Coronary Arterial Disease

S Chapter 60
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Anat: Normal coronary a. vasculature
 Drainage
The venous circulation can be divided into three
systems:-
• the coronary sinus and its tributaries
• the anterior right ventricular veins, and
• the thebesian veins.
Understanding the anatomy of the coronary
sinus is essential for placing the retrograde
cardioplegia cannula during CPB.
Physiology and Regulation of Coronary
Blood Flow
• Aortic pressure is a driving force in the
maintenance of myocardial perfusion.
• Autoregulated over wide po ranges (70-180
mmHg)
• Normal coronary blood flow: 0.7-0.9 mL/g of
myocardium per min. (about 225 mL/min)
• 75% oxygen extraction, :. coronary sinus blood is
the most deoxygenated blood in the body
• 4 -7 fold increase in flow with increased demand
• 60% blood flow occurs during diastole
– basis for exercise-induced stress tests
• Flow limited oxygen supply
Physiology and Regulation of Coronary
Blood Flow
Mechanisms for increased blood flow with
increased demand
1. Coronary vasodilation
– Mediated by local metabolic neurohumoral factors
2. When a transient occlusion to the coronary
artery is released, blood flow immediately
rises to exceed the normal baseline flow.
The mechanism for vasodilation and reactive
hyperemia is endothelium-dependent
ATHEROSCLEROTIC CORONARY A. DISEASE
The process begins early in the patient’s life.
– Most susceptible: Epicardial conductance vessels
– Least susceptible: Intramyocardial arteries
Risk factors include:
a. elevated plasma levels of total cholesterol and
LDLc
b. Cigarette smoking
c. hypertension, DM, advanced age
d. low plasma levels of HDLc
e. FHx of premature coronary a. disease (CAD).
ATHEROSCLEROTIC CORONARY A. DISEASE
Pathogenesis
Etiology: endothelial injury induced by an
inflammatory wall response and lipid
deposition.
Stages of the disease:
1. early lipid deposition
2. plaque formation
3. plaque rupture, and then
4. coronary artery thrombosis.
ATHEROSCLEROTIC CORONARY A. DISEASE
Pathogenesis
• Not all plaque ruptures are symptomatic;
– this is dependent on the thrombogenicity of the
plaque’s components.
• Rupture of a vulnerable plaque may be
spontaneous or caused by
– extreme physical activity
– Severe emotional distress
– exposure to drugs
– cold exposure or
– acute infection.
ATHEROSCLEROTIC CORONARY A. DISEASE
Fixed Coronary Obstructions
• Account for >90% of patients with symptomatic
IHD/ advanced coronary atherosclerosis
• Atherosclerotic plaques of the coronary aa. are
concentric (25%) or eccentric (75%).
• …when the cross-sectional area of the vessel has
decreased by 75% or more, coronary blood flow
is significantly compromised (Poiseuille’s law).
– Clinically, the onset of exertional angina.
• 90% reduction in luminal diameter
– Resting angina.
Clinical Presentation
• Angina (most common symptom)
• Dyspnoea
– Above symptoms typically are exacerbated or
incited by effort but subsequently resolve with
rest.
• “Unstable angina”:
– encompasses resting angina, new-onset angina,
and accelerated angina.
– usually indicative of severe ischemia and
impending MI.
Approx. 15% of patients with CAD do not
present with angina.
Clinical Presentation
“acute coronary syndrome (ACS)”:
constellation of clinical symptoms that
represent MI:
• crushing chest pain
– may be associated with nausea, diaphoresis,
anxiety, and dyspnea.
• dizziness, fatigue, and vomiting
– Symptoms of hypoperfusion.
Clinical Presentation
• HR and BP: may be initially normal
– increase in response to the duration and severity
of pain.
– Loss of BP is indicative of cardiogenic shock and
indicates a poorer prognosis.
Atleast 40% of ventricular mass involved.
• Sudden onset of a non-perfusing ventricular
rhythm, such as ventricular tachycardia or
fibrillation.
– first manifestation of CAD in 40% of patients
Clinical Presentation : MI
• Prehospital mortality rate for an acute MI
(AMI) is approximately 50%.
• Of those patients who reach the hospital,
another 25% die during the hospital stay.
• Another 25% die in the first year afterward.
Mechanical complications of MI include
– acute ventricular septal defect (VSD)
– papillary m. rupture
– free ventricular rupture.
Usually occur approx. 7 -10 days after the initial MI.
Physical Examination
Systemic manifestations of atherosclerosis:
• Eye examination may reveal a copper wire
sign, retinal hematoma or thrombosis 20 to
vascular occlusive disease, and HTN.
• Corneal arcus and xanthelasma are features
noticed in cases of hypercholesterolemia.
Sequelae of CAD
Physical Examination
Sequelae of CAD
• Abnormal neck vein pulsations, which may be
seen in patients with second- or third-degree
heart block or CHF.
• Bradycardia—a subtle presentation of ischemia
involving the right coronary territories and a
possible sign of heart block
• Weak or thready pulse suggestive of ectopic or
premature ventricular beats
• Third heart sound that is noted with elevated left
ventricular filling pressures/CHF
• Fourth heart sound, which is commonly heard in
patients with acute and chronic CAD
Physical Examination
Sequelae of CAD
• Mitral regurgitant heart murmurs caused by
ischemic papillary muscles
• Ejection systolic murmur indicative of aortic
stenosis, which can contribute to coronary
ischemia
• Holosystolic murmurs caused by ventricular
septal rupture
• Manifestations of CHF
• rales, hepatomegaly, RUQ (abdominal)
tenderness, ascites, and marked peripheral and
presacral edema
Physical Examination
Vascular exam
• thorough vascular evaluation for any patient
with CAD
– atherosclerosis is a systemic process.
• If surgery is being planned, evaluate
extremities for any previous surgical scars or
fractures
– these could potentially preclude vein harvest.
 Diagnostic Testing
Biochemical Studies
• Creatinine kinase m. and brain subunits (CK-
MB) and troponin T or I
– should be assessed at least 6 to 12 hours apart.
• CBC, comprehensive metabolic panel, and
lipid profile (total cholesterol, triglycerides,
LDLc, HDLc)
• Brain natriuretic peptide (BNP) and CRP
– Elevated levels suggest a worse outcome.
 Diagnostic Testing
Chest Radiography
• helpful in identifying causes of chest
discomfort or pain other than CAD.
• It identifies sequelae, such as cardiomegaly,
pulmonary edema, and pleural effusions, that
are indicative of heart failure.
• Evidence of calcification in the coronary aa.
– although suggestive of CAD, it is not reflective of
disease severity
 Diagnostic Testing
Resting Electrocardiography
• evaluated for evidence of left ventricular
hypertrophy, ST-segment depression or
elevation, ectopic beats, or Q waves.
– Persistent ST-segment elevation or an evolving Q
wave are consistent with myocardial injury and
ongoing ischemia
• Arrhythmias and conduction defects
– Suggestive of CAD and MI.
50% of ECGs obtained during chest pain at
rest will be normal
 Diagnostic Testing
Exercise Stress ECG
– to determine the patient’s ischemic threshold
Echocardiography
– to estimate ventricular wall abnormalities and the
ejection fraction.
Multidetector computed tomography (MDCT)
– allows imaging of the coronary arteries anatomy
MRI and Gadolinium MRI
Cardiac Catheterization and Intervention
 Diagnostic Testing
Cardiac Catheterization and Intervention
– gold standard for evaluating the anatomy of the
coronary aa.
– High-quality coronary angiography is essential for
identifying CAD and assessing its extent and
severity.
 Management
Coronary Artery Revascularization
Indications
1. Angina unresponsive to medical therapy
2. Unstable angina
3. Congestive heart failure with viable
myocardium
4. Cardiogenic shock
• These indications are managed preferably by
PCI.
 Management
Coronary Artery Revascularization
Indications
5. Left main stenosis >50%
6. Left main equivalent disease—a combination
of hemodynamically significant lesions
involving the proximal circumflex and LAD
territory
7. Concomitant triple-vessel CAD, EF <50%, and
diabetes
• These indications 5 through 7 are managed
preferably by surgical revascularization.
 Management
Coronary Artery Revascularization
Indications
8. Acute coronary occlusion after failed PCI
9. Mechanical complication of acute MI

These last two indications constitute surgical