Acute Coronary Syndromes Flashcards
Problems with supply
Epicardial Coronary artery obstruction
Microvascular obstruction
Epicardial Coronary artery obstruction
- Atherosclerosis
- Vaso-spasm
- Printzmetal angina - Embolus
- Extrinsic compression
Microvascular obstruction
- Atherosclerosis
- CT dz
- transplant vasculopathy
- Diabetic micro-angiopathy
- Micro-emboli-Kawasaki’s
Problems with demand
Increased Demand • Hypertension-high afterload • Aortic valve stenosis-fixed afterload • Peri-op-high catecholamines • Anemia • Tachycardia • Hyperthyroidism
Stable Ischemic Heart Disease: Presentation
- Exertional chest pain (or equivalent) that is chronic
- May be asymptomatic
- predictable angina pectoris
- Typically seen in the outpatient clinic setting
Stable Ischemic Heart Disease: Pathophysiology
- Obstructive(collaterals) or non-obstructive coronary artery plaque
- Intact fibrous cap
- Minimal platelet activation, inflammation or thrombus
•Other conditions: aorticstenosis, HOCM
Stable Ischemic Heart Disease: Clinical Integrated Assessment
Symptoms Prognostic Tests Diagnostic Tests Functional Capacity Risk Factors
Stable Ischemic Heart Disease: Angina Pectoris
Pain or discomfort in the chest caused by insufficient blood supply to the heart muscle
- Typically brought on by exertion or emotional stress
- Typically lasts 1-15minutes
- Relieved by rest
- Relieved by nitroglycerin
Stable Ischemic Heart Disease: Making the Dx
“Exertional and Predictable” indigestion  • Heaviness • Tightness • Squeezing • Burning can be misconstrued as • Choking • Radiating to the arms  Associated Symptoms • Weakness of the arms • Shortness of breath • Dizziness
Populations with silent myocardial ischemia
*Examples of anginal equivalents
10-40% of patients will be silent
Women, Diabetes, elderly
*fatigue, weakness, shortness of breath
Stable Ischemic Heart Disease: Risk Factors
- Tobacco use
- Diabetes mellitus
- Dyslipidemia
- Family history of CAD
- Hypertension
- Peripheral artery disease
- Renal Failure
- Inflammatory Diseases (RA, SLE, Psoriasis)
- Obesity
- Sedentary Lifestyle
Stable Ischemic Heart Disease: Diagnosis and Prognosis
Don’t need to know details just know that there are a lot of ways to do this
• Stress Testing
- Exercise/Pharmacologic
- ECG
- *Nuclear SPECT imaging
- *Echo stress test
- MRI
• Ventricular Function
- Echocardiogram
- Nuclear Imaging
- MRI/CT/CardiacCatheterization
- worse prognosis for those with low EF
• Coronary anatomy & physiology
- CT Angiography
- Cardiac Catheterization
- –Intravascular Ultrasound
- – Fractional Flow Reserve
Stable Ischemic Heart Disease: Exercise Stress Test (EKG)
- Limited sensitivity & specificity(70%)
- typically useful as a prognosis indicator when pre-test is intermediate: 50 year old male with 1 or 2 risk factors; not useful in say a morbidly obese person or a marathon runner
- Sensitivity/Specificity worse in women than men
- Diagnostic value of the test depends on“pre-test” probability of having coronary artery disease
EKG has ST depression for ischemia pattern
- combine with imaging to improve sensitivity and specificity
- nuclear scintigraphy (blood flow)
- echo (contractility)
Stress Echo
Real-time US study to determine wall motion (contractility) of individual regions of LV before and after exercise
Nuclear Stress imaging
IV radio tracer: thallium or technitium conjugated to organic compound (Sestamibi)
-taken up by myocardium in proportion to blood flow
What can be used in lieu of exercise to stress the heart?
Coronary vasodilators: adenosine and dipyridamole
hypercontractility agents: dobutamine
Invasive Coronary Angiography/Invasive cardiac catetherization
“gold standard” for diagnosing atherosclerotic coronary artery disease and assessing its severity
- simple test with low risk
- often outpatient
- catheters advanced from a percutaneous (“needle stick”) puncture in femoral artery to the heart and are used to inject a radio-opaque contrast into the right and left coronary arteries
- The flow of contrast through the arteries is recorded using X-ray cinematography
***Left ventricular function-assessed by measuring intra-cardiac pressures and by injecting contrast into LV to determine its size, shape and contractility
***However demonstrates only the lume; not sensitive to detect early, preclinical atherosclerosis where positive remodeling preserves the luminal dimensions, often despite extensive atherosclerosis
IV Ultrasound
invasive technique
arteries via a miniaturized ultrasonic piezo-electric crystal mounted in an angioplasty-type wire
very sensitive to detect the full extent of atherosclerosis in coronary arteries
***commonly employed clinically to measure vessel size and assess plaque burden
Fractional Flow Reserve
Invasive
cath lab to define the “functional” significance of a lesion
coronary guidewire mounted with a miniature pressure transducer is placed across the lesion
Maximum hyperemia via adenosine administration
FFR=(distal coronary pressure)/(proximal)
*during max hyperemia
FFR
Coronary CT angiography
newer, noninvasive approach to visualizing the coronary arteries
ID’s obstructive plaques, but can also detect non-obstructive calcifications in the coronary artery, which is diagnostic of the presence of coronary artery atherosclerosis
promising noninvasive technique; the lower spatial resolution, imaging related artifacts, higher radiation dose, and healthcare reimbursement issues have prevented universal adoption of this method
Stable Ischemic Heart Disease: treatment
Focus is on treating symptoms and preventing events (Death, MI, stroke, revasc.)
Stable Ischemic Heart Disease: Treating Symptoms
- Nitrates-vasodilator
- Calcium channel blockers
- vasodilator and decrease HR (decreasing demand) - Beta Blockers
- Decrease HR - Revascularization:
PCI (stents/angioplasty) CABG
Stable Ischemic Heart Disease: Preventing Events
- Lifestyle measures
- exercise
- diet/wt reduction
- smoking cessation - Anti-platelet meds
a) Aspirin
- 50% reduction in mortality for previous MI
b) clopidogrel and prasrugrel - Statins
- ACE-Inhibitors
- Thieonopyridine
- If considered to be very high risk (ie. stress testing)
then may consider
PCI (stents/angioplasty) and CABG
-PCI really only provides relief and does not decrease total rates of MI or death
CABG vs. Medical Therapy
Survival related to 2 main things: LV function and severity of CAD
Improved survival only for those with Left Main CAD or Severe 3 vessel disease + reduced LV fxn
*no benefit to low risk patients
Medical Therapy vs PCI
PCI did not reduce risk of death, MI, or other major event compared to medical therapy alone
Optimal Medical Therapy
- Smoking Cessation
- Total Dietary Fat / Saturated Fat
40 mg/dL - Triglyceride (secondary goal) 27.5
Goal: 10% relative weight loss - Blood Pressure
CABG vs. PCI
- similar CV events
* more revascularization for PCI
Acute Coronary Syndromes: Types and General Pathology
- Unstable Angina (UA)
- NSTEMI
- STEMI
Pathology: •Obstructive coronary artery plaque • Plaque rupture or erosion -thin fibrous cap w/large lipid pool • Platelet activation, inflammation, thrombus
Acute Coronary Syndromes Diagnostic tests
- EKG
2. Serum biomarkers: troponin I and T (hallmark of MI)
Why do plaques rupture?
• Mechanical factors (shear stress) • Endogenous factors (catecholamines) • Inflammation • Exogenous Factors (smoking)
Why do coronary arteries thrombose?
After rupture, lipid core is exposed:
• Activation of intrinsic clotting
- Tissue Factor
• Platelet activation
- Collagen
- von Willebrand Factor
- catecholamines
- smoking
• Endothelial dysfunction
- reduction in NO
- reduction in prostacyclin
- vasoconstriction
Platelet Activation
“Triggers” Just be aware that there are a lot and they mainly deal with platelet aggregation • Catecholamines • Cigarette smoking • Collagen • Tissue Factor • vWF
“Feed-back”-vicious cycle
• Adenosine Diphosphate
• Serotonin
• Thromboxane A2
*platelets activate extrinsic clotting path
Why is an acutely occluded artery not always a STEMI?
- Pre-formed collaterals
- Electrically silent area of myocardium affected
“Circumflex artery”
Acute coronary syndrome: angina pectoris
occurs at rest lasts >10 minutes
severe, new onset crescendo pattern
ACS: Emergency Assessment
• Characterize discomfort onset, character, severity • Identify risk factors • Physical Examination – signs of instability -Rule out other causes of chest pain • Cardiac Biomarkers (Troponin, CK-MB) • ECG (ST depression or ST elevation) • Rule out other causes of chest pain
TIMI Risk Score Criteria
Death, MI, Severe ischemia requiring revascularization
TIMI Risk Scores
0/1 — 4.7 percent 2— 8.3 percent 3— 13.2 percent 4— 19.9 percent 5— 26.2 percent 6— 40.9 percent
Unstable Angina/NSTEM Tx: Treating Symptoms
NTG + morphine
Unstable Angina/NSTEM Tx: Preventing Events:
Death, MI, stroke, revasc.
Anti-platelet therapy Anti-thrombin therapy Statins Beta-blockers ACE-Inhibitors Revascularization Lifestyle measures - exercise - diet/wt reduction - smoking cessation
Unstable Angina/NSTEM Tx: ACS and Antiplatelet Therapy: 2 types
- ASA/Aspirin
• irreversibly blocks the catalytic site of (COX-1) in platelets
• COX-1 is required for the metabolism of arachidonic acid to PGH2 which processed to thromboxane A2, a powerful promoter of platelet aggregation

2.P2Y12 Receptor Blockers
*Don’t worry about details, just know they inhibit platelet aggregation
• Irreversibly inhibits the low-affinity ADP receptor (P2Y12) on the platelet membrane.
• Inhibits the activation of the GpIIb-IIIa (directly inhibiting fibrinogen cross-linking)
Unstable Angina/NSTEM Tx: Anti-thrombins
Goal: prevent formation of thrombin
Be aware but don’t worry:
Unfractionated Heparin
Low Molecular Weight Heparin: Enoxaparin Direct thrombin Inhibitor: Bivalirudin Factor Xa Inhibitor: Fondaparinux
Unstable Angina/NSTEM Tx: Beta Blockers
Improved Survival Reduction in MI
Reduction in Stroke Reduction in HF
Reduction in Arrhythmia
Unstable Angina/NSTEM Tx:
- fibrinolytic therapy
- PCI/CABG
- No benefit, only harm
2. Indicated if high risk features; reduction in ischemic events
Unstable Angina/NSTEM Tx:Lifestyle Measures
- Exercise
- Diet
- Weight reduction
- Smoking Cessation
- Stress reduction
CARDIAC REHABILITATION
Focus for…
- Stable Ischemic Heart Disease
- Unstable Angina/NSTEMI:
1.Symptom Management
Preventing CV Events Selective Revascularization
- Preventing CV Events Greater role for Revascularization
(But no fibrinolytics)
Wave Front of Ischemic Death
- Necrosis
- Microvascular Injury Interstitial Hemorrhage
- Cessation of Microvascular Perfusion
histopathology: 22 h after chest pain onset
• Wavy fibers • Fibers separated by spaces • “Contraction bands” Ca2+ dependent-hypercontractile state -->contractile necrosis • Neutrophil infiltration
slide 76
histopathology: 7 days post MI
• Vacuoles within myocytes • Mononuclear cell and macrophage infiltration • Small vessel proliferation • Fibroblast proliferation
Slide 77
histopathology: 14 days post MI
Fibrosis–>patchy scar
Slide 78
Management of STEMI
- PROMPT Reperfusion
- ASA (aspirin)
- Thienopyridine (ie. clopidogrel)
- Cardiac Care Unit Care
- Statin
- Beta-blocker
- ACE-Inhibitor
- Cardiac Rehab
- Secondary Prevention
STEMI Reperfusion Therapy:
1. Fibrinolytic Therapy
Fibrinolytic (also called Thrombolytic) Therapy
- Amplifies activation of plasmin from plasminogen
- plasmin hydrolyzes fibrin
ie. streptokinase alteplase tenectaplase retavase
*****Problems**** • Failure to open infarct artery ~40% • Intracranial hemorrhage 1-2% because it causes systemic lysis • Contraindications up to 40% • Lytic outcomes consistently inferior to timely PCI
STEMI Reperfusion Therapy: Indications for PCI & timeframe
Indications:
- ST elevation of 1-2mm in two contiguous leads
- New onset Left Bundle Branch Block (controversial)
Timeframe: #1: Primary PCI – goal
Gusto IIb
30 day mortality if DTB:
a) 91 min
a) 1%
b) 3.7%
c) 4.0%
d) 6.4%
Summary of STEMI
- Goal of therapy?
- What interventions improve survival?
- Goal of therapy for STEMI is prompt reperfusion
Complications following MI
- Congestive heart failure
- Arrhythmias
- Cardiogenic Shock
- Post-MI Pericarditis
Post MI Ventricular Remodeling
“Time-dependent & dynamic structural alterations in the ventricle resulting from coronary occlusion and myocardial necrosis.”
*a lot of the meds given to MI patients are to prevent this remodeling
Pathophysiologic ans Biochemical Events Post MI
Myocyte death leads to: -inflammatory cascade -activation of RAAS -up-regulation of pro-inflammatory and pro-vasculatory things that contribute to remodeling
- early remodeling: wall thinning/dilatation
- myocyte hypertrophy
- late remodeling: fibrosis
slide 95
Why is the antero-apical region most vulnerable for infarct expansion?
- Thinnest area of myocardium
- Greatest curvature
- Greatest deforming forces
- Site of thrombus due to stasis
- Site of rupture
Ventricular Arrhythmias
Post MI ventricular fibrillation and ventricular tachycardia are common
•VF or VT after 48 hours predicts increased risk of sudden death
Cardiogenic Shock
Definition: Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume
- Pump failure (massive infarction of >40% myocardium)
- Myocardial rupture
- papillary muscle – causes severe mitral regurgitation
- ventricular septum – causes severe L to R shunt
- free wall rupture – causes pericardial tamponade
• Prognosis is very poor:
up to 80% in hospital mortality
Post MI Pericarditis
- Definition
- Peri-infarction Pericarditis
- Late Pericarditis (Dressler’s)
Not common anymore since we’re getting good at early reperfusion therapy
Definition:
• Inflammation of the parietal pericardium following transmural infarct
• Sharp, pleuritic, positional chest pain sharp-not like MI pain
• Pericardial friction rub
- Peri-infarction Pericarditis
• Common
• Symptoms
