CORONARY HEART

DISEASE

Satjit Bhusri, MD
Cardiologist
Lenox Hill Hospital
JEFF CHIANFAGNA RPA-C
LECTURE OVERVIEW
 Chronic Ischemic Heart Disease
 Chronic Stable Angina
 Silent Myocardial Ischemia
 Variant (Prinzmetal’s) Angina
 Acute Coronary Syndromes
 Unstable Angina
 Non-ST-segment elevation MI (NSTEMI)
 ST-segment elevation MI (STEMI)
 Sudden cardiac death (SCD)
CORONARY CIRCULATION
 Left main  2 branches (LAD & CXA)
 LAD located in IV groove giving off diagonal &
perforating branches
 CXA goes left & posterior into AV groove
 RCA in right AV groove  2 branches (marginal &
PDA)
 No connections bt major vessels, however smaller
perforating branching arteries are joined by
anastomotic channels
 With gradual large vessel occlusion, smaller
collateral vessels  in size
 CORONARY ATHEROSCLEROSIS
& PATHOGENESIS OF CAD

 Atherosclerosis is MC cause of CHD

 Atherosclerotic plaque disruption is the most
common cause of MI
 More than 90% of pts with CHD have evidence of
coronary atherosclerosis
 Most pts with CHD have 1 or more stenotic lesions
of 75% or greater
 Plaque formation can affect 1 or all of the major
epicardial coronary arteries
STABLE vs. UNSTABLE PLAQUES

 Fixed (stable) plaques obstruct blood flow & have

thick fibrous caps
 Unstable (vulnerable) plaque have a thin fibrous
cap
 Rupture depends on (1) size of lipid core &
thickness of fibrous cap (2) presence of
inflammation with plaque degradation (3) lack of
SM cells with impaired healing & plaque
stabilization
 Triggers for plaque rupture?
 CHRONIC STABLE ANGINA
 Definition  symptomatic paroxysmal CP or P
sensation due to transient ischemia
 Associated with fixed coronary obstruction
producing a disparity in coronary blood flow &
metabolic demands of the myocardium
 Stable angina is initial manifestation of IHD in
50% of pts with CHD
 Angina is usually precipitated by situations that 
work demands of the heart
 CHRONIC STABLE ANGINA
 Sxs  CP is steady, heavy, P, squeezing, or
suffocating; precordial or substernal with or w/o
radiation to L-shoulder, jaw, both arms or other
areas of the chest; Levine’s sign
 Many pts report fixed thresholds for pain onset,
others report day to day & time of day variations
 CP relieved within minutes by rest or SL nitro
 Anginal “ equivalents” are dyspnea, fatigue &
faintness
CHRONIC STABLE ANGINA
 Risk factors  ???
 PE  often normal, but may reveal evidence of
atherosclerosis at other sites; fundoscopic may
reveal  light reflexes & AV nicking; palpation
may reveal cardiomegaly or abnormal PMI;
auscultation may uncover bruits, S3, S4
 Labs Dx usually made from Hx & PE, however
routine labs should be ordered
 CXR  cardiomegaly? sgs of HF?
 CHRONIC STABLE ANGINA
 EKG  usually normal at rest unless previous
ischemic injury has occurred
 Stress testing  widely used test for dx of IHD;
performed using either standard EKG, echo, or
nuclear imaging; monitors sxs, BP, EKG, wall
motion defects or perfusion deficits before, during &
after physical exercise or pharmacological induced
cardiac exertion
 +EKG stress test  CP, severe SOB or fatigue,
dizziness,  in SBP >10 mmHg, ST-segment
depression >2mm or an arrhythmia
 ST-
segment
depression
 CHRONIC STABLE ANGINA
 Coronary arteriography
 Indications (1) stable angina with severe sxs despite
medical therapy & who are being considered for
revascularization (2) sxs that present diagnostic
difficulties & there is a need to confirm or r/o IHD
(3) pts w/ known angina who have survived cardiac
arrest (4) pts w/ angina & evidence of LV
dysfunction (5) pts judged to be at  risk of having a
coronary event based on stress testing
 CHRONIC STABLE ANGINA
 Management  education, Tx RF & comorbidities,
adaptation of activity, drug therapy, consider
revascularization
 Drug therapy
 Nitrates  systemic venodilators which  myocardial wall
tension & O2 demand
 B-blockers   O2 demand by inhibiting the  in HR, BP,
& myocardial contractility
 CCB  vasodilators producing
 Antiplatelet drugs  ASA or Clopidogrel
 Ranolazine  sodium channel blocker used with a
BB or as a substitute for a BB
 CHRONIC STABLE ANGINA
 Coronary revascularization  performed in pts
with severe sxs despite medical therapy & pts with
severe ischemia on stress testing
 Percutaneous transluminal coronary angioplasty
(PTCA)  balloon dilatation w/ stent deployment;
usually reserved for pts with 1-2 vessel involvement with
normal LV function
 Coronary artery bypass grafting (CABG)  surgical
vessel anastomosis using IMA, SV, or RA; indicated in
pts with: left main coronary artery stenosis, 3 vessel
disease + EF<40%, 2 vessel disease with >75% stenosis
in LAD, or vessel blockages that cannot be reached by
catheters
SILENT MYOCARDIAL ISCHEMIA
 Definition  ischemia without anginal pain
 Etiology  atherosclerosis or vasospasm
 3 populations (1) asymptomatic pts w/o CHD
evidence (2) MI survivors that continue to have
myocardial ischemia (3) pts w/ angina who also have
episodes of silent ischemia
 Explanation for painless episodes is unclear
 Can lead to ischemic cardiomyopathy
 Tx  depends on extent of ischemia, comorbidities,
age, occupation, & RF
 PRINZMETAL’S ANGINA
 Caused by vasospasm of coronary arteries, however
in most instances vasospasms occur in the presence
of nearby plaques
 Pathogenesis of vasospasm is uncertain
 CP usually occurs during rest or may awaken the pt
from sleep; serious arrhythmias can occur during
anginal episodes
 Pts are typically younger with fewer CV RFs
 EKG demonstrates ST-segment elevation
 Mainstay of tx is SL nitroglycerin & CCBs
 ACUTE CORONARY
SYNDROMES (ACS)
ACS includes:
 Unstable angina
 Non-ST-segment elevation (non-Q-wave)
myocardial infarction (NSTEMI)
 ST-segment (Q-wave) myocardial infarction
(STEMI)
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI
 UA defined as CP or angina equivalents with at least
1 of 3 features: (1) occurs at rest (2) severe & new
onset (3) more severe, prolonged, or frequent than
previously
 UA referred to as “ preinfarction syndrome”
 NSTEMI is established if a pt with clinical features of
UA develops evidence of myocardial necrosis as
reflected in elevated cardiac biomarkers
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI

 Pathophysiology  decrease in O2 supply or increase

in myocardial O2 demand
 4 contributing pathophysiologic processes for UA: (1)
plaque rupture or erosion w/ superimposed
nonocclusive thrombosis (2) dynamic obstruction due
to vasospasm (3) progressive & rapidly advancing
atherosclerosis (4)  myocardial O2 demand and/or 
supply
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI
 Clinical manifestations  substernal CP w/
radiation to neck, L-shoulder or L-arm; or anginal
“ equivalents” ; PE similar to stable angina & may
be unremarkable; with large area of ischemia or
NSTEMI, the physical findings can include
diaphoresis, pale cool skin, sinus tachycardia, S3,
S4, rales, & sometimes hypotension
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI
 EKG  ST-segment depression and/or T-wave
inversion
 Cardiac biomarkers  NSTEMI pts have  CK-
MB and Troponin I
 Diagnostic pathways  clinical hx, EKG, cardiac
markers, & stress testing
 Goals (1) recognize or ROMI (2) evaluate for rest
ischemia (3) evaluate for significant CAD
 HIGH OR CHEST PAIN,
LOW LIKELIHOOD ATYPICAL
INTERMEDIATE
ISCHEMIA PAIN
LIKELIHOOD

RECURRENT OBSERVE
PAIN +EKG/ CARDIAC
MARKER MARKERS &
EKG

NO RECURRENT PAIN -EKG/ MARKER

+ STRESS EXERCISE OR - STRESS

TEST PHARMACOLOGIC TEST
STRESS TESTING
(+/- IMAGING)

ADMIT TO DISCHARGE
UA/STEMI TX HOME & FOLLOW
PATHWAY UP WITH PMD
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI
Medical Tx  anti-ischemic & antithrombotic
 Anti-Ischemic Tx
 Nitrates  SL 1st, if pain persists after 3 doses given Q5
minutes, then IV nitro should be given
 B-blockers  IV Metoprolol followed by PO with a
targeted HR of 50-60 bpm
 CCBs  (Verapamil or Diltiazem) recommended in pts
who have persistent or recurrent sxs after full dose
nitrates & B-Bs or any C/I to B-Bs
 If pain persists, then administer morphine sulfate
 ARBs or ACE-I & statins for long-term prevention
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI
 Antithrombotic Tx
 ASA  chewable aspirin should be initial tx
 Clopidogrel (Plavix)  ADP inhibitor; combo of ASA &
Plavix recommended for pts who are not at excessive risk
for bleeding
 Heparin  UFH or LMWH should be added to ASA &
Plavix: LMWH appear to be superior
 GP IIb/IIIa inhibitors  used for high-risk pts when an
invasive management is intended (PCI); includes
Abciximab, Eptifibatide, & Tirofiban
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI
INVASIVE VS. CONSERVATIVE STRATEGY
 Benefit of early invasive tx in high-risk pts with
multiple RFs
 Invasive  pre-treat 1st , then coronary
angiography is done w/i 48 hours of admission,
followed by PCI or CABG
 Conservative  anti-ischemic & antithrombotic
therapy followed by “ watchful waiting”
 UNSTABLE ANGINA &
NON-ST-ELEVATION MI
LONG TERM MANAGEMENT
 Risk factor modification
 Stop smoking
 TLC
 BP control
 Tight glycemic control
 B-blockers
 Statins & ACE-I (plaque stabilization)
 ASA & Plavix x 9-12 months, followed by ASA
thereafter
 ST-SEGMENT ELEVATION MI

 AMI is one of the MC dx in hospitalized pts

 650,000 new & 450,000 recurrent AMIs annually
 30% early (30 day) mortality rate; more than ½ of
deaths occur before pt reaches hospital; 1 of every
25 surviving pts die in the 1st year after AMI
 30-40% AMIs affect RCA, 40-50% affect LAD &
the remainder affect the LCX
 ST-SEGMENT ELEVATION MI

 Pathophysiology  vessel injury & plaque rupture

followed by thrombotic occlusion
 Occurs when plaque fissures or ruptures & when
conditions favor thrombosis, so that a mural
thrombus forms at rupture site & leads to coronary
artery occlusion
 STEMI may also be caused by coronary emboli or
spasm & a wide variety of systemic inflammatory
diseases
 ST-SEGMENT ELEVATION MI
 Amount of damage depends on:
 Territory supplied by affected vessel
 Is vessel totally occluded?
 Duration of occlusion
 Quantity of blood supplied by collateral vessels
 Demand for O2 of affected myocardium where blood
supply has suddenly been limited
 Native factors that can produce early spontaneous lysis of
occlusive thrombus
 Adequacy of perfusion in infarct zone when flow is
restored in the occluded artery
 ST-SEGMENT ELEVATION MI

 Clinical presentation  deep, visceral, heavy,

squeezing, or crushing substernal CP w/ or w/o
radiation; diaphoresis, N/V, anxiety, palpitations,
sense of impending doom
 Proportion of painless STEMIs is greater in pts
with DM & it increases with age
 Elderly pts may present with sudden onset of SOB
which may progress to pulmonary edema
ST-SEGMENT ELEVATION MI

 PE  anxiety, pallor, diaphoretic & cool

extremities; tachy or bradycardia, hypo or
hypertension, PMI may be difficult to palpate, +S3
or S4,  intensity of S1, a mid or late systolic
murmur or pericardial friction rub may be present;
pts with large infarcts may have rales or sgs of
shock; fever wouldn’t be expected acutely, but
may be present during the first week of recovery
 ST-SEGMENT ELEVATION MI

 EKG  total occlusion produces ST-segment

elevation; most pts with ST-segment elevation
develop Q waves
 When a thrombus is not totally occlusive or there is
a rich collateral network, no ST-segment elevation
is seen
 ST-SEGMENT ELEVATION MI
 Where is the infarct ??
 Lateral wall  leads I, aVL, V5, V6 (LCX artery)
 Inferior wall  leads II, III, aVF (RCA or PDA)
 Anterior  leads V2, V3 (LCA or LAD diagonal branch)
 Septal  leads V1 & V2 (LCA and/or LAD septal branch)
 Anteroseptal  leads V1 – V4; (LCA & LAD or left
main)
 Posterior  ST-segment depression in leads V1, V2, V3
or V4; involves RCA or LCX artery
 ST-SEGMENT ELEVATION MI

 Serum cardiac markers  proteins released in large

quantities from necrotic heart muscle
 Troponin I & Troponin T  gold standard cardiac
markers for MI; rises w/I 4-8 hrs
 Total CK or CPK  rises w/i 4-8 hrs & generally returns
to nl by 48-72 hrs; lacks specificity
 CK-MB  more specific over total CK in that it is not
present in significant extracardiac tissue
 Myoglobin  1st marker released during AMI, lacks
specificity & is rapidly excreted in the urine
 ST-SEGMENT ELEVATION MI

 Cardiac imaging
 2D-echo  wall motion defects, EF, pericardial effusions,
aneurysms; cannot distinguish between old & new infarcts
 Doppler echo  VSDs & mitral regurgitation (2
complications of STEMI)
 Myocardial perfusion scans  used less than echo b/c
more difficult to obtain acutely; infarcted tissue displays
irreversible ischemic deficits; cannot distinguish between
old & new infarcts; not specific for dx of AMI
 ST-SEGMENT ELEVATION MI
MANAGEMENT
 ASA  chewable; other anti-thrombotic agents are heparin
& GP IIB/IIIA inhibitors
 O2  give 2-4L/min of O2 via nasal canula
 Nitroglycerin  SL X 3 doses; if CP continues or ongoing
ischemia on EKG, then IV nitro
 Morphine  2-4 mg IV Q5 minutes
 B-Bs  Metoprolol 5mg Q5 min X 3; 15 min after last
dose 50mg PO QID X 48 hrs, then 100mg BID
 ACE-I  given w/i 24 hrs to all pts who are
hemodynamically stable w/ STEMI
 All pts with AMI get B MONA
BBs  HR which
prolongs diastole
and increases
myocardial
perfusion
 ST-SEGMENT ELEVATION MI

MANAGEMENT STRATEGIES
 1 tool for screening pts & making triage
decisions is initial EKG; with ST-segment
elevation of at least 2 mm in 2 contiguous
precordial leads or 1 mm in 2 limb leads, strongly
consider reperfusion therapy
 Deciding between PCI & fibrinolysis depends on
capabilities of the facility
 ST-SEGMENT ELEVATION MI
 Limitation of infarct  central necrosis area occurs
w/ AMI; fate of surrounding ischemic tissue
improved by restoration of perfusion,  O2 demand,
preventing accumulation of noxious metabolites &
reperfusion injury
 Timely reperfusion prevents ischemic & injured
zones from becoming infarct zones
 Maintain balance between O2 supply & demand w/
pain control,  tachycardia & HTN extends time
“ window” for myocardial salvage
 ST-SEGMENT ELEVATION MI

 Primary PCI  restores perfusion when carried

out in 1st few hrs; more affective than fibrinolysis
when performed by experienced operators &
associated w/ better short & long-term clinical
outcomes
 Compared w/ fibrinolysis, primary PCI is
preferred when available especially if dx is in
doubt, cardiogenic shock is present, sxs present
for >2-3 hrs
 ST-SEGMENT ELEVATION MI
 Fibrinolysis  fibrinolytics should ideally be
initiated w/i 30 min of presentation (door-to-needle
time < 30 min); includes tissue plasminogen
activator (tPA), streptokinase, tenecteplase (TNK) &
reteplase
  infarct size, limits LV dysfunction &  incidence
of serious AMI complications
 Pts tx w/i 1-3 hrs of onset of sxs benefit most,
modest benefits are seen w/i 3-6 hrs & mild benefit
appears possible up to 12 hrs
 ST-SEGMENT ELEVATION MI
 Absolute contraindications to fibrinolysis
 Hx of cerebrovascular hemorrhage at any time
 Nonhemorrhagic CVA w/i the last year
 Marked HTN (SBP >180 and/or DBP >110)
 Suspicion of aortic dissection
 Active internal bleeding (excluding menses)

 Relative contraindications
 Anticoagulants, recent (<2 wks) invasive or surgical
procedure, known bleeding disorder, pregnancy,
hemorrhagic eye condition
 Complications
 Hemorrhage
ST-SEGMENT ELEVATION MI

 Post AMI hospital phase management

 Coronary care units  continuous cardiac monitoring
 Activity  bedrest for 1st 12 hrs; 2nd or 3rd day pts
typically can ambulate in room & to shower
 Diet  NPO or clear liquid diet for 1st 4-12 hrs
 Bowels  stool softeners are recommended; laxatives
may be necessary
 Sedation  helps withstand the periods of inactivity;
commonly used agents are benzos
 ST-SEGMENT ELEVATION MI

 AMI complications
 Ventricular dysfunction  LV undergoes series of
remodeling changes in infarcted & non-infarcted segments
when left untreated leads to HF
 Heart failure  results from infarction of 20-25% of LV
and will result in congestive lung sgs & sxs
 Cardiogenic shock  extreme form of HF; results with
>40% infarction of LV or MV dysfunction
 RV infarction  inferoposterior AMI can progress to RV
infarction causing sgs/sxs of right HF
 ST-SEGMENT ELEVATION MI

 AMI complications
 Acute MR ischemia or papillary muscle rupture
 Arrhythmias  most deaths due to fatal arrhythmia
occur in the 1st few hrs after AMI; other arrhythmias
include VPCs, idioventricular rhythms, SVTs, sinus
bradycardia & AVB
 Hypovolemia  results from  fluid intake during acute
illness, vomiting due to AMI or narcotic medications,
fluid loss due to prior diuretics
 Myocardial rupture  LV free wall rupture occurs in
<1% of pts & usually results in immediate death
 ST-SEGMENT ELEVATION MI
 AMI complications
 Recurrent CP  25% of pts w/ AMI; requires prompt
angiography & possible revascularization or repeat
fibrinolysis
 Pericarditis  pericardial pain are frequent in pts w/
transmural STEMI; managed w/ ASA
 Thromboembolism 10% of pts; emboli originate from
LV mural thrombi
 LV aneurysm  describes dyskinesis or local expansile
paradoxical wall motion on echo; true aneurysms are
composed of scar tissue; complications include HF,
emboli, & arrhythmias
 SUDDEN CARDIAC DEATH
 Definition  unexpected death due to cardiac
causes acutely (generally 1 h of sx onset) in a
person w/ known or unknown cardiac disease in
whom no previously diagnosed fatal condition is
apparent
 350,000 individuals annually; in many
individuals SCD is the 1st clinical manifestation of
IHD
 More than 80% of SCD events occur in
individuals with CAD
 SUDDEN CARDIAC DEATH
 Pathophysiology  lethal arrhythmia; although
ischemia can impinge on conduction system &
create instability, in most cases the arrhythmia is
triggered by electrical irritability of myocardium
distant from conduction system that is induced by
ischemia or other cellular abnormalities
 Precipitating causes: VHD, DCM, HCM, isolated
hypertrophy, myocarditis, pulmonary HTN,
congenital heart defects
 SUDDEN CARDIAC DEATH
 M & M  survival usually depends on setting,
presence & timely use of AED & BLS, rapid EMS
arrival & performance of ACLS
 History  obtaining a hx from family members or
witnesses is necessary to gain insight into events
surrounding SCD; pts at risk for SCD may have sxs
of IHD; a hx of LV impairment (EF <30-35%) is
the single greatest RF for SCD
 SUDDEN CARDIAC DEATH
 PE  survivors have variable PE findings
depending on co-morbidities
 Labs/Diagnostic studies  ROMI work-up &
imaging studies will be obtained to evaluate
cardiac & coronary structure & fx
 TX  life-saving tx of acute life-threatening
arrhythmias depends on ability to reverse these
rhythms; survivors need long-term medical
therapy & may need mechanical revascularization
procedures