3. Current evidence shows that the steps leading up to MI begin with atherosclerotic changes of the coronary arterties, known as coronary artery disease (CAD; Elendu et al., 2023; Paulino, 2024). Deposits of lipids and cholesterol, known as plaque, accumulate within the layers of the vessel walls.
4. Etiology
5. Men are slightly more likely to report chest pain as their chief complaint versus women.
6. Men are more likely to be diaphoretic than wormen.
7. Women report more nausea, vomiting, shortness of breath, fear of dying, and pain in neck/jaw compared to men.
8. Diagnostics & Tests
9. speeds up plaque accumulation in coronary arteries
10. changes inflammatory response
11. cellular damage from oxidative stress
12. The longer time it takes to establish reperfusion, the more myocardium is sacrificed. It is imperative that reperfusion is achieved with careful consideration in order to avoid reperfusion injuries.
13. Cardiomyocyte injury triggers a cascade of cellular responses that lead to inflammation. Cytokines, such as interleukin 1 and TNF-a, along with immue cells, flood the area, leading to greater tissue damage (Paulino, 2024). https://pubmed.ncbi.nlm.nih.gov/38395114/
14. Prolonged myocardial ischemia progresses to myocyte death, known as infarction.
15. The sudden occlusion of blood flow causes myocardial ischemia. Mitochondria within the cardiomyocytes are unable to produce ATP effectively; anaerobic metabolism leads to increase in intracellular ROS production.
16. The spilling of plaque contents is the catalyst for a cascade of events that lead to thrombus formation. As the forms, it quickly grows to block the artery.
17. As the encapsulated plaque gows, it becomes increasing unstable and vulnerable to rupture.
18. Pathophysiology (Elendu et al., 2023) https://pmc.ncbi.nlm.nih.gov/articles/PMC10615529/
19. Complications
20. Patient Education
21. Dyslipidemia
22. Smoking Tobacco (Parmar et al., 2023) https://pmc.ncbi.nlm.nih.gov/articles/PMC10208588/
23. Hypertension
24. Gender
25. Genetic Predisposition
26. Age
27. Cardiac biomarkers, such as troponin I and creatine kinase MB (CK-MB) increase in the circulating blood. Elevated troponin is seen as soon as three hours after infarct; CK-MB begins to increase at hour six (Elenud et al., 2023; Hjort et al., 2023; Paulino, 2024) https://pubmed.ncbi.nlm.nih.gov/36565198/
28. Stressors
29. elevated emotional/physical stress is commonly reported in the days leading up to MI; more research is needed to understand the mechanism of stress triggering MI (Chan et al., 2023) https://www.ajconline.org/action/showPdf?pii=S0002-9149%2823%2900616-1
30. According to Shulte and Mayrovitz (2023), 70% of MIs occur in males and at a younger age compared to females. https://pmc.ncbi.nlm.nih.gov/articles/PMC10182740/
31. Abberant serum lipid levels are linke(d to plaque deposits within coronary atery walls (Alloubani et al., 2021). Nitric oxide levels are altered by elevated LDL, causing endothelial damage (Paulino, 2024). https://pmc.ncbi.nlm.nih.gov/articles/PMC8950504/ https://pubmed.ncbi.nlm.nih.gov/38395114/
32. At least 28 genes have been identified to predict a predisposition for MI (Tirdea et al., 2022) https://pmc.ncbi.nlm.nih.gov/articles/PMC9738549/
33. Cardiac and immune changes that occur with age make the elderly more vulnerable to MI (Appel et al., 2021). https://www.sciencedirect.com/science/article/pii/S2468867320301115?ref=pdf_download&fr=RR-2&rr=921832ea59d26175
34. There is a notable difference between the genders and the symptoms they report experiencing leading up to and during MI. Both genders report chest pain/pressure upon arrival at the clinical setting (Dekleva et al., 2024; Schulte & Mayrovitz, 2023) https://pubmed.ncbi.nlm.nih.gov/39685777/ https://pmc.ncbi.nlm.nih.gov/articles/PMC10182740/
35. Chronic increases mechanical stress on vasculature and compromises integrity of endothelium (Konstantinou et al., 2019). Paulino (2024) reports that lipid metabolism is altered in hypertensive individuals. https://pmc.ncbi.nlm.nih.gov/articles/PMC8030564/ https://pubmed.ncbi.nlm.nih.gov/38395114/
36. Reperfusion Injury
37. Paradoxical outcome of reperfusion in which inflammation proliferates myocardial damage following successful reperfusion, sometimes contributing to half of the final area of infarct (Sanchez-Hernandez et al., 2020).
38. Oxygen
39. Meidcations
40. Increase available oxygen which reduces patient's effort during event
41. Opioids for pain management during event (Sanchez-Hernandez et al., 2020).
42. Heparin to prevent the formation of additional clots (Elendu et al., 2023)
43. Cardiac Catheterization
44. Aspirin with either clopidogrel, ticagrelor, or prasurgrel to prevent platelet aggregation in vessels as well as on any stents that may be placed (Elendu et al., 2023; Sanchez-Hernandez et al., 2020).
45. Percutaneous Coronary Intervention (PCI) to physically remove the blockage (Elendu et al., 2023)
46. Angiontensin Converting Enzyme (Ace) Inhibitors mitigate ventricular remodeling and reduce risk of heart failure (Elendu et al., 2023)
47. Surgical Intervention
48. Coronary Artery Bypass Grafting (CABG) is done when other interventions, such as PCI, are not viable for the patient and the severity of the case. It is also used when there is elevated risk for serious complications (Shi & Smith, 2018). According to Shi and Smith (2018), the procedure bypasses occluded vessels and restores cardiac bloodflow by gratfting in vessels harvested from elsewhere.
49. Beta-Blockers to prevent arrhythmias and reduce strain on infarct by lowering heart rate, reducing blood pressure, and decreasing the demand for oxygen (Elendu et al., 2023)
50. Thrombolytic drugs such as tissue plasminoge activator (TPA) when PCI is not available; dissolve the obstructing clot (Elendu et al., 2023; Sanchez-Hernandez et al., 2020).
51. Cardiogenic Shock
52. Systemic loss of perfusion leading to multi-organ failure; occurs in 5-10% of MI patients; high mortality rate (Samsky et al., 2021)
53. Arrhythmias
54. Ventricular Remodeling
55. As the LV is affected, the inflammatory response leads to remodeling of the ventricular tissue. Ventricular hypertrophy results which often leads to congestive heart failure (Elendu et al., 2023)
56. Result from remodeling of cardiac tissue (Elendu et al., 2023)
57. Providers should stress the importance of lifestyle changes, including making better dietary choices, increasing activity level, smoking cessation. It has been found that dedication to cardiac rehabilitation programs greatly improves prognosis and mitigates recurrences (Brust et al., 2024; Elendu et al., 2023) According to Brust et al. (2024), it is best to provide education at varying opportune times during all phases of their cardiac care recovery versus all at once prior to discharge from inpatient care.
58. Typically, infarction affects the left ventrical (LV). This is due to the nature of cardiac vasculature. According to Paulino (2024), the most commonly occluded coronary artery is the left coronary artery (LAC), followed by the right (RCA), and then the circumflex branch. Most of the left ventricle is perfused downstream of the LCA. Occlusion of the RCA causes infarct of the posterior aspect of the LV. Finally, the damage from circumflex occlusion appears on the lateral aspect of the LV wall. https://pubmed.ncbi.nlm.nih.gov/38395114/
59. Treatments
60. Commonly known as a "heart attack".
61. Myocardial infartction (MI) is one of the leading causes of death globally (Elendu et al., 2023; Paulino, 2024). MI occurs when blood flow to myocardial tissue is obstructed leading to prolonged localized myocardial ischemia. This anoxic state leads to myocyte damage and death. The area of injury is known as an infarct. MI arises from coronary artery disease caused by one or a combination of many etiologies. Rapid diagnosis of MI quickly after onset of symtpoms helps salvage the greatest amount of cardiac tissue and preserver as much cardiac function as possible. Several complications can follow MI, including death. Current treatments range from pharmacological to physical therapy and lifestyle changes. Patient education remains critical in managing after MI to prevent recurrence and other cardiovascular and related pathology.
62. Electrocardiogram is the first-line non-invasive standard for determining cardiac ischemic changes (Chow et al., 2021; Elendu et al., 2023). This test also determines if there is ST-segment elevation, which helps guide clinical decision-making (Elendu et al., 2023).
63. Cardiac biomarkers found at elevated levels in the blood are reliable indicators of cardiac tissue inflammation (Hjort el al., 2023)
63.1. Troponin >99% of upper limit; approximately 3 standard deviations above mean normal value (Kott et al., 2022)
63.2. pro-B-type natriuretic peptide (NT-proBNP): Rule out: <300 ng/L; Rule in: age < 50; >450 ng/L; Rule in: age 50–75; >900 ng/L; Rule in: age > 75; >1800 ng/L (Kott et al., 2022)
63.3. creatine kinase-MB (CK-MB); (ratio of CK-MB:CK)100 is =/>2.5%, MI likely (Wu et al., 2020)
