Coronary Artery Disease

Coronary Arteries

• Sit like a “crown” on the heart

• feed the myocardium

The Coronary Arteries are the first branch of the:

Ascending Aorta

Where do the coronary arteries originate from?

• at Sinus of Valsalva

  • dilated portion of the Ao root

  • in area of RCC and LCC respectively

What does the LMCA branch into?

1. Circumflex (LCX)

2. Lt Anterior Descending (LAD)

Circumflex (LCX) (Obtuse Marginal A)

• passes through Lt coronary Sulcus

  • will anastomose with RCA

What artery does the Lt Coronary Sulcus give rise to?

Obtuse Marginal A

What does the Lt Anterior Descending (LAD) (Ant Interventricular CA) course through?

Ant Intervent Sulcus

What artery does the LAD give rise to?

Lt Diagonal A

The RCA bifurcates into:

1. Posterior Descending

2. Right Marginal (A-V nodal)

How does the Rt Coronary Artery (RCA) travel through the heart?

Travels in rt coronary sulcus to posterior / inferior aspect of heart

What artery does the RCA anastomose with?

LCX

The LAD supplies blood to:

• Ant Septal wall

• Ant wall

• Mid Inf Sep

• Apical Septal wall

• LV apex

  • Apical Lateral wall

  • Apical Inferior wall

• Apical Cap

• Portion of RV

  • ant pap m.

The Left Circumflex supplies blood to:

• Inf Lat wall

• Ant Lat wall

• Lat wall (apex)

• LA

What wall do both the LAD and LCX both supply?

Apical Lateral wall

What wall do both the LAD and RCA both supply?

Apical Inferior wall

The Right Coronary Artery supplies:

• Basal Inf Septal Wall

• Inferior wall

  • may supply PMPM (of LV)

• RV free wall

• RV apex

• RA

What are the effects of CAD?

• Ischemia

• Infarction

• LV Diastolic dysfunction

• Decreased systolic wall thickening

• segmental wall motion abnormalities

Ischemia

Blood deficiency supply due to constriction or obstruction of blood vessels

Infarction

• tissue death (necrosis) that is caused by a local lack of oxygen following the cessation of blood supply

  • MI → myocardial infarction

    • MI is considered part of a spectrum

What spectrum is MI considered a part of?

Acute Coronary Syndrome (ACS)

LV Diastolic Dysfunction

• impaired relaxation / decreased compliance of the LV

• LV filling pressure (LVEDP) increases immediately following occlusion

What does LV diastolic dysfunction cause?

• Reduced early diastolic filling

  • LA must now work harder to move blood

    • perform PW Dp of MV inflow and Pulmonary Veins and TDI

Decreased Systolic wall thickening

• Occurs at MI location / Impaired systolic function

  • should correlate with diseased CA

The location and severity of decreased systolic wall thickening may vary depending upon:

• RCA / LCA dominance

  • rt - 48%

  • Left - 18%

  • Balanced - 34%

• collateral circulation

• presence and severity of stenosis in other CA’s

What is the cause of segmental wall motion abnormalities?

Decreased perfusion

What does decreased systolic wall thickening present as?

Segmental Wall Motion Abnormalities (WMA)

Segmental Wall Motion Abnormalities

• perfusion at rest is maintained until 90% blockage occurs

• perfusion w/ exercise ceases with 50% blockage

What are all of the ways you can describe WMA’s?

• Normal

• Hyperkinetic

• Hypokinetic

• Akinetic

• Dyskinetic

• Tardokinetic

• Scarred

Hyperkinetic

Over-active contraction

Hypokinetic

Under active contraction

Akinetic

No activity / contraction

Dyskinetic

Motion in wrong direction during contraction → paradoxical SM

Tardokinetic

Late activity / contraction

Scarred WMA

• thin, akinetic myocardium

  • usually due to MI

• More echogenic than surrounding tissue

• Hinge point

Hinge Point

• common area for LV aneurysm formation

• Where scar tissue borders normal myocardium

5 Point WM Scoring Index

• Normal or Hyper-contractile segment

• Hypokinesis

• Akinesis

• Dyskinesis

• Aneurysmal

How do we calculate the 5 Point WM Scoring Index?

• add total together

• Add total and divide by 17 for Score Index

  • 1.0 = normal function

  • >1.0 = WMA’s present

Does a lack of WMA exclude the possibility of CAD?

• NO

  • Collaterals may be present

  • WMA may not be seen at rest

• However, the pretense of regional WMA is highly sensitive to which vessel may be involved in the ischemic process

What is the timeline of CAD events?

• LV tissue damage

  • Seen w/ naked eye 15 hrs after Coronary Occlusion

  • Histological changed occur within 6 hours

• At 3 weeks scar tissue has started forming

  • LV wall thickness has decreased

• Over next 2 months scar tissue continues to become firmer and denser

• Area appears thin, dense, echogenic and akinetic

What are other imaging modalities to observe CAD?

• Cardiac Cath

• CTCA

Cardiac Cath

• Gold standard

• Adv: can Tx during test

  • Balloon/stent

CTCA

• computed

• Non invasive

Echocardiography

• useful for locating effects of Acute MI

  • Immediately following vessel occlusion, WMA’s may be seen by Echo

  • Valuable ER tool

    • TPA administration

      • Has a brief window of time d

TPA administration during an echocardiogram will not work for:

Chronic ischemia

Echo is used to:

• locate LV injury

  • Such as acute MI or chronic ischemia

• Assess extent of the disease

• Assess rest of LV

During an echo, you assess the extent of disease using:

• Scoring wall segments

  • higher sum = greater amount of ischemic myocarditis

  • Index >1.0 = greater amount of ischemic myocarditis

Following an acute MI, how should the LV walls appear as?

• un-affected walls should demonstrate compensatory hyperkinetic WM

  • if not, global CAD

What are major pitfalls of echo?

• subjective

  • d/t eyeballing EF

• difficult to perform

  • master views and images first

What are the pitfalls for diagnosing WMA’s?

• should compare w/ previous studies

  • helps determine chronic or acute

• “Tethering Effect”

  • effect of hypokinesis on adjacent wall segments

    • “weighs-down” connected (normal) walls

What are the pitfalls for diagnosing WMA’s?

• Stunned Myocardium

• Hibernating Mocardium

• Will benefit from Tx

Stunned Myocardium

• d/t periods of ischemia too brief for necrosis

  • <20 mins

• ischemic muscle is still viable but not functioning

  • often recovers to normal function over time

    • especially is reperfused in timely manner

  • can take days to weeks to return to normal function

Hibernating Myocardium

• viable muscle not functioning

  • d/t chronic ischemia

  • when it is reperfused it may function again

Risk factors of CAD include:

• HTN

• Pre-eclampsia

  • up to 30 yrs s/p

• Migraine sufferers who experience ‘aura’

  • visual disturbances

  • flashing lights

• Diabetes

  • Gestational

• Obesity

• Hyperlipidemia

• sourc of atheroma

• SMoking

• Poor dental health Family Hx

Risk factors of CAD include:

• Age

• Gender

• BC

• HRT

• Stress

• physical inactivity

• Hyperproteinemia

  • CRP

  • vWF & Fibinogen

  • Lp(a)

• abnormal heart rhythm

How does birth control affect CAD?

high doses decrease HDL (good lipids) and increase LDL and BP

C-reactive protein (CRP)

A marker of inflammation in blood vessels

von Willebrand factor (vWF) & Fibrinogen

Proteins linked to blood clotting activity

The signs of CAD include:

• CP

• angina

• MI

• sudden death

• cardiogenic shock

Cardiogenic shock

• Myocardial damage resulting in decreased CO

• Causes:

  • hypotension

  • pulmonary edema

How does CAD appear on an EKG?

• ST segment - T wave changes

  • elevated ST = acute MI

  • Depressed ST seg / inverted wave = chronic ischemia / infarc

• abnormal Q waves

  • may indicate chronic MI

• Watch for any EKG changes

Methods of treating CAD include:

• Reduce risk factors

• CABG

• Thrombolysis

  • TPA

• PTCA → balloon angioplasty

• Coronary tent

• Laser

• Anti-anginal meds

  • nitroglycerine tablet

What treatments of CAD are percutaneous coronary intervention (PCI)?

PTCA (balloon angioplasty) and Coronary Stent

What are potential complications of a MI?

• ↑ LVEPD (Diastolic dysfunction)

• Pericardial effusion

• LV aneurysm

• LV pseudoaneurysm

• Ventricular septal rupture

• LV thrombus

• Papillary muscle dysfunction

• CHF & cardiogenic shock

Increased LVEDP in response to MI:

• diastolic dysfunction

  • occurs immediately after CA occlusion

    • causes reduced early diastolic filling

  • LA must now work harder to move blood

What does diastolic dysfunction in response to MI result in?

• Restrictive Filling Pattern

  • stage III LVDD

Pericardial Effusion

• Fluid around the heart

  • increased volume w/in one “potential space” created by visceral and parietal pericardium

What is the cause of pericardial effusion?

Pericarditis

There are 2 forms of pericardial effusion following MI:

1. Acute response to MI

2. Delayed form

What is the acute pericardial effusion response to MI?

Inflammation in response to trauma

What is they delayed form of pericardial effusion?

Dressler’s Syndrome - occurs 2-10 weeks following MI

LV Aneurysm

A bulge in LV wall that persists in systole and diastole w/ reduced wall thickness and dyskinesis

Where does LV aneurysm typically affect in the heart?

Any LV wall, including IVS and Inferior wall → most common at apex

When does LV aneurysm typically occur in response to MI?

2-4 weeks s/p

LV Pseudoaneurysm

• Result of LV free wall rupture

  • blood trapped in pericardium, forming a contained, pulsing hematoma

    • clotted blood forms the walls preventing hemopericardium

Ventricular Septal Rupture

Rupture of IVS resulting in abnormal communication between Lt and Rt heart

How does Ventricular Septal ruture appear on an echocardiogram?

• high velocity, turbulent jet

  • Lt to Rt shunt

    • when normal pressures exist

What is the best modality to diagnose a ventricular septal rupture?

CFI → in a subcostal view

LV Thrombus

• most often form in the apex

  • may occur anywhere in LV

What are LV thrombus’s always associated with?

WMA’s + low EF

What is papillary muscle dysfunction a common cause of?

MR s/p MI

Papillary Muscle Dysfunction

• MI may result in:

  • WMA’s, fibrosis, scarring, & pap m thinning

• LV dilation causes map’s and chordae to stretch away from MV annulus

  • causes MV “tenting” and incomplete closure

A severe consequence of papillary muscle dysfunction may include:

• Papillary muscle rupture

  • eccentric MV motion

  • acute severe MR

  • surgical ER

CHF

When >23% of the LV is infarcted

Cardiogenic shock

• Systemic shock due to inadequate cardiac output

• likely to result when >40% of the LV is infarcted