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Broken Hearts - Putting the Pieces Together

Underwriting CAD

Valerie R. Kaufman, MD

MUD Meeting, 1/30/17

Reinsurance Group of America

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Agenda

Anatomy/Physiology/Pathophysiology review

Epidemiology overview

Preponderance of the evidence

Reconciling discordant test results

Practice guidelines and appropriate use criteria (AUC)

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Review of Anatomy, Physiology and Pathophysiology

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By Coronary.pdf: Patrick J. Lynch, medical illustratorderivative work: Fred the Oyster (talk)adaption and further

labeling: Mikael Häggström - Coronary.pdf, CC BY-SA 3.0,

https://commons.wikimedia.org/w/index.php?curid=9967381

Heart: Exterior

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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%

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Structure of an Artery

Intima

Media

Adventitia

Endothelium

Lumen

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Stable Obstructive Plaque

Thick Cap

Small Lipid

Core

Calcium

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Nonobstructive Vulnerable Plaque

Large

Lipid Pool

Thin Cap

Inflammation

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Epidemiology

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Epidemiology

CAD death rate has fallen since 1968

About 15.5 million Americans ≥ 20 years of age have CAD

In 2013

• CAD caused 370,000 deaths

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

Nearly 1 million coronary events each year

Estimated an additional 160,000 silent MIs each year

About 34% of coronary events are fatal

Mozaffarian D, Benjamin EJ et al on behalf of the American Heart Association Statistics Committee and Stroke Subcommittee. Heart disease and stroke statistics – 2016 update: a report from the American Heart Association. Circulation 2016;133.

US Data

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Underwriting CAD

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The Heart: a complex organ

• Myocardium

• Conduction system

• Heart valves

• Aorta and arterial

tree

• Coronary arteries

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Underwriting Cardiac Disease – The Evidence

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Putting the Pieces Together . . .

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Case Study #1: 1000 Piece Puzzle

2011 Cardiology note

• FH of early CAD

• H/O HTN, high chol, pre-diabetes

• On statin, BP meds, ASA and metformin

• TC 123, HDL 32

• HgbA1c 5.9%

• 2010 stress echo negative for ischemia, aortic sclerosis and mild aortic insufficiency

• No chest pain or other cardiac symptoms

• BP 140/86

61 year old man, nonsmoker

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Case Study #1 (cont)

2014: progressive dyspnea on exertion for last 3 months

• CAC 2857

• Nuclear stress o Resting EKG with nonspecific ST changes

o Upsloping ST depression and PVCs with hypertensive response.

o Perfusion scan showed partially reversible inferoapical defect and reversible anteroapical defect.

• Cath o LVEDP 26, LVEF 60%

o Left main coronary – moderate calcification with 10-20% distal disease

o Ramus is small caliber with mild disease

o LAD is very tortuous with severe calcification and diffuse 20-30% disease at the midsection

o Circumflex is co-dominant with mild disease proximally and in the 2 small OM branches

o RCA has 30% disease at the midsection

• BP meds adjusted


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Follow up 3/15, 9/15 – no new symptoms, no testing

Current insurance labs

• HgbA1c 7.5%

• TC 147, HDL 33

• NTproBNP 60

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Case Study #1: Considerations

Enormous CAD burden with CAC nearly 3000

Despite near-maximal risk factor modification program since prior to 2011, had progression of disease with symptoms in 2014

MPI showed multiple perfusion defects

Cath showed extensive disease, but apparently not obstructive

BP not well controlled until last year; EKG abnormal - ? LVH

Now frankly diabetic with HgbA1c of 7.5%

Still relatively young at age 61


Risk Level: Very High

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Case Study #2: Missing Pieces?

Had cardiac cath in 2012 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 2012 was negative, and echo showed normal LV function with LVEF 60%

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


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Is he still on his medications?

What are his risk factors like? (Are the medications effective in reducing risk factors)

Is he diabetic?

Do we have a current EKG?

Do we have NTproBNP?

What do we know about symptoms and functional state?

Does he have any other medical issues?

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Is he still on his medications? YES

What are his risk factors like? (Are the medications effective in reducing risk factors) Chol 150, HDL 55, BP 126/78

Is he diabetic? NO HgbA1c on insurance labs is 5.4%

Do we have a current EKG? YES, it is normal

Do we have NTproBNP? NO

What do we know about symptoms and functional state? Has had regular, alternating PCP and Cardiology visits. No new cardiac symptoms and remains very active.

Does he have any other medical issues? Nothing ratable.

So, should we postpone, or can we assess?

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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 Associati on of Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thorac ic Surgeons. J Am Coll Cardiol 2012;60:e44-164.

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

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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 Associati on 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.


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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

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 Thor acic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2012;60:e44-164.


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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

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 Associati on of Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thorac ic Surgeons. J Am Coll Cardiol 2012;60:e44-164.

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: Postpone or Offer?

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 and normal

Consider offering with currently

available evidence

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Case Study #3: Preponderance of the Evidence

History of

• DVT following hip surgery (no details) as teenager

• PE after rotator cuff surgery in 2010; on low dose ASA

• Negative cardiac cath (don’t know why done) about 2008

• Negative stress test 2011

• GERD, not on any treatment

3/16: Went to ER due to off and on atypical chest pain x 3 weeks. Concerned about possible recurrent PE

• EKG normal; troponins negative

• CTA negative for PE


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3/16 evaluation

• Stress MPI:

o 10.3 METs, peak heart rate 144, peak BP 188/76

o Resting EKG normal, no chest pain

o No ST changes or arrhythmias

o Nuclear scan showed a small fixed defect in the mid anterior wall most consistent with old infarct. No evidence of reversibility. Normal wall motion, with EF of 61%

• Resting echo

o LV normal size, normal wall thickness, normal wall motion, EF 60%

o Valves normal

• Discharge summary noted “CAD, new diagnosis”. Begun on atorvastatin and metoprolol, continue ASA

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Case study #3: Preponderance of the Evidence

In Favor of MI

Weighing against MI

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Case study #3: Putting it all together

Mildly increased risk, but likely not due to CAD

MI is possible, but unlikely

History of 2 thromboembolic episodes, both provoked by surgery

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Case Study #4: Muddy Waters?

12/11 Chest pain

• EKG abnormal with nonspecific ST-T changes

• Stress echo o Equivocal ST changes on EKG portion

o Mild LVH (walls 1.2 and 1.2) and mild diastolic dysfunction

o Normal LVEF and wall motion before and after stress

2/15 Screening coronary artery calcium (CAC) score: 1451 (90 th = 1294)

5/15 Occasional nonexertional chest pain

• EKG unchanged

• Resting echo said to be unchanged, but LV walls 1.4 and 1.3, LA 4.6

• Stress test again with equivocal ST changes

• MPI with mostly fixed inferior perfusion defect, possibly due to diaphragmatic attenuation

67 year old man, nonsmoker, BMI 36, treated HTN

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Case Study #4: Questions/Considerations?

Does he have CAD?

Is the CAD causing his chest pain?

Are the stress tests suggestive of ischemia?

What about the LVH?

Any concerns about the combination of LVH and CAD?


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Case Study #4: Muddy Waters

LVH

• Appears to have worsened between 2011 and 2015

• Check BP control

• Could explain EKG changes

CAD

• CAC > 90th percentile

• Resting EKG abnormal

• Equivocal stress EKG changes

• Stress echo normal 12/11

• MPI equivocal 5/15

LVH + CAD = synergistically unfavorable

Moderately increased risk due to combination of impairments

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Take Aways

Consider all the evidence and try to “put the puzzle together” to get a clear perspective on the risk at hand: “preponderance of the evidence”

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Give more weight to the more predictive or specific pieces of evidence. 2

Evidence-based clinical guidelines are becoming more important in determining how and when clinical testing should be done 3

Abnormalities of more than one component of cardiac function are often additive and can be synergistic 4

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