ISCHEMIC HEART DISEASE (IHD)

Medicine 2
Dr. Sofia Black
September 13, 2014

MYOCARDIAL OXYGEN SUPPLY

CLINICAL SCENARIO
A 55 y/o female consulted OPD because of effort-related chest pain. She is a known
hypertensive, diabetic, previous smoker and non-compliant to medications. Physical exam
showed BP= 140/100, CR= 60 bpm, RR 18/min, BMI of 30.
ISCHEMIC HEART DISEASE

Inadequate oxygen supply

Increase oxygen demand
Imbalance: supply < demand
Myocardial ischemia
o Where the imbalance happen
o Obstructive atherosclerotic disease of epicardial vessel

Most common cause

o Inadequate perfusion of coronaries
Previously known as Coronary artery disease
o Term used in Europe
o In PHIC they accept ischemic heart disease but not CAD

EPIDEMIOLOGY

Most common, serious, chronic life threatening disease

PATHOLOGY

Coronary arteries

PATHOPHYSIOLOGY
MYOCARDIAL OXYGEN DEMAND

Heart rate
o increase HR increase oxygen demand on a background of inadequate
supply
Myocardial contractility
o More contraction increase oxygen demand
Myocardial wall stress/ tension
o Frank Starling law

Increase LV end diastolic volume in Left ventricular pressure

increased forceful contractility up to a limit

Overstretching increase wall tension increase contractility

increase oxygen demand failure will not be elastic
breakage

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Oxygen carrying capacity of blood (by hemoglobin)

o Level of inspired oxygen

High altitude higher elevation low oxygen

o Pulmonary function

Dysfunctional pulmonary system (ex. COPD and bronchial

asthma has decrease oxygenation) secondary Myocardial
ischemia
o Hemoglobin concentration

Low hemoglobin concentration (ex. anemia) normal blood

flow but oxygen content is low
Blood flow: occurs during Diastole
o Relaxation

Impairment of relaxation impairment in the flow and supply

o Blood flow goes to coronaries when the heart relaxes
o Abnormal Diastolic dysfunction is the EARLIEST SIGN of Ischemia

ECG and contractility may be normal but diastolic function is

abnormal IHD

CORONARY ARTERIES

3 Large epicardial arteries

o Left coronary artery (from the aorta)

Divides into two: (1) Left anterior descending artery and (2)
Left circumflex artery
o
(3) Right coronary artery (from the aorta)

Large epicardial vessels Obtuse marginal 1 and 2 vessels Pre-arteriolar

arteries myocardium Arteriolar and intramyocardial capillary vessels

Orifices that originate from the aorta behind aortic valve

o Aortic valve has 3 cusps:
Right coronary cusp Where the right coronary artery came from to the
right coronary sinus
Left coronary cusp
Where the Left coronary artery/left main coronary
artery came from
Non-coronary cusp
CONDUCTANCE VESSEL

Large epicardial coronary arteries

Constriction and relaxation
Abnormal constriction:
o Prinzmetal angina (unknown etiology): Epicardial coronary arteries are
abnormally vasospastic without atherosclerosis
o No relaxation, remain vasoconstricted (but theres still a chance to dilate)

RESISTANCE VESSELS

Major determinants of coronary resistance coronary flow

The absence of evidence is not an evidence of absence Carl Sagan

Smaller vessels from epicardial vessels:

o Pre-arteriolar vessels

From obtuse marginal vessels

o Arteriolar vessels
o Intramyocardial capillary vessels

Intramyocardial arteriole

Abnormal constriction

Seen in Diabetic patients

Failure of dilatation, remain vasoconstricted (NO chance to

dilate again)

Microvascular ischemia pathophysiology in diabetic

patients
Capable of auto-regulation

Side Notes:
*coronary angiogram (gold standard for IHD in the past) can show normal results for IHD
*microvascular circulation are not seen in coronary angiogram only the large epicardial
vessels
CORONARY ATHEROSCLEROSIS
MAJOR RISK FACTORS (3 FACTORS QUALIFY A PERSON TO BE AT RISK )
MODIFIABLE

Cigarette smoking
o Nicotine accelerates the position of cholesterol
o Acts as a catalyst: deposit the cholesterol

Hypertension
o Sheer stress to capillary wall endothelial dysfunction

Diabetes mellitus
o High sugar inflammation and endothelial dysfunction

Low HDL

High LDL
NON-MODIFIABLE

Family history of premature CHD

o Male <55 y/o
o Female < 65 y/o

Age
o Male 45 y/o
o Female 55 y/o
o *No longer true due to food chain (unhealthy food)

Male gender

Lifestyle risk factors

o Obesity (BMI >30 kg/m2)
o Physical inactivity

Endothelial dysfunction
o Atherogenic diet
#KAFC #LML #DAB #LGTM #DACM MEDICINE BATCH 2016

Emerging risk factors

o Lipoproteins: Apo B
o Homocysteine
o Pro-thrombotic

By Oral contraceptive pills

o Pro-inflammatory

Patients with IHD and STD: (+) for Chlamydia on autopsy

(plaque contains chlamydia)
o Impaired fasting glucose

Slight innervation of fasting blood glucose

Not diabetic yet, waiting to be diabetics, diabetics in the

process increase glucose in the vascular system intraendothelial dysfunction

INITIATION OF ATHERO SCLEROSIS (IN ORDER)

Initial stage: fatty streak formation

o As early as 10 years old and above
o Fatty stage formation in utero

Maternal blame cholesterol of the mother goes to the child

Lipoprotein oxidation tunica intima
Non enzymatic glycation
Leukocyte recruitment
Foam cell formation
o Leukocytes transforming to macrophages and phagocytize oxidized LDL
Atheroma evolution (it takes time)
o Involvement of arterial smooth muscle
o Blood coagulation thrombosis
o Micro vessel formation
o Plaque evolution

ATHEROSCLEROSIS A PROGRESSIVE DISEASE

The absence of evidence is not an evidence of absence Carl Sagan

(Refer to the picture)

Atherosclerosis

Progressive disease

Atheros: porridge (cholesterol)

Scleros: hardening

A lot of oxidized LDL will become a soft porridge rupture attract platelet
thrombus formation

CORONARY ARTERY
METABOLIC REGULATION

Decrease in oxygen carrying capacity

o Good supply but the oxygen is depleted
o Severe anemia

No hemoglobin to carry oxygen

Free oxygen in the blood cannot be used because it is not

bound to Hemoglobin
o Carboxyhemoglobinemia

Carbon monoxide (CO) poisoning: competing with oxygen in

hemoglobin

Ex. Sleeping inside the car with engine on

Painless death

Regulates oxygen supply

CORONARY ATHEROSCLEROSIS

AUTO REGULATION

Regulates coronary blood flow

Vasodilation and vasoconstriction
o As long as there are no blockages

*Coronary arteries extract the most oxygen in the blood for consumption
CAUSES OF ISCHEMIA

Reduction in the lumen of the coronary artery

o Atherosclerosis

Arteries distal to plaque are vasospastic

Decrease lumen decrease perfusion to myocardium

o Coronary artery spasm

Prinzmetal angina
o Arterial thrombi

From a ruptured plaque proximally thrombus dislodge

distally smaller vessels (Intramyocardial vessels)
o Coronary emboli from infective endocarditis

Vegetation from right coronary valve dislodge to right

coronary artery

Left coronary valve left coronary artery

Increase oxygen demand with limited blood flow (not totally obstructed)
o LVH due to aortic stenosis

Arteries are patent but supply is not enough during systole and
diastole due to fixed obstruction in aortic valve
o Hypertension

There is Left Ventricular hypertrophy

Increase the demand when there are hypertrophied

muscles because the supply is decreasing
o Hyperthyroidism

Due to increased HR
o Fever

Due to increased HR

#KAFC #LML #DAB #LGTM #DACM MEDICINE BATCH 2016

Epicardial coronary artery

o Major site of atherosclerotic disease
Main affectation: Tunica intima
Major risk factor: Endothelial dysfunction
o Whole cascade of atherosclerosis proceeds
o Bottom-line of all the risk factorS
o Does not happen overnight
o Vasoconstriction
o Luminal clot formation
o Monocytes and platelet interaction
o Atherosclerotic plaque formation

When it ruptured Acute coronary syndrome

Sub-intimal fat collection

Smooth muscle cell proliferation

Fibroblast and intercellular matrix

Major risk factorS
o High LDL
o Low HDL
o Cigarette smoking
o Hypertension
o DM

*The good cholesterol (HDL), the bad cholesterol (LDL) and the ugly cholesterol (triglycerides)
ISCHEMIC HEART DISEASE (AGAIN)

Critical obstruction: 70%

o Myocardial ischemia
o Do intervention: angioplasty (single vessel) or bypass (multiple vessel
disease)
o *But MI can also occur in <70%

Due to rupture of the plaque thrombus formation (give antiplatelets)

3

The absence of evidence is not an evidence of absence Carl Sagan

Asymptomatic Ischemic Heart Disease

o Coronary atherosclerosis: 20 year-old post mortem studies

EFFECTS OF ISCHEMIA

Abnormal muscular contraction and relaxation

o Contraction but no relaxation

Relaxation (coronary blood flow)

Patient complains of chest pain, fatigue, SOB

Aging heart will be fibrotic (stiff heart) heart failure

LV failure
o Ejection fraction is low: <40%
o Systolic HF: no contraction
o Diastolic HF: no relaxation
Mitral regurgitation
o Involvement of the papillary muscles ischemia incompetent mitral
valve

BIOCHEMICAL EFFECTS

No oxygen Glucose to lactate lactic acidosis

o When myocardium is in an acidic medium it will not contract systolic

Myocardial necrosis
o The heart cant survive with a lactic environment
Angina pectoris

dystaxia

*32 ATPs in the Krebs cycle

ELECTRICAL EFFECTS

MECHANICAL

MANIFESTATION

Repolarization abnormalities
o STTWC: ST wave depression and T wave inversion
Electrical instability
o Arrhythmias
o Most dreaded
o Ventricular tachycardia

Male >50; female >60

Chest discomfort (typical)
o Retrosternal pain
Levine sign
o Fist clenched on sternum

*Chest paint equivalent/atypical chest pain

ANGINA

Cardiac origin
o Atypical chest pains in the elderly

Epigastric pain

Choking sensation
Crescendo-decrescendo
o Crescendo going up; decrescendo going down
Duration
o 1-5 minutes, 10 minutes at the most
Radiation
o Below mandible and above the umbilicus
o Epigastric pain CAN BE an inferior myocardial infarction (diaphragm
irritation)
Location
o Retrosternal is the MC description

PRECIPITATING FACTOR S

Exertion
Emotion
Rest
o Chest pains at rest: Severe IHD
o Obstruction is severe

Arteries clogged >70%

GRADING OF SEVERITY OF ANGINA

CANADIAN CARDIAC SOC IETY CLASSIFICATION

For IHD chest pain

STABLE ANGINA PECTORIS

Episodic clinical syndrome

Transient myocardial ischemia
o When it becomes persistent it becomes ACS
70% males in before menopausal stage

CLASS
I
II
III
IV

ONSET OF CHEST PAIN

Chest pain with more than ordinary activity
Chest pain on ordinary activity
Chest pain on less than ordinary activity
Chest pain at rest

*New York Heart Classification: Heart Failure and Chest Pain

4

#KAFC #LML #DAB #LGTM #DACM MEDICINE BATCH 2016

The absence of evidence is not an evidence of absence Carl Sagan

RISK FACTORS

Modifiable and Non-modifiable

ASSOCIATED COMORBID CONDITIONS

CVD, TIA, PAD, CKD, stroke

Atherosclerosis is not only on the heart but also systemic
o Ex. kidneys = renal failure

PHYSCIAL EXAMINATION

Most are normal

Evidence of atherosclerosis
o Abnormal aneurysm
o Carotid bruit, PAD
o Xanthomas (yellow deposition of the fat), xanthelasmas
Risk factors for atherosclerosis

Fundoscopy
o

Atherosclerotic retinopathy

Thick vessel wall

o Hypertensive retinopathy

With papilledema

Plain hemorrhages

Copper wiring
Signs of anemia and pallor
Signs of aortic stenosis
o Heart: left ventricular fibrillation and systolic ejection murmurs
o Palpation of the radial pulse: Weak pulse

*even if there are normal test proceed to exercise stress testing

DIAGNOSTIC TEST OF I HD
EXERCISE STRESS TESTING

Most widely used

To prognosticate IHD and in patients for angiogram and bypass
Problem: Symptom limited
Sensitivity = only 70% are detected (30% are missed)
o 85% if with post MI
Heart rate limited

CONTRAINDICATON OF E XERCISE STRESS TEST

Angina at rest within 48 hours

Unstable rhythm
o Atrial fibrillation and fast ventricular response

Severe aortic stenosis = definite contraindication!!!

Acute myocarditis
o Prone to arrhythmias

Unstable heart failure

Active infective endocarditis

o Embolization of vegetation
*If exercise stress testing is normal but patient still has episodic chest pains proceed to
cardiac imaging
*Dobutamine Stress Test for patients who are unable to exercise
CARDIAC IMAGING

LABORATORY EXAMINATION

ECG
o A normal ECG does not rule out disease
o Accurate only in 30%
o Arrhythmias
Chest X-ray
o Heart enlargement: sign of Congestion
Urinalysis
o To know Comorbid diagnostics or risk factors (ex. glycosuria=DM,
glomerulonephritis=HTN)
Lipid profile
o HDL, LDL, TG
Blood glucose
o FBS: 126 = Diabetes
o RBS: 200 = Diabetes
o Impaired blood sugar
Hemoglobin/Hematocrit
o Anemia

#KAFC #LML #DAB #LGTM #DACM MEDICINE BATCH 2016

Myocardial perfusion scan

o Let the patient exercise then inject a radioactive

There is perfusion defect

o Physiologic
o Once it is normal it means normal
o If (-) cardiac scan but (+)myocardial perfusion scan = microvascular
ischemia
Echocardiography
o A normal result does not say youre really a normal patient
o EF: <40%: poor prognosis

CORONARY ANGIOGRAPHY

Done when ALL things failed like medical management and the patient still has
chest pains
Gold standard before the discovery of intramyocardial ischemia
Invasive
5

The absence of evidence is not an evidence of absence Carl Sagan

INDICAITONS FOR CORO NARY ANGIOGRAPHY

Chronic Stable Angina (CSA) severely symptomatic despite treatment

Diagnostic difficulty
o To know if CAD or malingerer

Cardiac arrest survivors

(+) non-invasive testing with LV dysfunction

o Treadmill stress test

High risk patients

o Admitted for acute coronary syndrome (ACS)
o Symptoms in careers involving safety of others (pilots, bus drivers)
o Male >45, female >55 undergoing valve surgery

For patients with rheumatic heart disease

o High risk on stress test

Mets (measure of oxygen consumption)

If result is <7 METS (Metabolic Equivalent of Tasks)

Normal person should reach 7 METS

Primary goal: Increase patients quality of life
Secondary goal: Prolong life
CT ANGIOGRAPHY

Conductance vessels only

o Intramyocardial vessels not seen
Less invasive

IHD: PROGNOSTIC INDI CATORS

Age
o The older the poorer the prognosis
Functional state of the LV
o Ejection fraction 40% (poor prognosis)
Location and severity of occlusion
o Left main artery involvement

Patient is not sent home

Widow or orphan maker lesion

o The more proximal the poorer the prognosis

*Nuclear scan: physiologic

*Echocardiography, cardiac MR scan and cardiac PET scan: anatomic
#KAFC #LML #DAB #LGTM #DACM MEDICINE BATCH 2016

The absence of evidence is not an evidence of absence Carl Sagan

TREATMENT OF IHD

Class IIb

MANAGEMENT PLAN

Evidence of therapy less established, No other options available, <50%, Good study
Class III
Dypirimole
Used before as anti-platelet
Therapy
not
Can cause coronary steal syndrome (normal cells steel
useful; Harmful
from the deceased myocardium)
Increase perfusion to normal arteries only
Induces more ischemia
Diagnostic procedure only
Chelation therapy
Alternative medicine/Herbal medicines
Dissolve the plaque not true!!!

Explanation and reassurance

o Anxiolytics Diazepam
o Explain that there is no time to be dependent on these drugs
Identification and treatment of aggravating factors
o Family counseling
Activity adaptation
o Dont go beyond the capacity of the heart

If Treadmill test showed 7 METS then do not prescribe 7 METS

(only prescribe 70% of the metabolic requirement)

Climbing the stairs: 4 METS

Climbing a mountain: 11 METS

Walking for 5 kilometers: 7-10 METS

DRUG THERAPY
GUIDELINES FOR TREATMENT OF CSA
Class I
Aspirin (anti-platelet)
Used before for headache
(+) Evidence of Beta blockers
Drug Efficacy
Decrease HR
Decrease O2 consumption
Calcium antagonist
If patient has allergies, asthma or has history of asthma
Decrease HR, coronary vasodilator
Do not give with EF of less than 40%
Sublingual nitrates
Decrease preload and vasodilator
Decrease wall tension and wall stress decrease oxygen
demand
Lipid lowering
Anti-cholesterol drugs
STATINS to be taken for life
Control LDL and HDL
Risk modification
Walk
Class IIa
Clopidogrel
When aspirin is contraindicated in cases of allergy and
Evidence in favor
ulcers
of therapy
Long acting calcium antagonist
Instead of beta blockers in cases of asthma
>50%
positive Long acting nitrates and beta blockers
effect of the drug

#KAFC #LML #DAB #LGTM #DACM MEDICINE BATCH 2016

TREATMENT OF RISK FACTORS TO IMPROVE OUTCOME

Class I
Smoking cessation
Treatment of dyslipidemia
Total cholesterol: 160 mg/dL
LDL: 70-100 mg/dL
Treatment of hypertension
Ideal weight and exercise
(Ht in cm 100) 10% of answer IBW
Aerobic exercise not isometric (weight lifting increase myocardial
oxygen demand)
ACE inhibitors
DOC
Have different effects at different dosages
Hypertension: Captopril 50mg BID
LV remodeling: Captopril 25 mg tab OD
High levels: anti-hypertensive
Low levels: for ischemia and remodeling
Low fat diet
Treatment of DM
Class IIb
Folate therapy
Not a first line treatment
Improve hemoglobin
Intervention directed for psychological stress
Class III
Hormonal replacement therapy
After menopause there is higher risk because estrogen cannot be
replaced
Increased chance of developing cervical and breast cancer
Treatment of depression
Chelation therapy
Vitamin E and C
Supplement
Antioxidant
7
Herbal medicines
The absence of evidence is not an evidence of absence Carl Sagan

INTERVENTION WITH FAILURE OF MEDICAL MANAGEMENT

CORONARY REVASCULARIZATION

Percutaneous coronary intervention

o Angioplasty with stent
Coronary artery bypass grafting

ASYMPTOMATIC ( SILENT) ISCHEMIA

Continuous ambulatory ECG monitoring will show ischemia

o Holter monitoring
Increase risk for cardiovascular events
o Patients wont take the medications
Treatment of risk factors: hypertension and diabetes
o Diabetic patients usually present with asymptomatic chest pain
No manifestation of chest pain

PRINZMETALS VARIANT ANGINA

Uncommon form of unstable angina

Recurrent severe ischemia
Episodic focal spasm
ECG changes transient ST elevation
Treatment
o Nitrates vasodilator
o Calcium antagonist vasodilatation of coronary arteries

Side Notes:
*Lowest incidence of CAD is in Japan
*Bypass can be done in MI but not in stroke (brain is dead)

#KAFC #LML #DAB #LGTM #DACM MEDICINE BATCH 2016

The absence of evidence is not an evidence of absence Carl Sagan