Myocardial Infarction and Stroke Flashcards
(33 cards)
What are the 3 layers of tissue that constitute the heart?
- Pericardium:
- Fibrous (outer layer)
- Serous (parietal which is fused to the fibrous layer and then visceral which is closer to the heart) - Myocardium:
- Made up of with cardiomyocytes: striated, branching, centrally located nuclei and intercalated discs - Endocardium:
- Lining of heart made up of endothelial cells
What is myocardial disease>
- Myocardial disease is coronary insufficiency due to atherosclerosis, where the luminal cross-sectional area of the coronary artery is decreased by more than 75%
What are the two manifestations of myocardial disease?
- Angina pectoris: due to gradual occlusion of the coronary artery
- Myocardial infarction: due to sudden occlusion of the coronary artery
What are some risk factors for IHD?
HARD risk factors:
- High levels of blood lipids (e.g. LDL)
- Hypertension (BP > 140/95 mmHg)
- Cigarette smoking
- Diabetes mellitus
- Genetics (influence HDL: LDL levels)
SOFT risk factors:
- Hormonal factors e.g. increased incidence after menopause in women
- Obesity
- Sedentary lifestyle
- Stress
Are hard risk factors for IHD additive or multiplicative?
- Hard risk factors for IHD are multiplicative
e. g. A hypertensive, diabetic smoker has a 20x increased risk of atherosclerosis compared to someone without these risk factors (5 x 2 x 2 = 20)
What are the clinical effects of atherosclerosis?
- Intermittent ischaemic effects
- Angina pectoris (chest pain)
- Intermittent claudation (reduced blood flow to legs)
- Neurological impairment
- Secondary hypertension
What does an atherosclerotic lesion consist of?
- In atheroscleroris the tunica intima (connective tissue layer) becomes thickened and enlarged by an atheroma/atherosclerotic lesion
- Atherosclerotic lesions consist of a fibrous cap (made up of collagen) and a lipid core (synthesised by foam cells)
What are some risk factors for atherosclerotic plaque rupture?
- Thin fibrous cap (decreased collagen synthesis and increased collagen degradation by MMP)
- Large lipid pool
- Decrease in amount of smooth muscle in plaque
- Rupture of an atheroma frees the contents of the atheroma which can cause disease such as MI and stroke by causing emboli
What is a partial occlusion and its symptoms?
- The more mild presentation of IHD, due to a luminal size reduction due to atherosclerosis
- Manifests as transient pectoral angina (particularly due to exertion)
What is the general chronology of atherosclerotic plaque formation?
- Normal artery
- Fatty streak appears due to LDL deposition in lamina intima
- Macrophages are recruited to the area where they form foam cells that deposit more lipids into the lipid core and cause the plaque to progress
- Fibrosis occurs which forms the fibrous cap- making a fibrotic plaque
- The fibrotic plaque continues to accumulate lipids within the lipid core causing more occlusion of the artery (this is typically when clinical events begin to occur)
- Due to MMP degradation of the fibrous cap or excessive lipid core content- the plaque may rupture causing platelet aggregation leading to MI, stoke or peripheral ischemia
What is a complete occlusion and its symptoms?
- Occurs when a previously atherosclerotic vessel becomes completely occluded usually due to the effect of a superposed thrombosis
Symptoms:
- Causes persistent chest pain un-related to cardiac workload
- Also called myocardial infarction when it occurs in the coronary arteries
What are the sequelae of myocardial infarction?
- Sudden death (due to extensive necrosis of cardiac muscle)
- Death within two days (due to shock or heart failure)
- Congestive heart failure resulting in pulmonary oedema (as the heart does not have sufficient capacity to pump blood out of lungs)
- Fibrosis and healing after 6 weeks (normal cardiac muscle is replaced with fibrotic tissue)
- Pericarditis after 6 weeks (acute inflammation within the pericardium causes the pericardium to rub on the heart resulting in a friction rub)
What localisation of myocardial infarctions is most likely to cause a secondary stroke?
- Subendocardial and transmural infarcts can both stimulate thrombosis in the left ventricle which can lead to a thromboembolism that can cause stroke
What are the types of typical arterial occlusions?
- Left anterior descending coronary artery occlusion:
- Causes extensive necrosis in anterior wall of LV and apex of heart
- Most common (50% of MIs) - Right coronary artery occlusion:
- Causes necrosis in posterior wall of LV
- 30% of MIs - Left Circumflex Coronary Artery Occlusion:
- Causes necrosis on lateral wall of LV
- 20% of MIs
What Investigations are done to diagnose MI?
- ECG: a change in ECG recording patterns e.g. a pathological Q wave, can be indicative of injury to the heart
- Troponin blood test: increase in concentration in blood after infarcts due to cell death
- Cardiac Enzymes: Creatinine phosphokinase (CDK), Lactic dehydrogenase (LDH), HDH and SGOT are all elevated after MI
- Blood Lipids: High blood cholesterol and LDL/HDL ratio is indicative of cardiac disease
- Full Blood Examination: Raised neutrophil count (response to necrotic tissue) and also increase in RBC mass (to aid in carrying oxygen to compensate for less effective heart)
- Chest X-Ray
How is ischaemic heart disease managed?
ACUTE:
- Defibrillation
- Fluid replacement (IV saline)
- Pulmonary oedema management (morphine)
- Furosemide (to increase urine output)
- O2 therapy
- Inotropic agents (increase ventricular output)
- Acute coronary thrombolysis (e.g. streptokinase given within 3 hours to treat atherosclerosis of coronary artery)
- Analgesia
- Antiarrthymics: to restore rhythm to heart
LONG TERM:
- Antithrombotic medication e.g. aspirin or warfarin
- Lifestyle changes
- Rehabilitation
What is the likelihood of the most common consequences of stroke?
- 30% of patients survive with no disability
- 30% that survive 1 year will have severe disability (dependent at 6 months)
- 30% die within 1 year
- 5% of survivors per year have a stroke recurrence
- 3% of survivors per year have a MI
What is the respective contribution of ischaemic heart disease and stroke to mortality in Australia?
- IHD is the highest cause of mortality
- Stroke is the second highest cause of mortality (but highest cause of morbidity)
What are the two types of stroke?
- Ischaemic Stroke:
- 80% of strokes
- Occurs when a thrombosis or embolism becomes lodged in a cerebral vessel and occludes the vessel
- All tissues supplied by that vessel or downstream vessels become ischaemic - Haemorrhagic Stroke:
- 20% of strokes
- Due to rupture of cerebral blood vessel resulting in bleeding into the brain
- Has a more severe outcome
What are the causes of ischamic stroke?
- Embolism:
- A clot formed elsewhere e.g. heart or cartotid artery, that travels to the cerebral blood vessels and becomes lodged and occludes the vessel
- Most common cause - Thrombosis:
- A blood clot forms on an atherosclerotic narrowing of a large cerebral artery
What are the causes of hemorrhagic stroke?
- Hypertension (intracranial BP becomes too high)
- Thrombocytopenia (causes excessive bleeding)
- Weakening of the blood vessels:
- Aneurysm
- Arteriovenous malformation
- Cerebral amyloid angiopathy
What are the fundamental aims of stroke management?
- Acute treatment: remove the clot or stop the bleeding
2. Long term: reduce the probability of another stroke occurring
What are the different pathological features that occur due to an ischaemic stroke?
- Ischaemic core:
- The area where blood flow is reduced to <15% of normal, it is the area affecting the territory proximal to the site of the occlusion
- If the occlusion is in place for long enough, there will be irreversible tissue damage and death of cells in this area
- Ischaemic penumbra:
- The area where the blood flow is reduced to between 15%-40% of normal (limited blood flow is still occurring)
- In this area, the tissue is stressed and is on the verge of tissue damage and death
- It is imperative to attempt to rescue the ischaemic penumbra, as the damage to these cells is not irreversible. If blood flow is restored, the penumbra can be prevented from becoming a larger ischaemic core or damaged and dead tissue
How does ischemia cause neuronal injury and cell death?
- When cells are starved of oxygen and glucose they become stressed, when this occurs in neurons they enter a state known as excited toxicity
- This involves: excessive release of glutamate from cells (which can cause neuronal overstimulation and thus neural toxicity)
- Influx of calcium into neurons occurs, causing calcium overload- which causes perturbation of intracellular signalling pathways