myocardial infarction case study ppt

Myocardial Infarction (MI) Case Study (45 min)

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Definition of Myocardial Infarction (MI)

Myocardial infarction, commonly known as a heart attack, is a critical medical event that occurs when the blood supply to the heart muscle is severely reduced or completely blocked. It is a leading cause of death worldwide and a significant public health concern.

Introduction to Myocardial Infarction (MI)

This nursing case study aims to provide a comprehensive understanding of myocardial infarction by delving into its various aspects, including its pathophysiology, risk factors, clinical presentation, diagnostic methods, and management strategies. Through the exploration of a fictional patient’s journey, we will shed light on the intricate nature of this life-threatening condition and highlight the importance of early recognition and intervention.

Background and Significance of Myocardial Infarction

Myocardial infarction is a sudden and often catastrophic event that can have profound consequences on an individual’s health and well-being. Understanding its underlying mechanisms and risk factors is essential for healthcare professionals, as timely intervention can be life-saving. This case study not only serves as a learning tool but also emphasizes the critical role of medical practitioners in identifying and managing myocardial infarctions promptly.

Pathophysiology of Myocardial Infarction

A crucial aspect of comprehending myocardial infarction is exploring its pathophysiology. We will delve into the intricate details of how atherosclerosis, the buildup of plaque in coronary arteries, leads to the formation of blood clots and the subsequent interruption of blood flow to the heart muscle. This disruption in blood supply triggers a cascade of events, ultimately resulting in the death of cardiac cells.

Risk Factors of Myocardial Infarction

Understanding the risk factors associated with myocardial infarction is vital for prevention and early detection. This case study will examine both modifiable and non-modifiable risk factors, including age, gender, family history, smoking, high blood pressure, diabetes, and high cholesterol levels. Recognizing these risk factors is instrumental in developing effective strategies for prevention and risk reduction.

Clinical Presentation Myocardial Infarction

Recognizing the signs and symptoms of myocardial infarction is crucial for timely intervention. We will present a fictional patient’s experience, illustrating the typical clinical presentation, which often includes chest pain or discomfort, shortness of breath, nausea, lightheadedness, and diaphoresis. Through this patient’s journey, we will highlight the importance of accurate symptom assessment and prompt medical attention.

Diagnostic Methods for Myocardial Infarction

Modern medicine offers various diagnostic tools to confirm a myocardial infarction swiftly and accurately. This case study will explore these diagnostic methods, such as electrocardiography (ECG), cardiac biomarkers, and imaging techniques like coronary angiography. By understanding these diagnostic modalities, healthcare professionals can make informed decisions and initiate appropriate treatments promptly.

Management Strategies for Myocardial Infarction

The management of myocardial infarction involves a multidisciplinary approach, including medication, revascularization procedures, and lifestyle modifications. We will discuss the fictional patient’s treatment plan, emphasizing the importance of reestablishing blood flow to the affected heart muscle and preventing further complications.

Nursing Case Study for Myocardial Infarction (MI)

Having established a foundational understanding of myocardial infarction, we will now delve deeper into Mr. Salazar’s case, tracing his journey through diagnosis, treatment, and recovery. This in-depth examination will shed light on the real-world application of the principles discussed in the introduction, providing valuable insights into the clinical management of myocardial infarction and its impact on patient outcomes.

Mr. Salazar, a 57-year-old male, arrives at the Emergency Department (ED) with complaints of chest pain that began approximately one hour after dinner while he was working. He characterizes the discomfort as an intense “crushing pressure” located centrally in his chest, extending down his left arm and towards his back. He rates the pain’s severity as 4/10. Upon examination, Mr. Salazar exhibits diaphoresis and pallor, accompanied by shortness of breath (SOB).

What further nursing assessments need to be performed for Mr. Salazar?

• Heart Rate (HR): The number of heartbeats per minute.
• Blood Pressure (BP): The force of blood against the walls of the arteries, typically measured as systolic (during heartbeats) and diastolic (between heartbeats) pressure.
• Respiratory Rate (RR): The number of breaths a patient takes per minute.
• Body Temperature (Temp): The measurement of a patient’s internal body heat.
• Oxygen Saturation (SpO2): The percentage of oxygen in the blood.
• S1: The first heart sound, often described as “lub,” is caused by the closure of the mitral and tricuspid valves.
• S2: The second heart sound, known as “dub,” results from the closure of the aortic and pulmonic valves.
• These sounds provide important diagnostic information about the condition of the heart.
• Clear: Normal, healthy lung sounds with no added sounds.
• Crackles (Rales): Discontinuous, often high-pitched sounds are heard with conditions like pneumonia or heart failure.
• Wheezes: Whistling, musical sounds often associated with conditions like asthma or chronic obstructive pulmonary disease (COPD).
• Pulses refer to the rhythmic expansion and contraction of arteries with each heartbeat. Common pulse points for assessment include the radial artery (wrist), carotid artery (neck), and femoral artery (groin). Evaluating pulses helps assess the strength, regularity, and rate of blood flow.
• Edema is the abnormal accumulation of fluid in body tissues, leading to swelling. It can occur in various body parts and may indicate underlying conditions such as heart failure, kidney disease, or localized injury. Edema assessment involves evaluating the degree of swelling and its location.
• Skin condition (temperature, color, etc.)

What interventions do you anticipate being ordered by the provider?

• Oxygen therapy involves administering oxygen to a patient to increase the level of oxygen in their blood. It is used to treat conditions such as respiratory distress, and hypoxia (low oxygen levels), and to support patients with breathing difficulties.
• Nitroglycerin is a medication used to treat angina (chest pain) and to relieve symptoms of heart-related conditions. It works by relaxing and widening blood vessels, which improves blood flow to the heart, reducing chest pain.
• Aspirin is a common over-the-counter medication and antiplatelet drug. In the context of myocardial infarction (heart attack), it is often administered to reduce blood clot formation, potentially preventing further blockage in coronary arteries.
• A 12-lead EKG is a diagnostic test that records the electrical activity of the heart from 12 different angles. It provides information about the heart’s rhythm, rate, and any abnormalities, helping diagnose conditions like arrhythmias, heart attacks, and ischemia.
• Cardiac enzymes are proteins released into the bloodstream when heart muscle cells are damaged or die, typically during a heart attack. Measuring these enzymes, such as troponin and creatine kinase-MB (CK-MB), helps confirm a heart attack diagnosis and assess its severity.
• A chest X-ray is a diagnostic imaging procedure that creates images of the chest and its internal structures, including the heart and lungs. It is used to identify issues like lung infections, heart enlargement, fluid accumulation, or fractures in the chest area.
• Possibly an Echocardiogram

Upon conducting a comprehensive assessment, it was observed that the patient exhibited no signs of jugular vein distention (JVD) or edema. Auscultation revealed normal heart sounds with both S1 and S2 present, while the lungs remained clear, albeit with scattered wheezes. The patient’s vital signs were recorded as follows:

• BP 140/90 mmHg SpO 2 90% on Room Air
• HR 92 bpm and regular Ht 173 cm
• RR 32 bpm Wt 104 kg
• Temp 36.9°C

The 12-lead EKG repor t indicated the presence of “Normal sinus rhythm (NSR) with frequent premature ventricular contractions (PVCs) and three- to four-beat runs of ventricular tachycardia (VT).” Additionally, there was ST-segment elevation in leads I, aVL, and V2 through V6 (3-4mm), accompanied by ST-segment depression in leads III and aVF.

Cardiac enzyme levels were collected but were awaiting results at the time of assessment. A chest x-ray was also ordered to provide further diagnostic insights.

In response to the patient’s condition, the healthcare provider prescribed the following interventions:

• Aspirin: 324 mg administered orally once.
• Nitroglycerin: 0.4 mg administered sublingually (SL), with the option of repeating the dose every five minutes for a maximum of three doses.
• Morphine: 4 mg to be administered intravenously (IVP) as needed for unrelieved chest pain.
• Oxygen: To maintain oxygen saturation (SpO2) levels above 92%.

These interventions were implemented to address the patient’s myocardial infarction (heart attack) and alleviate associated symptoms, with a focus on relieving chest pain, improving oxygenation, and closely monitoring vital signs pending further diagnostic results.

What intervention should you, as the nurse, perform right away? Why?

• Apply oxygen – this can be done quickly and easily and can help to prevent further complications from low oxygenation.
• Oxygen helps to improve oxygenation as well as to decrease myocardial oxygen demands.
• Often it takes a few minutes or more for medications to be available from the pharmacy, so it makes sense to take care of this intervention first.
• ABC’s – breathing/O 2 .

What medication should be the first one administered to this patient? Why? How often?

• Nitroglycerin 0.4mg SL – it is a vasodilator and works on the coronary arteries. The goal is to increase blood flow to the myocardium. If this is effective, the patient merely has angina. However, if it is not effective, the patient may have a myocardial infarction.
• Aspirin should also be given, but it is to decrease platelet aggregation and reduce mortality. While it can somewhat help prevent the worsening of the blockage, it does little for the current pain experienced by the patient.
• Morphine should only be given if the nitroglycerin and aspirin do not relieve the patient’s chest pain.

What is the significance of the ST-segment changes on Mr. Salazar's 12-lead EKG?

• ST-segment changes on a 12-lead EKG indicate ischemia (lack of oxygen/blood flow) or infarction (death of the muscle tissue) of the myocardium (heart muscle). 
• This indicates an emergent situation. The patient’s coronary arteries are blocked and need to be reopened by pharmacological (thrombolytic) or surgical (PCI) intervention.
• Time is tissue – the longer the coronary arteries stay blocked, the more of the patient’s myocardium that will die. Dead heart tissue doesn’t beat.

Mr. Salazar’s chest pain was unrelieved after three (3) doses of sublingual nitroglycerin (NTG). Morphine 5 mg intravenous push (IVP) was administered, as well as 324 mg chewable baby aspirin. His pain was still unrelieved at this point

Mr. Salazar’s cardiac enzyme results were as follows:

Troponin I 3.5 ng/mL

Based on the results of Mr. Salazar's labs and his response to medications, what is the next intervention you anticipate? Why?

• Mr. Salazar needs intervention. He will either receive thrombolytics or a heart catheterization (PCI).
• Based on the EKG changes, elevated Troponin level, and the fact that his symptoms are not subsiding, it’s possible the patient has a significant blockage in one or more of his coronary arteries. 
• It seems as though it may be an Anterior-Lateral MI because ST elevation is occurring in I, aVL, and V 2 -V 6 .

Mr. Salazar was taken immediately to the cath lab for a Percutaneous Coronary Intervention (PCI). The cardiologist found a 90% blockage in his left anterior descending (LAD) artery. A stent was inserted to keep the vessel open.

What is the purpose of Percutaneous Coronary Intervention (PCI), also known as a heart catheterization?

• A PCI serves to open up any coronary arteries that are blocked. First, they use contrast dye to determine where the blockage is, then they use a special balloon catheter to open the blocked vessels. 
• If that doesn’t work, they will place a cardiac stent in the vessel to keep it open.[ /faq]

[faq lesson="true" blooms="Application" question="What is the expected outcome of a PCI? What do you expect to see in your patient after they receive a heart catheterization?"]

• Blood flow will be restored to the myocardium with minimal residual damage.
• The patient should have baseline vital signs, relief of chest pain, normal oxygenation status, and absence of heart failure symptoms (above baseline).
• The patient should be able to ambulate without significant chest pain or SOB.
• The patient should be free from bleeding or hematoma at the site of catheterization (often femoral, but can also be radial or (rarely) carotid.

Mr. Salazar tolerated the PCI well and was admitted to the cardiac telemetry unit for observation overnight. Four (4) hours after the procedure, Mr. Salazar reports no chest pain. His vital signs are now as follows:

• BP 128/82 mmHg SpO 2 96% on 2L NC
• HR 76 bpm and regular RR 18 bpm
• Temp 37.1°C

Mr. Salazar will be discharged home 24 hours after his arrival to the ED and will follow up with his cardiologist next week. 

What patient education topics would need to be covered with Mr. Salazar?

• He should be taught any dietary and lifestyle changes that should be made.
• Diet – low sodium, low cholesterol, avoid sugar/soda, avoid fried/processed foods.
• Exercise – 30-45 minutes of moderate activity 5-7 days a week, u nless instructed otherwise by a cardiologist. This will be determined by the patient’s activity tolerance – how much can they do and still be able to breathe and be pain-free?
• Stop smoking and avoid caffeine and alcohol.
• Medication Instructions
• Nitroglycerin – take one SL tab at the onset of chest pain. If the pain does not subside after 5 minutes, call 911 and take a second dose. You can take a 3rd dose 5 minutes after the second if the pain does not subside. Do NOT take if you have taken Viagra in the last 24 hours.
• Aspirin – take 81 mg of baby aspirin daily
• Anticoagulant – the patient may be prescribed an anticoagulant if they had a stent placed.  They should be taught about bleeding risks.
• When to call the provider – CP unrelieved by nitroglycerin after 5 minutes. Syncope. Evidence of bleeding in stool or urine (if on anticoagulant). Palpitations, shortness of breath, or difficulty tolerating activities of daily living.

Linchpins for Myocardial Infarction Nursing Case Study

In summary, Mr. Salazar’s case highlights the urgency of recognizing and responding to myocardial infarction promptly. The application of vital signs, EKG, cardiac enzymes, and medications like aspirin, nitroglycerin, and morphine played a pivotal role in his care. Diagnostic tools like echocardiography and chest X-rays contributed to a comprehensive evaluation.

Nurses must remain vigilant and compassionate in such emergencies. This case study emphasizes the importance of adhering to best practices in the assessment, diagnosis, and management of myocardial infarction, with the ultimate goal of achieving favorable patient outcomes.

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Case study 1: acute myocardial infarction

Published by Shanon Hunter Modified over 9 years ago

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Patient Case Presentation

Patient presentation.

Mr. Smith is a 60-year-old Caucasian male, who presents with 8/10 chest pain after working out. He just quit smoking and started a new workout and diet program after recently retiring. He has noticed some chest and shoulder discomfort with working out that usually resolves with rest, but decided to come to the emergency department because this episode was unrelenting and more severe. Mr. Smith describes his current pain as severe and sharp, and also complains of nausea and shortness of breath. Vital signs are HR: 110 BP: 150/90 RR: 30 Temp 97.6 O2 Sat: 92% on 2L nasal cannula, EKG shows ST segment elevation in leads II, III and AVf. Labs were drawn, including an elevated troponin (4.23 ng/ml), and slightly elevated white blood cell count (13.6 × 10 9 /L) .

Past Medical History

Type II diabetes (age 47), dyslipidemia (age 33), atherosclerosis (age 52), hypertension (age 49), obesity (age 33), viral pneumonia (age 29), hiatal hernia (age 28), peptic ulcer disease (age 41)

Family Medical History

Mother (deceased) – atrial fibrillation (diagnosed at age 45), died of MI (age 65)

Father (83) – obesity, type II diabetes (diagnosed at 50), COPD (diagnosed at 55)

Social History

Smoker (20 pack years), worked in an office sitting at a desk his whole career (35 years), recently began working out at his local gym since retiring this year.

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Myocardial Infarction

Jan 04, 2020

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Myocardial Infarction. Dr Isazadehfar. Background. Myocardial Infarction is the rapid development of myocardial necrosis by a critical imbalance between oxygen supply and demand to the myocardium. Classification. Acute coronary syndromes include ST-elevation MI (STEMI)

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Presentation Transcript

Myocardial Infarction Dr Isazadehfar

Background Myocardial Infarction is the rapid development of myocardial necrosis by a critical imbalance between oxygen supply and demand to the myocardium

Classification • Acute coronary syndromes include ST-elevation MI (STEMI) Non ST-elevation MI ( NSTEMI) Unstable Angina • Cardiac markers in circulation indicates myocardial infarction and help categorize MI and is a useful adjunct to diagnosis

Classification • Anatomic or morphologic Transmural= Full thickness Non- transmural= Partial thickness • ECG Q wave MI Non Q wave MI Does not distinguish transmural from a non- transmural MI as determined by pathology

Prevalence • Increase in the proportion of NSTEMI compared to STEMI

History The history is critical in making the diagnosis of MI and sometimes provide only the only clues that lead to the diagnosis in the initial phase of presentation

History • Chest Pain- anterior precordium tightness • Pain may radiate to jaw, neck and epigastrium • Dyspnea - angina equivalent, poor LV function • Nausea/abdominal pain with posterior MI • Anxiety

History • Nausea with and without vomiting • Diaphoresis or sweating • Syncope or near syncope • Elderly present with MS changes, fatigue, syncope or weakness • As many as half of MI are clinically silent

Physical exam • The physical exam can often be unremarkable • Hypertension • Hypotension • Acute valvular dysfunction may be present • Rales • Neck vein distention

Physical • Third heart sound may be present • A fourth heart sound poor LV compliance • Dysrhythmias • Low grade fever

Causes • Most frequent cause is rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation • Coronary artery vasospasm • Ventricular hypertrophy • Hypoxia • Coronary artery emboli

Causes • Cocaine • Coronary anomalies • Aortic dissection • Pediatrics Kawasaki disease, Takayasu arteritis • Increased afterload which increases myocardial demand

Risk factors for atherosclerosis • Age • Male gender • Smoking • Hypercholesterolemia and triglyceridemia • Diabetes Mellitus • Poorly controlled hypertension • Type A personality

Risk factors for atherosclerosis • Family History • Sedentary lifestyle

Differentials • Acute coronary syndrome • Anxiety • Aortic stenosis • Asthma • Cholecystitis and biliary colic • Cholethiasis • COPD

Differentials • Aortic Dissection • Endocarditis • Esophagitis • Shock • Myocarditis • Pericarditis • Pulmonary embolism

Mechanisms of Myocardial damage The severity of an MI is dependent of three factors • The level of the occlusion in the coronary • The length of time of the occlusion • The presence or absence of collateral circulation

Cardiac Biomarkers • Cardiac biomarkers are protein molecules released into the blood stream from damaged heart muscle • Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury • These biomarkers have a characteristic rise and fall pattern

Troponin T and I • These isoforms are very specific for cardiac injury • Preferred markers for detecting myocardial cell injury • Rise 2-6 hours after injury Peak in 12-16 hours Stay elevated for 5-14 days

Creatinine Kinase ( CK-MB) • Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB) • Increased in over 90% of myocardial infraction • However, it can be increased in muscle trauma, physical exertion, post-op, convulsions, and other conditions

Creatine Kinase (MB) • Time sequence after myocardial infarction Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2 days • MB2 released from heart muscle and converted to MB1. • A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injury

Myoglobin • Damage to skeletal or cardiac muscle release myoglobin into circulation • Time sequence after infarction Rises fast 2hours Peaks at 6-8 hours Returns to normal in 20-36 hours • Have false positives with skeletal muscle injury and renal failure

Renal Failure and Renal Transplantation • Diagnostic accuracy of serum markers of cardiac injury are altered in patients with renal failure • Cardiac troponins decreased diagnostic sensitivity and specificity in patients receiving renal replacement therapy • Current data show levels of troponin I are unaltered while levels of troponin T may be elevated

CBC • CBC is indicated if anemia is suspected as precipitant • Leukocytosis may be observed within several hours after myocardial injury and returns to levels within the reference range within one week

Chemistry Profile • Potassium and magnesium levels should be monitored and corrected • Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization

C-reactive Protein (CRP) • C- reactive protein is a marker of acute inflammation • Patients without evidence of myocardial necrosis but with elevated CRP are at increased risk of an event

Chest X-Ray • Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax) • Chest radiography also reveals complications of myocardial infarction such as heart failure

Echocardiography • Use 2-dimentional and M mode echocardiography when evaluating overall ventricular function and wall motion abnormalities • Echocardiography can also identify complications of MI ( e.g. Valvular or pericardial effusion, VSD)

Electrocardiogram • A normal ECG does not exclude ACS • High probability include ST segment elevation in two contiguous leads or presence of q waves • Intermediate probability ST depression • T wave inversions are less specific

Localization of MI • ST elevation only • Inferior wall- II, III, aVF • Lateral wall_ I, aVL, V4-V6 • Anteroseptal- V1-V3 • Anterolateral- V1-V6 • Right ventricular- RV4, RV5 • Posterior- R/S ratio >1 in V1 and T wave inversion

Therapy The goals of therapy in AMI are the expedient restoration of normal coronary flow and the maximum salvage of functional myocardium

Antiplatelet Agents • Aspirin at least 160mg immediately • Interferes with function of cyclooxygenase and inhibits the formation of thromboxane • ASA alone has one of the greatest impact on the reduction of MI mortality. • Clopidogrel, ticlopidine, have not been shown in any large scale trail to be superior to Aspirin in acute MI

Supplemental Oxygen • Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and other tissues may be diminished • Supplemental oxygen should be administered to patient with symptoms and or signs of pulmonary edema or pulse oximetry readings less than 90%.

Nitrates • IV nitrates to all patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI • Primary benefit vasodilator effect • Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium • Vasodilatation reduces myocardial oxygen demand and preload and afterload

Beta-blockers • Recommended within 12 hours of MI symptoms and continued indefinitely • Reduces Myocardial mortality by decreasing arrythmogenic death • Decrease the rate and force of myocardial contraction and decreases overall oxygen demand

Unfractionated heparin • Forms a chemical complex with antithrombin III inactivates both free thrombin and factor Xa • Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with alteplase

Low-molecular weight heparin • Direct activity against factors Xa and IIa • Proven to be effective in treating ACS that are characterized by unstable angina or non ST- elevation MI • Their fixed doses are easy to administer and laboratory testing to measure their therapeutic effect is not necessary makes them attractive alternative of un-fractionated heparin

Thrombolytics • Indicated with MI and ST segment elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset LBBB, who present less than 12 hours but not more than 24 hours after symptom onset • The most critical variable in achieving successful fibrinolysis is time form symptom onset to drug administration

Thrombolytics • As a class the plasminogen activators have been shown to restore coronary blood flow in 50-80% of patients • Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, coagulopathy • Retaplase slightly higher angiographic patency but did not translate into survival benefit • Intracranial bleed risk major drawback

Percutanous Coronary Intervention • Alternative if performed by skilled operator in an experienced center • Standard is a “ door to balloon” time of 90 minutes • PCI can successfully restore coronary blood flow in 90 to 95% of MI patients • PCI definitive survival advantage over fibrinolytics for MI patients who are in cardiogenic shock

Surgical Revascularization • Emergent or surgical revascularization in setting of failed PTCA in patients with hemodynamic instability and coronary anatomy amendable to surgical grafting • Also indicated of mechanical complications of MI including VSD, free wall rupture, or acute MR • Carries a higher risk of perioperative mortality than elective CABG

Lipid Management • All post MI patients should be on AMA step II diet ( < 7% of calories from saturated fats) • Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try to lower levels to <100 mg/dl • Recent data indicate that all MI patients should be on statin therapy, regardless of lipid levels or diet

Long term Medications • Most oral medications instituted in the hospital at the time of MI are continued long term • Aspirin, beta blockers and statin are continued indefinitely • ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or diabetes

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Myocardial Infarction and Complete Heart Block in a Patient With Anomalous Origin of the Left Coronary Artery From the Pulmonary Artery (ALCAPA)

Muhammad umer riaz gondal.

1 Internal Medicine, Reading Hospital, West Reading, USA

Devi Parvathy Jyothi Ramachandran Nair

2 Internal Medicine, Tower Health Medical Group, West Reading, USA

3 Cardiology, Reading Hospital/Tower Health, West Reading, USA

Muhammad Zafar

4 Cardiology, Reading Hospital, West Reading, USA

Muhammad Asad Hanif

Brian mccauley.

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital malformation. We present a case of an elderly patient with ALCAPA presenting with complete heart block and non-ST-elevation myocardial infarction years after diagnosis and surgical correction. An 81-year-old female with a history of ALCAPA presented to the emergency department with chest pain and progressive mental deterioration. She was bradycardic and hypotensive. An electrocardiogram revealed a complete heart block. Troponin was 4.04 ng/mL. She received atropine and underwent transcutaneous pacing. Left heart catheterization revealed complete occlusion of the mid-left circumflex artery, which was intervened with balloon angioplasty and chronic total occlusion of the right coronary artery. She was supported with temporary transvenous pacing, did not require further pacing support, and was discharged home. Previous records unearthed that in 1988 she had presented with syncope and was diagnosed with ALCAPA, filling from right-to-left collaterals with large and ectatic coronaries. At the time, she underwent surgical correction with excision of the left coronary from the pulmonary artery and reimplantation in the left coronary cusp along the posterior aorta. She had remained asymptomatic after her surgery until this presentation. ALCAPA is extremely rare in adults. Insufficient collaterals to the left ventricle cause inadequate blood supply, leading to ischemia in adults, predisposing them to arrhythmias and risk of sudden death. Adults with ALCAPA remain at increased risk of adverse cardiac events later in life, requiring long-term monitoring.

Introduction

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA), also known as Bland-White-Garland syndrome, is a rare childhood congenital cardiac malformation with a high infant mortality rate. It accounts for 0.25-0.5% of all congenital heart disorders, with the incidence reported as 1/3,00,000 [ 1 ]. The congenital anomaly carries a high risk of infant mortality, with up to 90% reported in the first year of life without surgical correction [ 2 ]. Elderly survivors are rare, with our patient presenting with complete heart block and non-ST-elevation myocardial infarction years after diagnosis and surgical correction.

This article was previously presented as a meeting abstract at the 2024 American College of Cardiology (ACC) meeting on April 6th, 2024.

Case presentation

An 81-year-old female with persistent atrial fibrillation and ALCAPA presented to the emergency department with chest pain. Chest pain was substernal, crushing, and severe, with no radiation. Her previous medical records revealed that in 1988 she had presented with syncope and ventricular ectopy and was diagnosed with ALCAPA after an urgent catheterization, filling from right-to-left collaterals with large and ectatic coronaries. At the time, she underwent surgical correction with excision of the left coronary from the pulmonary artery and reimplantation in the left coronary cusp along the posterior aorta. The patient had remained asymptomatic from a cardiovascular standpoint until the age of 45 years when she was first diagnosed with ALCAPA. After her surgical correction, she led a regular, healthy life with close follow-ups until this recent presentation.

In the emergency room, vitals included a heart rate of 42 bpm and blood pressure of 86/40 mmHg. Her mental status progressively deteriorated. An electrocardiogram revealed a complete heart block (CHB) (Figure ​ (Figure1 1 ).

Troponin was high at 4.04 ng/mL. Her blood work was unremarkable, including infectious workup and thyroid stimulating hormone (TSH) (Table ​ (Table1). 1 ). The patient received two doses of atropine and transcutaneous pacing for her CHB. An emergent left heart catheterization revealed a calcified and aneurysmal left anterior descending artery, with a complete occlusion of the mid-left circumflex artery. It also showed chronic total occlusion of the right coronary artery (RCA). She was supported with temporary transvenous pacing. Percutaneous balloon angioplasty was performed on the left circumflex artery, and her CHB was deemed likely due to transient ischemia of the AV node from the occlusion of the left circumflex artery (providing collaterals to the RCA) (Figures ​ (Figures2, 2 , ​ ,3). She 3 ). She did not require further pacing support and was discharged home with optimal acute coronary syndrome (ACS) management.

In ALCAPA, the left coronary artery arises from the pulmonary artery and carries deoxygenated blood to the left side of the heart. ALCAPA is classically divided into two types, infantile and adult-onset, based on the age of onset and symptom presentation [ 3 ]. The amount of collateral circulation between the RCA and LCA determines the extent of ischemia and symptoms. The hallmark of the adult form of ALCAPA is the significant collateral circulation between the RCA and LCA and retrograde perfusion of the left ventricle through the RCA [ 4 ]. However, over time, these collaterals are often insufficient to supply the left ventricle adequately, which can lead to subendocardial ischemia. Thus, they are at an increased risk of ventricular arrhythmia. Adults can, therefore, present with sudden cardiac death.

Approximately 90% of patients have sudden cardiac death at the age of 35 years [ 5 ]. Adult patients can remain asymptomatic or present with heart failure, angina on exertion, and mitral regurgitation. Only 10-15% of patients survive to adulthood [ 6 ]. Over the age of 50 years, survival is rare [ 7 ]. A literature review by Yau et al., involving 153 cases, revealed the average reported age of ALCAPA patients was 41 years, with the oldest being 83 years. While ventricular arrhythmias, syncope, or sudden death were observed in 17% of these patients, angina, dyspnea, or palpitations were the presenting symptoms in 66% of them, and 14% of the patients were asymptomatic [ 1 ]. There were a few case reports of ALCAPA patients presenting in their 70s [ 8 , 9 ]. We did not encounter any patient in their 80s with ALCAPA in our literature search.

Our patient was diagnosed with ALCAPA at the age of 46 years, as she had presented with syncope and ventricular ectopy. Before the advent of advanced radiographic technology, ALCAPA was usually diagnosed with coronary artery angiography, which is the gold standard for diagnosis [ 10 ]. The primary modalities include 2D transthoracic echocardiography and color Doppler flow imaging. Other imaging modalities that provide direct visualization of coronary artery anatomy with 3D reconstruction are CTA and cardiac magnetic resonance (CMR).

The prevalence of adult individuals with ALCAPA syndrome has significantly increased as a result of recent developments in non-invasive cardiac imaging [ 1 ]. According to the 2018 American Heart Association/American College of Cardiology and 2020 European Society of Cardiology guidelines, once ALCAPA is diagnosed, surgical correction is recommended to restore double coronary circulation [ 11 ]. Early surgical correction is recommended in adults, given that they are at increased risk of sudden cardiac death. A study by Kanoh et al. comparing long-term postoperative outcomes of ALCAPA patients revealed that adult-type ALCAPA patients had a higher risk of major adverse cardiac events, including arrhythmias and cardiac death compared to infant-type ALCAPA because of irreversible left ventricular remodeling caused by long-term chronic myocardial ischemia [ 12 ].

Conclusions

ALCAPA is a rare congenital cardiac anomaly, and early diagnosis is essential for long-term survival. Postoperative ALCAPA patients require long-term follow-up as chronic myocardial damage can lead to adverse consequences, such as our patient who presented with non-ST-elevation myocardial infarction (NSTEMI) and complete heart block. Our case raises awareness of the association of ALCAPA with acute coronary syndrome and complete heart block.

Disclosures

Human subjects: Consent was obtained or waived by all participants in this study.

Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following:

Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work.

Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work.

Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Author Contributions

Concept and design:   Muhammad Umer Riaz Gondal, Devi Parvathy Jyothi Ramachandran Nair, Smit Shah, Muhammad Zafar, Muhammad Asad Hanif, Brian McCauley, Earl Hope

Acquisition, analysis, or interpretation of data:   Muhammad Umer Riaz Gondal, Devi Parvathy Jyothi Ramachandran Nair, Smit Shah, Muhammad Zafar, Muhammad Asad Hanif, Brian McCauley, Earl Hope

Drafting of the manuscript:   Muhammad Umer Riaz Gondal, Devi Parvathy Jyothi Ramachandran Nair, Smit Shah, Muhammad Zafar, Muhammad Asad Hanif, Brian McCauley, Earl Hope

Critical review of the manuscript for important intellectual content:   Muhammad Umer Riaz Gondal, Devi Parvathy Jyothi Ramachandran Nair, Smit Shah, Muhammad Zafar, Muhammad Asad Hanif, Brian McCauley, Earl Hope

Supervision:   Brian McCauley, Earl Hope

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Open Access

Peer-reviewed

Research Article

Association of IL13 polymorphisms with susceptibility to myocardial infarction: A case-control study in Chinese population

Roles Formal analysis, Methodology, Resources, Writing – original draft

Affiliation Department of Cardiology, Qinghai Province Cardiovascular and Cerebrovascular Disease Specialist Hospital, Xining, Qinghai, China

Roles Formal analysis, Investigation, Writing – original draft

Affiliation Department of Coronary Heart Disease, Qinghai Province Cardiovascular and Cerebrovascular Disease Specialist Hospital, Xining, Qinghai, China

Roles Conceptualization, Supervision, Writing – review & editing

* E-mail: [email protected]

• Rong Chen, 
• Qiaoling Bao, 
• Xiaofeng Ma

• Published: August 1, 2024
• https://doi.org/10.1371/journal.pone.0308081
• Peer Review
• Reader Comments

Inflammatory cytokines play a major role in the pathogenesis of myocardial infarction (MI). Although information on the importance of interleukin 13 (IL13) in human MI is limited, it has been well documented in the mouse model. Genetic variation in the IL13 gene has been associated with the structure and expression of the IL13. In the present study, we hypothesized that IL13 common genetic variants would be associated with a predisposition to the development of MI.

Materials and methods

The present study enrolled 305 MI patients and 310 matched healthy controls. Common genetic polymorphisms in the IL13 gene (rs20541, rs1881457, and rs1800925) were genotyped using the TaqMan SNP genotyping method. Plasma levels of IL13 were measured using an enzyme-linked immunosorbent assay (ELISA).

In MI patients, minor alleles of the IL13 rs1881457 and rs1800925 polymorphisms were less common than in healthy controls [rs1881457: AC (P = 0.004, OR = 0.61), C (P = 0.001, OR = 0.66); rs1800925: CT (P = 0.006, OR = 0.59)]. Further haplotype analysis of three studied SNPs revealed a significant association with predisposition to MI. Interestingly, IL13 rs1881457 and rs1800925 were linked to plasma levels of IL13: the reference genotype had higher levels, heterozygotes were intermediate, and the alternate genotype had the lowest levels.

Conclusions

In the Chinese population, IL13 (rs1881457 and rs180092) variants are associated with different plasma IL13 levels and offer protection against MI development. However, additional research is required to validate our findings in different populations, including descent samples.

Citation: Chen R, Bao Q, Ma X (2024) Association of IL13 polymorphisms with susceptibility to myocardial infarction: A case-control study in Chinese population. PLoS ONE 19(8): e0308081. https://doi.org/10.1371/journal.pone.0308081

Editor: Andrea Da Porto, University of Udine, ITALY

Received: April 24, 2024; Accepted: July 16, 2024; Published: August 1, 2024

Copyright: © 2024 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All minimal data are in the manuscript. if further info is required, request can be directed to the corresponding author.

Funding: The author(s) received no specific funding for this work.

Competing interests: The authors have declared that no competing interests exist.

Abbreviation: MI, Myocardial infarction; SNP, Single nucleotide polymorphism; HWE, Hardy-Weinberg equilibrium; ELISA, Enzyme-linked immunosorbent assay; IL, interleukin; TNF, tumor necrosis factor; STEMI, ST-Elevation Myocardial Infarction; NSTEMI, Non-ST-Elevation Myocardial Infarction; ECG, Electrocardiogram

Introduction

Myocardial infarction (MI) is a serious form of coronary artery disease (CAD) that results from the occlusion of a coronary artery, impairing blood supply to the heart muscle. Despite significant advances in the understanding and treatment of cardiovascular diseases, MI remains a major public health concern worldwide. A recent meta-analysis revealed the global prevalence of MI is around 3.8% below 60 years old individual and the prevalence is 9.5% in older age group (>60 years) [ 1 ]. The mortality rate has increased in Chinese populations both in rural and urban areas in between 2002 to 2016 [ 2 ]. MI can be categorized as either STEMI or NSTEMI based on ECG changes. STEMI involves a complete obstruction of a coronary artery, which is indicated by ST-segment elevation on an ECG, necessitating immediate reperfusion therapy. On the other hand, NSTEMI results from a partial blockage and presents without ST elevation but with other ECG changes, which are managed with medications and, in some cases, percutaneous coronary intervention. In the context of MI, STEMI is more commonly observed than NSTEMI [ 3 ]. Both types of MI require prompt medical attention to prevent heart damage and improve patient outcomes. The multifaceted aetiology o MI includes complex interactions between genetic predisposition and environmental factors [ 4 ]. Numerous environmental factors and host genetic factors have been demonstrated to impact cytokines and the immune response in humans [ 5 ]. Cytokines are critical in the pathophysiology of MI, as they mediate the inflammatory response that follows cardiac tissue injury [ 6 ]. These small, signaling proteins are secreted by immune cells, endothelial cells, and other cell types in the heart, orchestrating a complex series of events aimed at limiting damage and initiating repair [ 7 ]. During an MI, cytokines such as interleukins, tumor necrosis factor-alpha (TNF-α), and chemokines are rapidly increased, contributing to both protective and detrimental effects [ 8 ] and facilitate leukocyte infiltration, modulate cell survival and apoptosis, and influence myocardial remodelling [ 9 ]. A recent study found differences in inflammatory molecules between ST elevation myocardial infraction (STEMI) and non STEMI clinical phenotypes, which are distinguished by elevated methylene diphosphonate (MDP), macrophage inflammatory protein-1β (MIP-1β), and TNF-α [ 6 ]. Additionally, cytokine levels were related to blood flow through the infract related artery [ 6 ]. Interleukin-13 (IL-13), is a pro-fibrotic cytokine that is secreted by various immune cells, including T cells, B cells, and macrophages. This cytokine plays a crucial role in the Th2 immune response, a process that is triggered by the activation of T helper 2 cells. These cells release a range of cytokines, such as IL-4, IL-5, and IL-13, which promote B cell activation, class switching to IgE production, and the recruitment of eosinophils [ 10 ]. Although IL-13 was initially thought to play a role in allergic responses, it has gained increasing attention due to its involvement in a variety of immune processes and diseases. The cytokine exerts multiple and diverse biological effects on different cell types or tissues and is responsible for immune cell differentiation, proliferation, and inflammatory responses [ 10 ]. In the MI mouse model, dynamic expression of IL13 has been reported; after the incidence of MI, the levels significantly increased, reaching a peak on day three and then declining until day seven, when they increased again [ 11 ]. However, another research group found that upregulation began on day 7 and continued until day fourteen [ 12 ]. Surprisingly, investigations on the role of IL13 in MI patients are very limited and in a study lower levels have been reported [ 13 ].

Genetic variations can influence gene expression, protein function, and susceptibility to different disease risks [ 14 ]. Functional variations in the IL13 gene have been linked with different types of cardiovascular diseases [ 15 ]. Although various genome-wide association studies have been carried out in diverse populations, no notable genetic association between the IL13 gene and susceptibility to develop MI has been identified [ 16 , 17 ]. Given that differential IL13 levels have been observed in MI patients and functional genetic variants play a role in regulating IL13 levels, we hypothesized that common genetic variants affecting plasma IL13 levels would be linked to the pathogenesis of MI in the Chinese population. Till date several single nucleotide polymorphisms (SNP) in IL13 gene have been reported to be linked with wide range of clinical diseases ( https://www.ncbi.nlm.nih.gov/clinvar/?term=IL13[gene ]). However, three SNPs (rs20541, rs1881457 and rs1800925) have been studied most frequently based on their functional relevance. The human IL13 gene, which consists of 5 exons and 4 introns, is located in the long arm of the fifth chromosome (q31.1). The IL13 rs20541 polymorphism is found in the fourth exon, which is a result of a transition mutation (A>G) that alters the amino acid sequence of the IL13 protein at the 130 th codon (Glycine to Arginine). The other two genetic variants are situated in the promoter region of IL13 gene (rs1881457: A-1512C; rs1800925: C-1111T) and are presumed to alter the expression of IL13 [ 18 ]. In addition, the significance of IL13 polymorphisms has been documented in clinical phenotypes that serve as risk factors for MI, such as type-1 diabetes mellitus, hypertension, and dyslipidemia. Specifically, in Kuwaiti children, the rs20541 variant was associated with susceptibility to T1DM [ 19 ]. Conversely, genetic variants in the IL13 gene failed to demonstrate an association with T1DM in Filipino [ 20 ], British [ 21 ], and Thai populations [ 22 ]. Moreover, the rs1800925 and rs1881457 polymorphisms have been shown to be linked to hypertension in the Korean population [ 23 ]. Based on the functional significance of these genetic polymorphisms, case-control studies in various populations have been conducted to investigate their association with MI susceptibility. In the Iranian population, rs1881457 heterozygotes provided protection against the development of MI, but no significant link between MI susceptibility and the rs20541 polymorphism was found [ 24 ]. In contrast, the IL13 rs20541 variant increased the risk of MI in Greek Cypriot males [ 25 ].

Given the importance of IL13 in the pathogenesis of MI and the possibility of genetic variants influencing IL13 levels, we hypothesized that the common IL13 genetic variant would be associated with susceptibility/resistance to MI. We conducted a hospital-based case-control study in the Chinese population to investigate the possibility of an association between IL13 variants and MI.

Study design

The study used a hospital-based case-control design to investigate the genetic association between common variations of the IL13 gene and the susceptibility or resistance to MI in a Chinese cohort. The report of this study adhered to the STREGA guidelines.

The present study was conducted on the patients enrolled in the Department of Cardiology, Qinghai Province Cardiovascular and Cerebrovascular Disease Specialist Hospital, from January 2017 to December 2022. Other baseline parameters such as hypertension, hypercholesterolemia, hyperglycemia, and coronary artery disease were also explored in the included MI patients. Age, sex and gender-matched healthy controls hailing from similar geographical locations were considered healthy controls without any history of heart-related issues. All healthy controls were subjected to blood pressure measurement and different biochemical tests such as cholesterol and blood sugar levels, and subjects with higher BP (more than 120 mm Hg for systolic and 80 mm Hg for diastolic), cholesterol (total >200 mg/dL, LDL >100 mg/dL, HDL<40 mg/dL for eman and 50 mg/dL for women, triglycerides > 150 mg/dL), or sugar levels (fasting blood glucose > 99 mg/dL and HbA1c >5.7%) were not included in the present study. The study protocol was approved by the institutional ethical committee of Qinghai Province Cardiovascular and Cerebrovascular Disease Specialist Hospital, and informed written consent was obtained from each participant. In situations where patients were unable to provide informed consent due to their medical condition, consent was obtained from legally authorized representatives, including family members or legal guardians. The IEC reviewed and approved the study protocol, including this consent process (IEC/2016/156). If patients subsequently regained capacity, they were informed and requested to provide direct consent. About 5 ml of intravenous blood was collected from MI (within six hours of the MI onset) and healthy control subjects with anticoagulants.

Sample size calculation

The sample size for the study was calculated a priori to ensure that an adequate number of cases and controls were enrolled. The GPower v3.1.9.7 software was utilized for the sample size calculation. To achieve a power of 90% with an effect size of 0.15 and an alpha error probability of 0.05, the analysis indicated that 630 subjects were needed. Consequently, the study was designed to include 315 cases and an equal number of healthy controls in the investigation of the genetic association.

IL13 genotyping

Whole genomic DNA was isolated from the whole blood by QIAamp Blood mini kit according to the manufacturer’s instructions (QIAGEN, Germany). DNA quantity and quality were assessed using a NanoDrop 2000 spectrophotometer (Thermo Fisher Scientific, Waltham, MA, USA) and agarose gel electrophoresis. Genotyping of common IL13 gene polymorphisms (rs20541, rs1881457 and rs1800925) were carried out by TaqMan Genotyping assays kit (Thermo Fisher Scientific, Catalog number: 4351379) ( https://tools.thermofisher.com/content/sfs/manuals/TaqMan_SNP_Genotyping_Assays_man.pdf ). Details of the probe are given below: rs20541, C___2259921_20 , Context Sequence [VIC/FAM] TTAAAGAAACTTTTTCGCGAGGGAC[A/G]GTTCAACTGAAACTTCGAAAGCATC , rs1881457: C__11740467_10 , Context Sequence [VIC/FAM]TACAGATTAGGAAACAGGCCCGTAG[A/C]GGGGTCACACGGCCAAGTAGCGGCA , rs1800925, C___8932056_10 , Context Sequence [VIC/FAM]GGTTTCTGGAGGACTTCTAGGAAAA[C/T]GAGGGAAGAGCAGGAAAAGGCGACA . The genotyping reactions comprised the genomic DNA template, TaqMan Genotyping Master Mix, and the specific primer/probe combination. These reactions were performed using a real-time PCR thermal cycler, with an initial denaturation step at 95°C for 10 minutes, followed by 40 cycles of denaturation at 95°C for 15 seconds and annealing/extension at 60°C for 1 minute. The fluorescence signals were detected and analyzed. To ensure the accuracy and reliability of the genotyping results, positive and negative controls were included in each run. Genotype calling was accomplished based on the allelic discrimination plot. Each sample was considered for genotyping in duplicate and considered for analysis only in case of concordant observation. Subjects who were unsuccessful in genotyping were excluded from the present investigation.

Plasma IL13 quantification

Plasma levels of IL-13 were measured by enzyme-linked immunosorbent assays (ELISA) according to the manufacturer’s instructions (Invitrogen, Catalog no: BMS231-3, https://www.thermofisher.com/document-connect/document-connect.html?url=https://assets.thermofisher.com/TFS-Assets%2FLSG%2Fmanuals%2FMAN0016602_231–3_HuIL-13ELISA_UG.pdf ). The plasma samples, which were collected and stored at -80°C until analysis, were thawed on ice before use. To prepare a standard curve, the standards were reconstituted with distilled water and serially diluted (1:2) on seven tubes, such that the highest concentration of the standard remained at 100 pg/mL and the lowest was 1.6 pg/mL. The precoated microplate wells were properly washed, and the pre-prepared standards were applied in duplicate wells. Two wells were used as blank wells and were only filled with assay buffer. 50 microliters of assay buffer were applied to all sample wells, and an equal amount of samples were applied to the wells in duplicate. Fifty microliters of conjugate mixture were added to all wells, and the plate was incubated at room temperature for two hours. After incubation, the plate was washed thrice properly and proceeded to the color development step using TMB as a substrate solution. The reaction stopped ten minutes later, and absorbance was measured at 450 nm. The concentrations of IL-13 in the samples were determined by interpolation from the standard curve.

Statistical analysis

All statistical analysis was performed by GraphPad Prism v9 (GraphPad Software, Boston) using the default setting. The allele and genotype frequency was calculated by manual counting. The distribution of genotypes with references to Hardy Weinberg equilibrium (HWE) was explored using the Microsoft Excel program. The Fisher exact test compared the prevalence of genotype and allele in different clinical categories. The Fisher exact test is a reliable method for obtaining precise test results in small sample sizes. It calculates the exact probability value and the confidence interval of the observed data for measuring the association [ 26 ]. Bonferroni correction is a technique used to correct the significance level for multiple comparisons, aiming to reduce the likelihood of false positives. It entails dividing the desired significance level (α) by the number of comparisons (n), thereby creating a more stringent threshold (α/n) [ 27 ]. In the current analysis, three SNPs were examined, and the significance levels were adjusted using the Bonferroni correction method. A P value less than 0.016 (0.05 divided by 3) was considered statistically significant. The haplotype construction and comparison of their distribution among MI patients and healthy controls were executed by SNPAlyze software Version 8.1.1 employing the default setting (DYNACOM Co. Ltd. Japan). The software uses a permutation test for the comparison of haplotype frequencies among two groups. The mean plasma IL13 levels in healthy controls and MI patients were compared by student’s t-test. The association of IL13 polymorphism with the plasma levels of IL13 was explored by one-way analysis of variances (ANOVA). For the comparison of cytokine among cases and controls or within different genotypes of IL13 polymorphisms, a P value less than 0.05 was considered statistically significant.

Baseline characteristics of patients and controls

The baseline characteristics of patients and controls are shown in Table 1 . In the present study, a total of 305 MI patients (Male: 189, Female: 116) were enrolled. In addition, 310 age and gender-matched (male: 195, female: 115) healthy controls were considered. The mean age of patients was 56.65 years, and healthy controls were 55.35 (p = 0.31). Hypercholesterolemia (58%) was more frequent among MI patients, followed by hyperglycemia (53%) and hypertension (52%). About one-third of the total MI patients had coronary artery diseases. Interestingly, the family history of cardiovascular diseases or smoking habit was more frequent in the MI patients compared to the healthy controls. While the excessive alcohol consumption rate was comparable among MI patients and controls.

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https://doi.org/10.1371/journal.pone.0308081.t001

MI patients displayed higher levels of IL-13 compared to healthy controls

Based on the availability of plasma samples, a total of 224 plasma samples were quantified for plasma levels of IL13, including each of 112 patients and controls, by ELISA. As shown in Fig 1 , the MI patients displayed significantly higher mean levels of IL13 compared to healthy controls (p<0.0001).

Levels of IL-13 were quantified by ELISA in plasma of MI patients (n = 112) and healthy controls (n = 112). The mean IL13 levels were compared by student’s t test. The MI patients displayed higher levels of IL13 compared to the healthy controls. A P value less than 0.05 considered as significant.

https://doi.org/10.1371/journal.pone.0308081.g001

Distribution of IL13 polymorphisms in healthy controls

In the present investigation, we genotyped three common gene polymorphisms in the IL13 gene (rs20541, rs1881457, and rs1800925) by TaqMan genotyping assays. Although we have enrolled 328 MI patients and 322 healthy controls for the present study, 310 cases and 305 healthy controls were successfully genotyped for IL13 polymorphisms. The prevalence of these polymorphisms is demonstrated in Table 2 . GG genotype (56%) of rs20541 polymorphism was more frequent than heterozygotes (34%) and AA type (10%). The genotype distributions did not match HWE (χ 2 = 6.03, p = 0.01). For the other two gene polymorphisms (rs1881457 and rs1800925), the reference genotypes (AA: 47%, CC: 63%) were more frequent than heterozygotes (AC: 44% and CT: 32%) and alternative genotypes (CC: 7% and TT: 5%), respectively. The distribution of genotypes for rs1881457 (χ 2 = 0.21, p = 0.64) and rs1800925 (χ 2 = 0.54, p = 0.46) polymorphisms were in line with the HWE. The HWE holds substantial implications in population genetics, serving as a foundational model for comprehending the genetic composition of populations. It posits that allele and genotype frequencies in a population remain constant from generation to generation in the absence of evolutionary influences, such as selection, mutation, migration, genetic drift, and non-random mating. HWE offers a null hypothesis for detecting evolutionary forces acting on a population, and any departure from it can indicate the presence of these forces, thereby providing insights into the evolutionary dynamics at play [ 28 , 29 ].

https://doi.org/10.1371/journal.pone.0308081.t002

IL13 polymorphisms (rs1881457 and rs1800925) are associated with MI

The distribution of IL13 polymorphisms (rs20541, rs1881457, and rs1800925) was explored in MI patients and healthy controls. Details are depicted in Table 2 . Genotypes and allele distributions were comparable in patients and controls for IL13 rs20541 polymorphism. However, the heterozygotes of rs1881457 and rs1800925 polymorphisms were more frequent in healthy controls than the MI patients (rs1881457: p = 0.004, OR = 0.61; rs1800925: p = 0.006, OR = 0.59). Similarly, the alternate allele of rs1881457 polymorphism (C) was also highly prevalent in healthy controls compared to MI patients (p = 0.001, OR = 0.66), indicating the alternate allele’s protective nature against the development of MI in the Chinese population. However, the prevalence of the alternate genotypes for rs1881457 and rs1800925 polymorphisms was comparable among MI patients and healthy controls.

Association of rs20541, rs1881457, and rs180092 haplotype with MI

Haplotype frequency was calculated and compared among the MI patients and healthy controls by SNPAlyze software, and the results are shown in Table 3 . Haplotype rs20541-rs1881457-rs1800925, G-A-C (p = 0.02), and A-A-C (p = 0.01) were more frequent in MI patients than healthy controls. In contrast, the haplotypes G-C-C (p = 1E-3), A-C-C (p = 9E-3), G-A-T (p = 0), and A-A-T (p = 2E-3) were more prevalent in controls than in MI patients.

https://doi.org/10.1371/journal.pone.0308081.t003

Plasma levels of IL13 linked with IL13 polymorphisms

To explore the functional relevance of the studied SNPs in the IL13 gene, plasma levels of IL13 were quantified by ELISA, and possible association with different genotypes of IL13 was explored. As shown in Fig 2 , the rs1881457 and rs1800925 polymorphisms were linked with plasma levels of IL13. The wildtype of rs1881457 and rs1800925 polymorphisms displayed significantly higher levels of IL13 compared to their respective heterozygotes and homozygous mutants. Heterozygotes had intermediate levels of IL13 ( Fig 2A and 2B ). Interestingly, a similar pattern of association between IL13 polymorphisms and plasma levels of IL13 remained valid still after separating MI patients ( Fig 2C and 2D ) and healthy controls ( Fig 2E and 2F )

Plasma levels of IL13 were quantified in MI patients (n = 112) and healthy controls (n = 112). Mean IL13 levels in different genotypes of rs1881457 (a) and rs1800925 (b) in the pooled clinical categories (MI patients and healthy controls) were compared by ANOVA. Further, an association of rs1881457 and rs1800925 polymorphism with IL13 was explored in MI patients (c and d) and healthy controls (e and f). A P value <0.05 is taken as statistically significant.

https://doi.org/10.1371/journal.pone.0308081.g002

Discussions

The current hospital-based case-control study found a significant link between IL13 common gene polymorphisms (rs1881457 and rs180092) and MI risk. Furthermore, a substantial relationship was found between plasma IL13 levels and IL13 promoter variants (rs1881457 and rs180092). To the best of our knowledge, this is the first study to investigate the possible association of IL13 polymorphism with the development of MI in the Chinese population.

The role of IL13 in MI has been widely investigated in experimental model systems, but data are limited from human subjects. Dynamic IL13 levels have been demonstrated in mice models in relation to the time period after the incidence of the MI. The levels significantly increased and reached the highest levels on the third day and, after that, started declining until day seven, and then further increased [ 11 ]. However, other reports showed an upregulation of IL13 after the seventh day and continued until day fourteen [ 12 ]. In the present study, we observed about four folds of elevated IL13 in MI patients compared to healthy controls. Most of the patients enrolled in the present study just after the incidence of MI (within six hours), possibly that could be the reason for higher levels of IL13 in the plasma levels. Further, it has been well documented that elevated IL13 is essential for the cardio-protective effect [ 11 ].

There have been limited investigations into the role of IL13 common variants in the development of MI. The homozygous mutant of the rs20541 polymorphism has been linked to MI susceptibility in Greek Cypriot males [ 25 ]. In contrast, the Iranian population rs20541 failed to show such an association [ 24 ], which is consistent with the findings of the current study. In the Iranian population [ 24 ] and in the current study, heterozygotes of IL13 rs1881457 polymorphisms are associated with protection against MI development. Furthermore, the other polymorphism, rs1800925, demonstrated the protective nature of heterozygotes, which were highly prevalent in healthy controls. The precise mechanism by which the variant protects against the development of MI is unknown. Both IL13 (rs1800925 and rs1881457) polymorphisms are located in the intron region. Although these regions are typically not translated into proteins but can affect gene expression by altering splicing patterns, transcription factor binding, or RNA stability. Intronic variants can lead to alternative splicing, exon skipping, or the inclusion of aberrant exons, which may disrupt protein function and contribute to disease [ 30 – 32 ]. The two IL13 polymorphisms (rs1800925 and rs1881457) were possibly linked to plasma levels of IL13, and the intermediate production of IL13 cytokines may protect against the development of MI. The current study has several advantages over previous studies, including i) a larger number of participants and ii) genotyping and quantification of plasma IL13 in each sample.

HWE provides a theoretical framework for predicting the expected frequencies of genotypes in a large, randomly mating population where no evolutionary forces are at play. Any departure from this equilibrium can signal the presence of evolutionary forces, such as natural selection, mutation, migration, genetic drift, or non-random mating. We found a deviation of IL13 rs20541 polymorphism genotypes from HWE in this study. HWE deviation has been linked to factors such as population stratification, genotyping error, and selection pressure [ 33 ]. We recruited healthy controls from a similar ethnic group and geographical area, reducing the possibility of population stratification. Using stringent genotyping technology, we eliminated the possibility of error in the genotyping method. The deviation could be attributed to the selection pressure provided by different infections [ 34 – 37 ]. Importantly, IL13 rs20541 polymorphism has been linked with susceptibility to pulmonary tuberculosis [ 38 ], Schistosoma mansoni infection [ 39 ], hand, foot, and mouth diseases [ 40 ], further strengthening its possibility of the beneficial selection of genetic variants in the studied population.

The current study has revealed a significant role played by IL13 in the pathogenesis of MI. The genetic variations within the IL13 gene, specifically rs1881457 and rs180092, were observed to have varying levels of plasma IL13 and were found to offer protection against the development of MI. Although the precise mechanism linking the genetic mutants to plasma levels of IL13 is not yet fully understood, understanding the potential mechanism could provide valuable information on the underlying mechanisms of atherosclerosis and plaque instability, which are key factors contributing to MI. Identifying specific IL-13 polymorphisms associated with increased MI risk or severity could aid in risk stratification and the early detection of at-risk individuals. Furthermore, IL-13 genetic profiling may help personalize treatment strategies, such as anti-inflammatory therapies or targeted interventions to modulate immune responses, to improve outcomes and prevent recurrent cardiovascular events. Overall, the study of IL-13 gene polymorphism holds promise for enhancing risk assessment, prognosis prediction, and therapeutic interventions in the context of MI and cardiovascular disease management. Although the current study successfully demonstrated the significance of the IL13 genetic variant in MI, it is essential to acknowledge the limitations of the investigation. One limitation is that the Chinese population is a mixed group comprised of various ethnic and sub-population groups. The sample size used in the study may not be sufficient, which warrants further investigation with a larger sample size. Additionally, the study only examined three SNPs in the IL13 gene, so the role of other variants in the predisposition to MI remains unknown. Moreover, the current case-control study did not explore the mechanism of how the genetic variations in the IL13 gene alter the expression of mRNA or respective protein levels. Furthermore, the frequency distribution of IL13 rs20541 genotypes did not conform to the expectations of the HWE, thus rendering the interpretation of the relationship between haplotype and MI cautious.

Based on the observations of this study, future research should concentrate on elucidating the molecular mechanisms underlying the protective effect of IL13 genetic mutants and exploring how IL13 variants modulate gene expression and inflammatory pathways in cardiovascular tissues. Employing transgenic animal models and cellular systems can provide deeper insights into the functional impact of these polymorphisms. Large-scale epidemiological studies are necessary to confirm these findings across diverse populations and understand the gene-environment interactions that influence MI risk. Furthermore, investigating the potential of IL13 polymorphisms as biomarkers for risk stratification and personalized medicine could significantly impact cardiovascular care, leading to targeted prevention and therapeutic strategies.

The IL13 gene variants rs1881457 and rs180092 have been linked to varying plasma levels of IL13 and offer protection against the development of MI in the Chinese population. This finding adds to the existing body of research on genetic factors influencing MI risk, and it sheds light on the possible role of IL13 in cardiovascular health. To better comprehend the importance and applicability of these gene variants, further investigations are needed in diverse populations, including those with different ethnic backgrounds. These studies are crucial for validating the findings and determining the broader relevance of IL13 variants in the global context of MI prevention and treatment.

Acknowledgments

Authors would like to thanks all participants of the study for their voluntary contribution and involvement in the research.

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• 10. de Vries JE, Carballido JM. Interleukin-13. In: Henry HL, Norman AW, editors. Encyclopedia of Hormones. New York: Academic Press; 2003. p. 470–8.

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Article Contents

Introduction, summary figure, case presentation, lead author biography, supplementary material, data availability.

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Thrombus inside the channel of patent foramen ovale revealed by optical coherence tomography imaging in a patient with myocardial infarction

Conflict of interest: None declared.

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Xing-ye Wang, Lu He, Xue-gang Xie, Xiao-qin Liu, Yu-shun Zhang, Thrombus inside the channel of patent foramen ovale revealed by optical coherence tomography imaging in a patient with myocardial infarction, European Heart Journal - Case Reports , Volume 8, Issue 7, July 2024, ytae304, https://doi.org/10.1093/ehjcr/ytae304

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Myocardial infarction (MI) caused by patent foramen ovale (PFO)-based paradoxical embolism is rare, and there are few case reports in the literature.

Here, we report a case of MI in which optical coherence tomography revealed in situ thrombi in the PFO channel.

In addition to paradoxical embolism, in situ thrombus may also be one of the pathogenic mechanisms of PFO in patients with MI.

In young patients with myocardial infarction, in situ thrombus attached to patent foramen ovale may be the source of coronary artery embolism.

Optical coherence tomography can clearly visualize microthrombus and can be used to find the source of thrombus.

Patent foramen ovale (PFO) occurs in 20–34% of the general population, with most of them being asymptomatic. 1 The closure of PFO is maintained through the pressure gradient between the left and right atria. However, during actions such as coughing, squatting, or defecating, this pressure gradient can reverse owing to a transient increase in right atrial pressure, leading to opening of PFO and occurrence of a right-to-left shunt (RLS). Consequently, substances such as microemboli from the venous system can enter the arterial system, 2 a phenomenon called paradoxical embolism. Patent foramen ovale is most commonly associated with paradoxical embolism and clinically plays an essential role in the pathogenesis of several conditions, including stroke, migraine, and decompression sickness. 1

In addition to paradoxical embolism, Yan et al . 3 , 4 found thrombi in the PFO fissure using optical coherence tomography (OCT) in patients with cryptogenic stroke but not in asymptomatic PFO patients. The authors speculated the involvement of in situ thrombi in the pathogenesis of stroke. Patent foramen ovale can lead to intracranial infarction and rare extracranial embolisms such as myocardial infarction (MI), which has a rare incidence of ∼0.65%. 5 However, in situ thrombi inside the PFO channel have rarely been reported in patients with MI. 6 Here, we present a case of MI with thrombi inside the PFO channel detected using OCT.

A 50-year-old woman who presented with one episode of chest pain lasting 3 min, accompanied by a 2-year history of hypertension, was admitted to the outpatient clinic of a local hospital, where electrocardiogram revealed normal findings, and she discharged home without medication.

One week later, she returned to the local hospital’s emergency department for sudden and severe chest pain persisting without relief for 40 min. Electrocardiogram indicated ST-segment elevation in the V1 to V4 leads and elevated myocardial enzyme spectrum. She was diagnosed with acute MI, and emergency coronary angiography was conducted, but no apparent stenosis was found in the vessels. Unfortunately, no other abnormalities were found at the local hospital. She was discharged with routine medication for primary prevention of coronary heart disease, including aspirin, clopidogrel, and atorvastatin.

Two months later, she experienced headache attacks approximately once or twice a week, prompting admission to our hospital. A detailed medical history revealed that her headaches had been occurring for 2 years, combined with well-controlled high blood pressure. The coexistence of MI with normal coronary arteries and recurrent headaches led us to explore a potential association, prompting a series of diagnostic tests. Cranial magnetic resonance imaging showed no abnormalities (see Supplementary material online, Figure ). After 24 h Holter monitoring, no atrial fibrillations or other arrhythmias were revealed. Transthoracic echocardiography revealed no abnormalities except for oblique shunt over the atrial septum ( Figure 1A ). Contrast transthoracic echocardiography examination indicated sustained RLS ( Figure 1B ). Transoesophageal echocardiography showed a PFO channel with 2.6 mm height and 9.3 mm length ( Figure 1C ). Venous ultrasound of the lower extremity showed no thrombosis, and coagulation testing yielded normal findings. The Caprin Assessment was used to evaluate the thromboembolic risk, and the patient received a score of 1 (for age 50 years), placing her in the low-risk group. Based on the patient’s history, a possible coronary artery embolism secondary to PFO was considered. Before initiating PFO occlusion treatment, coronary angiography was repeated at our centre, confirming normal coronary artery ( Figure 2A and B ).

Images of echocardiogram: ( A ) Oblique shunt on atrial septum was revealed by transthoracic echocardiography; ( B ) contrast transthoracic echocardiography shows a large right-to-left shunt; ( C ) anatomy of patent foramen ovale indicated by transoesophageal echocardiography.

A and B present normal coronary angiography images.

Given the absence of evidence supporting paradoxical embolism, we suspected in situ thrombosis. Optical coherence tomography was performed with the patient’s consent. The OCT catheter was advanced ∼1 cm beyond the left atrial opening of the foramen ovale fissure. When the contrast agent was injected through a guiding catheter to clear the blood in the fissure, the catheter was withdrawn to the right atrial of the PFO tunnel (see Supplementary material online , Video S1 ). Optical coherence tomography revealed three white thrombi in the channel, with a calculated thrombus area of 0.19 mm 2 and total thrombus volume of 0.13 mm 3 . Additionally, we found an endocardial discontinuity in the tunnel ( Figure 3A and B , Supplementary material online , Video S2 ).

( A ) and ( B ) present images of optical coherence tomography, star refers to white thrombi and arrow endocardial discontinuity.

To prevent recurrence of embolic events, we chose a 25 mm Amplatzer PFO closure device to close her PFO. At the 6-month follow-up, the patient was in good condition, with resolution of headache and no recurrence of chest pain. The patient provided consent for the publication of this report and its associated data.

MI is a serious cardiovascular emergency and the leading cause of death worldwide. 7 Reduced blood flow due to rupture or erosion of vulnerable plaques and formation of thrombus in the coronary artery are the main mechanisms of its pathogenesis. 8 , 9 Although MI caused by a paradoxical embolism is a rare, exclusive diagnosis, other potential causes of MI, such as coronary atherosclerosis, vasospasm, heart valve defects, and atrial fibrillation, should be systematically excluded. When paradoxical embolism is highly suspected after eliminating the above reasons, it is necessary to find evidence of an abnormal embolism, including an abnormal intracardiac or extracardiac shunt. MI caused by an intracardiac shunt mainly involves an atrial septal defect and PFO. 2 Unlike other intracardiac shunts, PFO exhibits slow or stable blood flow in the unhealed fissure between the septum primum and septum secundum, creating a conducive environment for in situ thrombus formation. These thrombi may subsequently enter the arterial circulation through an RLS, causing embolism events.

In patients with PFO-related stroke, the incidence of detectable thrombus in the lower limb and pelvic veins is only ∼11%, 10 indicating that the source of most clots remains unknown. An in situ thrombus in the PFO tunnel has always been a hypothetical source of thrombus. 11 Using OCT, Yan et al . found that, in addition to being a thrombus pathway itself, the tunnel of PFO-related stroke patients is the site for in situ thrombus formation. In contrast, no thrombi were found in the tunnel of asymptomatic PFO patients, and in situ thrombi are likely to be the pathogenic mechanism of PFO. 4 As a pioneering study, the researchers only included patients with PFO-related stroke and migraine, excluding those with extracranial infarction caused by PFO, which is rare in clinical setting. 5 In situ thrombi inside the PFO channel in patients with MI have rarely been reported. 6 In our patient, white thrombi were attached to the PFO channel, and the endocardial surface was irregular, which is consistent with the conclusion of Yan et al. 4

Based on the primary mechanism of MI pathogenesis, clinical treatments for acute MI mainly focus on restoring blood flow, including primary percutaneous coronary intervention and thrombolysis. 12 However, if MI is due to a paradoxical embolism, the management strategy may not be completely consistent. Manual aspiration thrombectomy and avoidance of stent implantation is beneficial. Additionally, beta-blockers and angiotensin-converting enzyme inhibitors may be used in cases of reduced left ventricular ejection fraction, whereas antiplatelet or statin therapy may not be necessary. Anticoagulant therapy has been used to treat venous thrombosis. 13 Despite the absence of evidence from randomized controlled trials on PFO closure in MI induced by PFO, finding from a large multicentre case–control study have shown equivalent efficacy of PFO closure in treating peripheral embolisms, including MI, compared to intracranial infarction. 14 Blocking the RLS caused by the PFO may emerge as the preferred strategy, supported by remission of symptoms in patients after PFO closure.

In patients with MI considered to be caused by PFO, in situ thrombus within the PFO fissure can be revealed on OCT, which represents another pathogenic mechanism that deserves further investigation.

Professor, MD, Vice President of Cardiovascular Hospital, and leader of the Department of Structural Heart Disease, The First Affiliated Hospital of Xi’an Jiaotong University.

Supplementary material is available at European Heart Journal – Case Reports online.

Consent: Written informed consent to publish the clinical details and images of the patient was obtained, in line with the COPE best practice guidelines.

Funding: None.

All available data was presented within the manuscript.

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Causal relationship between breakfast skipping and myocardial infarction: Two-sample Mendelian randomization

Affiliations.

• 1 Department of Cardiology, The First Hospital of Shanxi Medical University, School of Medicine, Shanxi Medical University, Taiyuan, China.
• 2 Department of Cardiology, The Second Hospital of Shanxi Medical University, School of Medicine, Shanxi Medical University, Taiyuan, China.
• PMID: 39058860
• PMCID: PMC11272345
• DOI: 10.1097/MD.0000000000038895

While observational studies suggest a connection between skipping breakfast and myocardial infarction (MI), the causal nature of this relationship is unclear. This study aims to investigate the genetic causal relationships between breakfast skipping and MI through Mendelian randomization (MR). Employing genetic data from a public genome-wide association study, this research focuses on genetic variations linked to breakfast skipping and MI. The primary analytical method was the inverse variance-weighted approach, complemented by additional methods like MR-Egger, weighted median, and mode analyses. It also includes heterogeneity and horizontal pleiotropy tests such as the Cochrane Q test, MR-Egger intercept, and MR-PRESSO tests, with a leave-one-out analysis for enhanced sensitivity assessment reliability. The study discovered a notable association between breakfast skipping and an increased risk of MI (odds ratios: 1.34, 95% confidence intervals: 1.03-1.76, P = .027). The test revealed no heterogeneity or multiplicity, and the sensitivity analysis confirmed the robustness of the results. Our MR analysis suggests that habitual breakfast skipping might elevate the likelihood of MI, underlining the importance of regular breakfast consumption in potentially mitigating heart attack risks.

Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

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Conflict of interest statement

The authors have no conflicts of interest to disclose.

The flow diagram of this…

The flow diagram of this Mendelian randomization (MR) study. IVW = inverse variance…

Scatter plot of breakfast skipping…

Scatter plot of breakfast skipping and myocardial infarction.

Forest plot of breakfast skipping…

Forest plot of breakfast skipping and myocardial infarction.

Funnel plot of breakfast skipping…

Funnel plot of breakfast skipping and myocardial infarction.

Analysis of breakfast skipping and…

Analysis of breakfast skipping and myocardial infarction by the leave-one-out method.

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