229814.pptLiver disease in and heart failure pregnancy

Liver disease in pregnancy

1. CORONARY HEART
DISEASE
JEFF CHIANFAGNA RPA -C
Satjit Bhusri, MD
Cardiologist
Lenox Hill Hospital

2. 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)

4. 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

7. 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

9. 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?

12. 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

13. 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

15. 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?

16. 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

17. ST-
segment
depression

19. 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

21. 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

22. 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

26. 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

27. 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

28. 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)

29. 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

30. UNSTABLE ANGINA &
NON-ST-ELEVATION MI
Pathophysiologydecrease in O2supply or
increase in myocardial O2demand
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 O2demand and/or supply

31. 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

32. UNSTABLE ANGINA &
NON-ST-ELEVATION MI
EKG ST-segmentdepression 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

33. OBSERVE
CARDIAC
MARKERS &
EKG
HIGH OR
INTERMEDIATE
LIKELIHOOD
ATYPICAL
PAIN
CHEST PAIN,
LOW LIKELIHOOD
ISCHEMIA
EXERCISE OR
PHARMACOLOGIC
STRESS TESTING
(+/-IMAGING)
ADMIT TO
UA/STEMI TX
PATHWAY
DISCHARGE
HOME & FOLLOW
UP WITH PMD
+ STRESS
TEST
-STRESS
TEST
RECURRENT
PAIN +EKG/
MARKER
NO RECURRENT PAIN -EKG/ MARKER

34. UNSTABLE ANGINA &
NON-ST-ELEVATION MI
Medical Txanti-ischemic & antithrombotic
Anti-Ischemic Tx
NitratesSL 1
st
, 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

35. 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

37. 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 1
st
, 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”

38. 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

39. 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 1
st
year
after AMI
30-40% AMIs affect RCA, 40-50% affect LAD
& the remainder affect the LCX

40. 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

42. 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

43. 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

44. 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

45. 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

48. 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

50. 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1
st
marker released during AMI, lacks
specificity & is rapidly excreted in the urine

52. 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

53. 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

54. BBs HR which
prolongs diastole
and increases
myocardial
perfusion

55. 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

56. ST-SEGMENT ELEVATION MI
Limitation of infarctcentral necrosis area
occurs w/ AMI; fate of surrounding ischemic
tissue improved by restoration of perfusion, 
O2demand, 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

59. ST-SEGMENT ELEVATION MI
Primary PCIrestores perfusion when
carried out in 1
st
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

60. 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

61. 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

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

63. 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

64. ST-SEGMENT ELEVATION MI
AMI complications
Acute MRischemia or papillary muscle rupture
Arrhythmiasmost deaths due to fatal arrhythmia
occur in the 1
st
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

68. 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

72. 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 1
st
clinical
manifestation of IHD
More than 80% of SCD events occur in
individuals with CAD

73. 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

75. 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

76. 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