Ischemic Heart Disease Flashcards
Distinguish between stable to unstable ischemic heart disease presentations.
• Stable:
o Exertional chest pain (or equivalent) that is chronic
o May be asymptomatic
o Typically seen in outpatient setting
o Pathophysiology:
• Obstructive or non-obstructive coronary artery plaque
• Intact fibrous cap
• Minimal platelet activation or thrombus
• Unstable/ Acute coronary syndrome
o Unstable angina or Non-ST elevation MI or ST elevation MI
o Pathophysiology:
• Obstructive coronary artery plaque
• Plaque rupture or erosion
• Platelet activation, inflammation, and thrombus
Discuss stable ischemic heart disease in terms of clinical presentation & pathophysiology
• Clinical presentation
o Angina pectoris: pain or discomfort in the chest caused by insufficient blood supply to the heart muscle
• Usually brought on by exertion or emotional stress
• Typically lasts 1-15 minutes
• Relieved by rest or nitroglycerin
• Predictable
o Atypical symptoms in special populations: women, diabetics, elderly
• Ex. “silent” ischemia, fatigue, weakness, SOB
• Pathophysiology
o Common: from fixed, obstructive atherosclerotic plaque affecting coronary arteries
o Other: aortic stenosis, hypertrophic cardiomyopathy, isolated coronary vasospasm
Discuss stable ischemic heart disease in terms of diagnosis
o Patient history – most important part!
o Electrocardiogram
• With ischemia:
• Changes in T wave
• Displaced ST segment
• Q wave if prior MI
• With stable angina: resting ECG is normal
o Exercise stress testing
• Confirm diagnosis of angina pectoris or evaluate atypical chest pain
• CAD with horizontal or down-sloping depression or elevation of ST segment
• Stress ECG: limited (70%) sensitivity and specificity (worse in women)
• Diagnostic value depends on “pre-test” probability
• So most useful when pre-test probability is intermediate
• To improve electrocardiographic sensitivity and specificity:
• Stress nuclear scintigraphy
• Echocardiogram
• Can establish risk stratification to estimate prognosis
• High risk CAD: chest pain or electroCG changes at low level of exertion, exercise-induced hypotension, malignant ventricular arrhythmias, large areas show reduced perfusion or contractility
o Invasive Coronary angiography
• Gold standard to diagnose atherosclerotic CAD and assess severity
• Determine suitability for revascularization
o Intravascular ultrasound
• Invasive
• Sensitive method to detect full extent of atherosclerosis
o Fractional flow reserve
• Invasive
• Defines functional significance of a lesion
o Coronary CT angiography
• Non-invasive
• Identifies plaques and calcifications
Discuss stable ischemic heart disease in terms of treatment
o Life-prolonging measures:
• Lifestyle modifications
• Anti-platelet medications
• BP reduction and plaque modifying medications
o Relieve symptoms
• Drugs: Nitrates, Ca2+ channel blockers, Beta blockers
• Revascularization (if patient very high risk or non-responsive to other treatments):
• Percutaneous coronary intervention (PCI)
o Balloon angioplasty and stenting
o Improve symptoms but don’t reduce rates MI or death since CAD is a diffuse disease
• Coronary artery bypass grafting (CABG)
o Considered if patient is refractory to medial therapy, has 3-vessel disease with depressed LV function, and has no contraindications to surgery
o Improved survival with greater severity of CAD and left ventricular function
Describe unstable ischemic heart disease or “acute coronary syndromes” in terms of clinical presentation & pathophysiology
• Clinical presentation
o Unstable angina, Non-ST elevation or ST elevation MI
o Occurs at rest
o Lasts >10 minutes
o Severe, new onset
o Crescendo pattern
• Pathophysiology
o Obstructive coronary artery plaque
o Plaque rupture or erosion
• Vulnerable plaque
• Thin fibrous cap
• Large lipid pool
• Susceptible to plaque rupture or erosion
o Platelet activation
• Triggered by catecholamines, cigarette smoking, collagen, tissue factor, vWF
• Positive feed-back from adenosine diphosphate, serotonin, thromboxane A2
• Serotonin and thromboxane A2: smooth muscle agonists → vasoconstriction → further arterial narrowing
• Platelets (tissue factor) activate extrinsic clotting pathway
• Ends with prothrombin → thrombin
• Thrombin cleaves fibrinogen to fibrin
• Organizes platelets = more resistant
o Endothelial damage/dysfunction: reduces NO and prostacyclin (inhibitors of platelet activation)
o Inflammation
o Thrombus
• Activation of intrinsic clotting (tissue factor)
• Platelet activation (collagen, von Willebrand Factor, catecholamines, smoking)
• Endothelial dysfunction (reduced NO or prostacyclin, vasoconstriction)
Types unstable angina
o Unstable angina
• Angina at rest, new angina (higher risk if within past 2 weeks), increasing/accelerating angina
• 12 lead ECG
• No biochemical evidence of myonecrosis
• Usually artery is NOT 100% occluded
• Generally triggered by plaque rupture
o NSTEMI
• 12 lead ECG: T inversion, no ST elevation
• Cardiac enzymes show myonecrosis
• Usually artery is NOT 100% occluded
• Generally triggered by plaque rupture
o STEMI
• 12 lead ECG: ST elevation, Q waves if not treated quickly
• Lots cardiac enzymes → necrosis
• Usually artery is 100% occluded
o ***Acutely occluded artery not always a STEMI
• Pre-formed collaterals
• Electrically silent area of myocardium affected (circumflex artery)
Describe unstable ischemic heart disease or “acute coronary syndromes” in terms of diagnosis
o Emergency assessment
• Characterize discomfort onset, character, severity
• Identify risk factors
• Physical exam
• Cardiac biomarkers (troponin, CK-MB)
• ECG (ST depression or elevation) to determine if STEMI
• Rule out other causes of pain
o UA/NSTEMI risk stratification
• TIMI risk score:
• Age ≥65
• Presence of at least 3 other CHD risk factors
• Prior coronary stenosis of ≥50%
• Presence of ST segment deviation on ECG
• At least 2 angina episodes in prior 24 hours
• Elevated serum cardiac biomarkers
• Use of aspirin in prior 7 days
• Scoring (death, MI, severe ischemia requiring revascularization <14 days)
• Score 0-2 → 4.7- 8.3%
o Stress test first
o Managed conservatively: lifestyle modifications, statin therapy, anti-anginal therapy
• Score 3-7 → 13.2-40.9%
o Cath first (fibrinolytic therapy if not possible)
o Managed aggressively
o Also have lifestyle modificiations and pharmacotherapy for prevention
Describe unstable ischemic heart disease or “acute coronary syndromes” in terms of treatment
o To prevent death, MI, stroke, revascularization:
• Bed rest and narcotics to minimize O2 demand, decrease work needed of heart
• Anti-platelet therapy
• Aspirin (ASA): irreversibly blocks catalytic site of COX-1 in platelets (needed for metabolism of AA → PGH2 → thromboxane A2, a promoter of aggregation)
• P2Y12 receptor blockers: irreversibly inhibits low-affinity ADP receptor (P2Y12) on platelet membrane; inhibits activation of GpIIbIIIa complex
• GpIIbIIIa inhibitor: directly prevents fibrinogen cross-linking
• Anti-thrombin therapy
• Unfractionated heparin
• Low molecular weight heparin (enoxaparin) = more predictable anticoagulant effect
• Direct thrombin inhibitor (bivalirudin)
• Factor Xa inhibitor (fondaparinux)
• Statins
• Lower risk of future events
• Convert vulnerable plaques to more stable ones
• Beta-blockers
• Increase post-MI survival
• Nitrates:
• Veno- and arteriolar vasodilators → reduce preload and afterload → reduces ventricular wall stress → reduces O2 demand
• Dilates local arterioles, minimizes arterial spasms → increase O2 supply
• Supplemental O2
• ACE-inhibitors
• Revascularization
• Lifestyle modifications (diet, exercise, wt reduction, smoking cessation)
o Unstable angina/NSTEMI treatment
• Fibrinolytic therapy: no benefit, only harm
• PCI/CABG: indicated if high risk features, reduces ischemic events
o STEMI treatment
• Prompt reperfusion
• First: primary PCI if done in <90 minutes
• Less mortality if done sooner
• But <25% hospital perform PCI
• Second: fibrinolytic therapy: goal <30 minutes
• Fibrinolytic/thrombolytic therapy to activate plasmin (hydrolyzes fibrin)
• Problems:
o ~40% failure rate to open infarct artery
o Intracranial hemorrhage 1-2%
o Contraindications up to 40% (predisposition to internal bleeding eg. Recent stroke or head trauma, recent major surgery)
o Lytic outcomes consistently inferior to timely PCI
• So rescue PCI if not work
• ASA
• P2Y12 receptor blocker
• Cardiac care unit care
• Statin
• Beta blocker
• ACE inhibitor
• Cardiac rehab
Discuss complications that can result following myocardial infarction.
• Congestive heart failure and post-MI remodeling
o Early phase (<72 hrs)
• Inflammatory neutrophil infiltration, MMP activation, degradation of collagen, myocyte slippage → wall thinning
• Stroke volume changes when infarct affects >20% ventricular mass
o Late (>72 hrs)
• Stretching and thinning of scar → enlarges ventricle, decreases function
o Antero-apical region most vulnerable for infarct expansion:
• Thinnest area
• Greatest curvature
• Greatest deforming forces
• Site of thrombus due to stasis
• Site of rupture
• Arrhythmias
o Post MI ventricular fibrillation and tachycardia common
o Presence after 48 hours = increased risk of sudden death
• Cardiogenic shock: decreased CO and evidence of tissue hypoxia
o Pump failure (typically >40% LV mass infarcted)
o Myocardial rupture:
• Papillary muscle: causes severe mitral regurgitation
• Ventricular septum: causes severe L to R shunt
• Free wall rupture: causes pericardial tamponade
o Poor prognosis: (80% mortality)
• Post-MI pericarditis
o Inflammation of parietal pericardium after transmural infarct
o Sharp, pleuritic, positional chest pain
o Pericardial friction rub
o Early phase
• Common
• Symptoms <few></few> • Usually transient
• Tx: NSAIDs
o Late (Dressler’s)
• Very rare
• Symptoms weeks/months post MI
• Immune complex mediated
• Fever, myalgias
• Tx: NSAIDs, steroids, colchicine
