Nursing Diagnoses for Myocardial Infarction (MI): A Comprehensive Guide for Nurses

Introduction

Acute Myocardial Infarction (MI), commonly known as a heart attack, remains a leading cause of mortality globally, particularly in developed nations. Affecting millions worldwide and causing over a million deaths annually in the United States alone, MI is a critical condition requiring immediate recognition and intervention. It is broadly classified into two main types: Non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Unstable angina, while similar to NSTEMI, is distinguished by the absence of elevated cardiac markers.¹,²,³

Myocardial Infarction is characterized by irreversible damage to the heart muscle resulting from oxygen deprivation. This ischemic event impairs both diastolic and systolic heart function, predisposing patients to arrhythmias and a host of serious complications. Timely reperfusion of the heart to restore blood flow is paramount. Outcomes are significantly improved when treatment is initiated within six hours of symptom onset.

Diagnosis of MI is established when at least two of the following criteria are present:

Clinical symptoms indicative of ischemia.
New ST-segment changes on an electrocardiogram (ECG) or the presence of a new left bundle branch block (LBBB).
Development of pathological Q waves on the ECG.
Imaging evidence of new regional wall motion abnormalities.
Identification of an intracoronary thrombus during autopsy or angiography.

Effective nursing care is crucial in managing patients with MI. An accurate nursing diagnosis forms the foundation for planning and implementing patient-centered care to address the complex needs associated with this condition.

Common Nursing Diagnoses for MI

Nurses play a pivotal role in the care of patients experiencing a myocardial infarction. Identifying appropriate nursing diagnoses is essential for guiding interventions and achieving positive patient outcomes. Here are some of the most common nursing diagnoses relevant to patients with MI:

Acute Pain: Cardiac chest pain, or angina, is a hallmark symptom of MI, resulting from myocardial ischemia. This pain can be severe and distressing, often described as crushing, squeezing, or pressure-like.
Activity Intolerance: Myocardial damage reduces the heart’s pumping efficiency, leading to decreased cardiac output and oxygen supply to meet metabolic demands during activity. This results in fatigue, dyspnea, and weakness with exertion.
Fear/Anxiety: The sudden onset of chest pain, coupled with the life-threatening nature of MI, understandably induces significant fear and anxiety in patients and their families. Fear of death, uncertainty about the future, and the unfamiliar hospital environment contribute to this emotional distress.
Risk for Decreased Cardiac Output: Damage to the myocardium directly impairs the heart’s ability to pump effectively, leading to reduced cardiac output. Arrhythmias, structural damage, and cardiogenic shock can further compromise cardiac function.
Risk for Ineffective Tissue Perfusion (Cardiac, Peripheral, Cerebral): Reduced cardiac output and potential thrombus formation can compromise tissue perfusion. Cardiac tissue perfusion is directly affected by the MI, while peripheral and cerebral perfusion may be compromised due to decreased systemic circulation.
Risk for Excess Fluid Volume: Heart failure, a potential complication of MI, can lead to fluid retention. Reduced cardiac output and compensatory mechanisms like the renin-angiotensin-aldosterone system contribute to sodium and water retention, increasing the risk of fluid overload.
Deficient Knowledge: Patients often lack adequate understanding of MI, its causes, risk factors, treatment, and necessary lifestyle modifications for secondary prevention. This knowledge deficit can hinder adherence to treatment plans and lifestyle changes post-discharge.

Alt text: Gross pathology specimen of a heart showing myocardial infarction in the left ventricle and interventricular septum, with left ventricular hypertrophy indicated by an asterisk.

Causes of Myocardial Infarction

The primary cause of acute myocardial infarction is a significant reduction in coronary blood flow, leading to a critical imbalance between myocardial oxygen supply and demand. This ischemia occurs when the heart muscle does not receive enough oxygen-rich blood. The most frequent underlying cause is the rupture of atherosclerotic plaques in coronary arteries. This rupture triggers thrombus formation, acutely obstructing blood flow.

While atherosclerosis is the predominant etiology, other less common causes include:

Coronary Artery Embolism: Emboli originating from other parts of the body can lodge in coronary arteries, causing sudden blockage. This accounts for a small percentage of MI cases. ⁴,⁵
Cocaine-Induced Ischemia: Cocaine use can induce coronary vasospasm and increase myocardial oxygen demand, leading to ischemia and MI, especially in younger individuals.
Coronary Artery Dissection: A tear in the inner layer of a coronary artery can restrict blood flow and cause MI. This is less common but can occur spontaneously or be associated with certain conditions.
Coronary Vasospasm: Spasm of coronary arteries can temporarily but severely reduce blood flow, causing angina and potentially MI, even in the absence of significant atherosclerosis.

Risk Factors for Myocardial Infarction

Atherosclerosis is the major underlying pathology in approximately 70% of fatal MI events. Consequently, risk factors for atherosclerosis are also primary risk factors for MI. Notably, modifiable risk factors are responsible for a vast majority of myocardial infarctions – around 90% in men and 94% in women.

Modifiable Risk Factors:

Cigarette Smoking: Smoking significantly damages blood vessels, promotes plaque formation, and increases the risk of thrombosis.
Physical Inactivity: Lack of regular exercise contributes to obesity, hypertension, and dyslipidemia, all of which increase atherosclerosis risk.
Hypertension: High blood pressure puts excessive strain on arteries, accelerating atherosclerotic processes and increasing the risk of plaque rupture.
Obesity: Excess body weight, particularly abdominal obesity, is linked to insulin resistance, dyslipidemia, and hypertension, thereby increasing MI risk.
Dyslipidemia: Elevated total cholesterol, LDL cholesterol, and triglycerides, along with low HDL cholesterol, are major contributors to atherosclerosis.

Non-Modifiable Risk Factors:

Age: The risk of MI increases significantly with age as atherosclerosis progresses over time.
Sex: Men generally have a higher risk of MI at younger ages than women. However, after menopause, women’s risk increases and eventually becomes comparable to men’s.
Family History: A family history of premature coronary artery disease indicates a genetic predisposition to atherosclerosis and MI. ⁶,⁷

Assessment of Myocardial Infarction

The clinical presentation of acute myocardial infarction can vary widely. A thorough history and physical examination are essential, although findings can be inconsistent. The history should focus on the characteristics of the chest pain, including onset, quality, location, radiation, and associated symptoms. Diaphoresis (sweating) and bilateral arm pain radiating from the chest are strongly associated with MI, particularly in men.

Common Associated Symptoms:

Lightheadedness or dizziness
Anxiety or a sense of impending doom
Cough
Choking sensation
Diaphoresis (sweating)
Wheezing
Irregular heart rate or palpitations

Physical Examination Findings:

The physical exam should focus on vital signs, general appearance (noting diaphoresis), lung sounds, and cardiac auscultation.

Heart Rate: May be tachycardic (rapid), bradycardic (slow), or reveal arrhythmias like atrial fibrillation or ventricular arrhythmias.
Pulses: Unequal pulses may suggest aortic dissection, a differential diagnosis.
Blood Pressure: Usually elevated initially, but hypotension (low blood pressure) may be present in cases of cardiogenic shock.
Respiratory Rate: Tachypnea (rapid breathing) is common. Fever is not typical of uncomplicated MI and may suggest other conditions.
Neck Veins: Distended neck veins may indicate right ventricular failure, often associated with inferior MI.
Cardiac Auscultation: Possible findings include lateral displacement of the apical impulse, soft S1 heart sound, palpable S4 heart sound, or a new mitral regurgitation murmur. A loud holosystolic murmur radiating to the sternum may indicate ventricular septal rupture, a serious complication.
Lung Auscultation: Wheezing and rales (crackles) may be present if pulmonary edema has developed secondary to heart failure.
Extremities: May be cool, clammy, and exhibit cyanosis (bluish discoloration) or edema (swelling).

Evaluation and Diagnostic Tests

Prompt and rapid 12-lead electrocardiogram (ECG) testing is crucial for all patients presenting with chest pain or symptoms suggestive of MI. It’s important to note that women, elderly patients, and individuals with diabetes may present with atypical symptoms. Women may experience abdominal pain, dizziness, or fatigue rather than classic chest pain. Elderly patients may primarily present with shortness of breath. Any of these presentations should prompt immediate ECG evaluation. ⁸,⁹,¹⁰

Electrocardiogram (ECG):

The ECG is highly specific for MI, particularly STEMI (95% to 97%), but less sensitive (approximately 30%). Repeat ECGs and the use of right-sided and posterior leads can improve sensitivity. “Hyperacute T waves,” peaked T waves on ECG, are often an early sign of ischemia and can precede ST-segment elevation.

STEMI Diagnosis: ST-segment elevation greater than 2 mm in two contiguous leads is highly indicative of STEMI. The location of ST elevation helps identify the affected coronary artery and myocardial region (inferior: leads II, III, aVF; septal: V1, V2; anterior: V3, V4; lateral: I, aVL, V5, V6). Reciprocal ST depressions in opposite anatomical regions are also frequently observed.

ECG Challenges: Diagnosing STEMI via ECG can be challenging in patients with pre-existing left bundle branch block (LBBB) or pacemakers. Sgarbosa criteria are used to aid in STEMI diagnosis in these complex cases. Isolated ST elevation in lead aVR in the appropriate clinical context can indicate left main coronary artery occlusion, a high-risk condition. Wellens’ waves, deeply biphasic T waves in leads V2 and V3, are predictive of proximal left anterior descending artery occlusion, which can lead to extensive anterior wall MI.

NSTEMI Diagnosis: Patients with NSTEMI may not have ST-segment elevation. ECG findings in NSTEMI can be subtle, including ST-segment depressions, T-wave inversions, or may even be normal. Serial ECGs are helpful to detect dynamic changes. Clinical decision tools like the HEART score, incorporating clinical suspicion, risk factors, ECG findings, and troponin levels, assist in risk stratification for NSTEMI.

Cardiac Biomarkers:

Cardiac Troponins: Cardiac troponins are the preferred and most specific biomarkers for myocardial injury. Elevated troponin levels, particularly in serial measurements, are crucial for diagnosing MI, especially NSTEMI, where ECG changes may be non-diagnostic.

Other Laboratory Tests:

Complete Blood Count (CBC): To assess overall hematologic status.
Lipid Profile: To evaluate modifiable risk factors for atherosclerosis.
Renal Function Tests: To assess baseline renal function, important for medication management and contrast use during procedures.
Metabolic Panel: To evaluate electrolytes and glucose levels, providing a general metabolic assessment.

Medical Management of Myocardial Infarction

Immediate medical management is critical in both STEMI and NSTEMI.

Initial Management (STEMI and NSTEMI):

Aspirin: Immediately administer chewable aspirin (160-325 mg) to inhibit platelet aggregation and thrombus propagation.
Intravenous Access: Establish intravenous access for medication administration.
Oxygen Supplementation: Administer supplemental oxygen if oxygen saturation is below 91%.
Pain Management: Opioids (e.g., morphine) can be used for pain relief if needed, in addition to sublingual nitroglycerin, provided blood pressure is adequate. ¹¹,¹²,¹³

STEMI-Specific Treatment:

Reperfusion Therapy: Immediate reperfusion is the cornerstone of STEMI treatment.
- Percutaneous Coronary Intervention (PCI): Emergent PCI is the preferred reperfusion strategy if available within 90 minutes of STEMI diagnosis. Prior to PCI, patients receive dual antiplatelet therapy (aspirin and a P2Y12 inhibitor like ticagrelor) and intravenous heparin infusion. Glycoprotein IIb/IIIa inhibitors or direct thrombin inhibitors may be administered during PCI.
- Fibrinolytic Therapy: If PCI cannot be performed within 90 minutes, intravenous thrombolytic agents (e.g., alteplase, tenecteplase) should be administered to dissolve the thrombus and restore blood flow. Fibrinolysis should ideally be initiated within 120 minutes of symptom onset.

NSTEMI-Specific Treatment:

Medical Management: Stable NSTEMI patients without ongoing symptoms may be initially managed medically with antiplatelet agents and anticoagulants.
PCI: PCI is typically performed within 24-48 hours of admission for NSTEMI patients and can improve in-hospital mortality and reduce length of stay. Emergent PCI is indicated for NSTEMI patients with refractory ischemia, hemodynamic instability, or electrical instability.

Discharge Medications:

Upon discharge after MI, patients are typically prescribed a combination of medications for secondary prevention:

Aspirin: For long-term antiplatelet therapy.
High-Dose Statin: To lower cholesterol levels and stabilize atherosclerotic plaques.
Beta-Blocker: To reduce myocardial workload, heart rate, and blood pressure.
ACE Inhibitor or ARB: Especially for patients with heart failure, hypertension, or diabetes, to improve ventricular remodeling and reduce mortality.

PCI, if planned, should ideally be performed within 12 hours of symptom onset. Fibrinolytic therapy, if chosen, should be administered within 120 minutes. Parenteral anticoagulation, in addition to antiplatelet therapy, is recommended for all MI patients.

Nursing Management of Myocardial Infarction

Nursing care is integral to the management of patients with MI, focusing on monitoring, symptom management, and patient education. Based on the nursing diagnoses identified, key nursing interventions include:

ECG Monitoring: Obtain a 12-lead ECG daily and with any changes in patient condition, to detect arrhythmias, ischemia, or re-infarction.
Intravenous Access: Ensure two large-bore IV lines are in place for rapid medication and fluid administration.
Cardiac Enzyme Monitoring: Monitor serial cardiac enzyme levels (troponins) to assess myocardial damage.
Initiate Acute MI Protocols: Promptly implement established protocols for acute MI management, including medication administration and reperfusion strategies.
Pain Management: Administer pain medications as ordered, such as morphine, and monitor pain relief and side effects.
Nitroglycerin Administration: Administer sublingual nitroglycerin (0.4 mg) as ordered for angina, monitoring blood pressure closely.
Oxygen Therapy: Provide supplemental oxygen if pulse oximetry is less than 94% on room air, and monitor oxygen saturation.
Cardiologist Consultation: Ensure timely consultation with a cardiologist for specialized management and treatment decisions.
Vital Signs and Hemodynamic Monitoring: Monitor vital signs (heart rate, blood pressure, respiratory rate, temperature), daily weight, and urine output to assess hemodynamic stability and fluid balance.
Anticoagulation Administration: Administer heparin or other anticoagulants as ordered, particularly for STEMI patients, and monitor for bleeding complications.
Post-Cardiac Catheterization Care: If the patient undergoes cardiac catheterization or PCI, meticulously check the groin or radial artery access site for hematoma formation and assess distal pulses in the affected limb.

Alt text: Infographic illustrating myocardial infarction warning signs in women, emphasizing atypical symptoms like shortness of breath, nausea, and back or jaw pain, from the U.S. Department of Health and Human Services Office on Women’s Health.

When to Seek Immediate Medical Help

Educating patients on when to seek immediate medical attention is crucial for improving outcomes in MI. Patients should be instructed to seek help for the following:

Persistent Hypotension (low blood pressure)
Nausea and Vomiting, especially if new or worsening with chest pain
Continuing or Worsening Chest Pain, despite rest or nitroglycerin
Loss of Distal Leg Pulses, suggesting embolization or severe circulatory compromise
Sudden Change in Mental Status, indicating decreased cerebral perfusion
Continuing Oxygen Desaturation (low oxygen levels)
New Onset Tachycardia or Arrhythmias (rapid or irregular heartbeats)
Sudden Onset of a Loud Heart Murmur, which could indicate new mitral regurgitation or ventricular rupture.

Outcome Identification and Goals of Nursing Care

The primary goals of nursing care for patients with MI are focused on improving physiological stability and promoting recovery. Expected outcomes include:

Improved Breathing Pattern and Respiratory Function
Relief of Chest Pain and Angina
Improved Tissue Perfusion and Hemodynamic Stability
Patient Able to Regain Pre-MI Functional Status to the Extent Possible

Monitoring and Ongoing Assessment

Continuous monitoring is essential to detect complications and evaluate treatment effectiveness. Key monitoring parameters include:

ECG Monitoring: Continuous ECG monitoring for arrhythmias and ischemic changes.
Cardiac Enzyme Levels: Serial measurements of cardiac troponins to track myocardial damage.
Oxygenation Status: Pulse oximetry to monitor oxygen saturation.
Vital Signs: Frequent monitoring of heart rate, blood pressure, respiratory rate.
Pain Assessment: Regular assessment of chest pain intensity, characteristics, and response to interventions.
Peripheral Vascular Assessment: Palpation of leg pulses to assess peripheral perfusion.
Auscultation: Auscultation of the chest for rales (crackles) indicating pulmonary edema and for new heart murmurs suggesting valvular dysfunction or structural complications.

Coordination of Interprofessional Care

Optimal management of acute myocardial infarction necessitates a collaborative, interprofessional team approach. This team typically includes:

Cardiologist: The lead physician, guiding overall management, reperfusion strategies, and long-term planning.
Cardiac Surgeon: For potential surgical interventions, such as coronary artery bypass grafting (CABG) in select cases.
Interventional Cardiologist: Performs PCI procedures.
Intensivist or Critical Care Physician: Manages critically ill patients, particularly those with complications like cardiogenic shock.
Cardiac Rehabilitation Specialist: Develops and implements cardiac rehabilitation programs post-MI.
Critical Care or Cardiology Nurses: Provide specialized nursing care, monitoring, and medication administration.
Pharmacist: Reviews medications, ensures appropriate dosing, checks for drug interactions, and provides patient education on medications. [Level 5]
Physical Therapist: Assists with early mobilization and functional recovery.
Social Worker: Facilitates discharge planning, home care arrangements, cardiac rehabilitation enrollment, and connects patients with support services.

Nursing Role in Coordination of Care:

Nurses are central to coordinating care, especially in the acute phase. Key nursing responsibilities include:

Early Recognition and Triage: Rapidly identify patients with MI symptoms at triage and communicate urgently with the interprofessional team.
Time-Sensitive Interventions: Ensure timely implementation of reperfusion strategies (PCI or fibrinolysis).
ICU Monitoring: Provide vigilant monitoring in the intensive care unit (ICU) for early detection and management of life-threatening complications.
Communication and Collaboration: Maintain clear and consistent communication with all team members regarding patient status, changes, and needs.
Patient and Family Education: Provide comprehensive education to patients and families about MI, treatment, medications, risk factor modification, and cardiac rehabilitation.
Discharge Planning: Collaborate with the team to ensure safe and effective discharge planning, including medication reconciliation, follow-up appointments, and referral to cardiac rehabilitation.

Pharmacist’s Role: Pharmacists play a crucial role in medication management, ensuring appropriate drug selection, dosing, and identifying potential drug interactions. They also provide essential patient education regarding medications, enhancing medication adherence. [Level 2]

Outcomes and Prognosis

Despite advances in treatment, acute myocardial infarction continues to have a significant mortality rate. A substantial proportion of patients die before reaching the hospital, and a further percentage die upon arrival or within the first year post-MI. Readmission rates within the first year are also high. Prognosis is influenced by factors such as ejection fraction (a measure of heart pumping function), patient age, and co-existing medical conditions. Patients who undergo timely revascularization (PCI or CABG) generally have better outcomes than those who do not. The most favorable prognosis is associated with early and successful reperfusion and preservation of left ventricular function. ¹⁷,¹⁸,¹⁹ [Level 2]

Health Teaching and Health Promotion

Patient education is paramount for long-term management and secondary prevention of MI. Key areas for health teaching include:

Healthy Diet: Emphasize a heart-healthy, low-salt diet rich in fruits, vegetables, and whole grains, and low in saturated and trans fats.
Medication Adherence: Stress the importance of taking prescribed medications as directed, including aspirin, statins, beta-blockers, and ACE inhibitors.
Weight Management: Encourage maintaining a healthy body weight through diet and exercise.
Physical Activity and Cardiac Rehabilitation: Recommend regular physical activity and enrollment in a cardiac rehabilitation program to improve cardiovascular fitness and promote recovery.
Risk Factor Control: Educate on managing blood pressure, blood glucose, and lipid levels through lifestyle modifications and medications.
Smoking Cessation: Strongly advise against smoking and provide resources for smoking cessation.
Regular Follow-up: Emphasize the importance of regular follow-up appointments with their healthcare provider.

Alt text: Electrocardiogram demonstrating Pardee waves indicative of acute myocardial infarction (AMI) in inferior leads II, III, and aVF, with reciprocal changes in anterolateral leads, highlighting ECG interpretation for nurses.

Risk Management Strategies

Effective risk management is crucial for preventing recurrent cardiac events. Key strategies include:

Promptly Report Chest Pain: Instruct patients not to disregard chest pain and to seek immediate medical attention if it occurs.
Vital Sign Monitoring: If vital signs are abnormal, ensure prompt referral to a cardiologist.
Laboratory Monitoring: If laboratory parameters are abnormal, consult with a physician immediately for appropriate management.

Discharge Planning Considerations

Comprehensive discharge planning is essential for a smooth transition home and continued recovery. Key elements include:

Reinforce Health Teaching: Reiterate key aspects of health teaching, including diet, medications, activity, and risk factor modification.
Promote Physical Activity: Encourage ambulation and gradual increase in physical activity levels as tolerated.
Medication Management: Ensure patients understand their medication regimen and have prescriptions filled.
Scheduled Follow-up: Arrange follow-up appointments with their cardiologist and primary care provider.
Smoking Cessation Support: Provide continued support and resources for smoking cessation if needed.

Evidence-Based Nursing Practice Issues

Evidence consistently demonstrates that earlier treatment of MI leads to better patient outcomes. Nurses play a vital role in early recognition of symptoms and ensuring timely intervention. Aggressive risk factor reduction is also evidence-based and crucial for improving long-term outcomes after MI.

Review Questions (for self-assessment and learning reinforcement)

(Note: Review questions are for educational purposes and not included in the rewritten article for the target website.)

References

1.Nascimento BR, Brant LCC, Marino BCA, Passaglia LG, Ribeiro ALP. Implementing myocardial infarction systems of care in low/middle-income countries. Heart. 2019 Jan;105(1):20-26. PubMed: 30269080

2.Barberi C, van den Hondel KE. The use of cardiac troponin T (cTnT) in the postmortem diagnosis of acute myocardial infarction and sudden cardiac death: A systematic review. Forensic Sci Int. 2018 Nov;292:27-38. PubMed: 30269044

3.Alaour B, Liew F, Kaier TE. Cardiac Troponin – diagnostic problems and impact on cardiovascular disease. Ann Med. 2018 Dec;50(8):655-665. PubMed: 30265127

4.Massberg S, Polzin A. [Update ESC-Guideline 2017: Dual Antiplatelet Therapy]. Dtsch Med Wochenschr. 2018 Aug;143(15):1090-1093. PubMed: 30060279

5.Scheen AJ. [From atherosclerosis to atherothrombosis : from a silent chronic pathology to an acute critical event]. Rev Med Liege. 2018 May;73(5-6):224-228. PubMed: 29926559

6.Berg DD, Wiviott SD, Braunwald E, Guo J, Im K, Kashani A, Gibson CM, Cannon CP, Morrow DA, Bhatt DL, Mega JL, O’Donoghue ML, Antman EM, Newby LK, Sabatine MS, Giugliano RP. Modes and timing of death in 66 252 patients with non-ST-segment elevation acute coronary syndromes enrolled in 14 TIMI trials. Eur Heart J. 2018 Nov 07;39(42):3810-3820. PMC free article: PMC6220126 PubMed: 30239711

7.Deng D, Liu L, Xu G, Gan J, Shen Y, Shi Y, Zhu R, Lin Y. Epidemiology and Serum Metabolic Characteristics of Acute Myocardial Infarction Patients in Chest Pain Centers. Iran J Public Health. 2018 Jul;47(7):1017-1029. PMC free article: PMC6119561 PubMed: 30182001

8.Haig C, Carrick D, Carberry J, Mangion K, Maznyczka A, Wetherall K, McEntegart M, Petrie MC, Eteiba H, Lindsay M, Hood S, Watkins S, Davie A, Mahrous A, Mordi I, Ahmed N, Teng Yue May V, Ford I, Radjenovic A, Welsh P, Sattar N, Oldroyd KG, Berry C. Current Smoking and Prognosis After Acute ST-Segment Elevation Myocardial Infarction: New Pathophysiological Insights. JACC Cardiovasc Imaging. 2019 Jun;12(6):993-1003. PMC free article: PMC6547246 PubMed: 30031700

9.Alquézar-Arbé A, Sanchís J, Guillén E, Bardají A, Miró Ò, Ordóñez-Llanos J. Cardiac troponin measurement and interpretation in the diagnosis of acute myocardial infarction in the emergency department: a consensus statement. Emergencias. 2018 Oct;30(5):336-349. PubMed: 30260119

10.Perera M, Aggarwal L, Scott IA, Logan B. Received care compared to ADP-guided care of patients admitted to hospital with chest pain of possible cardiac origin. Int J Gen Med. 2018;11:345-351. PMC free article: PMC6128279 PubMed: 30214268

11.Riley RF, Miller CD, Russell GB, Soliman EZ, Hiestand BC, Herrington DM, Mahler SA. Usefulness of Serial 12-Lead Electrocardiograms in Predicting 30-Day Outcomes in Patients With Undifferentiated Chest Pain (the ASAP CATH Study). Am J Cardiol. 2018 Aug 01;122(3):374-380. PubMed: 30196932

12.Jneid H, Addison D, Bhatt DL, Fonarow GC, Gokak S, Grady KL, Green LA, Heidenreich PA, Ho PM, Jurgens CY, King ML, Kumbhani DJ, Pancholy S. 2017 AHA/ACC Clinical Performance and Quality Measures for Adults With ST-Elevation and Non-ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Performance Measures. J Am Coll Cardiol. 2017 Oct 17;70(16):2048-2090. PubMed: 28943066

13.Larson EA, German DM, Shatzel J, DeLoughery TG. Anticoagulation in the cardiac patient: A concise review. Eur J Haematol. 2019 Jan;102(1):3-19. PubMed: 30203452

14.Bath PM, Woodhouse LJ, Appleton JP, Beridze M, Christensen H, Dineen RA, Flaherty K, Duley L, England TJ, Havard D, Heptinstall S, James M, Kasonde C, Krishnan K, Markus HS, Montgomery AA, Pocock S, Randall M, Ranta A, Robinson TG, Scutt P, Venables GS, Sprigg N. Triple versus guideline antiplatelet therapy to prevent recurrence after acute ischaemic stroke or transient ischaemic attack: the TARDIS RCT. Health Technol Assess. 2018 Aug;22(48):1-76. PMC free article: PMC6139477 PubMed: 30179153

15.Adamski P, Adamska U, Ostrowska M, Navarese EP, Kubica J. Evaluating current and emerging antithrombotic therapy currently available for the treatment of acute coronary syndrome in geriatric populations. Expert Opin Pharmacother. 2018 Sep;19(13):1415-1425. PubMed: 30132731

16.Stone GW, Ellis SG, Gori T, Metzger DC, Stein B, Erickson M, Torzewski J, Williams J, Lawson W, Broderick TM, Kabour A, Piegari G, Cavendish J, Bertolet B, Choi JW, Marx SO, Généreux P, Kereiakes DJ., ABSORB IV Investigators. Blinded outcomes and angina assessment of coronary bioresorbable scaffolds: 30-day and 1-year results from the ABSORB IV randomised trial. Lancet. 2018 Oct 27;392(10157):1530-1540. PubMed: 30266412

17.Lopes RD, de Barros E Silva PGM, de Andrade Jesuíno I, Santucci EV, Barbosa LM, Damiani LP, Nakagawa Santos RH, Laranjeira LN, Dall Orto FTC, Beraldo de Andrade P, de Castro Bienert IR, Alexander JH, Granger CB, Berwanger O. Timing of Loading Dose of Atorvastatin in Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndromes: Insights From the SECURE-PCI Randomized Clinical Trial. JAMA Cardiol. 2018 Nov 01;3(11):1113-1118. PMC free article: PMC6583055 PubMed: 30264159

18.Choi AR, Jeong MH, Hong YJ, Sohn SJ, Kook HY, Sim DS, Ahn YK, Lee KH, Cho JY, Kim YJ, Cho MC, Kim CJ., other Korea Acute Myocardial Infarction Registry Investigators. Clinical characteristics and outcomes in acute myocardial infarction patients with versus without any cardiovascular risk factors. Korean J Intern Med. 2019 Sep;34(5):1040-1049. PMC free article: PMC6718753 PubMed: 30257551

19.Piotrowicz R, Wolszakiewicz J. Cardiac rehabilitation following myocardial infarction. Cardiol J. 2008;15(5):481-7. PubMed: 18810728

20.Ruano-Ravina A, Pena-Gil C, Abu-Assi E, Raposeiras S, van ‘t Hof A, Meindersma E, Bossano Prescott EI, González-Juanatey JR. Participation and adherence to cardiac rehabilitation programs. A systematic review. Int J Cardiol. 2016 Nov 15;223:436-443. PubMed: 27557484

21.Contractor AS. Cardiac rehabilitation after myocardial infarction. J Assoc Physicians India. 2011 Dec;59 Suppl:51-5. PubMed: 22624283

22.Sjölin I, Bäck M, Nilsson L, Schiopu A, Leosdottir M. Association between attending exercise-based cardiac rehabilitation and cardiovascular risk factors at one-year post myocardial infarction. PLoS One. 2020;15(5):e0232772. PMC free article: PMC7213725 PubMed: 32392231

23.Aeyels D, Seys D, Sinnaeve PR, Claeys MJ, Gevaert S, Schoors D, Sermeus W, Panella M, Bruyneel L, Vanhaecht K. Managing in-hospital quality improvement: An importance-performance analysis to set priorities for ST-elevation myocardial infarction care. Eur J Cardiovasc Nurs. 2018 Aug;17(6):535-542. PubMed: 29448818

24.Schwaab B. [Cardiac Rehabilitation]. Rehabilitation (Stuttg). 2018 Apr;57(2):117-126. PubMed: 29216666

25.El Hajj MS, Jaam MJ, Awaisu A. Effect of pharmacist care on medication adherence and cardiovascular outcomes among patients post-acute coronary syndrome: A systematic review. Res Social Adm Pharm. 2018 Jun;14(6):507-520. PubMed: 28641999

Disclosure: Oren Mechanic declares no relevant financial relationships with ineligible companies.

Disclosure: Michael Gavin declares no relevant financial relationships with ineligible companies.

Disclosure: Shamai Grossman declares no relevant financial relationships with ineligible companies.

Disclosure: Kim Ziegler declares no relevant financial relationships with ineligible companies.

Alt text: Thumbnail image representing a figure, likely a Transesophageal Echocardiography showing a condition mimicking myocardial infarction, in a patient with pulmonary embolism, used for visual break and content relevance.