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Stable Ischemic Heart Disease, Screenshot 2025-01-29 at 10.32.29 PM :arrow…
Stable Ischemic Heart Disease
1. Intro
Definitions
angina pectoris
sx of chest pain believed to be cardiac related
chronic stable angina
predictable angina sx that occur with exertion/emotional stress and relieved by rest/medications
plaque present :arrow_right: increased flow limiting stenosis
when the plaque ruptures it leads to a
temporary
clot which leads to unstable angina
SIHD
narrowing of coronary arteries that affects the blood supply to the heart; tissue hypoxia aka low O2; pts don't necessarily have to have sx of angina to have SIHD
can be obstructive or non-obstructive (drug trials were done in obstructive)
chronic coronary syndromes
having plaque present, but it hasn't ruptured yet
2. Pathophysiology
supply vs demand
homeostasis of the heart is regulated by supply/demand "economics"; in SIHD the demand EXCEEDS the supply
coronary blood flow in exercise
microcirculation controls blood flow to the heart under normal conditions
when we exercise more blood flow is needed, vessels dilate, increased coronary blood flow
in SIHD, at rest, the vessel will be dilated slightly and then dilate a bit more during exercise
conclusion: there is a smaller change in vessel dilation bw rest and exercise in SIHD (>90% occlusion is needed to affect resting blood flow)
3. Diagnosis of SIHD
diagnostic tests
ECG
EST
increasing increments of stress on a treadmill to see if we can provoke chest pain that will bring on angina, to see if ECG changes
Myocardial Perfusion Imaging (MIBI / PET Scan)
nuclear scan comparing image of the heart at rest vs stress
Coronary Angiography
2D visual of the arteries using dye and X-ray; invasive bc it needs to be accessed through radial or femoral (near groin) artery; has too many A/E like perforation and bleeding
diagnostic criteria and differentiation
SIHD
pain with exertion/stress; ECG changes during exertion
acute coronary syndrome
pain at rest, for a log time; increased troponin in body; ECG changes always present
4. Goals of Therapy
improve prognosis
prevent MACE
improve sx/ QofL
and improve exercise tolerance and capacity
5. Treatment Strategies
Revascularization
Coronary Artery Bypass Grafting (CABG)
providing an alternate pathway for blood to flow through (literally adding a new fake artery
Percutaneous Coronary Intervention (PCI) aka "stenting"
stent is put in the coronary artery of the heart where the plaque is to improve flow
stents don't fix the problem bc atherosclerosis is a progressive disease; obstructive lesions cause more bad events, however non-obstructive lesions are more common, and stents can't fix those. a pt needs to be on meds for life for their SIHD, so the stent isn't the only thing they have to do and then be done.
Medical Therapy
Risk Factor Modification
control HTN, DM, cholesterol :pill: to delay onset of MI or SIHD; healthy weight, be active :weight_lifter: , stop smoking :no_smoking:
6. Medical Therapy
Symptom control (depending on severity of sx, frequency of attacks, impact on exercise, impact on QofL)
second line: CCB or long acting nitrates
third line: ranolazine
first line: BB
emerging therapies
combo therapy of these drugs shown to be more effective for sx control than single agent therapy
disease progression ('high risk pts)
antiplatelet therapy
clopidogrel
the CAPRIE trial tested high dose aspirin vs 75mg clopidogrel and found it was a bit better than aspirin at lowering stroke, MI, or vascular death but more expensive with the same a/e and indication
indicated for: pts with intolerance to aspirin
dual anti platelet therapy (DAPT)'
NOT indicated for most pts with stable disease
for high risk pts with low risk of bleeding, or that have multiple cardio events like CAD, CVA, PAD, or that are young
aspirin
all the pts we are treating are in the secondary prevention group because they've already done some sort of heart surgery due to a coronary issue
recall that aspirin is not for primary prevention
indicated for:
ALL
pts unless c/I
A/E: increased intracranial and GI bleed
dose: lowest effective dose
aspirin + rivaroxaban'
low dose Riva BID + aspirin low dose qd = lowest CV events seen, but highest rate of bleeding seen
should be used in high risk pts who are LOW bleeding risk
vascular protection
ACEi/ARBs
lowers progression of atherosclerosis. stabilizes plaque, protects the endothelium, breaks down clots; basically delays progression of CV events
indicated for: all pts with SIHD as long as no c/I
A/E: dry cough with ACEi, switch to ARBs; hyperkalemia and SCr rising initially
C/I: pregnancy, bilateral artery stenosis, hx of angioedema
statins
newer add-ons (colchicine, PCSK 9 inhibitors', SGLT2i')
7. Beta Blockers
Clinical Benefit
delayed/eliminated angina during exercise, decreased need for Nitro; decreased frequency of angina; AVOID acebutolol and stall because they can worsen angina due to unopposed alpha-blockade :red_cross:
initial choice for all pts with no C/I; reduced death and recurrent MI in pts who have already had an MI; BP should be above 100 systolic before initiating tx; HR should be above 60; titrate doses up until sx relief is achieved
MOA
reduces HR and contractility by lowering body's DEMAND for oxygen to the heart; decreases BP slightly by reducing CO and inhibiting renin; more filling time and ability to pump blood in the body
Anti-Ischemic Effects: lowered cardiac sympathetic tone (heart is contracting less, beating slower, conducting slower, and relaxing more); B1 recepetor is getting blocked
Normally, β₂-receptors in blood vessels promote vasodilation. Non-selective beta-blockers (which block β₁ and β₂) remove this β₂-mediated vasodilation, leaving only alpha-adrenergic vasoconstriction. This can lead to increased vasoconstriction and potentially worsen conditions like vasospastic angina
A/E
if high dose BB are stopped without tapering down, r
ebound tachycardia
can be expereinced
fatigue bc of lowered HR, depression, bradycardia, hypotn, heart block, bronchospasm, masked hypoglycemia, sweating, high TG and low HDL, impotence
C/I
asthma, COPD caution, secondary or tertiary heart block; decompensated heart failure; severe PAD; pheochromocytoma without alpha blockade
cario selective agents
atenolol, bisoprolol, metoprolol (these are all B1 selective aka cardio-selective)
if you push the dose of a B1 selective blocker too high,
it can start to block B2 receptors as well
, causing systemic effects, therefore not good to go too high with dosing
9. Nitrates
MOA
:arrow_down: venous dilation, preload, afterload (a bit) myocardial wall tension all are reduced, thereby lowering oxygen DEMAND
a reduced preload means that there is improved blood flow and flow distribution
:arrow_up: coronary vasodilation improves oxygen SUPPLY
nitrates get converted to NO (nitric oxide), then activates cGMP, decreasing cellular calcium and relaxing smooth muscle and causing vasodilation
rapid acting vs long acting
rapid
: for rescue tx of ALL PTS with angina (
max 3 sprays after 5 min increments, then call 911 if angina sx still don't go away
)
long acting
: second line therapy in combo with CCB or BB for prophylaxis (prevention)
A/E
nitrate free period of 8-12 hours is required
headache, dizzy, hypotn, reflex tachycardia, nausea, flushing/rash (patches)
C/I
severe aortic stenosis (preload dependant, and nitrates decrease preload which wouldn't be good in these pt's case)
clinical effects
improved exercise tolerance, time to onset of angina, ischemic threshold ; comes in SL tablets, spray, tabs, transdermal patch (take off after 12 hour use)
D/I
sildenafil, vardenafil, tadalafil all inhibit the breakdown of NO, therefore keeping it at high cones in the body. space sildenafil/vardenafil 24h apart from nitro; space tadalafil 3-4 days apart from nitro
8. CCB
NDHP vs DHP
NDHP
:arrow_down: reduced HR and contractility therefore lowering oxygen DEMAND ; reduces conduction
DHP
:arrow_down: lowers arterial resistance and after load, therefore lowering myocardial wall stress and oxygen DEMAND
:arrow_up: increases coronary artery dilation and blood flow, and improves oxygen SUPPLY; involved in
PERIPHERAL vasodilation
MOA
competitive L-type CC antagonist; when calcium availability decreases because of these drugs, heart doesn't contract as much and can relax and dilate; works on SA and AV node as well as myocytes and smooth muscle
Clinical use
second line therapy after BB; good as a combo add-on; good for
coronary spams
; long acting CCB are good
initiating NDHP: same as BB criteria
initating DHP: make sure BP is adequate and titrate until sx relief is reached
titrating NDHP: until HR reaches 55-60 or until sx relief
A/E
short acting DHP
(like nifidepine regular release) can increase cardiac A/E like hypotn, tachycardia, heart block and decreased exercise tolerance
dizzy, fatigue, hypotn, tachycardia, heart block, constipation (
verapamil
), rash (
diltiazem
), flushing (
DHPs
), peripheral edema
C/I and D/I
avoid NDHP + BB combo because it can cause high risk of bradycardia as both drugs focus on lowering heart rate (DHP + BB is fine)
C/I: second or third degree heart block or sick sinus syndrome without a pacemaker (don't use NDHPs); hypotn, bradycardia (don't use NDHP),
heart failure WITH REDUCED EJECTION FRACTION (amlodipine CAN be used)
:check:
D/I: digoxin + NDHP combo can decrease heart rate and increase conc of digoxin --> take precaution
diltiazem :arrow_forward: 3A4 substrate and inhibitor
verapamil :arrow_forward: 3A4 substrate and inhibitor, 1A2 and 2C substrate, P-glycoprotein
felodipine :arrow_forward: 3A4 inhibitor
10. Ranolazine
MOA
:arrow_down: inhibits late sodium channel influx during depolarization in myocytes (delayed contraction); reduces intracellular Na, lowers Ca influx, lowers ventricular wall tension, lowers oxygen DEMAND
A/E
nausea, constipation, dizzy, headache, prolonged Qt interval
C/I
caution with pts CrCl <50; C/I in cirrhosis, CYP3A4
inducers
and
inhibitors
(
phenytoin, carbamazepine, rifampin,
ketoconazzole, clarithromycin
)
clinical effects
good for second line therapy in combo
dosed ER 500mg BID, then titrate to max 1000mg BID in 2-4 weeks post-initiation
11. Colchicine
MOA
anti-inflammatory; inhibits tubulin from being made; alters leukocyte response; not really seen in reality (only if pt had gout + angina); good as add on therapy with ASA, statins, ACEi
A/E
major diarrhea, neuropathy, bone marrow suppression, nausea, myalgia
C/I
narrow therapeutic index; many D/I with CYP3A4 substrates and P-glycoprotein; dose adjustments required in pts with cirrhosis, CrCl <30 and elderly pts
:arrow_left: slide 41 of notes summary of sx management
