coronary artery disease Flashcards
The endothelial cells lining the coronary arteries have
two major roles:
- Regulate vascular tone: vasodilation (e.g., nitric
oxide) and vasoconstriction (e.g., endothelin, angiotensin-converting enzyme [ACE]) - Prevent intravascular thrombosis: (e.g., prostacyclin, plasminogen)
Factors that can impair endothelial function:
- Hemodynamic (e.g., shear stress, hypertension
[HTN]) - Chemical (e.g., low-density lipoprotein [LDL],
modified LDL, homocysteine) - Biologic (e.g., viruses, bacteria, immune complexes)
how does atherosclerotic plaque form
- Begins with disruption of endothelial cell integrity
- Leukocytes, mostly macrophages, are then attracted to the site of disruption, where they collect lipids and coalesce to form a fatty streak
- Fatty streaks mostly consist of lipid-laden macrophages containing cholesterol ester droplets (atheroma)
- Chemoattractants (e.g., platelet-derived growth factor) then cause smooth muscle cells to migrate to the
atheroma, where they produce collagen and fibrous tissue that contribute to plaque formation, covered by a layer of connective tissue called the fibrous cap - Most acute coronary syndromes (ACSs) occur when the
fibrous cap ruptures, leading to thrombus formation
cardiology scale for ACS event
- stable angina
- unstable angina
- Nstemi
- stemi
Plaque characteristics, not size,
determine its vulnerability to rupture
a large, fibrotic plaque with a thick cap is more stable and less prone to
rupture than a small plaque with a soft lipid core and a thin fibrous cap.
- Reproducible angina symptoms (chest pain or pressure) of at least 2 months
- Precipitated by exertion or emotional stress.
- Relived by rest of nitroglycerin
angina pectoris
it is important to recognize that classic symptoms may be absent, and some demographic groups (women and patients with diabetes mellitus) may have atypical symptoms, including exertional dyspnea (if it presents any other way)
atypical angina
Presence of angina during strenuous, rapid, or prolonged ordinary activity
(walking or climbing the stairs).
Angina only with strenuous exertion class 1
tightness, heaviness, or gripping in the chest,
typical angina
white guy angina
Mild myocardial ischemia with no symptoms.
asymptomatic angina class 0
Slight limitation of ordinary activities when they are performed rapidly, after
meals, in cold, in wind, under emotional stress, during the first few hours
after waking up, but also walking uphill, climbing more than one flight of
ordinary stairs at a normal pace and in normal conditions
Angina with moderate exertion class 2
Having difficulties walking one or two blocks or climbing one flight of stairs at
normal pace and conditions.
angina with mild exertion class 3
No exertion needed to trigger angina
angina at rest class 4
- The fundamental problem is an imbalance between myocardial oxygen supply and
demand. - Insufficient coronary blood flow occurs when a plaque leads to arterial stenosis
- Anginal symptoms occur during periods of exercise or stress when increased myocardial
oxygen demand (e.g., from an increase in heart rate, contractility, afterload, or wall
stress) is not met because of impaired coronary blood flow. - There is endothelial dysfunction preventing adequate vasodilation during exercise, which
can occur in the absence of severe luminal narrowing
stable angina
independent risk factor for plaques
diabetes
strong risk factors for CAD
(2 or more, they have it)
1.Older age
2.Male
3.Postmenopausal females
4.Hyperlipidemia (high LDL low
HDL)
5.Cigarette smoking
6.Hypertension
7.Diabetes mellitus
8.Obesity or sedentary lifestyle
9.Family history of early CAD
how to diagnose stable angina
ECG
Approximately 50% of patients with chronic stable angina have a normal resting ECG
* Pathologic Q waves ( Old MI) and conduction system abnormalities (e.g., LBBB, left anterior fascicular block) increase the likelihood of having CAD
stress test
* Stress testing can help risk-stratify patients:
* The sensitivity of an exercise treadmill test is
approximately 70%, the specificity is approximately
80%
* Stress tests add little diagnostic information for
patients with either high or low pretest
probabilities for CAD
* Stress tests are most useful for diagnosing CAD in
patients with intermediate pretest probability
- Typically occur during physical exertion and
gradually resolve with exercise cessation - Symptoms can also occur in conditions that
increase oxygen demand (e.g., anemia, fever,
sepsis, thyrotoxicosis - Substernal chest pressure or burning (less common
to have sharp pain) - Pain may radiate to the upper extremities (left arm
more often than right arm), neck, jaw, or face - Associated symptoms include dyspnea,
diaphoresis, palpitations, and lightheadedness - Women, diabetics, and the elderly are more likely
to have atypical symptoms
symptoms of stable angina
different types of stress tests
- exercise
-meds that mimic exercise (dobutamine, adenosine) - nuclear imaging (thallium 201, technetium 99)
- echocardiography (stressing and doing echo)
- Noninvasive and quantitative assessment of
coronary artery calcification - Higher coronary artery calcium scores are
associated with increased risk of MI and death
Calcium score screening CT:
allows for direct coronary artery visualization of a beating heart with little motion artifact
* Most accurate noninvasive modality in ruling out CAD with a very high negative predictive value
(>95%)
* Less accurate in differentiating degrees of coronary artery stenosis greater than 50%; the positive
predictive value varies between 60 and 90
with dye
Coronary CT
angiography (CCTA):
- Considered the gold standard for diagnosing CAD
- Refer for cardiac catheterization if:
1. Need to confirm or exclude CAD
2. Medical therapy fails to relieve anginal
symptoms
3. History and noninvasive testing suggest high-risk
coronary anatomy
cardiac angiography
Treatment of Chronic CAD Decrease modifiable risk factors:
before Cath lab
- Address modifiable risk factors (e.g., lipid lowering, cigarette cessation)
- Treat Sleep Apnea
- Weight loss
- Correct illnesses that can precipitate or exacerbate angina (e.g., anemia, infection, thyroid disease)
Treatment of Chronic CAD (stable angina): Anti-anginal (pain)
(First-line therapy) both:
- β-Blockers
Reduce myocardial oxygen (O2) demand by decreasing heart rate, BP, and contractility - Nitrates
Major effect stems from venodilation, which
decreases cardiac preload, thereby decreasing wall stress and O2 demand
Very good at relieving angina and improving exercise tolerance but does not affect mortality
Treatment of
Chronic CAD:
Anti Thrombosis
Aspirin
* Reduces risk of MI and death
* All patients with CAD should be on aspirin unless there
is a clear contraindication
Clopidogrel
* Platelet P2Y12 receptor inhibitor.
* If Allergic to ASA
* Neither prasugrel nor ticagrelor has been studied in the
context of stable angina, and their role in managing this
condition remains to be established.
Treatment of
Chronic CAD:
Antihypertensive
Reduce BP <130/80
Beta Blockers:
* Increase dose till resting HR 55-60/minute
Calcium Channel Blockers:
* If BP not controlled or still symptomatic add long acting
CCB (Amlodipine)
ACE inhibitors
* Clear decrease in mortality and morbidity rates in
patients with left ventricular (LV) dysfunction (ejection
fraction [EF] <40%)
Treatment of
Chronic CAD:
Lipid Lowering
- High Intensity Statin
- If LDL still > 70 consider Ezetimibe
- PCSK9 inhibitors
Treatment of
Chronic CAD:
Revascularization
The major indication for revascularization in
chronic CAD is for relief of angina symptoms in
patients on optimal medical management
- In patients with stable CAD, PCI is quite effective in reducing angina, but it does not reduce the risk of death or MI
It has 2 components:
* 1-Percutaneous transluminal coronary angioplasty (PTCA), in which a balloon is used to split the atheromatous plaque and stretch the
artery.
* 2-Stent deployment, which provides a metal scaffold to help maintain artery patency
Revascularization
of chronic CAD-
Coronary artery
bypass grafting
(CABG):
- Recommended for patients with extensive CAD, patients with left main or three-vessel CAD.
- Revascularization with CABG results in decreased recurrence of angina, lower rates of MI, and fewer repeat revascularization procedures compared with PCI.
- Long-term (10-year) follow-up demonstrated a survival advantage with CABG compared with
medical therapy alone among patients with multivessel CAD and severe left ventricular dysfunction.
- Unstable angina (UA),
- Non–ST-segment elevation MI (NSTEMI),
- ST-segment elevation MI (STEMI)
Acute
Coronary
Syndrome
(ACS)
- Clinically like UA, but distinguished by evidence of myocardial necrosis (i.e., an elevation in serum cardiac enzymes)
- ECG does not show ST-segment elevation
- positive labs
Non ST
segment
Elevated
Myocardial
Infarction
(NSTEMI):
- Angina at rest (usually prolonged more than 20 minutes),
- New-onset exertional angina (i.e., angina with only mild exertion),
- Preexisting angina that has increased in frequency or duration or that is now brought on with less exertion than before.
- Post MI angina
unstable angina
- Presence of elevated cardiac enzymes
- ECG criteria that include greater than 1-mm ST- segment elevation in two or more contiguous limb
leads, or greater than 2-mm ST-segment elevation in two or more contiguous precordial leads - ST-segment elevation suggests total occlusion of the infarcted artery by thrombus; in contrast, most patients presenting with UA or NSTEMI do not have a totally occluded infarct artery
ST segment
Elevated
Myocardial
Infarction
(STEMI):
ST elevation
STEMI
ST depression
NSTEMI
- Larger, fibrotic plaques with thicker caps are less
prone to rupture than smaller plaques, which have
softer atherogenic lipid cores and thinner caps - Inflammation can lead to plaque instability and
rupture - Other factors can contribute to plaque
vulnerability, including shear stress and enzymatic
degradation, which both weaken the plaque cap
the vulnerable plaque
T inversion
NSTEMI
occurs when a vulnerable plaque ruptures,
leading to platelet activation and aggregation,
resulting in the formation of intracoronary
thrombus
ACS
- Following plaque rupture, thrombotic factors from
within the lipid core are exposed to the
bloodstream - Activated platelets then adhere to the vessel wall
when platelet glycoprotein binds to the von
Willebrand factor - Tissue factor is also released from the lipid core,
activating the coagulation cascade and leading to
thrombin formation, the most potent platelet
activator - Platelets stick to one another during the final
common pathway of platelet activation, when
platelets expose glycoprotein IIb/IIIa receptors that
bind to fibrinogen
formation of thrombus
- Variable ECG findings, including
having no abnormalities, - ST-segment depression,
- T-wave inversions
- Nonspecific ST-segment and T-
wave changes
UA and NSTEMI
- Characterized by greater than 1-
mm ST-segment elevation in two
or more contiguous limb leads,
or - Greater than 2-mm ST-segment
elevation in two or more
contiguous precordial leads
STEMI
Diagnosis &
Evaluation:
Cardiac
Enzymes (labs for ACS)
cardiac panel:
- Troponin T and I: highest sensitivity and specificity for detecting MI; appear within 4 hours; peak at
24 to 48 hours and decline slowly; remain detectable for up to 7 to 10 days - Creatine phosphokinase myocardial band (CPK-MB): first measurable in the bloodstream at 6 to 10 hours; peaks at 24 hours; baseline by 48 to 72 hours
- Lactate dehydrogenase: obsolete; increases at 24 to 48 hours and remains elevated for 10 days
- Myoglobin: one of the earliest enzymes released in the circulation during MI (2 to 3 hours), returns to normal within 24 hours; very low specificity
Unstable Angina
and Non–ST-
Segment
Elevation MI:
Risk stratification
- As a rule, it is most appropriate to treat low-risk
patients conservatively (i.e., noninvasive testing,
medical management). - More aggressive treatment (e.g., catheterization,
PCI) is the best choice for intermediate-risk and
high-risk patients
TIMI Risk Score (don’t memorize)
- know if high score = high mortality
- Age >65 years
- Three or more coronary artery risk factors
- Prior coronary stenosis ≥50%
- Two or more anginal events in past 24 hours
- Aspirin use in past 7 days
- ST-segment changes
- Positive cardiac markers
TIMI risk score, predicts 14-day death, recurrent MI, and urgent revascularization rates
- Findings include abrupt, severe, “tearing” chest
pain that radiates to the back or abdomen,
unequal pulses and BP in the upper extremities, or
a new murmur of aortic regurgitation - ECG can reveal ST-segment elevations if the
dissection involves one or more of the coronary
arteries (typically affects the right coronary artery
first) - Thrombolytics and anticoagulants are
contraindicated
aortic dissection
- Findings include chest pain that may be pleuritic or
is relieved by sitting up; pericardial friction rub may
be present - ECG may reveal diffuse ST-segment elevation and
PR interval depression - Thrombolytics and anticoagulants are
contraindicated
acute pericarditis
- Clinical clues include risk factors for PE (e.g.,sedentary or immobile patient status, history of deep venous thrombosis, leg trauma, or oral contraceptive use);
- Symptoms include sudden-onset chest pain and dyspnea
- ECG may show only sinus tachycardia, but classic findings include an S wave in lead I, Q wave in lead III, and T-wave inversion in lead III; can also present with new right bundle branch block or right axis deviation
pulmonary embolism
anti angina Management of UA & NSTEMI: (pain)
- Nitrates
- B-Blockers
- Morphine
Management
of STEMI
- Rapid recognition of a STEMI and immediate
initiation of reperfusion therapy are crucial. - The faster normal flow can be restored in the
occluded artery, the better the prognosis
Anti clot anti angina Management of UA & NSTEMI: (save lives)
- Anti-platelets*: aspirin
- Anti-coagulants*: heparin
- Statins
- ACE-I/ARB if EF <40%
- Percutaneous coronary
intervention
Management of STEMI:
Anti-angina:
- Nitrates
- B-Blockers
- Morphine
Management of STEMI: anti clot:
- Anti-platelets
- Anti-coagulants
- Statins
- ACE-I/ARB if EF <40%
- Thrombolytic
- Revascularization (PCI & CABG)
- Major advantages over thrombolytics:
- Higher reperfusion rates (greater than 90% success
rate of opening the occluded artery) - Decreased incidence of stroke
- More effective than thrombolytics in patients with
acute decompensated heart failure, cardiogenic
shock, and prior bypass surgery - Major disadvantages:
- Not available in all hospitals, and it may take too
much time to get the patient to the appropriate
facility
Management
of STEMI:
PCI
preferred method of
treating STEMI
- PPCI is the preferred method of
treating STEMI - The goal time from first medical contact
until PPCI is 90 minutes or less. - When the patient presents to a PCI-
capable hospital or can be transferred
from an index hospital to a PCI-capable
center quickly (time from first medical
contact to PPCI of ≤120 minutes)
when is thrombolytic therapy most effective
- Approximately 60% successful
- Most effective when given in the first 6 hours, but
can be given up to 12 hours after onset of chest
pain - After 12 hours, the risk/benefit is unfavorable
because the benefit decreases and the risk of
myocardial rupture increases
absolute contraindications of Management of STEMI: Thrombolytic
therapy
1.Any history of intracranial bleed
2.Known cerebral vascular lesion (e.g., AVM)
3.Known malignant intracranial
neoplasm
4.Ischemic stroke within 3 months
5.Suspected aortic dissection
6.Active bleeding or bleeding diathesis (excluding menses)
7.Closed-head or facial trauma within 3 months
