sanger heart & vascular institute symposium 2015 · sanger heart & vascular institute...

S a n g e r H e a r t & Va s c u l a r I n s t i t u t e S y m p o s i u m 2 0 1 5

Cardiovascular Update For Primary Care Physicians

Glen A Fandetti, MD, FACC, FSCAICardiovascular Medicine and Interventional Cardiology

Sanger Heart and Vascular Institute

Evaluation and Management of Acute Pulmonary Embolism

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Sanger Heart & Vascular Institute Symposium 2015

Disclosures

I have nothing to disclose

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Why is a Cardiologist speaking about Pulmonary Embolism (PE)?

• These patients often present with:– Chest Pain– Arrhythmias– Leg Pain and Edema– Hemodynamic Instability: Hypotension, Cardiac Arrest– Abnormal Cardiac Imaging Studies & Biomarkers

• VTE shared risk factors with many cardiac disease states:-Advanced age, Smoking, CHF, Diabetes, HTN, Sedentary lifestyle

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Burden of VTE (Venous Thromboembolism): Acute PE & DVT

VTE kills more people each year than breast cancer, HIV, and traffic accidents…combined1,2

– Estimates of >200,000 deaths each year in US attributable to DVT/PE1,3,4

– Affects 1/1000 people annually – ~600,000 hospitalizations annually in

the United States for DVT and/or PE5

– Healthcare costs associated with DVT/PE in 2011 are estimated to be up to $10 billion1

4

CDC Reported Causes of Annual Deaths in the United States

41,078

9406

36,216

100,000

0

20,000

40,000

60,000

80,000

100,000

120,000

BreastCancer

HIV TrafficAccidents

VTE2

*

2

2 1

CDC = Centers for Disease Control and Prevention.*An estimated 100,000 deaths each year are attributable to DVT/PE.1. Centers for Disease Control and Prevention. http://www.cdc.gov/NCBDDD/AboutUs/documents/NCBDDD_StrategicPlan_2‐10‐11.pdf. Accessed September 11, 2012. 2. Centers for Disease Control and Prevention. http://www.cdc.gov/nchs/data/nvsr/nvsr60/nvsr60_60_03.pdf. Accessed October 3, 2012. 3. Heit JA. Arterioscler Thromb Vasc Biol. 2008;28:370‐372. 4. Heit J et al. Blood. 2005;106:267A. 5. Centers for Disease Control and Prevention. MMWR. 2012;61(22):401‐404.

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There is Renewed Interest in Venous Thromboembolism (VTE) Management?

• Novel oral anticoagulants with FDA approved VTE indication• More Data from Large Scale Thrombolysis Trials

– PEITHO (NEJM 2014) • Increased Role For Cardiovascular Expertise:

– Echo imaging for Acute RV strain diagnosis– Analysis of cardiac biomarkers– Education: Pulmonary HTN and Venous disease– Evolving Endovascular Therapies for VTE

• Support for System Wide Best Practice Algorithms for Acute PE Care: CODE PE

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Cardiovascular Update For Primary Care Physicians 2015

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Case36 year old female on OCP for uterine fibroids w recurrent bleeding is 1 week s/p recent severe L ankle sprain.-Urgent care prescribed partial weight bearing . -She chose bedrest & develops L calf pain which progresses proximally-Office with PCP:

-Now describes R lower rib cage pain (thought secondary to her crutch)-Exam: Mild Respiratory distress, L leg/thigh swelling, RR-20O2sat 90% on RA, BP 108/80

……Next steps?

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Venous Thromboembolism (VTE)Diagnostic Testing Pathways

• Testing for DVT and PE involves 3 components:– Clinical risk assessment (probability)– Blood Tests (D-Dimer)– Vascular Imaging

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Case: ECG

ST‐ HR ~110

PE Evaluation and Diagnosis: Modified Wells

• Pretest probability:– Low (<2 points)– Intermediate (2-

6 points)– High (>6 points)

VARIABLE POINTS

S/S of DVT 3.0

HR >100 1.5

Immobilization (bed rest >/= 3d) OR surgery within 4 weeks

1.5

Prior DVT or PE 1.5

Hemoptysis 1.0

Malignancy (treated within the past 6 months or palliative

1.0

Other diagnoses less likely than PE 3.0

Evaluation and imaging is dependent upon estimated pretest probability (Modified Wells Criteria)

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Venous Thromboembolism (VTE)Clinical Risk Assessment

Patients with High or Intermediate risk can be treated while waiting for results of further diagnostic tests

-Patients with Low risk may not need imaging tests

DVT and PE are both VTE, but they are NOT the same• They have different clinical implications and one can be

present without the other• BUT…..

The Acute Treatment for both is essentially the same

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D-Dimer Testing• Elevated in plasma in the presence of acute

thrombolysis – Due to simultaneous activation of coagulation and fibrinolysis

• HIGH NEGATIVE PREDICTIVE VALUE– Normal D-Dimer renders acute VTE unlikely

• LOW POSITIVE PREDICTIVE VALUE– Fibrin split products are very common in a variety of conditions:

• Cancer• Inflammation• Bleeding • Trauma Positive D-Dimer unhelpful in this case

• Surgery• Necrosis

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Testing for DVTLower Extremity Duplex U/S

• First line• High sensitivity/specificity for

DVT– Whole leg >> Proximal veins only

• Can miss proximal (iliac) DVT– CTV if pretest probability high

• Widely available• Cost Effective

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Death

V T E R i s k F a c t o r s

Small DVT

Big DVT

PE

~10%

~50%

<5%

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resolve

30-50%

<5%

post-thrombotic syndrome

Death

V T E R i s k F a c t o r s

Small DVT

Big DVT

PE

~10%

~50%

<5%

thromboembolicpulmonary

hypertension

90%

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Venous Thromboembolism (VTE)• Vascular Imaging for PE

• Multi-Detector CT (MDCT)– Has replaced V/Q scanning for diagnosis of PE– High radiation dose is problematic – Iodinating contrast can be nephrotoxic

• Ventilation/perfusion (V/Q) lung scanning– Consider in:

• Pregnancy (perfusion only)• Severe CKD• Contrast Allergy

• Pulmonary Angiogram– For patients undergoing heart cath once ACS is ruled out– For planned endovascular intervention

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Testing for PEMDCT: Multi‐Detector CTA Gold Standard

Rapid, Sensitivity/Specificity>90%; assesses RV strain, PE burden; R/o tamponade & aortic dissection

PE

RV/LV Ratio

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CaseLabs: -Chem7-wnl, Hgb ~10.2-trop < .04-cBNP 30-D- Dimer >150

MDCT:R Lower Lobe segment PEPartially obstructedRV/LV <.8

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Acute PE – Risk Stratification• Not based solely on

radiologic findings• The presence of “lots” of

VTE isn’t enough to call it “massive”

• Need to determine clinical picture– Co-morbidities– Risk of hemodynamic

collapse• Syncope,shock arrest

– Cardiac arrest– Syncope

Risk Stratifying Acute PE

Cardiac Biomarkers

Trop I>.14 ng/mlcBNP >90 pg/ml

Clinical DataPESI Index

AgeRisk Factors

Vitals

RV StrainOn MDCT or Echo

RV/LV >.9&

Clot Burden and Location

Acute PERisk

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Mortality:

70-95% 20-50% 5-10% < 3%

Cardiac arrest

Clinical High Risk PE

(Massive)

Intermediate Risk PE

(Submassive)

Low-Risk PE(Nonmassive)

extensive PE hypotension overt RHF

extensive PE no hypotension

sPESI>1 RVD on echo Tp, BNP

~5% ~5% ~30% ~60%

Acute PE

BNP = brain natruiretic peptide; RHF = right heart failure; RVD = right ventricular dysfunction; Tp = troponin

sPESI=0 no RV strain nl Tp, BNPSubsegmental clot

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Cardiospecific Biomarkers• Troponin ‐ released from right ventricle Injury

• Cardiac BNP ‐ released from cardiac myocytesin response to elevated pressures

• A normal troponin and BNP can safely exclude high risk patients with a negative predictive value of 97‐100%

(Kucher et al; Circulation 2003;108:2191-4)

Trop I > .14 ng/ml

> 90 pg/ml

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RV Strain• An RV/LV ration of >.9 was shown to be and

independent predictive factor for HOSPITAL MORTALITY

• RV hypokinesis on baseline echo following PE with a ~40% higher mortality rate

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Echocardiogram: RV Strain

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Low Risk PE definition

• Patients with the lowest short‐term mortality in acute PE are those who are:– normotensive with normal biomarker levels

– no RV dysfunction on imaging– sPESI =0

She is not Low Risk because of sPESI >1

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Intermediate Risk (Submassive) PE definition

• Acute PE without systemic hypotension (systolic blood pressure 90 mm Hg) but with either:– RV dysfunction

• Hypokinesis• Dilitation: RV/LV diameter >.9 on MDCT or Echo• BNP >90 pg/ml • Appropriate ECG Changes (RBBB, etc.)

– Myocardial necrosis • Troponin I >.14ng/ml

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Intermediate Risk PE therapy• ANTICOAGULATION (AC)- HEPARIN

– AC therapy prevents further clot growth– Consider Single Drug NOAC’s for stable patients

• Oxygen supplementation• Telemetry monitoring

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Thrombolysis in Acute PE

• ‘The decision to administer a fibrinolytic agent in addition to heparin anticoagulation requires individualized assessment of the benefits vs risks’

• Potential Benefits:– Rapid resolution of symptoms (SOB, CP, distress)– Stabilization of CV/respiratory status w/out ventilator or pressor

support– Reduce RV damage and decrease pulm HTN– Harms: Major & Minor Bleeding

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Lysis and Intracranial hemorrhage:Efficacy at the cost of safety

Study Intracranial Hemorrhage (Fibrinolysis

Group)ICOPER(Goldhaber SZ, et al. 1999)

9/304 (3%)

PEITHO (Meyer G, et al. 2014)

10/506 (2%)

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The Larger the Dose, the greater the Risk!!!

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EKOS: Low Dose Ultrasound Facilitated Localized Thrombolysis.

Concept: Ultrasound causes reversible disaggregation and separation of un-cross-linked fibrin fibers, increasingthrombus penetration of thrombolyticdrugs.

ULTIMA Trial. Kucher N, et al. Circulation 2014;129:479-486.

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Endovascular Therapy for Acute PE

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Thrombolysis in Acute PE (PEITHO)

SubmassivePE* R

Standard therapy: IV heparin > 48 h LMWH overlapping with warfarin

Standard therapy + IV bolus tenecteplase

Follow-up

x 1 mo.N~1,000

2007-2010G. Meyer

Primary outcome: composite of all-cause mortality + hemodynamic collapse (CPR, sBP <90 >15 min) within 7 daysSecondary outcomes: death, hemodynamic collapse, recurrent symptomatic PE, stroke, major bleeding within 7days; death <30 days

*RV dysfunction on echo or CTPA + elev troponin but normal BP

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Case

• 18 hours after initiating LMWH, ptdeveloped excessive menstrual bleeding, diaphoresis

• Hgb Dropped to < 8• Otherwise, patient remained stable on tele

with improvement in her O2 Saturation • Anticoagulation d/c following

recommendation of OB/Gyn consult • Next step?

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Case: Retrievable Filter Placed

• Big Concern:• Up to 80% are NOT removed!

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Accepted Indication for an IVC Filter

Uncertain (controversial) indications: • Big DVT + poor cardiopul. reserve• “Recurrent” VTE/failure of Rx• Primary prophylaxis

Recent PROXIMAL DVT or PEPLUS an absolute contra-indication to full

anticoagulation

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Case: VideoFilter Retrieval

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High-Risk (Massive) PE definition

• Acute PE with: – Cardiac arrest / hemodynamic instability– sustained hypotension

• systolic blood pressure 90 mm Hg for at least 15 minutes OR requiring inotropic support not due to a secondary cause (arrhythmia, sepsis)

• Remember: The presence of “lots” of PE isn’t enough to call it “massive”

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Suspected High-Risk PE• Initial care should consist of:

– Systemic Anticoagulation ASAP– Supplemental oxygen for O2 sat <90%– Admit to the intensive care unit:

• Significant hypoxemia • Hemodynamic compromise

– Mechanical ventilation for respiratory failure– For Hypotension:

• IVF• Vasopressor Support

0%

10%

20%

30%

40%

50%

60%

70%

RVPO(Echo)

Hypotension Shock CPR

In‐Hospital M

ortality

Mortality Spectrum in PE

W Kasper. J Am Coll Cardiol 1997;30:1165‐1171/ Konstantinides

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Surgical Embolectomy• PE with shock without time for or

contraindication to systemic thrombolytic therapy (Grade 2C).

• RA clot/paradoxical (PFO) associated with VTE

• High mortality/morbidity but can be life saving

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Intraoperative Photo

R

L

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Who can help me with this

Acute PE?

ED Cards Pulm Hospitalis

t

Yawn…the trop & BNP seem too low to be serious.

Show me the data for

Rx of Submassive

PE.

Cards read the Echo, so….

Pre CODE PE

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Code PE Program:The Vision

– Increase Acute VTE Public Awareness– Seek multidisciplinary clinical input

• By phone (or bedside if emergent)– Identify clinical experts

• Multi-Specialty• Pharmacy• PCP/Outpatient Anticoagulation Clinics

– Utilize Best Practice Treatment Algorithms– Standardize Order Sets & CANOPY Notes– Create CHS Acute PE Registry– Track our Outcomes as New Treatment Strategies are

Implemented“A great way of improving relationships/collaboration among multiple specialties”

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Duration of Anticoagulation

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44%↓

JUPITER: Rosuvastatin Prevents VTE• VTE pre-specified secondary endpoint of

JUPITER– Symptomatic PE– Symptomatic DVT

• Rosuvastatin decreased occurrence of VTE

– 43% reduction VTE (p=0.007)– Significant reductions in both

provoked and unprovoked events– Driven by reduction in symptomatic

DVT• Postulated mechanisms

– Beneficial downstream effects of statins on the coagulation profile via effects on signaling proteins

– ↓ tissue factor, Factor II expression– ↓ Factors V, VII activation– ↑ protein C activity

N Engl J Med 2009; 360:1851.

LDL cholesterol < 130 mg/dL and hs‐CRP > 2 mg/L

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VTE & CODE PE Management 2015

• Know who is at risk for VTE• Make the correct Diagnosis• Rapid LMWH or UFH• Risk Stratify your PE patients using the proper tools• Treat the Subtype of PE appropriately….CODE PE• Attempt to define the duration of anticoagulation post PE

Statin• Ensure proper clinical follow-up

Thank you!

[email protected](m) 704‐975‐3199

sanger heart & vascular institute symposium 2015 · sanger heart & vascular institute...

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