Unstable ischemic coronary syndromes Flashcards
What is the leading cause of death in the US?
-CV disease
Define myocardial ischemia vs myocardial infarction
-ischemia: pathophysiologic state in which the myocardium is deprived of oxygen and is unable to adequately remove catabolic metabolites -infarction: metabolic of physiologic state denoting dead or dying myocardium.
Clinically a MI pertains to the _______ and ______ period.
-peri infarct and post-infarct
Continuum of acute coronary syndromes: _____-_______ cycle
-ulceration-thrombosis cycle
________ accounts for 50-60% of acute coronary syndromes and _______ account for 30-35%.
- plaque rupture
- plaque erosion: younger premenopausal women, different plaque composition
- these both can lead to intravascular thrombosis, vasoconstriction and spasm
Plaque instability is a consequence of what 3 things?
- relative fibrous cap thickness
- necrotic lipid core thickness
- remodeling index: macrophages secrete MMPs
T/F: the biggest plaques are the most prone to rupture
- false; depends more so on the proportion of fibrous cap to necrotic core
- 67% of rupture plaques have <70um cap thickness
Which 2 acute coronary syndromes are nearly impossible to distinguish clinically in the ER?
-high risk unstable angina and NSTEMI
High-risk unstable angina and NSTEMI
- both result from plaque instability and intracoronary thrombus formation
- both caused by a decrease in coronary artery blood flow
- myocardial cell damage is present with NSTEMI
- ECG changes in STEMI take longer to resolve
History, P/E, ECG, and biomarkers used to dx high-risk unstable angina and NSTEMI; which tells you the difference between these two?
- history: change in the anginal pattern or new onset of anginal type chest pain
- PE: may be normal or indicate hemodynamic compromise
- ECG: ST depresison or T wave inverstion
- Biomarkers tell the difference!!!: normal in unstable angina and elevated in NSTEMI!!
2 steps to differentiate between high-risk unstable angina from STEMI from NSTEMI
- ECG: ST elevation or depression/no persistent elevation; if elevated, it is a STEMI; if not, continue to #2
- Troponin levels: if negative, unstable angina, if positive, NSTEMI
Why is ECG so important in patients with acute coronary syndrome (give 2 reasons)
- can help dx what acute coronary syndrome they have: STEMI vs NSTEMI/unstable angina
- characteristics can determine prognosis. No ST or T wave change has better prognosis than T wave inversion than ST elevation than ST depression that ST elevation and depression
No change > T wave inversion only > STE only >STD only > STE and STD
Which troponins are used as ischemic vs infarction biomarkers and why? Where are these found within the cell?
- Troponin I and T, NOT C bc C is found also in skeletal muscle and is therefore not as sensitive
- found attached to actin filaments (remember they are here in striated muscle to block myosin binding unless calcium is present)
2 issues with troponin being a biomarker for infarctions
- are not present in blood for approx 4-6 hours after MI
- are also found floating freely in intracellular locations and thus can be released in non infarction injuries; indicate damage but not always infarction
Troponin and mortality
- cardiac troponin level elevation predicts increased mortalities 42 days in pts with ACS
- higher the concentration, the greater the mortality
- also saw increased 1 year survival in TnI negative ACS patients vs TnI+ patients
RIsk stratification of ACS
- high risk: at least 1 of the following must be present: prolonged (>20) rest pain, pulmonary edema, new or worsening mitral regurg with angina, rest angina with dynamic ST changes >/ 1 min, angina with S3 or rales, angina with hypotension
- intermediate: rest angina now resolves but not low likelihood of CAD, rest angina (<20 min or relieved with rest or nitroglycerin), angina with dynamic T wave changes, nocturnal angina, new onset CCSC 3 or 4 angina in past 2 weeks but not low chances of CAD; Q waves of ST depression 1 mm in many leads, age < 65 years
- low risk: increased angina frequency, severity or duration, angina provoked at a lower threshold, new-onset angina within 2 weeks to 2 months, normal or unchanged ECG
3 main categories of acute care of ACS
- anti-ischemic therapy meants to optimize supply and demand: nitroglycerin, B-blockers are main options, calcium channel blockers less so
- anti-thrombotics inhibit or reverse thrombus formation: antiplatelets (aspirin, INNs, glycoprotein 2b,3a receptor inhibitors and anticoagulants: heparin, direct thrombin inhibitors, factor Xa inhibitors; work well in combos
- reperfusion to treat underlying mechanism: PCI or CABG
______ antiplatelet therapy reduces ischemic events in ACS
-dual; but did see an increase in major bleeding
_________ reduce events when combined with PCI in ACS
-GPIIbIIIa
Other than when paired with PCI, GPIIbIIIa antagonists are more effective in a different subgroup of patients as well. Who?
-those with elevated troponin levels benefit more from GP3b2a therapy than do those with normal troponin levels
What was seen to be better: early invasive or conservative therapy in UA/NSTEMI?
-favor early invasive which were seen to lower all cause mortality, less non-fatal MIs and less recurrent UA
Compare effectiveness of reducing overall mortality in non-ST elevation ACS between medical therapy, PCI or CABG
- PCI is the best!! and least invasive!
- medical therpay and CABG are less effective and similar to eachother
Summary of STEMI-ACS
- early dx is crucial
- risk stratify early
- rx protocals depend on underlying pathophys and hemodynamic instability of pts
- thick about pt treatment strategies as acute, in-hopsital and long-term (preventative)
STEMI vs NSTEMI
- both are caused by unstable plaques and overlying thrombus formation leading to decreased blood flow and myocardial damage
- differentiated by the size of the affected vessel, extent of underlying coronary artery disease and presence of collateral blood vessels
- although clinical differentiation is on basis of ECG changes, there are important prognostic and therapeutic differences
OCT imaging in STEMI vs NSTEMI
- STEMI: larger ruptured cavity, thinner fibrous plaques, and red thrombus
- NSTEMI: smaller ruptured cavity and white thrombus
Clinical differences between STEMI and NSTEMIs
- STEMI are clinically more unstable as they are more extensive: greater CPK levels, greater decrease in LV function, greater incidence of CHF
- NSTEMI: have increased risk of recurrent ischemia
Mortality curves of STEMI vs NSTEMI
- similar within first 6 months, but then NSTEMI becomes greater risk of mortality over time
1. while STEMIs have greater immediate damage, NSTEMIs hold greater risk over time of repeated ischemic events
Symptoms accompanying infarcts
- may just be chest pain
- profound sweating, nausea, or arm/jaw pain
- shortness of breath due to: Pulmonary edema, acute mitral regurgitation, arrhythmias
- hypotension, esp worrisome in STEMIs
- pericardial chest pain
- WOMEN TEND TO NOT HAVE TYPICAL SXS
Physical findings during a MI
- may not demonstrate any
- cool and clammy skin
- elevated or decreased BP and/or HR; worry about cardiogenic shock
- increased JVP
- late systolic bulge
- S3 on cardiac exam
- mitral regurgitation
- pulmonary edema
- pericardial friction rub
3 roles of ECG in MI
- dx
- localize infarction
- aids in determining eventual size of the infarction
Sequential ECG changes in anterior MI
- ST elevation
- may be followed by q-wave; Inverted T wave
Acute care of STEMI
- time is of the essence
- anti-ischemic therapy: NTG, B blockers
- antithrombotics: antiplatelets and anticoagulants
- reperfusion to limit infarct size and reduce mortality: fibronolytics, PCI, CABG
What is the ideal option to chose when reperfusing a STEMI
-PCI if you have access to a cath lab within 90 minutes
myocardial necrosis
- result of an ACUTE interruption of CBF resulting in anoxia and anaerobic metabolism
- intracellular depletion of high energy phosphates and decrease in pH
- anaerobic products accumulation: K+, lactate, CO2, adenosine
- cell death and loss of myocardial membrane integrity
Correlation of time of reperfusion to MI size
- faster you can reperfuse, the smaller the infarct size
- each half hour delay is associated with 7.5% increase in mortality
Effect of vessel patency and mortality in STEMIs
-occluded vessels do worse than patent –> why reperfusion is huge in STEMIs!!
PCI vs thrombolysis in long-term clinical outcomes in STEMI
-PCI >>> thrombolysis
Determinants of extent of myocardial necrosis
- duration of MI/ischemia
- size of bed at risk
- degree of blood flow reduction
- presence of “ischemic preconditioning”
- presence of alternative sources of blood: collaterals, ventricular cavity, CABG
Best way to treat STEMIs
- establish blood flow as quickly as possible to the infarcted myocardium
- such aggressive approaches have decreased mortality rate of MI substantially
- PCI is better than thrombolytics if transfer to cath lab can be performed quickly
3 things that make up the spectrum of unstable CAD states aka acute coronary syndromes (ACS)
- unstable angina
- NSTEMI
- STEMI
- causes are similar and overlapping
MI is associated with ______ while UA is not.
-myocardial cell death
Therapy for UA and NSTEMI is geared toward __________ while therapy for STEMI is geared toward _________
- reducing risk of subsequent large MI
- reducing the on-going myocardial damage
