Institute of Cardiovascular Diseases

“Prof. Dr. George I.M. Georgescu”

CORONARY ARTERY DISEASE

Prof. Grigore Tinică, MD, PhD

Iași, 2018
 Lecture plan
• Introduction
• Anatomy of the coronary arteries
• Atherosclerosis
• Angina pectoris
• Myocardial infarction
• Myocardial revascularization
 CARDIOVASCULAR DISEASES
Cardiovascular diseases are a group of disorders of the heart and blood.
The most frequent cardiovascular disease in western countries is the coronary artery disease (CAD)
responsible for angina pectoris and myocardial infarction.
Main cause of death globally
17,3 millions deaths due to cardiovascular diseases (30% of total global mortality) 7,3 millions
caused by coronary artery disease and 6,2 millions by cerebrovascular disease (2008 statistics).
1/6 are younger than 65 yrs.

• Coronary artery disease: disease of the blood vessels supplying the heart muscle;
• cerebrovascular disease: disease of the blood vessels supplying the brain;
• peripheral arterial disease: disease of blood vessels supplying the arms and legs;
• rheumatic heart disease: damage to the heart muscle and heart valves from
rheumatic fever, caused by streptococcal bacteria;
• congenital heart disease: malformations of heart structure existing at birth;
• deep vein thrombosis and pulmonary embolism: blood clots in the leg veins,
which can dislodge and move to the heart and lungs.
• Heart valve diseases.
 CORONARY ARTERY DISEASE
Coronary artery disease (CAD) includes: stable angina, unstable angina,
myocardial infarction, and sudden coronary death.
The underlying mechanism involves atherosclerosis of the arteries of the
heart which generates an imbalance between the heart's oxygen
demand and supply.

Coronary artery disease

1. Atherosclerosis
2. Stable Angina
3. Unstable Angina and Acute Coronary Syndrome
4. Myocardial Infarction
 CORONARY ARTERIES

Left coronary artery branches

•left anterior descending artery (LAD)
– diagonal branches (D1, 2, etc)
– septal perforators (S1, 2, etc)
•circumflex artery (Cx or LCx) / ramus circumflex
– obtuse marginal branches (OM1, 2, etc)
•ramus intermedius artery (RI)

Right coronary artery branches (RCA)

•conus artery
•sinotubular artery
•acute marginal branches (A1 or AM1, 2, etc)
•inferior interventricular artery (posterior descending
artery, PDA)
 1. ATHEROSCLEROSIS
• Atherosclerosis = or hardening of the arteries, is a condition in
which plaque builds up inside the arteries. Plaque is made of
cholesterol, fatty substances, cellular waste products, calcium and
fibrin (a clotting material in the blood)
• Arteriosclerosis = is the thickening, hardening and loss of elasticity
of the walls of arteries,
• Arteriosclerosis is used as a generic term for arterial degeneration
and includes atherosclerosis.
• Multiple genetic and environmental factors (risk factors) contribute
to the development of atherosclerosis, a process initiated at an
early age.
• Depending on the involved arteries, atherosclerosis can lead to a
peripheral arterial disease, cerebrovascular disease, or coronary
artery disease.
 1. ATHEROSCLEROSIS  
Pathophysiology
+ C-reactive protein (CRP)
  Non-specific marker of inflammation
  Increased in many patients with CAD
  Chronic exposure to CRP associated with unstable
plaques and oxidation of LDL cholesterol
1.Fatty streaks
•Earliest lesions
•Characterized by lipid-filled smooth
muscle cells
•Potentially reversible
2. Fibrous plaque
•Beginning of progressive changes in the
arterial wall
•Fatty streak is covered by collagen,
forming a fibrous plaque that appears
grayish or whitish
•Result = Narrowing of vessel lumen
3. Complicated lesion
Continued inflammation can result in
plaque
•instability, ulceration, and rupture
•Platelets accumulate and thrombus forms
 1. ATHEROSCLEROSIS
Risk factors
Unmodifiable risk factors:
•Age – atherosclerotic lesions progress with age
•Heredity – stroke in familiy members <65 yrs
•Sex – males present a higher risk compared to females
Modifiable risk factors
•Smoking – major risk factor
•Diabetes mellitus – especially type II
•Dyslipidemia – increase of LDL-cholesterol, triglycerids are risk factors and HDL cholesterol has a protective role.
•Arterial hupertension - >140/90 mmHg
•Overweight – especially of android type
•Sedentarity
•Metabolic syndrome:
- Waistline > 102 cm for males and > 88 cm for females;
- Triglycerides level > 1,50 g/l; HDL-cholesterol < 0,4 g/l for males and < 0,5 g/l for females;
- Blood pressure > 130 / 85 mmHg ;
-à jeun glycemia > 1,1 g/l
New risk factors
•Hyperhomocysteinemia
•Fibrinogen level
•C-reactive protein (CRP) level
 1. ATHEROSCLEROSIS

Classification of lesions

•Type I: initial lesion with foam cells – in adolescents and young adults, foam cells
accumulation within intimal thickening area
•Type II: fatty streak with multiple foam cell layers
•Type III: pre-atheroma with extracellular lipid pools (young adult)
•Type IV–V: plaque with a lipid or necrotic core surrounded by fibrous tissue with possible
calcification (simple, uncomplicated plaque)
•Type VI: complex plaque with possible surface defect, haemorrhage, or thrombus
•Type VII: calcified plaque (stable, advanced age)
•Type VIII: fibrotic plaque without lipid core
 1. ATHEROSCLEROSIS
Plaque complications
1) Stenosis
2) Hemorrhage
3) Ulceration
4) Thrombosis
5) Calcification
6) Ectasia
 1. ATHEROSCLEROSIS
Treatment
1)Prevention: risk factors control
2)Medical:
– Antiplatelet drugs
– Statins to normalize (together with
diet) the level of LDL cholesterol 
– Antihypertensive drugs
3)Surgical or endovascular in case of vital
risk, occlusion or stenosis associated to a
significant functional impairment or
significant risk involving the life of an
organ or a limb.
 2. ANGINA PECTORIS
• Angina pectoris – commonly known as angina – is the sensation of
chest pain, pressure, or squeezing, often due to ischemia of the heart
muscle from obstruction or spasm of the coronary arteries.

• Symptoms - substernal chest pressure or tightening, frequently with

radiating pain to the arms, shoulders, or jaw. The symptoms may also
be associated with shortness of breath, nausea, or diaphoresis.

• Stable angina - reproducible pattern of anginal symptoms that occur

during states of increased exertion;
• Unstable angina pectoris (UA) - increasing frequency of symptoms or
as symptoms occurring at rest;
• Prinzmetal angina - transient coronary artery spasms, either at rest or
with exertion;
• Microvascular angina – disease of small vessels;
• Cardiac syndrome X - symptoms of angina pectoris without CAD or
spasm.
 2. 1. STABLE ANGINA
• Also called “Effort Angina”
• Discomfort is precipitated by activity (same level of effort)
• Minimal or no symptoms at rest
• Symptoms disappear after rest/cessation of activity/nitrate derivate administration.
• Inadequate relationship between myocardial oxygen demand and supply by the coronary circulation secondary to :
– 95% - tight atheromatous stenosis
– Primary reduction of coronary blood flow in case of spasm
– Rarely, increase in oxygen demand associated to inssuficient blood flow (« functional » angina in case of aortic
stenosis, anemia, arrhytmias, hyperthyroidism)
– Exceptionally:  »angina with normal coronary arteries", an entity incompletely understood
• Main evolutive risk – plaque rupture with endothelial denudation leading to vessel thrombosis – a stable plaque
becomes unstable with 3 possible consequences :
1. Sudden death
2. Myocardial infarction
3. Incomplete coronary thrombosis = Unstable angina
 3. ACUTE CORONARY SYNDROMES

Acute coronary syndromes (ACS) result from acute obstruction of a coronary artery
Characterized by angina symptoms not ceasing at nitrate derivate administration:

• Transmural (ST-elevation) myocardial infarction (STEMI) (Pain +, ECG + markers+)

• Non-transmural (non-ST elevation) myocardial infarction (non-STEMI) (Pain+, ECG - markers+)

• Unstable angina (Pain +, ECG -, markers – needs surveillance for 24h)

 3.1. UNSTABLE ANGINA
• Unstable angina - acute coronary syndrome (ACS) in which there is no detectable release of the enzymes and biomarkers of myocardial
necrosis.
• determined by sudden rupture of a plaque with thrombus formation. The thrombus suddenly diminishes blood flow through the
involved coronary artery.
• Symptoms -similar to those of myocardial infarction (MI) (chest pain or pressure , sweating, dyspnea , nausea, vomiting , dizziness or
sudden weakness, fatigue , pain or pressure in the back, neck, jaw, abdomen, or shoulders or arms).
– Symptoms that occur at rest; become suddenly more frequent, severe, or prolonged; a change from the usual pattern of angina;
and do not respond to rest or nitroglycerin.
– « de Novo » unstable angina: previously asymptomatic patient with no history of ischemic cardiovascular disease, suddenly
presents with frequent effort angina or angina at rest. The symptoms resemble those of stable angina but with longer episodes and
slower or incomplete cessation after nitrate derivate administration.
– « accelerated » unstable angina: patient with known CAD, previously well controlled with medical treatment, presents with above
described symptoms.
 3.2. MYOCARDIAL INFARCTION
• caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic
plaque that stimulates the formation of an intracoronary thrombus, which results in coronary
artery blood flow occlusion. If such an occlusion persists for more than 20 minutes, irreversible
myocardial cell damage and cell death will occur in the territory of the affected coronary artery.
• Diagnosis is confirmed by ECG and biological markers.
• Severity depends on the extension of necrosis. If necrosis is limited to a small area, the patient is
hospitalized and receives standard medical treatment.
• In case of STEMI infarction, the necrosis affects a larger area with typical ECG anomalies. This
type of MI needs urgent desobstruction treatment - thrombolysis (dissolves the thrombus) or
Percutaneous transluminal coronary angioplasty (PTCA) with stent implantation (mechanical
dezobstruction).
• 1/3 are fatal fatales whose half die within the first hour after the onset of symptoms (sudden
death) 5% occur in patients <40 yrs
• M>F before the menopause, M=F 5-10 years after the menopause
 3.2. MYOCARDIAL INFARCTION
• Symptoms +  troponin + CPK. This definition englobes STEMI and non-STEMI
Symptoms:
•Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax
•Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back
•Associated dyspnea or shortness of breath
•Associated epigastric discomfort with or without nausea and vomiting
•Associated diaphoresis or sweating
•Syncope or near syncope without other cause
•Impairment of cognitive function without other cause
THE SYMPTOMS DO NOT COMPLETELY RESPOND TO NITRATE DERIVATE ADMINISTRATION!
 3.2. MYOCARDIAL INFARCTION
ECG diagnosis
•On the ECG, we encounter ST segment alterations (« lesion ») and T wave alterations (« ischemia »);
•Each of the ECG signs is further classified into subendocardial or subepicardial but these terms are
essentialy descriptive without strict anatomical equivalent
Anatomical territory ECG derivation Responsible coronary
artery
Anteroseptal V1 à V3 LAD

Apical V4 et V5 Distal LAD

Lateral superior: DI, VL Circumflex, marginal,

inferior: V5,V6 diagonal

Inferior DII, DIII, VF Circumflex, RCA

Basal V7, V8, V9 + R V1,V2 RCA

Anterosepto-apical V1 - V4 or V5 LAD

Anterior extended V1 - V6, DI, VL LAD

Deep septal DII, DIII, VF, V1 à V4 LAD, RCA

Infero-basal DII, DIII, VF, V7 à V9 Circumflex, marginal

+/- RCA
Infero-lateral DII, DIII, VF, V5, V6 Circumflex, marginal
or RCA
Circumferential DII, DII, VF, VL, V1 à LM, proximal LAD
V6
 3.2. MYOCARDIAL INFARCTION
CARDIAC MARKERS

•Located in the myocardium.

•Released in cardiac injury.
– Myocardial infarction
• Proinflammatory Cytokines
– Non-Q-wave infarction • IL-6
– Unstable angina pectoris • Plaque Destabilization
– Other conditions affecting cardiac muscle • MPO
(trauma, cardiac surgery, myocarditis etc.) • Plaque Rupture
•Can be measured in blood samples. • sCD40L
• Acute Phase Reactants
• hs-CRP
• Ischemia
• IMA
• Necrosis
• cTnT
• cTnI
• Myocardial Dysfunction
• BNP
• NT-proBNP
 3.2. MYOCARDIAL INFARCTION
•AST (ASPARATATE AMINOTRANFERASE, widely distributed in hear, liver, skeletal muscle, kidney and RBCs, AST activity is
increased after myocardial infarction)
•LDH (LACTATE DEHYDROGENASE) is a hydrogen transfer enzyme that catalysis the oxidation of L-Lactate to Pyruvate. Both
total and LDH isoenzymes are elevated in myocardial injury
•CK (CREATINE KINASE). CK is a dimeric enzyme that regulates high energy phosphate production and utilization in contractile
tissues.
•CK-MB - represent 20 – 30 % of total CK in diseased cardiac tissue (sensitive)
•Myoglobin dosage- Serum levels increase within 2h of muscle damage, Excellent NEGATIVE predictor of myocardial injury
•Cardiac troponins - regulate the contraction of striated muscle. Troponin consists of 3 subunits troponin C, I, and T. Cardiac
Troponin I (cTnl) is a cardiac muscle protein and Cardiac Troponin T (cTnT) is present in fetal skeletal muscle, absent in adult
skeletal muscle cells.
Marker start Peak Duration of
elevation
LD-1 24 – 47 h 48 – 72 h 7 – 10 days
Total CK 3–8h 12 – 30 h 3 – 4 days
CK-MB 4–6h 24 h 48 – 72 h
CK-MB 2–3h 18 h < 24 h
isoforms
cTnI 6h 24 h 7 – 10 days
cTnT 6h 12 – 48 h 7 – 10 days
Myoglobin 2h 6–7h 24 h

IMA Few minutes 2–4h 6h

 3.2. MYOCARDIAL INFARCTION
Interventional diagnosis
Cardiac catheterisation is an invasive diagnostic procedure that provides important information about the structure and function of the heart. Coronary
angiography can be used to diagnose heart conditions, plan future treatments and carry out certain procedures.
Diagnostic part: identification and characterisation of coronary arteries lesions (stenosis, obstruction, etc.)
• Cuantification (percentage of lumen narrowing)
• Importance
• Localisation

•Therapeutic part:
– PTCA - endovascular procedure to widen narrowed or obstructed arteries. An empty, collapsed balloon, known as a balloon catheter, is passed over
a wire into the narrowed locations and then inflated to a fixed size. The balloon forces expansion of the stenosis (narrowing) within the vessel and
the surrounding muscular wall, opening up the blood vessel for improved flow, and the balloon is then deflated and withdrawn. After dilatation, a
stent is inserted to maintain the vessel opened.
 3.2. MYOCARDIAL INFARCTION

Complications :
•Arrhytmias: mainly during the first week, could be ventricular, supraventricular, or T du rythme
ventriculaires, supra ventriculaires ou de la conduction auriculo ventriculaire.
•Cardiac failure
•Reinfarction: re-occlusion after reperfusion. Increased risk of mortality if LVEF <40%, ischemia at low
physical exercise, complex ventricular arrhytmias.
•Mecanical complications:
-papillary muscle rupture,
-interventricular septum rupture – VSD,
-free wall rupture – cardiac tamponade.
•Parietal aneurysm formation.
 3.2. MYOCARDIAL INFARCTION
Treatment
•Goals
-to save patient’s life
    -to prevent reinfarction
-to limit the extent of myocardial infarction
-to salvage jeopardized ischemic myocardium
-to recanalize infarct-related arteries 
-pain relief
    -to prevent complications (arrhytmias, heart failure, mechanical)
Sequence
Pre-hospital care: aspirin, nitroglycerin, refractory/severe pain – morphine. Pre-hospital thrombolysis is indicated if the
time from the initial call to arrival at hospital is likely to be over 30 minutes.
Hospital: Hospitalize in coronary intensive care unit
Major analgesics for pain relief
Thrombolysis
Urgent revascularisation (PTCA or surgery)
Anti-GpIIb/IIIa
   Heparin i.v.
    Antiarrhytmic drugs
    Aspirin, Plavix
    Beta-blockers and ACE inhibitors (improve balance between myocardial oxygen supply and demand)
    Nitrogliceryn
    Diuretics
 4. CORONARY REVASCULARISATION
Percutaneous transluminal coronary angioplasty (PTCA)
Coronary artery bypass grafting (CABG)
Rotablator atherectomy
Laser angioplasty
 Percutaneous transluminal coronary
angioplasty (PTCA)
 PTCA - a catheter-based procedure used to establish coronary reperfusion.
 Angiography, which provides essential knowledge of the extent of coronary disease, is performed
prior to PTCA.
 In regard to STEMI, PTCA may then be performed as a primary intervention or as an intervention
after thrombolysis failure.
 In patients presenting with NSTEMI, PTCA is an appropriate revascularization strategy for
individuals with a favorable coronary anatomy and severe stenosis.
Angioplasty requires an access vessel, typically the femoral or radial artery or femoral vein to permit
access to the vascular system for the wires and catheters. The procedure is performed under local
anesthesia. In most cases, after balloon dilatation a stent is placed in order to maintain the vessel
opened.  
• Evidence suggests that primary PTCA is more effective than thrombolysis and should be
performed for confirmed STEMI, new or presumably new left bundle-branch block (LBBB), severe
congestive heart failure, or pulmonary edema if it can be performed within 12 hours of symptom
onset. Door-to-balloon time should be 90 minutes or less. PTCA is the treatment of choice in most
patients with STEMI.
• Primary PTCA should be attempted every time it is considered feasable.
• In Romania – national RO-STEMI program with less than 6 hours of symptom onset
 Percutaneous transluminal coronary
angioplasty (PTCA)
INDICATIONS
• Acute ST-elevation myocardial infarction (STEMI)
• Non–ST-elevation acute coronary syndrome (NSTE-ACS)
• Unstable angina
• Stable angina
• Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
• High risk stress test findings
• Angiographic indications include hemodynamically significant lesions in vessels serving viable myocardium (vessel diameter
>1.5 mm)
CONTRAINDICATIONS
• intolerance of chronic antiplatelet therapy
• the presence of any significant comorbid conditions that severely limit patient lifespan (relative)
• A Heart Team approach (involving interventional cardiologists and cardiac surgeons) should be used in patients with diabetes
and multivessel CAD and in patients with severe left main (LM) disease and a high Syntax score
• Unprotected LM disease (unprotected by collateral coronary blood flow or patent bypass grafts)
• Less than 50% coronary artery stenosis
• No sign of myocardial ischemia (clinical, paraclinical, lab)
• No cardiac surgery unit in the hospital in case of complications
• No adequate equipment
• No trained team
• Severe allergy to iodinated contrast
 Coronary artery bypass grafting (CABG)
Coronary artery bypass graft surgery - a surgical procedure in which one or more blocked coronary
arteries are bypassed by a blood vessel graft to restore normal blood flow to the heart. These grafts
usually come from the patient's own arteries and veins located in the leg, arm, or chest.

Indications
Asymptomatic or Mild Angina
Class I
CABG should be performed in patients who have significant LM stenosis or LM equivalent :
significant (≥70%) stenosis of the proximal LAD and proximal left circumflex artery (Level of Evidence:
A)
CABG is useful in patients who have 3-vessel disease. (Survival benefit is greater in patients with
abnormal LV function) (Level of Evidence: C)
Class IIa
CABG can be beneficial for patients who have proximal LAD stenosis with 1- or 2-vessel disease
(Level of Evidence: A)
Class IIb
CABG may be considered for patients who have 1- or 2-vessel disease not involving the proximal LAD
(Level of Evidence: B)
 Coronary artery bypass grafting (CABG)
Indications
Stable Angina
Class I
•CABG is recommended for patients who have significant LM stenosis or LM equivalent: significant (≥70%)
stenosis of the proximal LAD and proximal left circumflex artery. (Level of Evidence: A )
•CABG is recommended for patients who have 3-vessel disease or 2-vessel disease with significant proximal LAD
stenosis and either EF less than 0.50 or demonstrable ischemia on noninvasive testing. (Level of Evidence: A)
•CABG is beneficial for patients who have 1- or 2-vessel CAD without significant proximal LAD stenosis but with a
large area of viable myocardium and high-risk criteria on noninvasive testing and for patients with stable angina
who have developed disabling angina despite maximal noninvasive therapy, when surgery can be performed with
acceptable risk. If the angina is not typical, objective evidence of ischemia should be obtained. (Level of Evidence:
B)
Class IIa
•CABG is reasonable in patients who have proximal LAD stenosis with 1-vessel disease. (Level of Evidence: A )
•CABG may be useful for patients who have 1- or 2-vessel CAD without significant proximal LAD stenosis but who
have a moderate area of viable myocardium and demonstrable ischemia on noninvasive testing. (Level of
Evidence: B)
Class III
•CABG is not recommended for patients with stable angina who have 1- or 2-vessel disease not involving
significant proximal LAD stenosis, patients who have mild symptoms that are unlikely due to myocardial ischemia,
patients who have not received an adequate medical treatment, or patients with ≤50% stenosis.
 Coronary artery bypass grafting (CABG)
Indications
Unstable Angina
Class I
•CABG should be performed for patients with LM stenosis or who have LM equivalent (Level of Evidence: A )
•CABG is recommended for patients in whom PTCA is not optimal or possible and who have ongoing ischemia not
responsive to maximal nonsurgical therapy. (Level of Evidence: B)
Class IIa
•CABG is probably indicated in patients who have proximal LAD stenosis with 1- or 2-vessel disease. (Level of
Evidence: A)
Class IIb
•CABG may be considered for patients who have 1- or 2-vessel disease not involving the proximal LAD when PTCA
is not optimal or possible. (Level of Evidence: B)
Poor LV Function
Class I
•CABG should be performed for patients with LM stenosis, LM equivalent (A) or proximal LAD stenosis with 2- or
3-vessel disease (B)
Class IIa
•CABG may be performed in patients with significant viable noncontracting, revascularizable myocardium and
without any of the above anatomic patterns. (Level of Evidence: B)
Class III
•CABG should not be performed in patients without evidence of intermittent ischemia and without evidence of
significant revascularizable viable myocardium. (Level of Evidence: B)
 Coronary artery bypass grafting (CABG)

Contraindications
•CABG carries a risk of morbidity and mortality and is therefore not
considered appropriate in asymptomatic patients who are at a low risk of
myocardial infarction or death. Patients who will experience little benefit
from coronary revascularization are also excluded.
•Patients less likely to benefit from coronary revascularisation
•Several factors could increase morbidity and mortality (elderly, cancer)
and should be well balanced when considering CABG
 Coronary artery bypass grafting (CABG)
Preoperative evaluation
•Coronary angiography for coronary artery evaluation – dominance, stenosis topography, downsream vessel
quality
•Ventriculography for LV function evaluation
•Angiographic indication for surgery:
– severe stenosis (≥50% for LM and ≥70% for other coronary arteries)
– Proximal stenosis.
– good quality of downstream vessel.
– LVEF ≥ 20%.
LM stenosis is considered separately from other vessels.
Blood count, coagulation studies, blood group determination, measurement of serum electrolytes, urea,
creatinine and hepatic enzymes
12-lead ECG
Transthoracic echocardiography (TTE) is frequently used to define cardiac anatomy and assess ventricular
and valvular function
Chest X-ray
Carotid ultrasonography or angiography
Other exams depending on patient’s comorbidities and history
 Coronary artery bypass grafting (CABG)
Steps

•Conduit harvesting (saphenous vein, radial artery)

•Opening the thorax and exposing the heart (median sternotomy, lateral thoracotomy for
miniCABG)
Conduit harvesting (LIMA, RIMA)
•Extracorporeal circulation (ECC)
•Cardiac arrest (cardioplegia)
•CABG
•ECC interruption and restart of cardiac activity
•Postoperative reanimation
•Hospitalization and initiation of cardiac recovery
•Reeducation
 Coronary artery bypass grafting (CABG)

Positioning

•Supine, arms at patient’s sides

•Padded roll under the shoulders

•defibrillation

•Brushing: neck, thx, abdomen, lower limbs

•Thighs abduction / external rotation

 Coronary artery bypass grafting (CABG)

Harvesting of conduit (pedicled [in situ] or free graft)

•Saphenous vein (SVG)

•Radial artery (RAG)
•Left internal thoracic (mammary) artery (LIMA)
•Right internal thoracic (mammary) artery (RIMA)
•Right gastroepiploic artery
•Inferior epigastric artery
 Coronary artery bypass grafting (CABG)

SVG harvesting

•The SVG can be procured either via an open harvest

technique, starting from either the ankle or groin and using
a vein stripper, or via an endoscopic technique
•Avoid over distension and vein spasm
•Varicose veins are improper for harvesting
•The vein should be without twists, inverted and labeled for
grafting
 Coronary artery bypass grafting (CABG)

LIMA/RIMA harvesting

•Dissection starts in the 6th intercostal space

•Pedicled or skeletonized
•The distal end should not be divided until just
before the anastomosis
•Avoid sondage unless there is no bleeding at the
end cut
 Coronary artery bypass grafting (CABG)
Harvesting other grafts

Radial artery

Inferior epigastric artery

Gastroepiploic artery
 Coronary artery bypass grafting (CABG)
Cardiopulmonary bypass (CPB)
A CPB circuit consists of a systemic circuit for oxygenating blood and re-infusing blood into a patient's body; and a
separate circuit for infusing a solution into the heart itself to produce cardioplegia, and to provide myocardial
protection.
• Initiation: opening the venous line and de la ligne veineuse et drain the venous blood to the artificial system.
Blood circulation is provided in part by the LV and mostly by the artificial pump.
• Maintenance: systemic flow fully insured by the heart-lung machine. Hematose is performed by the
membrane oxygenator.
• Hypothermic cardioplegia: Immediate and sustained electromechanical quiescence (K, Mg, Ca,
bicarbonate to buffer acidosis, procaine), rapid and sustained homogenous myocardial cooling (4 - 8 °C),
maintenance of therapeutic additives in effective concentrations, periodic washout of metabolic inhibitor,
substrates (glucose, aspartate, glutamate), free radical scavenger (Mannitol).
• Discontinuation: de-aeration of heart cavities, warming, heart reperfusion, electric activity spontaneously
recovered during warming / electric shock

Cannulae
 Coronary artery bypass grafting (CABG)
Surgical technique
•the goal is the complete revascularization by bypassing all significant stenoses

•Patency is increased by grafting onto large vessels, with a good flow

•Anastomoses

•LIMA-LAD
•RIMA-LCX
•SVG – RCA, LCX
•Sequential anastomoses
•Y or T anastomoses
Coronary artery bypass grafting (CABG)
Exposure

Pericardial fixation on the left side T-shaped pericardial incision

 Coronary artery bypass grafting (CABG)
Exposure

Enuculeation of the heart – a prolene stitch on the posterior pericardium, on the right
side of the vertebra, halfway between inferior vena cava and pulmonary veins
(left) and normal wet spounge inserted between the tourniquet, V-shaped
(right)
 Coronary artery bypass grafting (CABG)
Exposure

Enuculeation of the heart - the V-shape spounge will be moved, so that the target
vessel stays in the middle of the V
 Coronary artery bypass
Type grafting
V (CABG)
Exposure

Enuculeation of the heart - patient placed in

Trendelenburg and turned towards the surgeon
 Coronary artery bypass grafting (CABG)
Anastomoses

LIMA-LAD anastomosis
 Coronary artery bypass grafting (CABG)
Anastomoses

Y anastomosis (LIMA-LAD, RA-LCX)

and SVG-TCA
 Coronary artery bypass grafting (CABG)
Anastomoses
•Free graft: implanted laterally in the ascending aorta and to the coronary artery downstream of the stenosis.
•Pedicled graft: proximal end left in place (in situ), distal anastomosis to a coronary artery
•Sequential anastomosis: technique to revascularize several coronary arteries using a single graft which is
implanted in the aorta and anastomosed artery side-to-side to 1-2 coronary arteries and finally end-to-side to the
2nd/3rd coronary artery
•Y/T anastomoses: free graft anastomosed proximally to another graft and distally to a coronary artery (end-to-
side)
 Coronary artery bypass grafting (CABG)
Anastomoses
Proximal anastomoses
•Implantation to the aorta in a lateral position in order to protect the graft in case of re-intervention
•The bevel of the vein has to be larger than the aortic opening

Distal anastomoses
•4-6 mm longitudinal incision in the coronary artery
•The bevel of the vein has to be larger than the coronary inicision
•The sutures are performed inside-out on the coronary artery and outside-in on the vein
 Coronary artery bypass grafting (CABG)
Graft evolution

Venous grafts
• Intimal hyperplasia is a universal finding after one month, but is not progressive
· At 1 year, the graft diameter approximates the recipient coronary diameter
· 10% close within the first few weeks if antiplatelet therapy is not used
· 10-year patency is about 50-60%
· Most grafts have evidence of atherosclerotic changes at 10 years

LIMA/RIMA
•Intimal hyperplasia also develops; the IMA is highly resistant to atherosclerosis
· 10-year patency is about 90%
· 5-10% develop late stenoses, but most of these do not progress to occlusion
· Controversy exist over its use as a sequential graft and for bilateral IMA grafting

Other grafts
•Long-term patency not yet conclusive on gastroepiploic, inferior mesenteric, and inferior epigastric arteries
· The free radial artery graft is being re-evaluated for long-term patency
 Coronary artery bypass grafting (CABG)
Results
•Effort capacity amelioration,
•LV Systolic function amelioration (especially in hypokinetic/akinetic areas)
•Increase of LVEF, RVEDV, decrease of motility alteration at 2 weeks after surgery (treadmill test,
ultrasound)

Free from angina

•60% of patients are free of symptoms
•Long-term symptoms recurrence (>10 yrs) – graft disfunction/occlusion or CAD progression
Free from myocardial infarction- > 95% at 5 yrs
Free from sudden death - >97% at 10 yrs
Poor preoperative LV function – risk factor for sudden death after surgery
CABG does not influence existing ventricular arrhytmias as most of them are caused by the presence of
scar tissue.
 Coronary artery bypass grafting (CABG)
Evolution
•Up to 75% of patients may have subtle neurologic deficits in the perioperative period
• Severe neurologic impairment occur in less than 1% of younger patients but up to 5% of patients over 70
•Current hospital mortality is about 3%, most from acute cardiac failure
•5-year survival is 88% and 10-year survival 75%
•IMA graft favorably affects the mid- and long-term survival (after 6 years)
•About 25% of all deaths after CABG are unrelated to ischemic heart disease or CABG

Mortality risk factors:

-Diminished LV function
-Unstable angina
-Acute hemodynamic instability after MI
-Operation within 1 week of acute MI
-Cardiogenic shock at time of operation
-Older age
-No LIMA-LAD anastomosis
-Prolonged myocardial ischemia
-incomplete revascularisation
 Coronary artery bypass grafting (CABG)

Redo CABG

•Avoid manipulating intact grafts

•90% of patients are free from redo surgery at 10 yrs
•SVG disfunction/occlusion is the most frequent cause for redo surgery
•Arterial graft usage reduces the number of redo interventions and increases the interval from
primary to redo CABG
•10 yrs survival after redo CABG around 65%
•PTCA can be used for graft disfunction
 Actual CABG
Goals
• Total arterial revascularisation
• Y, sequential anastomoses
• Complete revascularisation
• CPB( ↓ beating heart)
• Skeletonized LIMA to protect from sternal devascularisation
• Prolene 8/0 with magnifying glasses
New CABG techniques
• Beating heart CABG
• Minimally invasive CABG
• Endoscopic CABG
• Robotic CABG
 Beating heart CABG
Off-pump coronary artery bypass or "beating heart" surgery is a form of coronary artery bypass graft (CABG) surgery performed without cardiopulmonary
bypass.
Goal: achieve effective revascularization, as complete as possible in technical terms and safely for the patient, avoiding the onset of complications
induced by CPB and myocardial ischemia.
The improvement of heart stabilization equipment and surgical procedure, combined with better monitoring and better perioperative management, now
allow performing of this type of surgery.
It appears that beating heart surgery achieves results at least equal in terms of efficacy and reproducibility in patients with low or moderate surgical risk.
 MI CABG
Minimally invasive CABG

Conventional CABG

• 10 cm incisition without separation of the thoracic cage

• Beating heart intervention
 Advantages and disadvantages of minimally invasive
CABG
Advantages:
• Incision Size
• Surgery / Recovery time
• Cost
• Complications

Disadvantages:
• Maximum number of arteries grafted
• Lack of exposure / practices
• Highly skilled surgeons required
Endoscopic CABG

Port Access Solution:

• Perform grafting through 3 small
ports near armpit
• View procedure through scope in 4th
port in chest
• Attach heart-lung machine through
femoral artery/vein
• Stop heart with inflatable tip of a
guide wire
 Robotic CABG

• The first robotic assisted closed chest

by pass on a beating heart was
completed on September 24th, 1999, at
London Health Sciences Center

• The surgeon moves the camera

through voice-operated controls and
manipulates the surgical equipment
using a hand held joystick.