Ischemic

Heart Disease
Supervised by: Dr. Saifullah

Presented by:
Amir Farhan - 1129200919452
M Omar Hamwi – 1129200919503
Nurul Farhanim - 1129200919568
 Coronary Arteries and Regions of Heart Supply
Left main coronary artery (LMCA):
• It supplies blood to the left side of the heart muscle (the left
ventricle and left atrium)
 The left anterior descending artery - supplies blood to the
front of the left side of the heart.
 The circumflex artery - supplies blood to the outer side and
back of the heart.
Right coronary artery (RCA):
• It supplies blood to the right ventricle, the right atrium, and the
SA (sinoatrial) and AV (atrioventricular) nodes, which regulate
the heart rhythm.
 The right coronary artery divides into smaller branches -
the right posterior descending artery & the acute marginal
artery.
Two Main Coronary Arteries:  Together with the left anterior descending artery, the right
• Left main coronary artery coronary artery helps supply blood to the middle or
• Right coronary artery septum of the heart.
Plaque Formation & Rupture in Atherosclerosis
Plaque Formation
• Condition mechanisms elicited by LDL and the other causal factors are
multifaceted involve the lipoprotein retention, inflammatory cell
recruitment, foam cell formation, apoptosis and necrosis, smooth
muscle cell (SMC) proliferation and matrix synthesis, calcification,
angiogenesis, arterial remodeling, fibrous cap rupture, thrombosis, and
more.
• Complex interaction between these processes and a variable importance
of each process in the development of single plaques leading to
unpredictable progression rates, heterogeneous plaque morphology,
and variable clinical outcomes.
• Most plaques remain asymptomatic (subclinical disease), some become
obstructive (stable angina), and others elicit acute thrombosis and may
lead to an acute coronary syndrome (ACS).
Plaque Rupture
• Rupture of a thin cap and subsequent thrombosis may occur spontaneously, but
in some cases a temporary increase in emotional or physical stress provides the
final triggering of the event.
• Recognized triggers include physical and sexual activity, anger, anxiety, work
stress, earthquakes, war and terror attacks, temperature changes, infections, and
cocaine use.
• Also simple daily activities or the circadian rhythm of biological pathways may
determine the onset of ACS, which are most frequent in the morning.
• The triggering pathways may include activation of the sympathetic nervous
system with increased heart rate and blood pressure, leading to plaque rupture,
or increased coagulability and platelet reactivity, leading to an accentuated
thrombotic response on already ruptured plaques.
• It is important to note that even though triggers temporarily increase the relative
risk of ACS in susceptible persons, this means little for absolute risk because the
exposure is transient and often relatively infrequent.
Plaque Formation & Rupture in Atherosclerosis
Risk Factors of Cardiovascular Disease
Clinical Features of Angina
Angina is a type of chest pain caused by reduced blood flow to the heart.
Occur when there is mismatch between blood supply and metabolic
demand
Angina is a symptom of coronary artery disease

• Squeezing
• Pressure
• Heaviness
• Tightness
• Pain in the chest
• Feel like a heavy weight lying on the chest
PATHOPHYSIOLOGY
Angina is due to myocardial ischemia resulting from a transient and reversible
imbalance (mismatch) between myocardial oxygen demand and supply. This may
occur in the presence of a fixed stenosis or the result of a dynamic stenosis
(vasospasm) of the coronary arteries.

In ACS, the thrombotic component of the ruptured plaque dominates the overall
pathophysiological process and clinical picture.

Myocardial ischemia may also occur in the absence of chest pain or with atypical
symptoms (angina equivalent) such as dyspnoea, unexplained sweating, extreme
fatigue, or pain at a site other than the chest. This is more common in diabetics, the
elderly and in women.
Clinical Features of Angina
Different types of angina depends on the cause and whether rest or medication relieve symptoms.

Classical Angina/ Stable Angina:

• Chest pain described as heavy, tight or gripping.

• Pain is central or retrosternal.
• May radiate to the jaw, left shoulder or down left arm.
• Tends to occur with exercise or emotional stress.

Unstable Angina:

• Discomfort that feels like tightness, squeezing, crushing, burning, choking, or aching.
• Frequently occur during rest and does not easily go away when take medicine.
• Sweating
• Chest pain that may also feel in the shoulder, arm, jaw, neck, back, or other area.
Refractory Angina:

• Discomfort in the chest, such as heaviness, pressure, stinging, burning or choking sensations
• Chest pain that does not improve with deep breathing, coughing or changing positions
• Chest pain caused by exertion, eating, exposure to cold temperatures, or stress
• Pain in the upper abdomen, back, neck, jaw or shoulders
• Angina is not controlled by medical therapy

Vasospastic/ Variant Angina:

• Angina that occur without provocation, usually occur at rest during the overnight or early
morning hour
• Result of coronary artery spasm
• May spread to other parts of the body, such as the throat, arms, between the shoulder
blades, or stomach (may feel like an ulcer or indigestion)
• Gives a feeling of tightness, pressure, or heaviness
• Nausea and sweating
• Palpitations—rapid, irregular, or skipped heartbeats
Microvascular Angina:

• Patients have exercise-induced angina but normal or unobstructed

coronary arteries which on coronary angiography, CTCA
• chest pain during physical exertion, signs of reduced blood supply to the
heart during a stress test, and normal-looking arteries on an angiography.
• Myocardium shows an abnormal metabolic response to stress, consistent
with the suggestion that the myocardial ischaemia results from
abnormal dilator response of the coronary microvasculature to stress
• Difficulty in sleeping
Causes of Chest Pain
Cardiac Chest Pain vs Non-cardiac Chest Pain
Investigation of a Patient with Stable Angina
Investigation of a Patient with Stable Angina
Functional imaging tests - Chest Radiography
• show how the heart works under stress. Different tests can be used depending on the
circumstances and the person's preferences. Helpful in assessing cardiac size, pulmonary
vasculature and excluding certain non-cardiac causes of chest pain.

Exercise ECG
• a test that shows how the heart works while a person is exercising (walking on a treadmill or
using an exercise bike).

Preferably, the ECG should be done during an episode of chest pain.

The resting 12 lead ECG:

• usually normal - A normal resting ECG does not rule out CAD or myocardial ischemia.
• may show evidence of CAD such as pathological Q waves, left bundle branch block (LBBB), ST-
T abnormalities.
• may help to identify other causes of chest discomfort such as pericardial disease, dynamic ST-
T changes of coronary vasospasm, hypertrophic obstructive cardiomyopathy (HOCM).
CT coronary angiography (IF NEEDED, HIGH RISK)​
•uses a type of X‑ray called computed tomography (CT) scanning. Dye is injected into
the person's veins to show whether the coronary arteries are narrowed or blocked.​

Invasive coronary angiography (IF NEEDED, HIGH RISK)​

•X‑rays to see how dye (called contrast medium) moves through the arteries up to
the heart. This shows whether there are any narrowed or blocked arteries. It is
invasive because it involves a fine, hollow tube called a catheter being inserted
through the artery of the person's leg or arm and up to the heart.
Echocardiography (at rest) - IF NEEDED ONLY

Echocardiography is not a routine investigation in individuals suspected of having

CAD. In most of these individuals, the study is normal.

The echocardiogram, provides valuable information on LV function which is

important in risk stratification.

It is indicated in the:
• Presence of abnormal auscultatory findings
• Presence of abnormal resting ECG
• Assessment of LV function/regional wall motion abnormalities in patients with
shortness of breath and/or known CAD. It is a useful test to assess LV function
in individuals with hypertension and/or diabetes
• chest pain suspected to be due to CAD
References:
Exercise Tolerance Test, Stable Angina
Treatment, Acute Coronary Syndrome,
Cardiac Markers, ECG Changes, Acute
MI
Presented by: M Omar Hamwi – 1129200919503, B10, Y3
Exercise Tolerance Test (ETT)
• Exercise Tolerance Testing is defined as the
observation and recording of patient's
cardiovascular response to exercise.
• Involves monito ring of HR, BP, ECG.

• The exercise test complements the medical

history and the physical examination, and
it remains the second most commonly
performed cardiologic procedure next to
the routine ECG.
Purposes of Exercise Testing
• Exercise testing has been used for the provocation and identification
of myocardial ischemia for >6 decades
• Detection of coronary artery disease (CAD) in patients with chest
pain (chest discomfort) syndromes or potential symptom equivalents
• Evaluation of the anatomic and functional severity of CAD
• Evaluation of physical capacity and effort tolerance
• Evaluation of exercise-related symptoms
• Assessment of chronotropic competence, arrhythmias, and response
to implanted device therapy
• Assessment of the response to medical interventions
Exercise Physiology

• Sympathetic activation • Ventricular contractility

• Parasympathetic withdrawal • Peripheral resistance
• Vasoconstriction, except in- • TSBP,MBP,PP
1. Exercising muscles • DBP-no significant change
2. Cerebral circulation • Pulmonary vascular bed can
3. Coronary circulation • accommodate 6 fold CO
• Norepinephrine and Renin • CO - 4-6 times
release
• 02 extraction
 Contraindications of Exercise Tolerance Test
• Acute myocardial infarction (MI), within 2 days
• Ongoing unstable angina
• Prinzemetal angina
• Uncontrolled cardiac arrhythmia with hemodynamic compromise
• Active endocarditis, myocarditis or pericarditis
• Symptomatic severe aortic stenosis
• Decompensated heart failure
• Acute pulmonary embolism, pulmonary infarction, or deep vein Thrombosis
• Acute aortic dissection
• Physical disability that precludes safe and adequate testing
Drugs used Stable Angina
• Pharmacologically, the treatment of CAD focuses on the reduction of
myocardial oxygen demand
1) Nitrates e.g. Nitroglycerin & Isosorbide mononitrate : produce venous
dilation by relaxing smooth muscle, which decreases preload, and decrease
O2 demand by the heart
2) β blocker e.g. Atenolol : reduce myocardial O2 demand by decrease
heart rate and contractility
3) Calcium channel blocker e.g. Amlodipine, Verapamil : reduce Systemic
vascular resistance (SVR) and myocardial contractility.
4) Antiplatelet drugs e.g. aspirin: prevent thrombus formation in the
coronary vessels
5) Lipid lowering drugs e.g. Lovastatin: reduce the risk of heart attacks
Cont..
* Unstable angina in addition to nitroglycerine,
antiplatelet, use anticoagulant drugs such as Warfarin
* Acute myocardial infarction is treated with
thrombolytic agent. (see other slides for management)
Acute Coronary Syndrome (ACS)
• Definition: clinical spectrum of Coronary Artery Disease (CAD)
ranging from Unstable Angina (UA), non-ST segment Elevation
Myocardial Infarction (NSTEMI) to STEMI depending upon the
degree and acuteness of coronary occlusion (low blood flow
to heart).
• Pathophysiology: decreased blood flow to part of heart
musculature which is usually secondary to plaque rupture
(usually atheromatous) and formation of thrombus.
decreased blood flow ischemia infarction
Investigation of ACS

*Adapted from Amsterdam EA, Wenger N, Brindis RG et al. “2014 ACC/AHA Guidelines for the management of
patients with Non ST Elevation Acute Coronary Syndromes” Circulation. 2014;130:e344-e426.
 CARDIAC MARKERS
• Intracellular macromolecules 1.Troponin I & T (Tnl, TnT)
(proteins)_released from a heat muscle 2.Creatine kinase MB (CK-MB),
when it is damaged as a result of 3.Myoglobin (Mb)
myocardia infarction (MI). 4.Aspartate aminotransferase (AST)​
• They found in the blood. 5.Lactate dehydrogenase (LDH)
• They are normally present at all times, 6.B-type natriuretic peptide (BNP)
however, they are significantly elevated 7.C-reactive protein (CRP)
during a damage of the heart muscle. 8.Myeloperoxidase (MPO) ​
9.Ischemic modified albumin (IMA)
ST elevation myocardial infarction (STEMI)
• Acute chest pain and persistent ST elevation
• Total acute coronary occlusion
• Immediate reperfusion by primary angioplasty
Non ST elevation myocardial infarction (NSTEMI)
• Acute chest pain with or without ECG changes
• ECG: ST depressions, T-wave inversions
• Partial occlusion of a coronary artery
ST Elevation
Pathophysiology of acute MI
Classification of infarction of MI
• Transmural infarction- extend through the whole thickness
of the heart muscle and are usually a result of complete
occlusion of the area's blood Supply.
ECG findings: "ST elevation myocardial infarct" (STEMI)
• Subendocardial (nontransmural) infarction - involves a small
area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles.
ECG findings: "non-ST elevation infarct" (NSTEMI).
A transmural acute myocardial infarct, predominantly of the posterolateral
left ventricle (arrow). Note the myocardial hemorrhage at one edge of the
infarct that was associated with cardiac rupture, and the anterior scar
(arrowhead), indicative of old infarct.
Locating the MI within the heart
Locating the MI within the heart
Clinical features of Acute MI
• Angina (Radiating) • Anxiety, sleeplessness,
• Dyspnea hypertension or​
• hypotension, arrhythmia.​
• Fatigue
• Other symptoms include:
1) Diaphoresis
Note: Chest pain is less
2) Nausea frequent in women, their
3) Vomiting common symptoms are
weakness, fatigue &
4) Light-headedness dyspnea
5) Palpitation
Progression of MI seen on ECG
Reference
Complications of acute MI
1. Arrhythmias

Tachyarrhythmias

• Pulseless ventricular tachyarrhythmias

- Defibrillate immediately
- Early VF: within the first 48 hours and is due to electrical instability.
- Late VF: large infarcts and poor pump function and carries a poor prognosis

• Ventricular tachycardia (VT)

- arise from ischemia (within 48 hours) or from a myocardial scar due to the infarct (late onset)

• Atrial fibrillation (AF)

More commonly seen in the elderly and is associated with large infarcts.
It denotes a poorer prognosis and carries an increased risk of thromboembolism
Complications of acute MI
Bradyarrhythmias

• Sinus bradycardia
This does not require treatment unless associated with symptoms and/or
hypotension.
• Atrio-ventricular (AV) block


2. LV dysfunction and cardiogenic shock

- due to myocardial necrosis, myocardial stunning, atrial and ventricular arrhythmias or mechanical causes
such as acute septal rupture and valvular dysfunction

3. Right ventricular failure ( RVF)/infarction

- The clinical triad of hypotension, clear lung fields and elevated JVP in the setting of inferior STEMI is
suggestive of RV infarct

4. Mechanical complications
- Rupture of the left ventricular free wall, rupture of the interventricular septum, and acute mitral
Initial management of patient with acute MI
The following should be done immediately and concomitantly in the emergency
department:
1. Assessment and stabilisation of the patient’s haemodynamics.
2. One dose of sublingual glyceryl trinitrate (GTN) by tablet or spray if chest
pain persists (avoid if SBP < 90 mmHg).
3. 300 mg of soluble or chewable aspirin if not given earlier
4. Clopidogrel at a dose of 300 mg should be given, if not given earlier

Alternatively, the following may be given as loading doses if primary

percutaneous coronary intervention (PCI) is being considered:
1. 300-600 mg of clopidogrel
2. 180 mg of ticagrelor

Oxygen is administered in patients with hypoxaemia (SpO2 < 95% or PaO2 < 60
mmHg). Routine oxygen is not recommended in patients with SpO2 ≥ 95%.78-8
Clinical & ECG criteria for thrombolysis
therapy
Four criteria should be met before thrombolysis is initiated:
• definite clinical diagnosis of acute myocardial infarction
• short interval since the onset of symptoms:
• normally 12 hr
• treat up to 24 hr if ST elevation is persisting and the infarct is large
• ECG signs:
• regional ST elevation of >2 mm in chest leads and >1 mm in limb leads
• regional ST depression in cases of posterior infarction
• left bundle branch block
• no contraindications to thrombolysis present
 • known active bleeding source e.g. peptic ulcer,
active dyspepsia
• active menstruation
Contraindications • severe hypertension:
of thrombolysis - systolic more than 200 mm HG or diastolic more
therapy than 100 mm Hg
- must be sustained e.g. not responding to i.v. nitrates
• hypotension:
- systolic less than 90 mm Hg and not corrected by
atropine (if bradycardia) or other rhythm correction
• known or suspected aortic aneurysm
• On warfarin
Reperfusion Strategies- Angioplasty
Indications: widen blocked or narrowed coronary arteries
Angioplasty procedure:
1. A thin flexible tube called a catheter inserted into one of patient arteries
through an incision in groin, wrist or arm. This is guided to the affected
coronary artery using an X-ray video
2. When the catheter is in place, a thin wire is guided down the length of the
affected coronary artery, delivering a small balloon to the affected section
of artery.
3. This is then inflated to widen the artery, squashing fatty deposits against
the artery wall so blood can flow through it more freely when the deflated
balloon is removed.
If a stent is being used, this will be around the balloon before it's inserted.
The stent will expand when the balloon is inflated and remains in place
when the balloon is deflated and removed.
Coronary artery bypass graft (CABG)
 involves taking a blood vessel from another part of the body (usually the chest, leg
or arm) and attaching it to the coronary artery above and below the narrowed area
or blockage.

Indications for CABG— to improve

survival:
• Left main stem disease.
• Triple-vessel disease involving proximal
part of the left anterior descending.

Indications for CABG— to relieve

symptoms:
• Angina unresponsive to drugs.
• Unstable angina (sometimes).
• If angioplasty is unsuccessful
Adjunctive Therapies
All patients with STEMI receiving fibrinolytic therapy should receive:

• 300 mg aspirin
+ (Plus) loading dose:
75 mg of clopidogrel (> 75 years of age) or
300 mg clopidogrel (≤75 years of age)

• followed by a maintenance dose of 75-150 mg daily of aspirin long-term and 75

mg of clopidogrel daily. The duration of dual antiplatelet therapy (DAPT) should
be between 1 month to 1 year, the duration being a balance between the
ischaemic risks vs the bleeding risks.
Adjunctive Therapies (cont..)
All patients with STEMI undergoing Primary PCI should receive loading doses of:
• 300 mg aspirin
+ (Plus):
Ø 300-600 mg clopidogrel or
Ø 180 mg ticagrelor or
Ø60 mg prasugrel (after the coronary angiogram)

• This is followed by a maintenance dose of 75-150 mg daily of aspirin long-term and 75

mg of clopidogrel daily or 90 mg twice daily ticagrelor or 10 mg prasugrel daily.
Adjunctive Therapies (cont..)

• Patients who underwent PCI require DAPT for up to a year depending on

the thrombotic/ischaemic versus bleeding risks. In patients with high
bleeding risks, a shorter period of DAPT of 6 months may be considered.
• Medications that have been shown to improve survival if given early are:
ØACE-Is
ØARBs if ACE-I intolerant
Ø ß -blockers
ØMineralocorticoid Receptor Antagonists (MRA)
ØHigh dose statins.
 1. Medical evaluation.
• Initial evaluation: to check patient physical abilities, medical
limitations and other conditions patient may have.
• Ongoing evaluations: keep track of patient progress over time

2. Physical activity
Cardiac • low impact activities that have a lower risk of injury, such as
walking, cycling, rowing jogging, yoga (beneficial for cardiac
Rehabilitation health)
• proper exercise techniques, such as warming up and cooling
down
• muscle-strengthening exercises, such as lifting weights or other
resistance training exercises (increase your muscular fitness)

3.Lifestyle education. This involves support and education on

making healthy lifestyle changes, such as eating a heart-healthy
diet, exercising regularly, maintaining a healthy weight and quitting
smoking
 Important lifestyle interventions
include:
• cessation of smoking
Secondary • dietary modification
prevention – non - salt intake < 5g per day
pharmacological
• weight control
• physical activity
Secondary prevention - pharmacological

2. Lipid lowering drug

• Statins have been shown to
1. Anti-platelet agents: improve prognosis in patients
3. ß-blockers
• Aspirin - low dose aspirin 75- with stable CAD, the lower the
4. ACE-Is and ARBs
100 mg daily low-density lipoprotein
cholesterol (LDL-C) achieved,
the better the CV outcome