Atherosclerosis & Stable Ischemic Heart Disease Diagnosis ......2014 ESC/EACTS Guidelines on...

Smita Negi MD, FACC

Atherosclerosis & Stable Ischemic Heart Disease

Diagnosis, Treatment and Guidelines

Pretest Questions

• Board Review Question 1

56-year-old male Mr. SIHD with DSL and HTN and family history of CAD, remote history of smoking presents with chest pain symptoms ongoing for over 2 years, predictably brought on with exertion and relieved by rest. What findings in the plaque indicate stability?

1-Upregulation of matrix metalloproteinase

2-Predominance of macrophages

3-Fibrous cap > 130 microns

4-Neoangiogenesis

5- All of the above

6-None of the above

• Board Review Question 2

Mr. SIHD is well educated and does a lot of internet

research. He asks you “ Doc, what will be the first

sign of reduced blood supply to my heart muscles” ?

You reply-

1-T wave inversions on ECG with exercise

2-Chest pain with Creatinine Kinase of 600

3-Wall motion abnormalities on stress echo

4-Perfusion defect on nuclear stress test

5-All of the above at the same time

• Board Review Question 3

Mr SIHD is in your clinic and reports exertional chest

pain symptom. He reports good ET and goes to gym

every other day but has to cut back on his sessions

due to CP.

Current meds- HCTZ, Lisinopril, baby ASA

Vitals BP=134/72, PR-85/min

1-Coronary Angiogram

2-Dobutamine stress echo

3-Regadenosine Nuclear Stress test

4-Exercise ECG stress test

5-CMRI

6-Reassurance and RTC as needed.

• Board Review Question 4

You are in clinic and are called to the Stress

department by supervising tech.

Mr. SIHD was scheduled for an exercise ECG stress

test. He ran on treadmill for 2 minutes but started

complaining of knee pain. His HR is at 60% of

MPHR. No changes on ECG. BP is at 142/98. He

states he cannot go any further.

1-Continue with the test

2-CMRI

3-Schedule coronary angiogram

4-Regadenosine Nuclear stress test

5-This is a test negative for ischemia. Reassurance

and D/C from clinic

• Board Review Question

Mr. SIHD undergoes Pharmacological Nuclear

Stress test. Continues with exertional CP.

Vitals stable, on metoprolol, asa, Lipitor, Lisinopril.

1-CT Angiogram

2-Coronary Angiogram

3-Reassurance

4-Isosorbide mononitrate

5-Diltiazem

• Board Review Question

Mr. SIHD now s/p pharmacologic nuclear stress

test-negative for inducible ischemia. ASA, acei, bb,

long acting nitrate, statin. Despite max therapy,

continues with exertional CP.

Bp=102/72, hr-65/min, ECG-unchanged

1-Add HCTZ

2-Dobutamine stress echo

3-CT Angiogram

4-Coronary Angiogram

5-Reassurance and RTC in 1 year

• Board Review Question 5

Mr. SIHD undergoes LHC and PCI with 3.0 DES to

his proximal right coronary artery. He is started on

ASA and P2Y12 inhibitor. Since his PCI, much

improved.

Comes back to clinic in 6 weeks and wants to

undergo hernia repair surgery next month (2

months).

1-Hold ASA and P2Y12.

2-ASA and P2Y12 for 36 months.

3-ASA and P2Y12 for 6 months.

4-ASA and P2Y12 for 12 months.

5-ASA and P2Y12 lifelong

• Board Review Question 6

Mr. SIHD presents to clinic now 1 year later. He has

been sent for a preop clearance for his hernia sx by

your surgery colleague. He is now on ASA, Plavix,

metoprolol, Lisinopril and statin. Feels great, goes to

gym every other day (>120min/week) back to his

regular sessions.

BP-120/66, HR-64, ECG-unchanged

1-Pharmacologic Stress test.

2-Coronary CTA

3-Proceed with surgery.

4-Ranexa

5-Coronary Angiogram

Objective

• Atherosclerosis

– Pathogenesis

– Clinical presentation

• Stable ischemic heart disease

– Clinical presentation

– Diagnostics

– Treatment options

Deaths attributable to cardiovascular disease

Go A et al. Circulation 2014;129:e28-e292

Risk factors

Non modifiable• Age

• Gender

• Genetic

Modifiable• Hyperlipidemia

• Smoking

• Arterial hypertension

• Physical inactivity

• Diabetes mellitus

• Obesity

• Stable plaque • Unstable “vulnerable” plaque

seven types of vulnerable plaques

70%

Diagnostic criteria for vulnerable plaque

Major criteria.

Active inflammation (monocytes/macrophages and sometimes T-

cell infiltration)

Thin cap with large lipid core

Endothelial denudation with superficial plaque aggregation

Fissured plaque

Luminal stenosis > 90%

Minor criteria

Superficial calcified nodule

Intra plaque haemorrhage

Endothelial dysfunction

Outward (positive) remodelling

Vulnerable

Blood

Vulnerable

Myocardium

Vulnerable

Plaque

Vulnerable Patient

Coronary artery disease

•MI

•Angina

Cerebrovascular disease

•Stroke

•TIA

Peripheral artery disease

•AAA

•abdominal angina

•renal artery disease

•Intermittent claudication

•Rest pain, cold pulseless leg

Lower the incidence of CVD related deaths

Identification in vivo

Prevention of rupture

Non invasive methods Invasive methods

Computed tomography (CT)

Magnetic resonance (MRI)

Intravascular ultrasound (IVUS)

Optical coherence tomography (OCT)

Near infrared spctroscopy (NIRS)

Biomarkers

The Quest for the Vulnerable Plaque

179ACS

LAD

Angiography vs CTA for CAD

Motoyama et al. JACC 2007

Fibrous plaque

Positive remodelingSoft plaque

Angiography vs. Pathology

Natural History of CAD : Remodeling

IVUS

EEMLumen

MLA

Plaque burden

NIRS chemogram

NIRS and IVUS

Yellow = high probability of lipids

IVUS cross-section

External elastic membrane

Lumen diameter / areaLipid core burden index(LCBI)

STABLE ISCHEMIC HEART

DISEASE

• Characterised by transient myocardial ischemia

• Most commonly caused by obstruction of the

coronary arteries by atheromatous plaque

Stable ischemic heart disease

Physiology of coronary circulation

• Coronary blood flow is phasic with maximal flow in diastole.

• 75% of the oxygen delivered by coronary arteries isextracted by LV → limited oxygen extraction reservein coronary circulation.

• At 85% lumen diameter at maximum exercise, vasodilator reserve is exhausted → inadequate pressure distal to the stenosis → rest or exertional myocardial ischemia

Perfusion

Abnormalities

Systolic Dysfunction

Δ ECG

Angina

Diastolic Dysfunction

Duration and severity of ischemia

Nuclear Imaging

Stress Echo/MRI

Stress ECG

Ischemic Cascade

Spectrum of CAD Presentations

DefinitionIschemia

with activity

Ischemia without

necrosis

Necrosis

(nontransmural)Transmural necrosis

Diagnosis

Symptoms,

ECG,

Stress

testing

Negative Biomarkers Positive biomarkers

No ECG ST-segment elevationECG ST-segment

elevation

Treatment The Big 5 Invasive or conservative depending on riskImmediate

reperfusion

SIHD UA NSTEMI STEMI

Roger VL, Go AS, Lloyd-Jones DM, et al.. Circulation. 2011;123:e18-e209.

Classification of SIHD

• Chronic stable angina pectoris

Fixed

• Variant angina pectoris

(Vasospastic/Prinzemetal’s)

Dynamic/Spasm

• Asymptomatic myocardial ischemia

Diabetics

Radiation

Conditions Provoking or Exacerbating IschemiaIncreased Oxygen Demand Decreased Supply

NoncardiacHyperthermia AnemiaHyperthyroidism HypoxemiaSympathomimetic toxicity (e.g., cocaine use) AsthmaHypertension Chronic obstructiveAnxiety pulmonary diseaseArteriovenous fistulae Pulmonary hypertension

Interstitial pulmonary fibrosisObstructive sleep apnea

Cardiac Sickle cell diseaseHCM Sympathomimetic toxicityAortic stenosis (e.g., cocaine use)Dilated cardiomyopathy HyperviscosityTachycardia

Grading of angina pectoris

Work up for SIHD

• History- typical symptoms

• Laboratory evaluation

– dyslipidemia, hyperglycemia, renal disease etc.

• Resting ecg

• ECHO

• Stress testing

• CT angiography

EuroIntervention 2015;10:1024-1094 published online ahead of print September 2014

2014 ESC/EACTS Guidelines on myocardial revascularization

Who needs Stress Testing?

Mr. SIHD

Exercise Pharmacologic

1. ECG -

2. ECHO 4. Dobutamine Echo

3. Nuclear 5. Adenosine Nuclear

The 5 Common Cardiac Stress Testing Modalities

CAD CP algorithm

Evaluation

What are the Big 5 medications for

CAD?

1. Beta blockers

2. ASA/antiplatelet agents

3. Statins

4. Nitrates

5. Antihypertensive and other risk

factor medications

Braunwald’s Heart Disease, 7th Edition

Beta blockers

CA blockers

ACEI

NTG

NTG

ASA

Heparin

GPB’s

Statins

Ranolazine

Indications for revascularization in Stable CAD or

silent ischemia

EuroIntervention 2015;10:1024-1094 published online ahead of print September 2014

2014 ESC/EACTS Guidelines on myocardial revascularization

Atleast 2 antianginals

SYNTAX

CABG or PCI ? in Stable CAD

EuroIntervention 2015;10:1024-1094 published online ahead of print September 2014

2014 ESC/EACTS Guidelines on myocardial revascularization

EuroIntervention 2015;10:1024-1094 published online ahead of print September 2014

2014 ESC/EACTS Guidelines on myocardial revascularization

Thygesen, K. et al. Circulation 2007;116:2634-2653

Plalque Rupture

Spasm, low BP

Sudden Death, no CK

PCI related

Stent Thrombosis

CABG related

THANK YOU FOR

YOUR ATTENTION !