Intern Case Report Talitha Morton, PGY1 - PowerPoint Presentation

Slide1

Intern Case Report

Talitha Morton, PGY1

Slide2

CC: Chest pain

61 yr old male presented to ED w/ substernal

, non-radiating chest pressure

while walking that lasted approximately 30 minutes

.

Bilateral

arm numbness and

weakness.

Bilateral

LE edema last night. Now resolved.

Severe muscle aches x 1 month

Chest discomfort resolved

after taking Imdur. Did not take NTG SL d/t concern for

hypotension.

Denied

shortness

of breath, nausea or

diaphoresis. No

palpitations, orthopnea or PND. No

fever, chills or night sweats.

Compliant

with medications.

Slide3

PMHx

:

CAD

Recent MI

Recent cardiac arrest d/t sustained ventricular tachycardia s/p AICD implantation

HLD

GERD

Meds

:

ASA 81 mg

Effient 10 mg daily

Atorvastatin 40 mg daily

Diltiazem 120 mg daily

Imdur 30 mg daily

Protonix 40 mg daily

Slide4

Allergies

:

Lisinopril

Metoprolol

Surgical Hx

:

AICD

Social Hx

:

Former tobacco user; recently quit smoking

No alcohol or drug use

Family Hx

:

None

Slide5

Vital signs

:

T: 98.4

P: 68

BP: 124/64

RR: 18

O2: 98% RA

Labs

:

CBC:

H/H 12.6/36.4

CMP: unremarkable

Troponin:

0.20

BNP: 61.8

CK: 59

TSH: 0.38

FT4: 1.11

ESR/CRP:

35/8.6

UDS: +BZD. Confirmation test (-)

Slide6

Imaging

:

CXR: mild bibasilar interstitial prominence may be acute or chronic

Echo: LVEF 62%. Normal chamber size and wall thickness. Normal global systolic function.

Slide7

EKG

Slide8

Physical Exam:

Slide9

Started on heparin gtt and given ASA 325 mg in ED

Assessment/Plan:

NSTEMI

DAPT w/ ASA and Effient, heparin gtt, Imdur

and diltiazem and NTG SL prn

Start lisinopril . Hold beta-blocker.

Trend troponin

Echo and Cardiology consult

Obtain records from OSH

Myalgias

CK normal. Start Flexeril. Consider changing atorvastatin to pravastatin.

Hx of cardiac arrest d/t VT s/p AICD

HTN

HLD

Slide10

OSH medical records- EKG

Slide11

OSH medical records

Admitted 1 month prior to presentation to BSW with complaint of chest pain

Acute anterior wall STEMI with troponin peak 1.99

Coronary angiography

:

Left main

: no significant stenosis

LAD

: 100% proximal occlusion with TIMI 0 flow. DES x2 to LAD.

LCx

: no significant disease

RCA

: no significant disease

Echo

: LVEF 45%. Hypokinesis if apical septum, apex and mild hypokinesis of anterior wall

Discharged on ASA, statin, beta-blocker and ACEi

Slide12

Cont.

Repeat admission within one week after discharge with recurrent chest pain

NSTEMI

Coronary angiography:

LM

: 50% diffuse disease. Suspicious for residual dissection from previous stent placement.

DES x1 to LM

LAD

: patent stents

LCx

: 90% stenosis w/ TIMI 2 flow

DES x1 to LCx

Slide13

Cont.

On 2

nd

hospital day the patient experienced cardiac arrest due to VT/VF with “brief” resuscitation

EP study and AICD implantation for inducible VT/VF

Slide14

Cont.

Recurrent chest pain

after AICD placement:

Coronary angiography:

LM

: patent stent

LAD

: patent stents.

70-75% stenosis distal to stent. Improved to 30% with

IC

NTG. Residual area of spasm noted.

Diagonal

:

85% stenosis w/ TIMI 1 flow. Improved to TIMI 3 flow with IC NTG.

LCx

:

stent patent

1

st

OM

:

occluded w/ TIMI 0 flow. Improved to 30% stenosis and TIMI 3 flow with IC NTG.

Discontinue beta-blocker and start CCB and

nitrates.

Avoid ACEi and

beta-blockers

for

coronary vasospasms

.

Slide15

Hospital Day 2

No chest pain or shortness of breath. +myalgias.

Troponin 0.20



0.98



3.72



7.07

Cardiology recommendations:

Increase Imdur

60 mg daily and diltiazem 180 mg daily for hx of coronary vasospasm

Cont lisinopril to decrease endothelial inflammation

Change to

r

osuvastatin 10 mg daily. Statin therapy will reduced inflammation and reduce incidence of vasospasm.

Plan for coronary angiography

Slide16

Coronary angiography:

Triple-vessel CAD

Patent stents

of LM, proximal LAD and mid-LAD

Significant coronary artery spasm in

LCx. 70-80% stenosis improved to 30% after IC NTG.

20-30% stenosis of proximal and mid-RCA

Plan:

Optical coherence tomography (OTC) of

area of

LCx and mid-distal LAD w/ possible intervention given refractory vasospasms despite

aggressive medical

management

resulting myocardial necrosis and malignant dysrhythmias

Slide17

OCT and IVUS

Evaluate for atherosclerotic coronary disease

X-ray coronary angiography w/ contrast media

OCT and IVUS

: Utilizes light vs sound to create an image.

C

ontour of vascular lumen and allows for visualization of the vascular wall. Coronary angiography may be limited in assessment of the extent of atherosclerotic disease due to:

Diffuse atherosclerosis

:

No

focal encroachment

of

the lumen

Complex luminal shapes

: varying severity in multiple views

Compensatory enlargement

: preserve lumen contour

Information about plaque

extent, morphology,

distribution and composition (i.e. calcium) which may influence interventional approach

Extent of stent expansion and apposition against vessel wall

Due to

10-fold higher resolution,

OCT can visualize non-diseased vessels and sub-clinical atherosclerotic disease formation

Slide18

Optical coherence tomography (OCT)Three concentric layersElastic membrane (internal), media (middle) and external elastic lamina (outer) Intravascular ultrasound (IVUS)Three-layer appearance Intima (bright), media (dark) and adventitia (bright)

Slide19

OCT report:

LCx

: patent vessel with atherosclerotic plaque noted in area of spasm correlated with angiography

PCI w/ DES x1 to LCx

Mid-distal LAD

: No significant atherosclerotic disease in area of spasm correlated with angiography

Slide20

Hospital Day 3

Chest

pain x2

overnight that resolved spontaneously within minutes

Troponin

6.39



8.35



13.27

SBP 80-90s

Cardiology recommendations:

Start Ranexa 500 mg BID. Later increased to 1000 mg BID.

Monitor for worsening hypotension

Slide21

Hospital Day 4-5

No chest pain

overnight. Improved

muscles aches

.

Troponin 9.14



7.68



6.54

Cardiology recommendations:

Continue current regimen

Remained asymptomatic overnight. Discharged on hospital day 5.

ASA

and

Effient, Imdur, diltiazem, lisinopril, Ranexa, rosuvastatin

and NTG SL prn

Slide22

Follow-up

Twelve days later:

Admitted for lightheadedness, hypotension

and AKI

Reduced Imdur and lisinopril dosages

Three additional admissions over four months for NSTEMI presumably d/t coronary vasospasm

Repeat Echo:

Mildly

reduced LV systolic function with LVEF of 45-50% and

hypokinesis

of

antero

-apex c/w injury/ischemia

Slide23

Variant angina

Prinzmetal or vasospastic angina

First described by Prinzmetal et al. in 1959

Characteristics

:

Usually younger,

females

with w/o traditional risk factors for

CAD,

except tobacco

use

Episodes

of angina pectoris

, usually at rest and often between midnight and early morning. Usually lasting 5-15 minutes.

ST-elevation

on EKG

Focal spasm of smooth muscle layer of arterial

wall leading to

high-grade obstruction causing transient ischemia or

myocardial

infarction, in some

cases.

Absence

of high-grade coronary artery stenosis

Slide24

Pathogenesis

Vascular

smooth muscle hyper-reactivity

May be focal

,

more

than one site or diffusely

Normal vessel or at the site of atherosclerotic plaques

Vasoconstrictors that provoke spasm: acetylcholine, serotonin, histamine, noradrenaline and dopamine

Autonomic nervous system

Imbalance of vagal and sympathetic tone. Vagal tone often higher from midnight to early morning.

Endothelial

dysfunction as a predisposing factor

Microvascular dysfunction

Slide25

Risk Factors

Tobacco use*

Ephedrine-based

products

Cocaine

, marijuana, amphetamines, alcohol, butane and sumatriptan

Guide-wire or balloon dilation during PCI

Magnesium deficiency

Hx of vasospastic

disease

Migraines,

Raynaud’s phenomenon and aspirin-induced asthma

Slide26

Diagnosis

12-lead EKG

Acute episode:

Transient

ST –elevation in multiple leads (<15 mins)

TWIs, tall

and broad R

wave, absence

of S

wave, taller

T

wave, negative

U wave

Serial cardiac enzymes

Coronary angiography

:

T

ransient ST-elevation

At

least 50%

obstruction at

site of

spasm that

is

reversed

with

IC

NTG

Provocation tests:

Acetylcholine and hyperventilation (rarely used)

Slide27

Cont.

No

ST-elevation present

S

tress test

exclude obstructive coronary

disease

Most

will be normal. 10-30% exercise-induced spasm during stress test.

Ambulatory

EKG

D

etect

ST-elevation

with or without angina

Can also be used to assess efficacy of

therapy because asymptomatic episodes

are

common

Coronary angiography

: Indicated

with normal stress test and ambulatory EKG if high clinical suspicion for variant angina

Slide28

Differential Dx

Fixed

obstructive CAD

Hx consistent

with

variant angina

GERD with esophageal spasm

Cardiac X syndrome

Angina or angina-like

chest pain with

exertion and

normal

coronary arteries without evidence of vasospasm

.

EKG

: ST depression with EST

Proposed pathogenesis

:

Coronary microvascular dysfunction

“Sensitive heart” syndrome. Enhanced sensitivity to intracardiac pain.

Slide29

Differential Dx

ST-elevation

Acute pericarditis

Stress-induced cardiomyopathy

Non-cardiac chest pain w/ early repolarization

V

entricular

aneurysm post-MI

LVH

LBBB

Brugada

syndrome

Slide30

Management

Goal is to

reduce frequency of symptomatic episodes and serious complications

NTG SL

: reduce duration of episode and ischemia

Smoking cessation

Nitrates

and CCB

will prevent

vasoconstriction and promote

coronary artery

vasodilation

Long-acting

nitrates may lead to nitrate

tolerance

Indicated if continued symptoms on CCB or persistent asymptomatic episodes to reduce risk of ventricular

arrhythmia

CCBs

: nefedipine, diltiazem (240-360 mg daily) and verapamil

Statins

: prevent coronary

vasospasm; stabilize pl aques, decreased oxidative stress and inflammation and inhibit thrombogenic response

Slide31

Cont.

Magnesium

:

Single study

. Vasodilation with IV Mg and had reduced chest pain and ST-elevation with acetylcholine provocation

PCI

:

Possible

benefit in medically refractory vasospasm that is associated with mild to moderate obstructive CAD

and when the vasospastic

segment can be clearly identified

Recommend to avoid

:

Non-selective

beta-blockers

ASA at high doses d/t inhibition of prostacyclin production. ASA 81 mg in CAD is

still recommended

.

Triptans

Slide32

Complications

25% untreated patients: MI and arrhythmias

Acute myocardial infarction

Usually with

fixed-obstructive

CAD

Arrhythmias

Heart

block

RCA

Due to

AV-node ischemia

Ventricular tachycardia

LAD

Recommend

AICD placement in sudden cardiac arrest

Slide33

Cont.

VT with high-risk

features:

Fixed-obstructive

CAD

Large ST-elevation

Multi-vessel

spasm on

maximal

or

even submaximal

doses of

CCB

Refer for EP study/possible AICD

VT without high-risk

features:

Maximize CCB dose and refer

for EP study/possible AICD

Maximize

CCB dose and

monitor closely for

arrhythmias

Slide34

Prognosis

Infarct-free

survival at 10-years is >80%

Worse prognosis

associated with

obstructive CAD and multi-vessel

spasms

Slide35



The End



Slide36

References

Intravascular ultrasound, optical coherence tomography, and angioscopy of coronary circulation.http://www.uptodate.com/contents/intravascular-ultrasound-optical-coherence -tomography-and-angioscopy-of-coronary-circulation

. Published

1/28/2014.

Updated January

2015.

Accessed February

15, 2015.

Variant angina

. http://

www.uptodate.com/contents/variant-angina.

Published

unknown.

Updated

February 2015

. Accessed February 15, 2015.

Gaetano AL, Giulia C, Filippo C. Mechanisms of coronary artery spasm.

Circulation

. 2011;124:1774-1782.

Looi KL, Grace A, Agarwal S. Coronary artery spasm and ventricular arrhythmias.

Postgrad Med Journal

. 2012;88:465-471.