M&M

4/5/2011
 weed12.jpg

M&M
4/5/2011

Ikue Nakayama
PGY-3
HPI
 74 yo F

 Hx of HTN, HLD, heavy smoking, PVD, CAD s/p 2

stents (mLAD and D1) 2 yrs ago

 CP for 2wks, Precordial CP radiating to her L breast,

which also woke her up at 5am, relieved by SL NTG
 No DOE/PND/orthopnea/palpitation/N/V

 Started on nitro PRN, imdur and increased dose of BB

by outpt MD with relief of symptoms

 Presented to PAH for elective catheterization

PMHx
 HTN
 HLD

 CAD s/p multiple stents 2 yrs ago

 Carotid artery stenosis
 PVD

 Colon CA s/p resection 6 yrs ago

PSHx
 R carotid endarterectomy 2 yrs ago
 Colon CA resection 6 yrs ago
 TAH
 Appendectomy
Social Hx Allergy
 Smoking (25 ppy),  PCNhives
quit 4 wks ago
 No ETHO
Medicine
 ASA 81mg daily
 Plavix 75mg daily
 Zetia 10mg daily
 Metoprolol 25mg BID
 Imdur 30mg daily
 SL NTG PRN
 Forteo sub Q daily
Elective cath from Day stay Unit
(day 0)
 Premedication: ASA 325mg, Benadryl 50mg,
Famotidine 20mg

 Pre-lab: Hb 14.1, Cr 0.76, Plt 212, K 3.5 INR

1.0, PTT 27

 Lft heart cath from R femoral artery

 Initial VS: BP 100/75, HR 60(sinus), SpO2 96

 FYI---Forteo
recombinant human PTH (rhPTH)
manufactured using a strain of E. coli modified by recombinant DNA technology
has an identical sequence to human PTH

Indicated for Tx of High Risk for Fx

(1)Postmenopausal Women and Men with Osteoporosis with hx of osteoporotic fx, multiple risk
factors for fx, or patients who have failed other tx
(2) Men and Women with Glucocorticoid-Induced Osteoporosis at High Risk for Fx

Once a day
injection, one pen
last for a month
During cath procedure
 Dialudid 0.5mg IV, angiomax 7.5cc IV and 17cc/hr
given

 Multiple ballon inflation were performed to the 1st Diag

and mLAD lesions and 3 stents were inserted.

 Plavix 300mg PO given

 ACT 414 sec

 VSS stable throughout

Cath results
Hypertrophic
LV
EF >50%

RCA40% Diag 2X 70%->0%

stenosis stenosis s/p 2 stents
IVUS 11.4mm2 (atom 2.25-
12mmx2)

mLAD 70% and

75% ->0% stenosis
s/p 1 stent (atom
2.25-32mm)
Cath results
 IVUS (intravascular ultrasound)

 Specialized catheter with a ultrasound probe attached to the distal end of the catheter to to see from inside
blood vessels to visualized endothelium of blood vessels

 Used to determine both plaque volume within the wall of the artery and/or the degree of artery stenosis.

 The progressive accumulation of plaque within the artery wall over decades: vulnerable plaqueleads to MI and
stenosis

 E
.

specially useful when

angiographic imaging is
unreliable (lumen of ostial
lesions, multiple
overlapping arterial
segments); also used to
assess the effects of
treatments of stenosis
A little History
 In 1977, PTCA (balloon angioplasty) was introduced.

 By the mid-1980s, PTCA and CABG were being performed at

equivalent rates. PTCA restenosis was frequent (30–40%),
usually within the 1st year. In ~3% of PTCA cases, failure of
the dilation and coronary artery dissectionemergency CABG.

 In 1986, the first coronary stent in a human patient was

implanted. Stenosis reduced because the stent hold open the
artery and repaired dissections of the arterial wall.

 Early difficulties with coronary stents included a risk of early

thrombosis(1)Coating stainless steel stents with platinum or
gold (2) High-pressure balloon expansion of the stent (3)
aspirin, ticlopidine or clopidogrel
A little History cont’d
 Stents remained vulnerable to late restenosis caused by
neointimal tissue growth (Macrophages accumulate around the
stent, and nearby smooth muscle cells proliferate)(1) drug-
eluting stents (sirolimus, paclitaxel)
UFH and ACT(activated clotting time)
 UFH is the standard of care for procedural anticoagulation

 UFH has an unpredictable dose-response relationship

(1)activate platelets within the first few minutes of dosing
(2) bind to nonspecific cellular and protein(acute phase
reactants).

 Because of unpredictable pharmacokinetics, IV UFH requires

laboratory monitoring and dose adjustment.

 In the cardiac cath lab, the ACT has been used to monitor
UFH. Target ACT values are 250-300 secs (HemoTec device)
and 300-350 secs (Hemachron device).

 When GP IIb/IIIa receptor antagonists are used, the target

ACT is reduced to >200 seconds with either device.
PCI risks (1)
 Ischemia; The patient is usually awake during angioplasty
for symptoms monitoring. (CP can also occur because the
balloon briefly blocks off the blood supply to the heart.)

 MI (during and shortly after the procedure occurs in 0.3%)

 Heart muscle injury (elevated CK-MB, troponin I/T occur in

up to 30%)have been associated with higher risk of
death, subsequent MI and need for repeat PCI

 VF non-sustained VT

 Bleeding and hematoma from the insertion point in the

groin->As flow from the artery into the hematoma may
continue, pseudoaneurysm occurs
PCI risks (2)
 Infection at the skin puncture site

 Dissection of the access blood vessel (including aortic

dissection)less common/serious with the radial
artery access.

 Allergic reaction to the contrast dye

 Kidney dysfunction with pre-existing kidney disease

 Stroke
 Death( less than 2%)
PCI risks(3) Pseudoaneurysms

 cause pain, swelling and bruising

 Treatment Options

(1) none if small

(2) surgery
(3) place pressure over the puncture site (via mechanical
device or u/s guided)sedation or analgesia required
(4)injection of thrombin through the skin into the swelling.

1st line----compression
2ne line---thrombin injection if compression fails.
Coagulation cascade inhibitors
Warfarin---pesticide against rats/mice;
used as a medication in the 1950s;
inhibit clot formation; best suited in
areas of slowly-running blood (veins,
the pooled blood behind valves and
dysfunctional cardiac atria.
Possibly a smaller risk of
bleeding.
Smaller risk of
osteoporosis and HIT
Heparin—usually
made from pig
Angiomax-- a specific and reversible direct
intestines, produced
thrombin inhibitor; short, potent, specific,
by basophils/mast
and a reversible; also inhibiting thrombin-
cells; prevents
mediated platelet activation and aggregation
clots formation
Used for angina, NSTEMI. STEMI or
and extension.(no
HIT undergoing PCI in conjunction with
break down of
ASA
exsiting clots--
unlike tPA).
 Anti-plt agents

They prevent
platelet
aggregation Integrilin –used during
and thrombus PCI or treat ACS
formation.

Persantine-- inhibits
thrombus formation
chronically and causes
vasodilation at high doses
over a short time.
After cath
 Brought to SCU. 2hrs later, pt c/o nausea. Found to have
SBP drop to 30s HR 50s

 NSS 2L bolus as well as Dop and Neo drip

startedresponded

 ACT 220s Hb 10.8(14.1)

 EKG: no EKG changes

 Stat TTE showed mod (1cm)* pericardial effusion, RV

collapase ?early sign of tamponade

 Transferred to ICU; need to place a catheter in pericardial

space for hemodynamic unstability
FYI
 Pericardial effusion size

Small-------<100ml, width <1cm, localized

Medium------100-500ml, width 1-2cm,
circumferential
Large-------- >500ml, width>2cm,
circumferential
TEE results
Cardiac tamponade
 Fluid begins to enter the pericardial space, pressure starts to
increase.

 Presses on the heart and forces the septum to bend into the
left ventricle. With each successive diastolic period, less and less
blood enters the ventriclesdecreased stroke volome
obstructive shock

 occurs when the pericardial space fills up with fluid faster than the
pericardial sac can stretch. (~100 ml)

 Causes: myocardial rupture (typically MI), cancer, uraemia,

pericarditis, retrograde aortic dissection, post heart surgery 2/2
clogged chest tube

 Treatment: pericardiocentesis (through the fifth intercostal space,

and aspirating fluid or emergency pericardial window (cut open the
pericardium to drain surgery is provided to seal later
Pericardial window
day 0

 3hrs post-cath, patient was brought back to cath lab

for draingae of pericardial fluid
 Found to have equalization of pressures210cc of
pericardial fluid removed. Wedge pressure found to
be low (~12) indicating need for further volume
resuscitation.
 PCWP is also useful in evaluating blood volume status when fluids are
administered during hypotensive shock. Goal is to maintains PCWP between
12-14 mmHg. If >20, pulm edema likely present.
Right cath result
 Pre tap  Post tap

PCW 15 12
PA 22/15 24/12
RV 22/15 24/8
Pericard 15 8
PA sat 59% 56%
day 0
 Pt was given 2l NS overnight and cont Dopamin
8cg/kg/min, Phenylephrine 60mcg/min

 7hrs post cath, BP 99/60, HR 80, no venous

engorgement

 Rt femoral cath to be flushed with heparin q8hrs

 ½” nitropast q6hrs to prevent coronary artery

vasoconstrition
day 0
 8hrs post-cath, Hb 7.9(1014)

 Increased requirement of Dopamin, Levophed,

Neo drips

 With tender LUQ abdomen, retroperitoneal

bleeding was suspected

 CTscan of abdmen/chest and 2unit RBC

transfusion arranged
day 1
 CT result
day 1(still midnight)
 12 hrs post-cath, Hb 6.4

 CT finding d/w IR-on call and coil embolization of L

hepatic artery planned

 A focal pseudoaneurysm found at the distal branchof

the L hepatic artery with evidence of active
extravasation

 D/t technical difficulty and small branches supplying

the pseudoaneurysm, particles infection instead of
micro-coil was selected.

 Vascular surgery consulted

Hepatic Embolization
 Embosphere®  Cleared by the FDA in 2000
for marketing in the U.S. for
hypervascularized tumors
and AVMs.

 Injecting agents, usually

particles, through a catheter
and into the blood vessels

 Since this product is uniform,

spherical shape and soft,
slippery surface, it is easy to
inject through small
catheters, resulting in a more
even distribution within the
vessel network.
day 1
 Still with abd pain with gurading and rebound (?peritoneal
irritation from bleeding)

 DA off and Pnenylephrine gradually weaned throuhout the day

 In/Out 7544(RBC1200)/1453(urine 1383)

 Hb 11.1 (after 4 units of RBC); on plavix 75 mg daily and ASA 325

mg daily (with EDS)

 Plt 78(272 pre cath); heparin sq held

 Femoral line taken out

 No fever, with WBC 15.7(band 7%) empiric abx after blood cx

taken (vanc, aztreonam, flagyl)
day 2
 Less abd pain with less tenderness

 Pressors weaned off completely

 No fever
 In/Out 5463(RBC 300)/1160(urine1080)
 WBC/Hb stable
 Elevated LFTs (AST 2382 ALT 1694, T-bil
1.2)

 Pericadial drain~80cc/daythe pig tail

catheter removed without complication
day 3
 Noted to be more SOB

 CXR c/w increased volume overloaded

 In over past 3 days, 12L net positive
 Lasix 20mg IV given

 LFTs trending down (AST 2382782 ALT 1694796)

 Afebrile, BCx 1/5 GPC in cluster-assessed as

contamination; cont emperic abx (bcx: staph hominis)
day 4
 Additional lasix 20mg IV for increased
SOB. Xopenex/advair added

 Encourage pulm toilet/OOB

 Paf with RVR noted  IV/PO metoprolol

restarted
day 6~d/c
 Transferred to SCU(day 6)

 Paf responded with IV metoprolol

 Repeated IV lasix as needed

 LFT trending down

 WBC/plt improved
 Hb stable

 Completed total of 7days of Abx

 Repeated CT(day 8) showed no evidence of bleeding

day 6~d/c
 Ongoing diarreha(day4~); c. diff (-) GI
consultrecent use of abx with Hb drop(hemo-
occult+) EGD, Flex sig perforemd

EGD: gastritis
Flex sig: no pseudomembraneous, no colitis

 TTE (day 8): minimal pericardial effusion

 Discharged!! (day 12)

Stent restenosis and
thrombosis
 In PCI, lumen enlargement is created by splitting the
atherosclerotic plaque stretching of the arterial
lining.

 The arteries response with injury-and-repair reaction.

-Initial 72 hrs: plt/fibrin deposition (acute inflammation)

-Over the next 2 wks: lymphocytes/macrophages replace

neutrophils. Proliferating vascular smooth muscle
cells make extracellular matrix form neointima
DES is not always safer(1)
 resolved the problem of restenosis (good!)

 reduced endothelialization (induced thorombus

formation), increased inflammation, and increased
peri-stent fibrin deposition effective anti-platelet
therapy is mandatory

 induce expression of tissue factor by sirolimus and

paclitaxel activation of the coagulation system.

 The polymers used to load DES cause inflammation

with eosinophilic cells (hypersensitivity reaction?
prothrombosis)
 DES is not always safer(2)
pre-DES era post-DES era
early stent thrombosis(<30-days)0.9% early stent thrombosis0.6%
late stent thrombosis(>30days) 0.65% late stent thrombosis0.7%.

At 6 months follow-up, stent thrombosis At 6 moths follow-ups, stent

70% incidence of death or MI thorombosis24% incidence of death,
69% with nonfatal MI

 Thrombosis may be quantitatively minor problem(0.5-2%)

 However, it has a major risk of MI and death. (Mortality due to
stent thrombosis: as high as 45 %)
 Thrombosis can happen at any time!
Managements for DES thrombosis
 Effective dual anti-platelet tx
(aspirin/clopidogrel) for 12 months. Aspirin for
life-long. (Gradual entothelial coverage of
stents)

 Stents coated with CD34-antibodies increase

and accelerate endothelial coverage.

 Furthermore, biodegradable stents? decrease

late and very late stent thrombosis
sudden occlusion of DES
 When plavix is stopped, even for a few days, some
patients experienced often fatal MI.

 A recent report appearing in the American Journal of

Cardiology suggests that stopping Plavix is more
dangerous than previously realized.

 For these patients discontinued antiplatelet therapy

during the first 12 months, nearly 30% of them
experienced stent thrombosis or death. (a risk which
was double that experienced by patients who
continued their antiplatelet tx).
Great areas of this case
 Patients were promptly evaluated and made a
proper judgement. (SCU/ICU transfer, stat
ETHO, transfusions)

 Even relatively rare complication—tamponade

and hepatic artery injury, they were detected
promptly and treated with a great team work
across the different specialities.

 Pt got better and discharged safely despite of

thoses adverse events!!
learning points from this case
 Cath procedure has life-threaten
complication and bleeding on
ASA/plavix/heparin can be very critical.

 However, EDS thrombosis is fetal stopping

plavix can be life-threaten as well.

 Sources of bleeding can be anywhere. Be

careful for patient’s new complain and
physical exams.
 Thank you for listening!
Special thanks to:
Dr Mahr, Dr Banka
Dr Haber, Dr Kempf

Dr Policastro,
Bora