaparin Anticoagulant;LMWH IV orSC 1mg/kg SC every 12 hours Adjust dose further for weight and creatinine clearance less than 30ml/minute.
TNKase Thrombolyticagent IV 30-50mg IV x 1 based on weight Use in STEMI if unable to do PCI.Goal door to drug time is 30 minutes.Improves mortality. Review inclusion criteria and contraindications.
Lisinopril Angiotensin converting enzyme inhibitor (ACE-inhibitor) PO 5mg PO daily Titrate and start within 24 hours, especially if ejection fraction EF < 40%
Valsartan ARB PO 80-320mg PO daily For ACE-inhibitor intolerant
Eptifibatide Glycoprotein IIb/IIa receptor antagonist IV ACS: Start: 180mcg/kg IV bolus, then begin infusion, 2 mcg/kg/minute IV. Max: 22.6mg/bolus; 15mg/hour infusion For PCI patients:Infuse up to 96 hours. Infuse 18-24 hours post-procedure.Non PCI patients:Infuse up to 72 hours.May use with ASA and heparin
Atorvastatin Statin PO 80mg daily

ACS: acute coronary syndrome

ASA: acetyl-salicylic acid

PO: per os

NC: nasal cannula

SL: sublingual

PRN: as needed

BP: blood pressure

IV: intravenous

PTT: partial thromboplastin time

LMWH: low molecular weight heparin

SC: subcutaneous

PCI: percutaneous coronary intervention

ACE-inhibitor: angiotensin converting enzyme inhibitor

TNKase: tenecteplase

EF: ejection fraction

ARB: Angiotensin receptor blocker

STEMI: ST elevation myocardial infarction

NSTEMI: non-ST elevation myocardial infarction

NTG: nitroglycerin

IV. What's the evidence?

Bolooki, HM, Askari, A. “Acute Myocardial Infarction”. .

Senter, S, Francis, G. “A New Precise Definition of Acute Myocardial Infarction”. . vol. 76. 2009. pp. 159-166.

Thygesen, K, Alpert, JS, White, HD. “Universal Definition of Myocardial Infarction”. . vol. 116. 2007. pp. 2634-2653.

Miranda, CH, de Carvalho Borges, M, Schmidt, A, Marin-Neto, JA, Pazin-Filho, A. “Evaluation of the endothelial glycocalyx damage in patients with acutecoronary syndrome”. Atherosclerosis.. vol. 247. 2016 Apr. pp. 184-184.

Eggers, KM, Lindahl, B, Melki, D, Jernberg, T. “Consequences of implementing a cardiac troponin assay with improved sensitivity at Swedish coronary care units: an analysis from the SWEDEHEART registry”. Eur Heart J. vol. 37. 2016 Aug 7. pp. 2417-24.

Breuckmann, F, Hochadel, M, Voigtländer, T, Haude, M, Schmitt, C, Münzel, T, Giannitsis, E, Mudra, H, Heusch, G, Schumacher, B, Barth, S, Schuler, G, Hailer, B, Walther, D, Senges, J. “The Use of Echocardiography in Certified Chest Pain Units: Results from the German Chest Pain Unit Registry”. Cardiology. vol. 134. 2016. pp. 75-83.

Ma, CP, Wang, X, Wang, QS, Liu, XL, He, XN, Nie, SP. “A modified HEART risk score in chest pain patients with suspected non-ST-segment elevation acute coronary syndrome”. J Geriatr Cardiol. vol. 13. 2016 Jan. pp. 64-9.

Ricottini, E, Madonna, R, Grieco, D, Zoccoli, A, Stampachiacchiere, B, Patti, G, Tonini, G, De Caterina, R, Di Sciascio, G. “Effect of High-Dose Atorvastatin Reload on the Release of Endothelial Progenitor Cells in Patients on Long-Term Statin Treatment Who Underwent Percutaneous Coronary Intervention (from the ARMYDA-EPC Study)”. Am J Cardiol. vol. 117. 2016 Jan 15. pp. 165-71.

Pan, Y, Tan, Y, Li, B, Li, X. “Efficacy of high-dose rosuvastatin preloading in patients undergoing percutaneous coronary intervention: a meta-analysis of fourteen randomized controlled trials”. Lipids Health Dis.. vol. 14. 2015 Aug 27. pp. 97

Paraskevaidis, IA, Iliodromitis, EK, Ikonomidis, I, Rallidis, L, Hamodraka, E, Parissis, J, Andoniadis, A, Tzortzis, S, Anastasiou-Nana, M. “The effect of acute administration of statins on coronary microcirculation during the pre-revascularization period in patients with myocardial infraction”. Atherosclerosis. vol. 223. 2012 Jul. pp. 184-9.

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