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Cardiology > Unstable ischemic coronary syndromes > Flashcards

Unstable ischemic coronary syndromes Flashcards

1
Q

What is the leading cause of death in the US?

A

-CV disease

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2
Q

Define myocardial ischemia vs myocardial infarction

A

-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.

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3
Q

Clinically a MI pertains to the _______ and ______ period.

A

-peri infarct and post-infarct

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4
Q

Continuum of acute coronary syndromes: _____-_______ cycle

A

-ulceration-thrombosis cycle

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5
Q

________ accounts for 50-60% of acute coronary syndromes and _______ account for 30-35%.

A
  • plaque rupture
  • plaque erosion: younger premenopausal women, different plaque composition
  • these both can lead to intravascular thrombosis, vasoconstriction and spasm
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6
Q

Plaque instability is a consequence of what 3 things?

A
  • relative fibrous cap thickness
  • necrotic lipid core thickness
  • remodeling index: macrophages secrete MMPs
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7
Q

T/F: the biggest plaques are the most prone to rupture

A
  • false; depends more so on the proportion of fibrous cap to necrotic core
  • 67% of rupture plaques have <70um cap thickness
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8
Q

Which 2 acute coronary syndromes are nearly impossible to distinguish clinically in the ER?

A

-high risk unstable angina and NSTEMI

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9
Q

High-risk unstable angina and NSTEMI

A
  • 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
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10
Q

History, P/E, ECG, and biomarkers used to dx high-risk unstable angina and NSTEMI; which tells you the difference between these two?

A
  • 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!!
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11
Q

2 steps to differentiate between high-risk unstable angina from STEMI from NSTEMI

A
  1. ECG: ST elevation or depression/no persistent elevation; if elevated, it is a STEMI; if not, continue to #2
  2. Troponin levels: if negative, unstable angina, if positive, NSTEMI
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12
Q

Why is ECG so important in patients with acute coronary syndrome (give 2 reasons)

A
  1. can help dx what acute coronary syndrome they have: STEMI vs NSTEMI/unstable angina
  2. 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

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13
Q

Which troponins are used as ischemic vs infarction biomarkers and why? Where are these found within the cell?

A
  • 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)
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14
Q

2 issues with troponin being a biomarker for infarctions

A
  1. are not present in blood for approx 4-6 hours after MI
  2. are also found floating freely in intracellular locations and thus can be released in non infarction injuries; indicate damage but not always infarction
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15
Q

Troponin and mortality

A
  • 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
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16
Q

RIsk stratification of ACS

A
  1. 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
  2. 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
  3. 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
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17
Q

3 main categories of acute care of ACS

A
  1. anti-ischemic therapy meants to optimize supply and demand: nitroglycerin, B-blockers are main options, calcium channel blockers less so
  2. 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
  3. reperfusion to treat underlying mechanism: PCI or CABG
18
Q

______ antiplatelet therapy reduces ischemic events in ACS

A

-dual; but did see an increase in major bleeding

19
Q

_________ reduce events when combined with PCI in ACS

A

-GPIIbIIIa

20
Q

Other than when paired with PCI, GPIIbIIIa antagonists are more effective in a different subgroup of patients as well. Who?

A

-those with elevated troponin levels benefit more from GP3b2a therapy than do those with normal troponin levels

21
Q

What was seen to be better: early invasive or conservative therapy in UA/NSTEMI?

A

-favor early invasive which were seen to lower all cause mortality, less non-fatal MIs and less recurrent UA

22
Q

Compare effectiveness of reducing overall mortality in non-ST elevation ACS between medical therapy, PCI or CABG

A
  • PCI is the best!! and least invasive!
  • medical therpay and CABG are less effective and similar to eachother
23
Q

Summary of STEMI-ACS

A
  • 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)
24
Q

STEMI vs NSTEMI

A
  1. both are caused by unstable plaques and overlying thrombus formation leading to decreased blood flow and myocardial damage
  2. differentiated by the size of the affected vessel, extent of underlying coronary artery disease and presence of collateral blood vessels
  3. although clinical differentiation is on basis of ECG changes, there are important prognostic and therapeutic differences
25
Q

OCT imaging in STEMI vs NSTEMI

A
  1. STEMI: larger ruptured cavity, thinner fibrous plaques, and red thrombus
  2. NSTEMI: smaller ruptured cavity and white thrombus
26
Q

Clinical differences between STEMI and NSTEMIs

A
  1. STEMI are clinically more unstable as they are more extensive: greater CPK levels, greater decrease in LV function, greater incidence of CHF
  2. NSTEMI: have increased risk of recurrent ischemia
27
Q

Mortality curves of STEMI vs NSTEMI

A
  • 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
28
Q

Symptoms accompanying infarcts

A
  • 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
29
Q

Physical findings during a MI

A
  1. may not demonstrate any
  2. cool and clammy skin
  3. elevated or decreased BP and/or HR; worry about cardiogenic shock
  4. increased JVP
  5. late systolic bulge
  6. S3 on cardiac exam
  7. mitral regurgitation
  8. pulmonary edema
  9. pericardial friction rub
30
Q

3 roles of ECG in MI

A
  1. dx
  2. localize infarction
  3. aids in determining eventual size of the infarction
31
Q

Sequential ECG changes in anterior MI

A
  • ST elevation
  • may be followed by q-wave; Inverted T wave
32
Q

Acute care of STEMI

A
  1. time is of the essence
  2. anti-ischemic therapy: NTG, B blockers
  3. antithrombotics: antiplatelets and anticoagulants
  4. reperfusion to limit infarct size and reduce mortality: fibronolytics, PCI, CABG
33
Q

What is the ideal option to chose when reperfusing a STEMI

A

-PCI if you have access to a cath lab within 90 minutes

34
Q

myocardial necrosis

A
  • 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
35
Q

Correlation of time of reperfusion to MI size

A
  • faster you can reperfuse, the smaller the infarct size
  • each half hour delay is associated with 7.5% increase in mortality
36
Q

Effect of vessel patency and mortality in STEMIs

A

-occluded vessels do worse than patent –> why reperfusion is huge in STEMIs!!

37
Q

PCI vs thrombolysis in long-term clinical outcomes in STEMI

A

-PCI >>> thrombolysis

38
Q

Determinants of extent of myocardial necrosis

A
  1. duration of MI/ischemia
  2. size of bed at risk
  3. degree of blood flow reduction
  4. presence of “ischemic preconditioning”
  5. presence of alternative sources of blood: collaterals, ventricular cavity, CABG
39
Q

Best way to treat STEMIs

A
  1. establish blood flow as quickly as possible to the infarcted myocardium
  2. such aggressive approaches have decreased mortality rate of MI substantially
  3. PCI is better than thrombolytics if transfer to cath lab can be performed quickly
40
Q

3 things that make up the spectrum of unstable CAD states aka acute coronary syndromes (ACS)

A
  • unstable angina
  • NSTEMI
  • STEMI
  • causes are similar and overlapping
41
Q

MI is associated with ______ while UA is not.

A

-myocardial cell death

42
Q

Therapy for UA and NSTEMI is geared toward __________ while therapy for STEMI is geared toward _________

A
  • reducing risk of subsequent large MI
  • reducing the on-going myocardial damage

Cardiology (27 decks)

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