Ischemic Heart Disease Dr. Mohd. Aslam - PowerPoint Presentation

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Ischemic Heart Disease

Dr. Mohd. Aslam

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Ischemic heart disease

Ischemic heart disease (IHD):

Is

a disease characterized by reduction

of blood

supply of the heart muscle, usually due to coronary

artery occlusion

1- Angina

Stable Angina

Unstable Angina

Variant Angina

Decubitus angina

Nocturnal angina

2- Myocardial infarction

STEMI

NSTEMI

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Definitions

Acute coronary syndrome is defined

as myocardial

ischemia due to

myocardial infarction

(NSTEMI or STEMI) or unstable angina

Unstable angina is defined as angina at

rest, new

onset exertional angina (<2 months

), recent

acceleration of angina (<2 months),

or post

revascularization angina

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Epidemiology:

• Most common cause of cardiovascular morbidity and mortality

• Atherosclerosis and thrombosis are the most important pathogenetic mechanisms.

• Peak incidence of symptomatic IHD is age 50-60 (men) and 60-70 (women)

M>F

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Etiology:

1- Decreased coronary blood flow due to mechanical obstruction

such as:

Atheroma

Spasm of coronary artery

Thrombosis

Embolism

Coronary artreritis

2- Increased myocardial oxygen requirement :

Increased cardiac output

:Thyrotoxicosis

Myocardial hypertrophy: aortic stenosis , hypertension

3- Decreased flow of oxygenated blood :

Anemia

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Angina pectoris

Is a clinical syndrome characterized by paroxysmal chest pain due to transient myocardial ischemia . It may occur whenever there is imbalance between myocardial oxygen supply and demand the most common cause is atherosclerosis .

However angina may also develop in aortic stenosis and hypertrophic cardiomyopathy even there is no coronary atheroma.

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Angina symptoms

Chest pain or discomfort

Pain in your arms, neck, jaw, shoulder or back accompanying chest pain

Nausea

Fatigue

Shortness of breath

Anxiety

Sweating

Dizziness

Chest pain or discomfort is usually felt as:

pressure

heaviness

tightening

squeezing

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Stable Angina

Atherosclerotic coronary artery disease

occurs when the heart has to work harder than normal,

during exercise

Typical: retrosternal chest pain, tightness or discomfort

Radiating to left(± right) shoulder/arm/

neck/jaw

Brief duration, lasting <10-15 min

Associated with diaphoresis, nausea, anxiety

Typically relieved by rest and nitrates

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precipitated by the " E's"Emotional stress

Exertion

Exposure to very hot or cold temperatures

Eating ( Heavy meals)

And Smoking

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Variant Angina

A spasm in a coronary artery

Usually happens when you're resting, unrelated to exercise, relieved by nitrates

Typically occurs between midnight and 8 AM,

The coronary arteries can spasm as a result of:

Exposure

to cold

Emotional stress

Medicines

that tighten or narrow blood vessels

Smoking

Cocaine

use

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Unstable Angina

Due to spasm and partial obstruction of coronaries.

Occurs even at rest

Is unexpected (new onset)

Is usually more severe and lasts longer than stable angina, may be as long as 30 minutes

May not disappear with rest or use of angina medication

May lead to complete occlusion of vessel causing MI

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Myocardial Infarction

Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia (total obstruction)

Typical symptoms of myocardial infarction include

sudden chest

pain

shortness of

breath

nausea,

vomiting

palpitations, sweating

weakness, light-headedness

Collapse/syncope

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Ischemic Heart Disease

Heart

Disease due to ischemia due to any

cause:

• Coronary artery disease

• Hypertensive heart disease

• Syphilitic heart disease

• Aortic stenosis

• Hypertrophic Cardiomyopathy

•

Anemia

• Aortic dissection

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Coronary artery disease

• Any disease involving coronary artery that may lead to IHD

• Atherosclerosis

• Thrombus

• Embolism

• Inflammation-PAN

• CAD may be Asymptomatic

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Angina/ IHD

•

Due to either increased oxygen demand Or due to reduced oxygen supply

Increased oxygen demand due to hypertrophy of left or right ventricle

Causes of left ventricular hypertrophy

1. Concentric due to systemic HTN, Aortic stenosis

2. Asymmetrical –cardiomyopathy

Causes of right ventricular hypertrophy

1. Concentric due to pulmonary HTN, Pulmonary stenosis

2. Asymmetrical – right ventricular cardiomyopathy

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Angina/ IHD

Reduced oxygen supply due

to:

• Coronary artery obstruction due to Atherosclerosis, spasm, thrombosis, embolism, dissection, inflammation

Coronary osteal stenosis due to syphilis

Reduced hemoglobin

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Diagnosis

Dx of acute coronary syndrome is based on history, physical exam, ECG, cardiac enzymes

Patients can then be divided into several groups

Non-cardiac chest pain (i.e., Gastrointestinal, musculoskeletal, pulmonary embolus)

Stable angina

Unstable angina

Myocardial infarction (STEMI or NSTEMI)

Other cardiac causes of chest pain (i.e., aortic dissection, pericarditis)

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Diagnosis

Severe chest discomfort

Occurs at rest

Lasting >10 min

Recent onset (up to 2 weeks)

Crescendo pattern

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Coronary artery disease

presentation

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Pathophysiology of ACS

Plaque rupture and subsequent formation of

thrombus

– this can be either occlusive or non-occlusive (STEMI,

NSTEMI

, USA)

Vasospasm such as that seen in Prinzmetal’s angina,

cocaine use (STEMI, NSTEMI, USA)

Progression of obstructive coronary

atherosclerotic disease

(USA)

In-stent thrombosis (early post PCI)

In-stent

rest enosis

(late post PCI

Poor surgical technique (post CABG)

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Pathophysiology of ACS

Acute coronary syndromes can also be due

to secondary

causes

Thyrotoxicosis

Anemia

Tachycardia

Hypotension

Hypoxemia

Arterial

inflammation (infection, arteritis)

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Diagnostic tests

ECG

Echocardiography

Myocardial SPECT

Biomarkers – Troponin, CK-MB,

Myoglobin

CCTA

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Cardiac Biomarkers

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Pre-Test Probability

In the absence of abnormal findings on physical

exam, ECG

, or enzymes, the pre-test probability of

acute coronary

syndrome must be determined by

the clinician

A good history is crucial (is the chest pain typical

or atypical

; what are the associated symptoms)

Determination of risk factors is also crucial (male,

age

>55

, smoking, DM, HTN, FamHx,

hyperlipidemia,

known CAD)

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Coronary artery disease-Diagnosis

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Treatment of ACS

Aspirin is an

antiplatelet

agent that initiates

the irreversible

inhibition of

cyclooxygenase, thereby

preventing platelet production

of thromboxane

A2 and decreasing

platelet aggregation

Administration of ASA in ACS reduces

cardiac endpoints

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ACC/AHA Guidelines for Aspirin therapy

Aspirin should be given in a dose of

75-325 mg/day

to all patients with ACS unless there is

a contraindication

(in which case,

clopidogrel should

be given)

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Treatment of ACS; Clopidogrel

Clopidogrel is a potent antiplatelet agent

It should be administered to all patients

who cannot

take ASA

The CURE trial suggests a benefit to

adding Clopidogrel

to ASA/Heparin in patients going

for PCI

Give 300 mg loading dose followed by

75 mg/day

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ACC/AHA Guidelines for Clopidogrel therapy

Clopidogrel should be administered to patients

who cannot

take ASA because of hypersensitivity

or gastrointestinal

intolerance

In hospitalized patients in whom an

early, non interventional

approach is planned,

clopidogrel should

be added to ASA as soon as possible

on admission

and administered for at least 1 month

and up

to 9 months.

Do

not use clopidogrel if there is

any possibility

patient may be candidate for CABG

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Treatment of ACS; Nitrates

Nitroglycerin is considered a cornerstone of

antianginal therapy

, despite little objective evidence for

its benefit

Benefit is thought to occur via reduction in

myocardial O2

demand secondary to venodilation

induced reduction

in preload as well as coronary

vasodilation

and afterload

reduction

Titrate to relief of chest pain; chest pain = death

of myocardial

cells

No documented mortality benefit

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Treatment of ACS; Beta blockers

Beta Blockers reduce myocardial

oxygen demand

by reducing heart rate,

contractility, and

ventricular wall tension

Administration of beta blockers in ACS

reduces cardiac

endpoints

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ACA/AHA Guidelines for Beta Blocker Therapy

Intravenous beta blockers should be

used initially

in all patients (without

contraindication) followed

by oral beta blockers with the

goal being

decrease in heart rate to 60 beats

per minute

A combination of beta blockers and nitrates

can be

viewed as first line therapy in all

patients with

ACS

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Treatment of ACS; Heparin

Heparin (unfractionated heparin or UFH)

has traditionally

been the mainstay of therapy

in acute

coronary syndromes as its efficacy

has been

documented in several large,

randomized trials

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Treatment of ACS; LMWH

More recent studies indicate that low

molecular weight

heparin is also effective in the

reduction of

end points such as myocardial infarction

or death

Some studies report that LMWH, when used

in combination

with ASA, may be superior

to continuous

infusion of Heparin

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ACA/AHA Guidelines for Heparin Therapy

All patients with acute coronary

syndromes should

be treated with a combination of

ASA (325

mg/day) and heparin (bolus followed

by continuous

infusion with goal of PTT

1-2.5X control

) or ASA and low molecular

weight heparin

unless one of the drugs

is contraindicated

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Treatment of ACS; ACE-Inhibitors

The best documented mechanism by

which these

agents act is to reduce

ventricular remodeling

over days to weeks after

myocardial damage

. However, there is data that a

mortality benefit

exists when these agents are used

early in

the course of ACS

Administration of ACE-I in ACS reduces

cardiac endpoints

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AHA/ACC Guidelines for ACE-Inhibitor Therapy

ACE-I should be administered to all patients

in the

first 24 hours of ACS provided

hypotension and

other clear cut contraindications are absent

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Treatment of ACS

; Statins

Statins may be of benefit in ACS

Possible mechanisms include

plaque stabilization

, reversal of

endothelial dysfunction

, decreased thrombogenicity,

and reduction

of inflammation

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TIMI Risk Score

Age >65 yrs

Daily ASA Therapy (>7 days prior to event)

Symptoms of Unstable Angina

Documented CAD (stenosis > 50%)

3 or more traditional cardiac risk factors

Elevated cardiac enzymes

ECG changes

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TIMI Risk Score

Score of 3 or less = low risk

Score of 4-5 = intermediate risk (use IIBIIIA)

Score of 6-7 = high risk (use IIBIIIA)

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Treatment of ACS; Emergent Revascularization

In the setting of STEMI primary PCI is

associated with

better outcomes than thrombolysis

Emergent PCI is also indicated in the setting of a new LBBB

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Conclusions; Treatment NSTEMI/USA

ASA

NTG

Beta Blocker

Heparin/LMWH

ACE-I

Statin

Clopidogrel

+/-

IIB/IIIA

inhibitors (based on TIMI risk score)

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Conclusions; Treatment

of STEMI

ASA

NTG

Beta Blocker

Heparin/LMWH

ACE-I

Clopidogrel

IIB/IIIA

i

nhibitors

Statin

Activate the Cath Lab!!!

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Coronary artery disease-Treatment

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Complications

Ventricular Dysfunction

Hemodynamic Assessment

Hypovolemia

Cardiogenic shock

Arrhythmias, conduction disturbances

Pericarditis

Aneurysm

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Conclusions; Approach to chest pain

Good History and Physical (note time

and duration

of symptoms)

Careful evaluation of ECG (compare to

previous when

possible)

Check Cardiac Enzymes

Monitor on Telemetry

Oxygen

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THANKS