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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
3
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.
5
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
6
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
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
10
The Coronary Arteries
Wikipedia, Patrick J. Lynch, medical illustrator
11
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
12
Coronary Arteries by CT
13
Structure of an Artery
Intima
Media
Adventitia
Endothelium
Lumen
14
Normal Resting State
DEMAND SUPPLY
15
Normal Coronary Reserve
DEMAND SUPPLY
16
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?
17
Stable Obstructive Plaque
Thick Cap
Small Lipid Core
Calcium
18
Inadequate Coronary Reserve
DEMAND
SUPPLY
19
Impaired Resting Function of Coronary Arteries
DEMAND
SUPPLY
20
Nonobstructive Vulnerable Plaque
Large
Lipid Pool
Thin Cap
Inflammation
21
Inadequate Coronary Reserve
DEMAND
SUPPLY
22
Ruptured Plaque with Thrombus
Large
Lipid Pool
Thin Cap
Inflammation
Thrombus
23
Acute Occlusion of Coronary Artery
DEMAND
NO SUPPLY
24
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.
25
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
26
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
27
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
30
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
31
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
33
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
34
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:
35
Case Study #1
36
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
38
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?
39
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???
40
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
41
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
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
42
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
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
43
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
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.
When new or worsening symptoms (not consistent with acute coronary syndrome)
44
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.
45
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
46
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
48
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
51
Case Study #3: Analysis
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
Case Study #4: Analysis
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
55
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
58
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
59
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
60
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
61
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
62
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
Severity of the CAD:
• 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
Case Study #6: Analysis
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
Case Study #7: Analysis
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
Case Study #8A: Analysis
Severity of the CAD:
• 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
68-year-old male, build 5.11.180, BP 138/82
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
Case Study #8B: Analysis
Severity of the CAD:
• One-vessel disease in a senior individual
• Recent normal stress test suggesting good exercise capacity
Would consider CAD as Limited
Severity of the COPD:
• 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
63-year-old male, build 5.9.210, BP 135/86
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
Severity of the CAD:
• Two-vessel disease and mild non-obstructive disease of the LAD
• Mildly overweight
Would consider CAD as Moderate
Severity of the COPD:
• 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
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Case Study #9A: Analysis
Severity of the CAD:
• 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
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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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Severity of the CAD:
• 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
Case Study #9B: Analysis
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
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Case Study #101/28/2017
4/13. He
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Case Study #10
1/28/2017
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Case Study #10: Analysis
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