Coronary Artery Disease (CAD)

• Coronary Artery Disease (CAD), also known as ISCHEMIC heart disease, narrows coronary arteries and increases the risk of angina and heart attacks.
• Heart disease is the 2nd leading cause of death in Canada.
• Approximately 1 in 12 Canadians have diagnosed heart disease.
• Underlying risk factors for CAD include:
• High blood pressure
• High blood sugars (diabetes)
• High cholesterol
• Smoking
• Ischemia is a restriction in blood supply, leading to a shortage of oxygen for cellular metabolism.
• Myocardial ischemia can result from:
• Coronary spasm
• Hypotension
• Dysrhythmias
• Decreased oxygen-carrying capacity of the blood (anemia)
• Myocardial cells become ischemic within 10 seconds of occlusion, altering aerobic metabolism and leading to anaerobic takeover and lactic acid accumulation.
• After several minutes, heart cells lose the ability to contract, which decreases cardiac output.
• Cardiac cells remain viable for 20 minutes under ischemic conditions.
• Time is muscle; rapid oxygen delivery is crucial.
• Multiple factors contribute to cardiac crime scenes.
• Pipe Problem: Atherosclerosis and plaque rupture.
• Inflammation
• Clotting cascade activation
• Endothelial remodeling.
• Problem: A clot obstructs coronary circulation.
• Not enough blood (hypovolemic shock).

Angina Pectoris

• It is a mismatch between myocardial demand for oxygen and supply.
• Normal function involves coronary blood flow increasing or decreasing through vasodilation or constriction.
• Healthy vessels dilate to increase blood flow when demand increases (exercise).
• Atherosclerosis in coronary arteries causes narrowing and decreased compliance, reducing the ability to adjust blood flow.
• Blood flow is impaired when coronary arteries narrow by 50%, compromising cellular metabolism when energy demand increases.
• Narrowing results from plaque formation, which can occlude the vessel lumen and limit coronary flow, resulting in coronary ischemia, especially during exercise.
• Ischemic heart cells send chemical messengers, causing chest pain.
• Evidence indicates this process also occurs in coronary arteries.

Types of Angina

Printzmetal's Variant Angina

• Unpredictable, can occur at rest.
• Results from vasospasm of one or more coronary arteries.
• Can happen with or without atherosclerosis.
• Causes sudden onset of sharp pain.

Stable Angina

• Caused by narrowing of coronary arteries due to atherosclerosis (plaques).
• Coronary arteries are unable to dilate due to atherosclerosis +/- inflammation.
• It is predictable, typically triggered with increased activity, and subsides at rest.
• Ranges from discomfort, tightness, heaviness, or pressure to severe pain.
• Women may present differently with feelings of unease, fatigue, and palpitations.
• Relieved with rest (decreased oxygen demand) and nitrates (vasodilators).

Silent Angina

• Mental stress-induced ischemia.
• Asymptomatic.
• Chronic stress causes a chronic inflammatory response, elevating inflammatory cytokines + hypercoagulability.
• Angina is a warning sign of myocardial ischemia.
• Chest pain may occur in different patterns, with gradual luminal narrowing/hardening or vasospasm at rest, but it can also be asymptomatic due to nerve dysfunction.

Angina Treatment and Interventions

• Aim to reduce cardiac demand.
• Rest, stop activity, or sit down.
• Keep calm.
• Aim to improve blood flow to the heart.
• Nitroglycerin spray/tab causes vasodilation.
  • Be aware of what is going to happen to blood presssure
  • Up to 3 doses can be given, 5 minutes apart.
• Remember that stable angina can become unstable quickly.
• Ruptured plaque = clot = occlusion.

Serious Crimes of the Heart: Spectrum of Acute Ischemic Events

• Unstable angina
• Non-ST Elevation Myocardial Infarction (non-STEMI)
• ST Elevation Myocardial Infarction (STEMI)

Unstable Angina

• Symptoms happen at rest and last longer than 20 minutes.
• New onset of exertion angina.
• Recent worsening of angina, happening more often and being more severe.
• Typically caused by atherosclerotic plaque disruption and activation of the inflammatory response.
• Ischemic stress can be seen on ECGs, but troponins are typically not elevated.
• Unstable angina is a warning sign of an impending myocardial infarction (heart attack).

Myocardial Infarction (MI)

• It is prolonged ischemia causing irreversible damage to heart muscle cells.
• CAD, myocardial ischemia and myocardial infarction (MI) form a pathological continuum that impairs the pumping ability of the heart.
• Heart muscle is deprived of blood nutrients and oxygen, causing persistent ischemia or complete occlusion, leading to acute coronary syndrome or MI.
• Part of a plaque is disturbed and activates the inflammatory response, leading to clot formation = occlusion.
• Rapid onset, and symptoms do not dissipate on their own.
• Size and location of the infarct determine the degree of damage.
• Atherosclerosis is the most common cause!
• Thrombus from an atheroma blocking the artery with inflammation involved.

Inflammatory Response Evidence

• Shearing forces (BP) can tear off the thin fibrous cap.
• Atherosclerotic plaque with a lipid-rich core and a thin fibrous cap:
• shear forces, inflammation, apoptosis, macrophage-derived degradative enzymes
• Rupture of plaque
• Thrombus formation over lesion plus vasoconstriction of vessel
• Acute decrease in coronary blood flow
• unstable angina or myocardial infarction
• Plaque core is rich in deposited oxidized LDL and triggers an inflammatory response -> release of inflammatory mediators (chemotaxis of leukocytes) + activation of plasma protein complement systems
• With sudden disruption of plaque these mediators secrete macrophage derived degradative enzymes causing apoptosis of cells at the edges of the lesion increasing injury and mediators
• Exposure of plaque contents activates the clotting cascade which increases platelet activation leading to thrombus forms quickly
• Vessel obstruction is further intensified by release of vasoconstrictors
• Thrombus and constriction = causes partial or complete obstruction of blood.

Timeline of the Crime

• Within 8-10 seconds of decreased blood flow, the myocardium becomes cool and cyanotic.
• Anaerobic metabolism kicks in (not sustainable).
• H+ and lactic acid accumulate rapidly, which suppresses conduction and contractile function (leads to HF).
• O2 deprivation causes electrolyte imbalances, and myocardial cells release catecholamines imbalances in SNS/PNS (irregular HR).
• Inflammatory mediators (pain, clotting, chemotaxis) are released.
• Angiotensinogen II is released in response to decreased blood flow to kidneys, leading to vasoconstriction
• Increasing afterload and increasing workload on the heart
• Irreversible damage to myocytes results if oxygen is not restored within 20 minutes.
• Dying cardiac cells release troponin, which is looked for in the blood of victims.
• ECG changes include ST segment elevation (bad sign) or other notable changes in multiple leads.
• Inflammatory response tries to clean up the mess and Leukocytes infiltrate the area within 24 hours and necrotic tissue is broken down
• Approximately 6 weeks are needed for necrotic tissue to be replaced with scar tissue which can not conduct electrical impulses and not contract OR relax

Degree of damage depends the following factors

• Time: Longer period without blood flow (oxygen) leads to more cardiac cells dying
• Artery blockage: Higher the artery blocked = more distal cells going without oxygen
• Collateral circulation: can help support areas of the heart and reserve some cells
• There is Zone of Infarction or Necrosis, can be hypoxic and can't function
• Hypoxic cells can't progress to cell death if recovered
• Ischemic cells can recover and resume normal functions
• Damage location depends on which artery is blocked

Statistical evidence:

• Reports show that most MYOCARDIAL INFARCTIONS involve all 3 layers of the heart and the majority involve the LEFT VENTRICLE!
• ECG Shows changes to conduction

Suspect: Non-ST Elevated MI

• ECG shows either ST depression or flipped T waves
• Infarction involves myocardium directly below the endocardium
• Partial thickness MI
• Depends on part of the heart to anticipate victim impact

Suspect: ST Elevated Myocardial Infarction 'STEMI'

• Infarction involves myocardium all the way from endocardium to epicardium
• Full wall thickness MI
• Elevations of segment on ECG = tombstone MI
• Has the highest risk of serious complications
• Needs Immediate interventions

Investigative Clues

• Acute Coronary Syndrome (ACS)

Stable Angina

• Increased demand causes discomfort due to stable atherosclerotic plaque without dilating the blood vessels
• Demand ischemia but no infarct
• Normal on EKG and troponins

Unstable Angina

• Plaque ruptures and blocks artery thrombus and angina at rest as well as increases rapidly in a short period of time
• Supply ischemia but no infarct
• May show Inverted T waves, or ST depression along ecg Normal of troponins

NSTEMI

• rupture and partial occlusion as well as causes and infarct to the subendocardial mycardium
• has inverted T waves, or ST depression shows
• Elevated troponins Subendocardial infarct

STEMI

• complete blockage to one of the vessels result a transmurdial injury
• EKG is normal in hyper acute twaves
• elevated in troponin
• transmural infarct

Investigation: Cardiac Biomarkers

• Released substances into blood tissues that are stressed, damaged or dying
• Elevated of troponin shows the possibility that can stay elevated for longer
• New tests can be useful in spotting lower levels Serial troponins are done and blood work a timed increments increases the confidence

Finding the Evidence Faster

• High level testing can pick up even the slighest damage and smaller infarctions AND so it can lead to spotting it sooner.

Cardiac Cell Consequences

• High level of inflammation, and structure and inflammation due to fibrin for the time it is needed(weeks) can result in permanent damage
• Electrolyte pumps need to work properly
• Heart is very high risk
• Hibernating mycardium can protect cardiac cells
• Electrolytes helps reduce the healing proccess.
• cardiac remodeling can be used to help treat or help with long term damage.
• Cardiac Remodeling Includes:
• Angiotension II and inflammatory cytokines
• After years to months following it, helps with loss in contractile function
• There are functional Changes such as altered ventricular compliance, decreased stoke volume, decreased in ejection fraction
• There are also treatments as ACE Inhibitors, Beta Blockers, even new treatments.

Signs and symptoms

• Feeling of presure, heaviness or burning in the chest
• Sudden Shortness of Breath
• Fatigue
• Nausea and indigestion
• Impending doom
• Upper Back and the arm or even Jaw

Investigate Tool

• Used to help see the signs such as heart diseases and arteries and cholesterol

Help Victim by:

• Reduce workload to the heart
• Improve blood Flow
• Lower Cardiac Demand
• Use vasocontrictors or ECG scans to check or relieve stress or blood flow.
• Give the victim oxygen along aspirin to help as well in the body.
• Check EKG Level
• Try to help calm down patient

Complications Post MI

• Deadly heart Rhythms due to ventricular damage
• Cardiogenic Shock Can lead to strokes
• Congestive Heart Fallure
• Necrotic tissue ruptures
• Cardiac/Stroke

Things for Investigation

• What are the consequences of heart damage, Is it possible that this occurs is a re-offense, Is this a common case.

Case Summaries

• Tell me about the heart using the correct terms and information so that the victim has high knowledge in these conditions