underwriting coronary artery disease · brief anatomy and physiology refresher ... co-morbid...

Underwriting Coronary Artery Disease

Jennifer Lockwood, CLU, FALU, FLMI, ACS

Technical Director, Large Case Underwriting

Valerie Kaufman, MD, FACC, DBIM

Vice President and Medical Director

September 2019

2

Brief anatomy and physiology refresher• Cardiac

• Coronary

Background• Epidemiology

• CAD pathophysiology

Case studies

Assessing CAD risk - tips and “tools of the trade”

Co-morbidities

Agenda

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PreTest!!! True or False?

1. CAD is the single leading cause of death in American women

2. In most individuals, the Right Coronary Artery supplies blood to part of the interventricular septum

3. Longstanding angina precedes most myocardial infarctions.

4. Obstruction of the Left Main Coronary artery is the most dangerous location.

5. Co-morbid rheumatoid arthritis, obstructive sleep apnea and/or testosterone supplementation do not add to CAD risk.

4

Anatomy of the Heart

Author: Ties van Brussel Wikipedia Author: ZooFari Wikipedia

The heart is fixed within the body by the major vessels attached to it and by the

fibrous skeleton provided by the heart valves and their supporting annuli. The

ventricles and atria are free to enlarge and contract against the fixed plane.

http://upload.wikimedia.org/wikipedia/commons/e/e0/Heart_diagram-en.svg

http://upload.wikimedia.org/wikipedia/commons/e/e0/Heart_diagram-en.svg

http://commons.wikimedia.org/wiki/User:ZooFari

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The conduction system of the heart consists of specialized fibers that are adapted to the conduction of the electrical impulse at a much faster rate than that of muscle tissue. The SA node generates an impulse which spreads throughout the atria and on to the AV node. The AV node reconstitutes the impulse and delays transmission to the ventricles to allow the atria to finish contracting.

Conduction System of the Heart

Author : Madhero88 - Wikipedia

http://commons.wikimedia.org/wiki/User:Madhero88

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Cardiac Cycle

Author: Kalumet, selbst erstellt, 28.11.2005. - Wikipedia

Electrical

• SA node fires

• Impulse spreads throughout atria and to AV node

• AV node reconstitutes/slows

• Impulse enters Bundle of His, bundle branches, Purkinje fibers

• Conduction system repolarizes

Mechanical

• Atria contract (systole)

• Pressure increases in ventricles, closing mitral and tricuspid valves; atria relax (diastole)

• Ventricles contract (systole); aortic and pulmonic valves open

• Ventricles relax (diastole), aortic and pulmonic valves close

• Mitral and tricuspid valves open and ventricles fill passively

• Atrial “kick” contributes 10-15% of cardiac output

http://commons.wikimedia.org/wiki/User:Kalumet

7

The Hard-Working Heart

The myocardium is constantly working

• Pumps about 5 liters of blood/minute

• About 100,000 heartbeats/day

• Pumps about 2,600 gallons of blood/day

The coronary arteries must provide adequate oxygen and nourishment

Cardiac reserve

• Cardiac output may be increased to as much as 35 liters/minute

• Normal coronary arteries can increase myocardial blood supply 5-6 fold if needed

• Early stages of disease of the heart often associated with reduced cardiac reserve

• Cardiac reserve diminishes with aging

• Atrial fibrillation reduces cardiac output by 10-15%

8

Categories of Cardiac Disease

Coronary artery disease

Valvular heart disease

Cardiomyopathy

Congenital heart disease

Hypertensive heart disease

Primary Arrhythmias

9

CAD Epidemiology

CAD death rate has fallen since 1968

16.5 million Americans ≥ 20 years of age have CAD

In 2014, CAD caused 364,000 deaths

• 207,000 in men

• 157,000 in women

• CAD was an underlying cause in about 1 of every 7 deaths

• Point of reference: 41,000 deaths due to breast cancer in 2014

Benjamin EJ, Blaha MJ, Chiuve SE et al on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics – 2017 update: a report from the American Heart Association. Circulation 2017;135.

US Data

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The Coronary Arteries

Wikipedia, Patrick J. Lynch, medical illustrator

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Coronary Artery Branches and Territory

Branches Supplies

Left Main Coronary

(LMCA)

• Left anterior descending (LAD)

• Left circumflex (LCx)

• Ramus intermedius

• Most of the left ventricle

Left Anterior

Descending (LAD)

• Septal perforators

• Diagonals

• Anterior, lateral and apical walls of left

ventricle

• Anterior 2/3 ventricular septum

• Right and left bundle branches

Left Circumflex

(LCx)

• Artery to SA node – 40%

• Obtuse (left) marginals

• Posterior Descending (PDA) – 15%

• Left atrium

• Lateral and posterior left ventricle

• Sometimes, the SA node

Right Coronary

(RCA)

• Artery to SA node – 60%

• Artery to AV node

• Acute (right) marginals

• Posterolateral

• Posterior descending (PDA) – 85%

• Right atrium

• Right ventricle

• SA node

• AV node

• Posterior 1/3 ventricular septum

• Posterior left ventricle

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Coronary Arteries by CT

13

Structure of an Artery

Intima

Media

Adventitia

Endothelium

Lumen

14

Normal Resting State

DEMAND SUPPLY

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Normal Coronary Reserve

DEMAND SUPPLY

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CAD Manifestations

Signs and symptoms

• Angina

• EKG changes

• Stress test abnormalities

• Acute events/Myocardial infarction

Coronary atherosclerosis

• Coronary artery calcium

• CT angiogram

• Coronary angiogram

How Does CAD Cause Mortality?

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Stable Obstructive Plaque

Thick Cap

Small Lipid Core

Calcium

18

Inadequate Coronary Reserve

DEMAND

SUPPLY

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Impaired Resting Function of Coronary Arteries

DEMAND

SUPPLY

20

Nonobstructive Vulnerable Plaque

Large

Lipid Pool

Thin Cap

Inflammation

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Inadequate Coronary Reserve

DEMAND

SUPPLY

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Ruptured Plaque with Thrombus

Large

Lipid Pool

Thin Cap

Inflammation

Thrombus

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Acute Occlusion of Coronary Artery

DEMAND

NO SUPPLY

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Acute Coronary Events

Acute coronary event = hospitalized MI or death

More than 1 million coronary events each year

Estimated to be an additional 165,000 silent MIs each year

About 36% of coronary events are fatal

Only 18% of MIs are preceded by longstanding angina

15-20% die of initial manifestation

Benjamin EJ, Blaha MJ, Chiuve SE et al on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics – 2017 update: a report from the American Heart Association. Circulation 2017;135.

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Diagnosis and Assessment of CAD

Anatomic Imaging

Coronary angiogram

CT angiogram

Coronary artery calcium score

Cardiac MR

Functional Tests

Stress tests

• Exercise

• Pharmacologic

Imaging with stress tests

• Myocardial perfusion imaging (MPI)

• Stress echocardiogram

Resting echocardiogram

Rhythm monitors

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Treatment of CAD

Goals

Reduce symptoms

Prevent complications

Slow progression

Types of Treatment

Risk factor modification

Medications

• Beta blockers

• Nitrates

Revascularization

• Percutaneous interventions (angioplasty, stents)

• CABG

Management of co-morbidities

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How Does CAD Cause Mortality?

Arrhythmias

Arrhythmias!

Arrhythmias!!!

Heart failure

Catastrophes

Pause It!

Assessing CAD Risk

Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of

Medicine 1 (2). DOI:10.15347/wjm/2014.010.ISSN 2002-4436. - Own work

https://en.wikiversity.org/wiki/WikiJournal_of_Medicine/Medical_gallery_of_Blausen_Medical_2014

https://en.wikipedia.org/wiki/Digital_object_identifier

https://doi.org/10.15347/wjm/2014.010

https://en.wikipedia.org/wiki/International_Standard_Serial_Number

http://www.worldcat.org/issn/2002-4436

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Factors Influencing Risk in CAD

Key Factors

Extent of disease

Left ventricular function

Risk factors

• Framingham: cholesterol, BP, smoking status

• Others: diabetes, activity, weight, inflammatory markers

Modifiers

Age at onset

Ischemia (symptoms, stress test results)

Arrhythmias

Co-morbidities

NTproBNP

Functional capacity

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Red Flags

Early onset of CAD before age 50

Very heavy atherosclerotic plaque burden

Left main coronary artery stenosis > 50%, not bypassed

Unstable symptoms or unfavorable stress test, not evaluated

Multiple procedures – indicative of disease progression

LVEF < 40% or left ventricular aneurysm

Recurrent or chronic heart failure

Significant ventricular ectopy or implanted cardioverter-defibrillator (ICD)

Comorbidities, such as diabetes, chronic inflammatory conditions, OSA

Uncontrolled risk factors, such as current smoking

Case Studies

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Case Study #1

53 year old man, nonsmoker

5’11”, 231 lbs. BP 136/88

Insurance labs: chol 145, HDL 45, ratio 3.2

HTN, CAD, low T

Meds: Losartan, atorvastatin, clopidogrel, ASA

Hospitalized for chest pain 8 months ago; had stent

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Case Study #1

8 months ago

• New onset of chest pain, called typical angina

• Treadmill exercise test was positive at 3 minutes into exercise

• Left heart catheterization (LHC) with coronary angiography and percutaneous coronary intervention (PCI)

Findings:

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Case Study #1

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Case Study #1: Analysis Does the description “One-Vessel CAD” adequately describe the plaque burden?

• 30% LAD

• 20-30% Ramus

• 30-40% LCx

• 95% in the RCA (stented)

How well are risk factors managed?

Any Red Flags?

The angiogram findings are more consistent with

moderate CAD rather than limited

Risk factors suboptimally managed

37

Case Study #2: Missing Pieces?

Had cardiac cath in 2016 due to chest pain with elevated troponin

• 80% stenosis mid LAD

• Nonobstructive disease in LCx and RCA

• LVEF 45% with anterolateral hypokinesis

• S/P stent in mid LAD

• Placed on statin, ASA and BP medication

Post-stent stress test in 2016 was negative, and echo showed normal LV function with LVEF 60%

Has had clinical follow up, but no follow up testing. Should we postpone?

56 year old man, nonsmoker

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Case #2

CASE SUMMARY

NSTEMI 2016

Stent in LAD; nonobstructive disease in LCx and RCA

Stress test 2016 - good exercise capacity, normal LV function, negative for ST changes and arrhythmias

Asymptomatic with regular clinical follow up

Good risk factor management

Important Questions How good is the information we have regarding symptoms

and activity?

Is he consistently taking his medications, and are the medications effective?

Is he diabetic?

Does he smoke?

Is there a current EKG?

Is there an NTproBNP?

Is this a good CAD case or a not-so-good one?

Should he have had a more recent stress test?

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Case Study #2: Important Questions

How good is the information? Very good. Has regular alternating PCP and Cardiology visits. No new cardiac symptoms and remains very active.

Are the medications effective in reducing risk factors? Yes. Chol 150, HDL 55, BP 126/78

Is he diabetic? No. HgbA1c on insurance labs is 5.4%

Does he smoke? No

Do we have a current EKG? No. Most recent EKG is from 2/18 (normal)

Do we have NTproBNP? Yes – favorable at 57

Good CAD case, but still no stress test.

Should we postpone???

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Follow Up for Stable Ischemic Heart Disease (IHD)

“After being treated, asymptomatic patients are typically at low risk for adverse events”

Key component in follow up: monitor symptoms

Frequency of visits – data sparse. Recommendations based on expert opinion

• May vary by local practice patterns, role of PCP, etc

• Every 4-6 months x 1st year

• Every 6-12 months thereafter if stable

Fihn SD, Gardin JM et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force, American Association of Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2012;60:e44-164.

2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline

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Follow Up of Stable IHD – Clinical History and Physical

History

• Response to therapy, adverse effects, adherence to recommendations

• Development of new conditions or changes in existing conditions

• Changes in symptom pattern

• Decreasing functional capacity

Physical exam

Blood Testing

EKG



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Follow Up Stress Testing in Stable IHD

“The data supporting follow up testing are sparse and insufficient to support routine, repeat testing in asymptomatic individuals”.

Could be considered

• Evaluation of incomplete revascularization

• Assessment of the adequacy of medical therapy

• Need to evaluate coronary status in anticipation of major noncardiovascular surgery



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Follow Up Stress Testing in Stable IHD

Exercise EKG testing

• If at least moderate physical functioning and no disabling comorbidity

• And an interpretable EKG

Stress echo or MPI

• If EKG not interpretable

• If previously required imaging with stress

• Known or at high risk for multivessel disease

Pharmacologic stress test if unable to exercise


When new or worsening symptoms (not consistent with acute coronary syndrome)

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Appropriate Use Criteria (AUC)

Developed “to support utilization of high-quality patterns of procedure use (i.e., appropriate use) while informing efforts to reduce use when benefits to patients are unlikely.”

An appropriate imaging study is one in which the expected incremental information, combined with clinical judgment, exceeds the expected negative consequences

Practice guidelines consistent with AUC

Appropriate, May be Appropriate, Rarely Appropriate

Wolk MJ, Bailey SR, et al. ACCF/AHA/ASE/ASNC/HFSA/HRS/SCAI/SCCT/SCMR/STS 2013 multimodality appropriate use criteria for the detection and risk assessment of stable ischemic heart disease. J Am Coll Cardiol 2014;63:380-406.

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Appropriate Use Criteria

Ex EKG Stress

MPI

Stress

Echo

Stress

CMR

CAC CCTA Cath

< 2 years after PCI R R R R R R R

≥ 2 years after PCI M M M M R R R

< 5 years after CABG R R R R R R R

≥ 5 years after CABG M M M M R R R

Asymptomatic, After Revascularization

Symptomatic, After Revascularization

Ex EKG Stress

MPI

Stress

Echo

Stress

CMR

CAC CCTA Cath

Eval of symptoms M A A A R M A

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Case Study #2: Analysis

Any indication of clinical change?

• No new symptoms

• Still taking medications, which appear to be effective

• No apparent change in functional status

• No new risk factors

• EKG unchanged through 2018

• Current NTproBNP favorable

Consider offering with currently

available evidence

47

Co-Morbid Conditions

Co-morbid means present in addition to main impairment

3 ways co-morbid conditions interact

• Overlap: such as Obesity and DM

• Additive: such as mild RA and CAD

• Multiplicative: such as COPD and smoking

Synergy: the working together of two or more things (muscles, drugs or diseases, for example) to produce an effect greater than the sum of their individual effects

2 + 2 doesn’t always = 4

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Important Co-Morbid Conditions for CAD

Diabetes mellitus

Smoking

Obstructive sleep apnea (OSA)

COPD/emphysema

Other atherosclerotic disease such as Peripheral Arterial Disease (PAD, PVD) and Stroke

Chronic inflammatory conditions

Other cardiac impairments, such as valvular disease and LVH

Any other conditions that either increase the cardiac workload, impede oxygenation, or adversely affect normal blood coagulability

49

Diabetes as a Co-Morbidity

What role does diabetes play as a risk factor, and how does it affect the CAD risk?

What are we looking for when considering a risk with CAD and diabetes?

50

Case Study #3

48-year-old male, build 6.1.195, BP 110/80

Part 2 indicates hx of DM and CAD

Current A1C at 9.5, HOS neg/normal

2 years prior had angioplasty (PTCA) to the LAD and RCA

Heart cath confirmed LAD and RCA disease

Found to have DM at time of CAD diagnosis

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Severity of the CAD:

• CAD in a relatively young individual – early onset

• PTCA to LAD and RCA

Would consider the CAD as moderate to severe

Severity of the diabetes:

• Duration of diabetes = 2 yrs.

• Control of the diabetes is fair to poor

• No known diabetic complications

Significant interaction between co-morbidities – at least

additive, possibly multiplicative. Overall High Risk

52

Case Study #4

6’1”, 221 lbs

On atorvastatin, B12, testosterone and tramadol

FH: father had heart problems and died at age 61

Labs: chol 117, HDL 41. Urine + for cotinine

L5/S1 decompression in 2014. No limitations, uses tramadol prn.

60 year old man, uses dip

53

Case Study #4

Screening CAC 528 in 2015 (around 90th percentile)

• Negative nuclear stress tests in 2015 and 2017

• Nuclear stress test 2019

o Exercised 8 minutes, 10.1 mets

o Heart rate increased from 69 at rest to 136 (85% PMHR).

o BP increased from 120/80 at rest to 160/100 at peak.

o No symptoms, ST changes or arrhythmias with exercise

o Nuclear scan showed a small reversible inferior defect

o LVEF 45% with inferior hypokinesis

Can you make an offer at this time?

54


Can we make an offer as is?

• Negative stress tests in the past; recent stress test now positive

• No cath/angiogram

• Nicotine user

Any concerns with the testosterone use?

Testosterone use may accelerate progression.

Nicotine use unfavorable. But no Red Flags.

Suggest moderately increased risk

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Case Study #4

What if there was an NTproBNP on insurance labs and it was 13 pg/ml?

What if the NTproBNP was 456 pg/ml?

56

Natriuretic Peptides

Family of peptides

First of the family identified in the 1980’s

Effects

• Natriuretic

• Diuretic

• Vasodilator

• ? Antiproliferative

Play role in • Regulation of blood pressure

• Regulation of plasma volume

• Attenuation of cardiac hypertrophy

57

Natriuretic Peptides

1983: Atrial (A-type) Natriuretic Peptide

• Made in the cardiac atria

• Normal hearts secrete very small quantities of ANP

• Elevated in those with LVH and mitral valve disease

1988: Brain (B-type) Natriuretic Peptide

• Discovered in pig brain

• Present in high concentrations in myocardium, mostly ventricular

• Secreted in relatively large quantities

• Elevated in many types of cardiac disease

1990: C-type Natriuretic Peptide

• Found in vascular endothelium

• Vasodilatory and anti-proliferative effects

Early 1990’s: Dendroaspis (D-type) Natriuretic Peptide

• Found in atrial tissue

• Functions similar to ANP

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B-Type (Brain) Natriuretic Peptides

Made and stored as a prohormone

When released, is cleaved into 2 fragments

• BNP – biologically active, short half-life

• NTproBNP – not biologically active, but long half-life and stable at room temperature

Released from myocardial cells in response to wall stress (pressure, stretch)

Initial use to differentiate cardiac vs. pulmonary cause for acute SOB

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NTproBNP Fun Facts

May be elevated in many types of cardiac disease – not just heart failure

• Atrial fibrillation

• Valvular heart disease

• LVH

• Cardiomyopathy

• CAD

May be before clinical onset of cardiac disease

• As much as 75% systolic dysfunction in the community is undetected

• About 500,000 people in the US have HCM, and most are unaware

Predicts all cause mortality, even after adjusting for traditional risk factors

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NTproBNP in Insurance Screening

Ability to predict occult cardiovascular disease and all cause mortality

Obtained by simple blood draw; stable in transit

Cost through insurance labs is acceptable

Increasing utilization in insurance screening

• Instead of stress tests

• As additional age and amount requirement

• ? Instead of EKGs

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Interpreting NTproBNP Results

“Normal” range varies by age and gender

Insurance labs use NTproBNP

BNP ≠ NTproBNP: different ranges

Different labs will use different normal ranges – use the actual value and your guidelines for interpretation

Two different scenarios

• NTproBNP obtained as an age-and-amount insurance requirement

• NTproBNP or BNP obtained by clinician due to a cardiovascular concern

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Risk Assessment with NTproBNP

Rate for underlying impairment

Elevated NTproBNP adds to the risk

• Consider additional debits when the NTproBNP is

o > 75 pg/ml in men

o > 175 pg/ml in women

• Risk becomes very high when NTproBNP is

o > 300 in men

o > 500 in women

Favorable values should also be considered

With known heart disease

63

Risk Assessment with NTproBNP

NTproBNP predicts all-cause mortality

Best studied in those age 50 and up

Identifies different risk than EKGs and not known if equivalent

Risk increases when the NTproBNP is > 150 pg/ml

Risk becomes very high when NTproBNP iso > 400 in men

o > 500 in women

Favorable values should also be considered

Without known heart disease

64

Case Study #4: Final Analysis

What if there was an NTproBNP on insurance labs and it was 13 pg/ml?

What if the NTproBNP was 456?

Slightly more favorable risk

Significantly higher risk – consider Decline

65

Sleep Apnea as a Co-Morbidity

How does sleep apnea affect your body and what impact does it have on a CAD risk?

When can we consider someone with CAD and sleep apnea?

66

Case Study #5A

55-year-old male, build 5.10. 250, BP 138/90

Part 2 indicates CPAP use for sleep apnea

5 years prior had a 3-vessel CABG

APS describes the sleep apnea as severe: AHI >70, 02 desat to 68%

Most recent visit indicates only partial compliance with CPAP, “doesn’t wear it every night”

CAD described as severe with bypass to the LAD, RCA and circumflex; also notes mild non-obstructive disease of the diagonal and posterior descending (PDA)

MVR: 2 careless driving violations in the past 2 years

67

Severity of CAD:

• Three-major-vessel disease with mild disease in two branch arteries

Would consider CAD as severe to very severe

Severity of OSA:

• AHI over 70, lowest 02 saturation 68%

• Non-compliance with treatment

Would consider the sleep apnea as severe

Case Study #5A: Analysis

High risk, suggest Decline

68

Case Study #5B

61-year-old female, build 5.6.150, BP 125/70

Part 2 reports using CPAP for 10 years; 2 years prior had a 1-vessel angioplasty

APS describes sleep apnea with an AHI of 19, lowest O2 desaturation 88%, and good compliance with CPAP nightly; feels rested, refreshed every morning

APS confirmed CAD history with PTCA of the obtuse marginal

69

Case Study #5B: Analysis


• Single-vessel disease involving 1 branch artery

Would consider the CAD as mild

Severity of the OSA:

• AHI of 19

• Compliant with treatment

Would consider this mild sleep apnea

Suggest adding debits for both

impairments

70

Case Study #6

55-year-old female smoker

Build 5.2.115, BP 150/93

Treated HTN and high cholesterol

FH: father died at age 46 due to MI; mother had CABG at age 60, lived to age 67. Two brothers (ages 52, 50) with coronary stents

Insurance labs: Chol 168, HDL 50

Stents to the LAD and RCA 2 years prior to application

71

Case Study #6

Echo (2 yrs ago):

• Normal LV size and EF (56%)

• Mild LVH with septum 1.3 and posterior wall 1.2

• Mild left atrial enlargement 4.3

• Minimal aortic sclerosis without stenosis

Stress test with nuclear imaging 18 months ago:

• Resting EKG with minor nonspecific ST-T changes

• Completed 6:42 min. without any symptoms or arrhythmias

• Borderline ST changes with exercise and hypertensive response

• Nuclear imaging negative

72


Severity of CAD:

• Obstructive CAD involving the LAD and RCA

• Nuclear stress test suggesting no ischemia

Would consider CAD as Moderate to Heavy

Risk factor profile:

• Early onset in a woman

• Unfavorable family history

• Smoker

• BP not well controlled

What about the LVH?

Complex case with CAD plus LVH plus

aortic valve disease. Suggest

discussion with M.D. for the appropriate

rating – possible high substandard

73

Chronic Inflammatory Conditions as a Co-Morbidity

How does chronic inflammation interact with CAD?

How should these conditions be handled when co-morbid with CAD?

74

Case Study #7

63 year old woman

5’3”, 143 lbs, BP 130/84

Long hx of RA, on etanercept (Enbrel)

2 years ago, had atypical chest pain

Coronary artery calcium score 750 (between 95-99th percentile; at 770 would be > 99th percentile)

CTA – scattered nonobstructive lesions in LAD, LCx and RCA

Atypical pain attributed to RA; no further episodes of chest pain

75


Manual says

• 90-94th percentile: rate as Limited CAD

• 95-99th percentile: rate as Moderate CAD

• > 99th percentile: rate as Heavy CAD

Would you rate as Moderate or Heavy?

But wait, the CTA showed only nonobstructive disease??

Consider bumping to Heavy CAD category due to

underlying RA and adding the RA and CAD ratings

76

COPD/Emphysema as a Co-Morbidity

How is COPD a risk factor, and what effect does it have on someone with CAD?

How should this combination of impairments be approached?

77

Case Study #8A

59-year-old female, build 5.4.210, BP 135/92

Part 2 mentions 2-vessel angioplasty 8 years prior and a 3-vessel CABG 2 years ago

Quit smoking at time of CABG – prior to that smoked 1½ packs/day

APS: COPD dx’d 5 years ago, FEV1 was 45%

No cardiac cath information reported

Most recent PE from last year indicated she had quit smoking years ago, but still smokes on an occasional/social basis

No current or recent pulmonary function tests

78



• History of multiple CAD procedures in a middle-aged individual

• Overweight with elevated blood pressure

Would consider CAD as Heavy

Severity of the COPD:

• Former 1 ½-packs-per-day smoker

• 5 years ago FEV1 was 45%, no subsequent PFTs available

• Admits to current social cigarette use

Would consider COPD severe, at best

High risk, unfavorable co-morbidities.

Consider Decline

79

Case Study #8B


Part 2 described single-vessel angioplasty 5 years ago and quit cigarette smoking over 10 years ago

APS confirmed no recent tobacco use

CXR from 3 years ago showed hyperinflation suggestive of COPD

PFTs last year were normal with an FEV1 >85%

Stress test completed this year also normal at 10:45 min. – asymptomatic with no ischemic changes

Currently walking 1-2 miles daily

80



• One-vessel disease in a senior individual

• Recent normal stress test suggesting good exercise capacity

Would consider CAD as Limited


• Former smoker over 10 yrs. ago

• COPD diagnosed by CXR only

• Recent PFTs normal with FEV1 >85%; exercising daily

Would consider COPD as mild

Suggest adding debits for both

impairments

81

Case Study #8C


Part 2 notes a hx of 2-vessel CABG 3 years ago

COPD diagnosed 5 years ago and currently using multiple medications including an occasional inhaler

APS confirms history of CABG 3 years ago to the RCA and obtuse marginal

Was also noted to have a mild non-obstructive lesion (<30%) of the LAD

Most recent stress test 2 years ago was negative

Past history of 1 pack per day cigarette use for 20 yrs., has not smoked in 5 years

Current FEV1 65%

82

Case Study #8C: Analysis


• Two-vessel disease and mild non-obstructive disease of the LAD

• Mildly overweight

Would consider CAD as Moderate


• Treated with multiple medications

• Former pack-per-day smoker x 20 yrs.

• Current FEV1 65%

Would consider COPD as moderate

Suggest discussing with

MD to determine

appropriate action

83

Peripheral Vascular Disease (PVD, PAD)

How does peripheral vascular disease impact someone with CAD?

When can we consider someone with PVD and CAD?

84

Case Study #9A

72-year-old male, quit smoking 2 years ago, with build 6.0.240, BP 142/93

Part 2 reports a 3-vessel CABG 5 years prior and a hx of treated/controlled HTN

APS confirmed 3-vessel CABG to the LAD, RCA and circumflex

The catheterization report also included moderate CAD in 2 branch arteries

Recent PE patient complained of severe aching and cramping in both legs when walking up inclines, resolving at rest

M.D. suggested an LE Doppler, which patient declined

85



• Three-vessel major artery disease and moderate disease in two branch arteries

• Quit smoking 2 years ago; current hypertension

Would consider CAD as very Heavy

Severity of the PVD:

• Complaints of bilateral leg pain with moderate exertion, resolving at rest

• Incomplete work-up for the leg pain

Would consider as moderate PVD at best

High risk, unfavorable co-morbidities.

Consider Decline

86

Case Study #9B

59-year-old female, build 5.9.165, BP 125/81, non-tobacco user

Part 2 notes 2-vessel angioplasty 3 years prior

APS confirmed angioplasty of the distal RCA and a diagonal artery branch artery

No other significant CAD

APS: PE exam last year notes patient is an avid jogger and reported aching in calves after running long distances; M.D. felt symptoms were probably from overexertion but offered additional testing, which was never completed

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• Two-vessel disease involving 1 major artery and 1 branch artery

Would consider CAD Moderate

Severity of the PVD:

• Active individual, but with calf pain after strenuous exercise

• No history of tobacco use

Would consider PVD as minimal to mild


Suggest adding debits for

both impairments

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Case Study #9C

66-year-old female, build 5.4.205, BP140/92, non-smoker

Part 2 includes hx of HTN controlled with Rx, and a 3-vessel CABG 4 years prior

APS reports CABG 5 years prior to the LAD, RCA and obtuse marginal

Last year’s stress test was negative at 9:41 min.; no ischemic changes, but with aching in her calves at peak exercise

Subsequent LE Doppler revealed mild distal PVD

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Case Study #9C: Analysis

Severity of CAD:

• Two major vessels and one branch artery disease

• Mildly overweight with hypertension

Would consider CAD as Moderate to Heavy

Severity of PVD:

• Aching in calves at peak exercise on recent stress test

• Lower extremity Doppler findings – mild distal PVD

Would consider PVD as mildSuggest adding debits

for both impairments

90

Case Study #101/28/2017

4/13. He

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Case Study #10

1/28/2017

92


Is the summary on the angiogram report - “mild to moderate CAD” consistent with the findings?

• Note “previously placed stents”

• Disease in all 3 vessels

To determine if the disease has progressed, would need to compare to original angiogram report

These findings are more consistent with Moderate – Heavy

CAD, noting the 1) prior interventions; and 2) diffuse disease

Consider possible disease progression

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General Underwriting Considerations

Utilize all available evidence – put the pieces together

Consider the preponderance of the evidence – what factors are most predictive in each situation

When asking for additional evidence, consider how it will impact risk assessment

Be sensitive to differences between insurance medicine and clinical medicine

Consider co-morbidities – is the sum greater than the parts?

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PreTest!!! True or False?

1. CAD is the single leading cause of death in American women

2. In most individuals, the Right Coronary Artery supplies blood to part of the interventricular septum

3. Longstanding angina precedes most myocardial infarctions.

4. Obstruction of the Left Main Coronary artery is the most dangerous location.

5. Co-morbid rheumatoid arthritis, obstructive sleep apnea and/or testosterone supplementation do not add to CAD risk.

TRUE

TRUE

TRUE

FALSE

FALSE

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Questions?

Time to Stop

underwriting coronary artery disease · brief anatomy and physiology refresher ... co-morbid...

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