Course Content
Cardio-respiratory 1
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TBL: Myocardial infarction

  1. Learning Outcome:


  • Describe the coronary arterial blood supply.


The heart is supplied with oxygenated blood through the coronary arteries, which branch off from the aorta just above the aortic valve. The right coronary artery (RCA) and the left main coronary artery (LMCA) are the two main branches of the coronary arteries.


The RCA supplies blood to the right ventricle, the bottom portion of the left ventricle, and the SA and AV nodes. The LMCA further branches into the left anterior descending (LAD) artery and the left circumflex artery (LCx). The LAD artery supplies blood to the front and side walls of the left ventricle, while the LCx supplies blood to the back of the left ventricle and the left atrium.


The coronary arteries also have smaller branches, known as arterioles, which supply blood to the capillaries within the heart muscle. The capillaries then deliver oxygen and nutrients to the heart muscle cells (myocardium) and remove waste products.

  1. Learning Outcome:


  • Explain the etiopathogenesis of ischemic heart disease including myocardial infarction.


Ischemic heart disease (IHD) is a condition in which the blood supply to the heart is reduced, leading to a decrease in oxygen and nutrient delivery to the heart muscle cells. IHD can lead to myocardial infarction (MI), or a heart attack, which occurs when a portion of the heart muscle dies due to a lack of blood flow.


The etiopathogenesis of IHD and MI involves a complex interplay between genetic, environmental, and lifestyle factors. Risk factors for IHD and MI include age, gender, genetics, high blood pressure, high cholesterol, smoking, obesity, diabetes, and a sedentary lifestyle.


The most common cause of IHD and MI is atherosclerosis, which is the buildup of plaque within the arterial walls. The plaque can narrow the lumen of the artery, reducing blood flow and increasing the risk of complications such as thrombosis and ischemia. Plaque rupture or erosion can lead to the formation of a blood clot, which can completely block blood flow to the heart muscle, leading to an MI.

  1. Learning Outcome:


  • Discuss the clinical significance of time-related changes of cardiac biomarkers in myocardial infarction.


Cardiac biomarkers are proteins that are released into the bloodstream following damage to the heart muscle cells. The most commonly used cardiac biomarkers in the diagnosis of MI are troponin, creatine kinase-MB (CK-MB), and myoglobin.


The clinical significance of time-related changes in cardiac biomarkers in MI lies in their ability to provide information on the timing and extent of myocardial damage. Troponin is the most sensitive and specific biomarker for MI and typically rises within 3-6 hours following an MI. It remains elevated for up to two weeks, allowing for the diagnosis of both acute and chronic MI.


CK-MB rises within 3-6 hours of MI and returns to normal within 48-72 hours, making it useful for diagnosing acute MI. Myoglobin is the earliest biomarker to rise following an MI, but it is not specific to cardiac muscle and can be elevated in other conditions.


The timing and pattern of biomarker elevation can also provide information on the location of the MI within the heart. For example, an elevation in the biomarkers specific to the right ventricle suggests that the MI occurred in the right coronary artery.

  1. Learning Outcome:


  • Describe the morphological changes in the myocardium in acute myocardial infarction.


Acute myocardial infarction (AMI) is characterised by the death of heart muscle cells (myocardium) due to a lack of blood flow. The morphological changes in the myocardium in AMI depend on the timing and extent of the infarction.


In the early stages of AMI, there is swelling and contraction band necrosis of the myocardial cells due to the influx of calcium into the cells. Within 12-24 hours, there is coagulative necrosis, which is characterized by a loss of nuclei and striations in the myocardial cells. Inflammatory cells, including neutrophils and macrophages, infiltrate the area and begin to remove the dead cells.


Over the next few days, granulation tissue forms, consisting of fibroblasts, myofibroblasts, and collagen. This tissue serves as a scaffold for the healing process. Within 1-2 weeks, the necrotic tissue is replaced by fibrous tissue, which can lead to scar formation.


The extent and location of the infarction can determine the functional impairment of the heart. If the infarction is small and confined to a specific region, there may be little functional impairment. However, if the infarction is large and involves a large portion of the heart, it can lead to heart failure and other complications.

  1. Learning Outcome:


  • Explain the pharmacological basis of the therapeutic uses of drugs for the treatment of myocardial infarction.


Drugs are used in the treatment of myocardial infarction to improve blood flow to the heart, reduce pain and discomfort, prevent further clot formation, and manage the risk of complications. Some commonly used drugs include antiplatelet agents, anticoagulants, thrombolytics, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins.


Antiplatelet agents such as aspirin and clopidogrel work by inhibiting the aggregation of platelets, which can reduce the risk of clot formation and further obstruction of blood flow to the heart. Anticoagulants such as heparin and warfarin can also reduce the risk of clot formation by inhibiting blood clotting factors.


Thrombolytic agents such as alteplase and reteplase can help to dissolve blood clots and restore blood flow to the heart. Beta-blockers such as metoprolol and atenolol can reduce the workload on the heart and decrease the risk of further damage to the heart muscle. ACE inhibitors such as lisinopril and enalapril can help to dilate blood vessels and reduce blood pressure, while statins such as atorvastatin and rosuvastatin can reduce cholesterol levels and the risk of further cardiovascular events.


The therapeutic use of these drugs is based on their ability to improve blood flow to the heart, reduce the risk of complications, and improve overall outcomes for patients with myocardial infarction.

  1. Learning Outcome:


  • Briefly discuss the life-threatening complications of myocardial infarction.


Myocardial infarction (MI) can lead to several life-threatening complications, including arrhythmias, heart failure, cardiogenic shock, and cardiac arrest.


Arrhythmias such as ventricular tachycardia and ventricular fibrillation can occur due to the disruption of the normal electrical conduction system of the heart. These arrhythmias can be life-threatening and require immediate medical intervention.


Heart failure can occur when the heart is unable to pump blood effectively due to damage to the heart muscle. This can lead to fluid buildup in the lungs and other tissues, causing difficulty breathing and other symptoms.


Cardiogenic shock can occur when the heart is unable to pump enough blood to meet the body’s needs, leading to a decrease in blood pressure and other symptoms. This can be a life-threatening complication that requires immediate medical attention.


Cardiac arrest can occur when the heart stops beating altogether, leading to a loss of consciousness and cessation of breathing. This is a medical emergency that requires immediate cardiopulmonary resuscitation (CPR) and defibrillation.

  1. Learning Outcome:


  • Describe the concept of early revascularization as a mean to salvage myocardium.


Early revascularization is a strategy used to salvage myocardium in patients with acute myocardial infarction (AMI). The goal of early revascularization is to restore blood flow to the heart as quickly as possible, minimizing the amount of damage to the heart muscle.


Early revascularization can be achieved through two main approaches: percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). PCI involves the use of a catheter to open blocked arteries and restore blood flow to the heart. CABG involves the use of a surgical procedure to bypass blocked arteries and restore blood flow to the heart.


The benefits of early revascularization include a reduction in mortality, a decreased risk of complications such as heart failure and cardiogenic shock, and an improvement in overall outcomes for patients with AMI.

  1. Learning Outcome:


  • Illustrate the role of biological and behavioural factors in the pathogenesis of coronary artery disease.


Coronary artery disease (CAD) is a complex disease with multifactorial causes. Biological factors, including genetics, inflammation, and metabolic disorders, can contribute to the development and progression of CAD. Behavioral factors, including diet, physical activity, and smoking, can also play a significant role.


Genetics can influence the development of CAD by affecting lipid metabolism, inflammation, and blood clotting. Inflammatory disorders such as rheumatoid arthritis and systemic lupus erythematosus have also been associated with an increased risk of CAD.


Metabolic disorders such as diabetes and obesity can also contribute to the development of CAD by promoting insulin resistance and dyslipidemia. Dyslipidemia, characterized by elevated levels of LDL cholesterol and triglycerides and decreased levels of HDL cholesterol, can lead to the buildup of plaque in the arteries.


Behavioral factors such as diet and physical activity can also play a significant role in the development of CAD. A diet high in saturated and trans fats, salt, and sugar can increase the risk of dyslipidemia and inflammation, while a diet high in fruits, vegetables, and whole grains can reduce the risk.


Physical activity can also help to reduce the risk of CAD by promoting weight loss, improving lipid metabolism and blood pressure, and reducing inflammation. Smoking is a major risk factor for CAD, as it can promote inflammation, reduce oxygen delivery to the heart, and increase the risk of blood clots.

  1. Learning Outcome:


  • Prepare an individual and population-level strategy to prevent the onset of coronary artery disease.


Preventing the onset of CAD requires a comprehensive approach that addresses both biological and behavioral factors. At the individual level, strategies can include maintaining a healthy diet, engaging in regular physical activity, quitting smoking, and managing chronic conditions such as diabetes and hypertension.


Population-level strategies can include promoting healthy lifestyle behaviors through public health campaigns, implementing policies to reduce salt and sugar intake, and providing access to healthy food and physical activity options. Screening programs can also be implemented to identify individuals at high risk of CAD, allowing for early intervention and treatment.


Other strategies include the use of medications such as statins and antiplatelet agents to reduce the risk of CAD in high-risk individuals, and the use of cardiac rehabilitation programs to improve outcomes for patients with CAD.


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