stable ischemic heart disease

for sihd what does everyoneee get

ada or plvavix

high intesity statin

SL nitroglycerin (NTG)

flu shot lol

what is ccd

• chronic coronary disease

• all the obstrucitve nad nonsobutrvive cornoary artery disease

obstructive ccd

narrowing of coronary artery due to plaque deposition

nonobstructive ccd

angina with nonobstructive coronary artiers (ANOCA)

what is IHD

ischemic heart disease

• lack of oxygen and/or no blood flow in myocardium

• disease means imbalance between o2 supply and o2 demand

what is presenting sign of IHD

angina in 50%+ patients

define ccs

chronic coronary syndromes

• can be reversible deficeit in supply/demand (stable ischemic heart disease)

• can be progressive and able to destablize at any. moment— ACS!

what is included in stable ischemic heart disease

• stable angina symptoms who are medically managed

• angian symptoms from coronary vasospasm or microvscular angina

what are the acute coronary syndromes

• unstable angina

• non ST-segment elevation MI

• ST segment elevation MI

the things that cannot be relieved by nitro and/or rest

how does ischemic heart disease (stable angina)

• angina

• coronary artery vasospasm or prinzmetal’s angina or vasospastic angina

• heart failure or arrthymias

• cerebrovascular accident or storke

• peripheral vascular disease

what is the STRUCUTRAL reason for SIHD?

what is the functional reason for SIHD?

• atheroscleorsis: damage to ENDOTHELIUM by plaque underneath (covered by fibrous cap)— can rupture which becomse UNSTABLE

• coronary artery vasospasm— coronary artery spasm (literal muscle contraction)

what are two main types of coronary arteries

• epicrdial coronary artieres— “conductance” vessels

• intramyocardial arterioles— “resistance” vessels— branch out into capillaries— react quickly when demand for oxygen chagnes

what forms the foam cells

macrophages that have swallowed up the fatty plaque

what is the LAD

• “widow maker” artery

• left anterior descending— supplies a LOT of blood to heart

what two factors inside the coronary arteries cause vasodilation

• nitric oxide

• endothelium-derived relaxing factor

damage to endothelium means cannot release NO

what is supple and demmand like in angina? what is causing the limit in one of these facotrs

angina occurs due to increased oxygen demand in limited ability to supply o2

• R1 (epicardial coronary artery) occlusion

what % occlusion of r1 (epicardial arteries) leads to UNSTABLE plaque

70%

how does body compensate for occluded r1 (epicardial artieres)

R2’s dilate

• so in excericse or stress they are maxed out and cannot expand anymore to supply more blood

what determinants myocardial oxy demand

• heart rate— beta blockers, ccbs

• contractility — bbs, ccbs

• ventricular volume (preload—stretch)

• ventricular pressure (afterload—squeeze)

what is systole? diastole

systole— heart pumping

• diastole— heart filing/relaxing

what is afterload

force heart is pushing against

• heart works harder’

• hypertrophy (the muscle GROWS)

what is preload

amount of blood returned to heart from suprieor vena cava into right atrium

• increase in volume means teh muscle in left ventricle has to do more work

what are NONcardiac reasons for decreases in o2 supply

• anemia (blood doesnt have enough oxygen)

• hypooxemia (not getting enough oxygen into the body, ie for asthma, sleep apnea)

• sickle cell disease

• Sympathomimetic toxicity (overload of SNS— ie OD, tumor, etc)—— hyperthyroidism

what effects preload

long acting nitrates

• venous side is preload

what are OTHER not-ascvd reasons for increases in O2 demand

aortic stenosis, hypertrophic cardiomyopathy, HTN

three big types of angina

• chronic stable angina

• unstable

• variant

what are three big symptoms of angina? (think PPR)

• pain — squeezing, suffocating/crushing sensation, pain in chest that radiate to neck

• predictable — precipitated by exertion or stress

• relieved— by rest or nitroglycerin

what normally causes variant angina

young, male, sometimes drug-user or smoker

• cocaine association

• smoking association— endothelium

how is angina presenting different in diabetics than other pops

• less pain bc of neuropathy

• higher risk of CV death

what are relevant labs ? what labs mostly mean?

normally are WNL— within normal limits

• CRP

• SCr

• Hgb

• Thyroid

• Troponins will be negative

these things really should be normal if its truly just an angina problem

what two pops most liekly to be misdiagnosed

• women— bc diagnosed as tummy troubles

• elderly— bc a lot of stuff going on

• diabetes— experience pain differently

what are looking for in past medical history

HTN

dyslipidemia

current smoker

DM

• also look at fam history, social history (drug use)

what are some tests that can actually be done on patients to rule out or determine pt risk

• cardiac specifc imaging— pet scan, ct scan

• chest x-ray— see if its heart falure

• ecg

• ett—exercise tolerance test—- pretty clear ind of increased demand not being met by supply— can be done with medication in elderly

• echo— may show ongoing myocardial injury— there is an invasive version called transesophageal

• cardiac catheterization (for pts with unacceptable symptoms)

will troponins be released in SIHD? why normally released

released when myocardial damage due to lack of blood supple

• NO not released

what do you need to have a MI diagnosis

positive troponins

clinical presentation of stable angina (slide 29)

• chest pain/sob/fatigue IN REPONSE to stress/exertion

• negative troponins

• predictable (same exertion causes it every time)

• relieved by nitrates (sublingual usually) or rest

how duration dif in stable vs unstable angina

10-15 minutes for stable

• longer for unstable angina

what is revascularization ? is this pref in angina

• NOT pref in angina

• revascularization is like CABG (coronary artery bypass grafting), stent (percutaneous coronary intervention), etc

• survival rates about teh same as just using meds, but can maybe have better sumptom improvement

what are some mechs by which cigs accelerate CVD

• platelet adhesion

• endothelial dysfunction

• vasoconstriction

goals of angina treatment

• symptom goal is relieve the angina

• mortality goal is lit don’t die lol

so we have mortality reducing drugs, and symptom relief drugs

what statins need take with food

JUST lovastatin

what statins must take PM

fluvastatin, lovastaitn, simvastatin, lovastatin ER is bedtime

what kind of fat should be avoided in sihd

trans fat

what are exercise recs

150 min/week of moderate intensity aerobic activity OR 75 min higher-intesity aerobic activity

• resistance for 2 or more days/week

  • set realistic goals! :)

in pts with SIHD what is goal ldl! and goal non-hdl

• ldl< 70

• non-hdl < 100 mg/dl

what are the 6As

ask, advicse, assess, assist, arrange, AVOID (avoid secondhand smoke)

so everyone is on statin pretty much in this patient pop. what could be added if very high risk

• zetia per IMPROVE-IT

• IF high risk, on max tolerated statin/ LDL-C at or less than 70 mg/dL

  • if STILL not controleld, can add PCSK9 inhib mAb

is ANY alcohol good for you

apparently NOT. all cancer related to imbibing (throat, gi, rectal— all the way down)

when in SIHD pts do you add icosapent ethyl (vascepa)

• fasating TG’s from 150-499

if SIDHD pts at high risk, what are lipid goals (think terat-resist ASCVD pts)

• LDL<55 mg/dL

• non-HDL< 85 mg/dL

major ASCVD EVENTS, high risk conditions (older, diabetes, HTN, smoker, CKD)

what are classes of meds that reduce mortality risk for SIHD? what is main principle behind this

main principle behind this is that drugs are used to decrease the risk factors for SIHD

• high-intensity statin (THIS IS LIT ASCVD SO)

• antiplatelets— aspirin, or clopidogrel if allergic

• HTN— so acei/arb if comorbid HTN/DM/CKD

• T2DM— so SGLT2i/GLP-1ags— with comorbidities

what are the two high intensity statins? what are their strengths? why high intesity

• high intenisyt bc decrease LDL by 50% or more

• atorvastatin 40-80 or rosuvatstatin 20-40

what is FIRST LINE for SIHD for HTN management

NON-pharm!

what is BP goal for HTN management for SIHD

<130/80 mmHg

so normalyl for HTN, thiazides, DHP-ccbs, ACEis and ARBs. BUT for HTN with CV trouble, what is pref

ACEis (have more data)

• then ARBs, esp if bradykinin with ACEis — cough, angioedema

which ACEi is best

nah they are all same

• you see lisinopril a lot bc its once a day (ex captopril is TID so like no one uses it)

what is A1C goal for SIDH pts with T2Dm

less than 7%

• BUT less than 8-8.5% for those over 65 yo

on slide 46, why is the lisinopril pref over hctz?

bc thepatient has stable ischemic heart disease

what are the two platelets used for prevention (piramry and secondary prevent)

aspriin (shortedn to ASA)

clopidogrel (for asa alllergy)

what is hte enzyme taht is required to get clopidogrel ot active form

clopidogrel !

clop dose for ½ prevention

75 mg daily

aspirin dosing for 1/ 2 prevent

75-100 mg qd (low dose which is 18 mg)

which ppi is ok to give iwth clop bc less cyp2c19 ?

pantoprazole (Protonix)

what are the two types of PCIs (stents given by catheter)

bare metal stent

drug-eluting stent

how long give dual-antiplatelet therapy after bare metal stent

• DUAL antiplate for 1 month (asa AND clop)

tyring to avoid re-thombosis of coronary artery

how long give dual antiplet thearpy after drug-eluting stent? then what give?

• 6 monts dual

• thennn given ASA or clop (usually for 6 months)

this is shown to decrease MACE and bleeding events! crazy work

what is added to ASA and clop to make triple theapry

DOAC!

when would you need TRIPLE therapy (dapt+doac which means asa+clop+riva or apix etc)

post MI or PCI WITH

• a fib

• mechanical heart valves

• - PE/DVT

what are two HARM things from guidlines in regards to SIHD (ccd) on DAPT?

• do not use prasugrel

• do not use NSAIDs

when is clop useful to ADD TO aspirin

onlyyy after PCI

how is triple therapy dosed over time

• DAPT for 1-3 weeks

• then DOAC with clop for 6 months

• then just DOAC

people using DAPT with sihd— what else can be given or protection what is this protection?

• can use PPIs

• to protection GI bleeding

• BUT ONLY IF COMPELLING IND— esp from stress

what is ccd?

chronic coronary disease

• means yes SIHD, must also includes ppl who are not currently having stable angina or myocardial ischemia but has happened in past

what do we want to do to FOR SYMPTOM REDUCTION

decrease myocardial o2 demand, or increase supply

what are the three drugs mainly for angina relief

beta blocker

CCB.

long acting nitrate

• note that you also have your SL nitroglycerin

how do beta blockers affect myocardial oxygen

decrease oxygen demand by decreasing heart rate and decreasing contracility

how do ccbs affect oxygen supply and demand

vasodilation and decreased heart rate

how do LONG-ACTING nitrates affect heart oxygen supply and demand

mostly decrease oxygen demand by decreasing preload, can slighlty increase oxygen supply by vasodilation

when do you add a second anti-anginal (BB, CCB, long act nitrate)?

if you still have symptoms

• try increasing dose of the first drug before you add another one

if you are on two or more anti-anginal durgs and STILL symptom, what to take

ranolazine

what are some LOW DOSE items for the anti-anginals

• BBs: MS is 25 mg; aten is 25 mg; carve 3.125 mg

• ccbs: amlop 2.5 mg; nife 30 mg

• LAN: isosorbide mononirtaes ER 30 mg; dinitrate 10 mg

are both ccbs and NON-dhp ccbs used in chronic cornary disease

YES

how is ccb and non-dhp ccb effect different

non-dhp (verampil/dilt)

• decrease demand by decreasing preload

ccb:

• dipines!

• mostly increase supply to heart by vasodilation of arteries — decreased afterload

ranolazine brand

ranexa

BB ad ef

bradycardia, hypotension

• Fatigue

• Dizziness

• Sexual dysfunction

which of our drugs would decrease oxygen DEMAND by decreasing HR

• Beta blockers

  • non-DHP ccbs (verapamil, dilt )

BB mech/benefit

• decrease HR by decreasing chronotrophy

• decrease contractilty (decrease inotrophy)

• decrease afterload/wall tension

when do beta blockers (which recall are used for symptom relief) NOT also help to reduce MACE

patietns with CCD (SIHD) wihtouttttt previous MI or LVEF under 50%

• this is reduced ejection fraction heart failure

what is chronotropy

heart rate

what is inotropy

contracitilyt — how hard heart can squeeze

what are the THREE beta blockers that ppl with angina (SIHD) and LVEF (reduced) ppl can get

metoprolol succinate, carvedilol, bisoprolol

• we don’t want BBs with ISA (instrict sympathomimetc acitivty— the only BB wiht this is pinodolol)

what is dromotropy

AV node conduction speed

which of our drugs for symptom relief decrease chronotrophy (HR) and contractility (inotropy)

beta blocker, verapamil/diltiazem

• work ON HEART

• decrease O2 demand!

WHAT DO YOU NEED TO CHECK before you change BB dose

BLOOD PRESSURE AND HEART RATE

• taper off as well

so how do dhp ccbs (amlodipine and others that work on periphery) and nitrates effect chronotropy (HR) and contractility (inotropy)

they DONT

• its mostly vasodilation

goal heart rate if on BB (like if its lower no use)

55-60 bpm

what is CI for BBs

prinzmetal’s (vasospastic, variant) angina

• can make spasm worse

names for prinzmetals

variant, vasospastic

what do the dhp do

• peripheral

  • reduces afterload— peripheral vasodilate

what do the n-dhp do ? ad ef

negative chronotrope, inotrope

• constipation, bradycardia