Angina Pectoris Complete

80
4/14/12  Angina Pectoris  Tutor : Prof. Dr. Nahed Baddour

Transcript of Angina Pectoris Complete

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Angina Pectoris

 Tutor : Prof. Dr. Nahed Baddour

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Angina Pectoris

ID number Name Topic

10-2-161 Muhammad Bin Misbah introduction about Ischemic heart disease

10-2-162 Muhammad Jailani Bin Mustafa risk factors of Ischemic heart disease

10-2-163 Muhammad Hazim Bin Zulkifli classification of Ischemic heart disease &introduction about angina

10-2-164 Muhammad Hasif Bin Ramli aetiology, morphology, pathogenesis of stable angina

10-2-165 Muhammad Hafiz bin Mohamad Radzi clinical features, fate or complications of stableangina

10-2-166 Muhammad Huzaifah bin Hassan aetiology, morphology, pathogenesis of unstableangina

10-2-167 Mohd Hafizuddin B Md Nasir clinical features, fate or complications of unstableangina

10-2-168 Mohd Ridwan Shahputra bin Shihabuddin aetiology, morphology, pathogenesis of variantangina

10-2-169 Muhammad Ridzwan bin Abd Aziz clinical features, fate or complications of variantangina

10-2-170 Mohamad Zaimey bin Zulmanaf differences between each type of angina and

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Angina Pectoris

introduction about Ischemicheart disease

Muhammad Bin Misbah

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• Definition: group of closelyrelated disorders resultingimbalance betweenmyocardial demand andvascular supply of oxygenated blood.

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Etiology of IschemicHeart Disease

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1) Decrease

coronary blood flow

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Coronaryatherosclerosis

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Aortic regurgitation &stenosis

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2) Increased

myocardial demand

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 Tachycardia 

Hypertrophy

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3) Factors thataggravate the

effects of ischemia

(hypoxia)

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cyanotic congenitalheart disease

 

advanced lun

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4) Diminishedoxygen carrying

capacity

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Anemia

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Angina Pectoris

classification of Ischemicheart disease &

introduction about angina

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Classification of IschemicHeart Disease (IHD)

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ANGINA PECTORIS• It is characterized by intermittent chest pain.•  The pain may radiate to the neck, back, down and left arm.

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ANGINA PECTORIS

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ACUTE myocardialinfarction (MI)

• MI, popularly called heart attack , is necrosis of heart muscleresulting from ischemia.

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ACUTE myocardialinfarction (MI)

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ECG CHANGES INMYOCARDIAL INFARCTION

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Chronic ischemic heartdisease

• Is essentially progressive heart failure as a consequence of ischemic myocardial damage.

 

•  The heart isenlarged.

• Moderate tosevere

atherosclerosis

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SUDDEN CARDIAC DEATH

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SUDDEN CARDIAC DEATH(SCD)• Sudden Cardiac Death (SCD) is most commonly defined as

unexpected death from cardiac causes either without

symptoms or within 1 to 24 hours of symptom onset•  The ultimate mechanism of SCD is most often a lethal

ARRYTHMIA, such as VENTRICULAR FIBRILLATION.

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Angina Pectoris

Risk factors of Ischemicheart disease

Muhammad ailani

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Hypertension (high bloodpressure)

• blood pressure can vary with activityand with age

• healthy adult generally has a systolicpressure reading between 120 and130 and a diastolic pressure readingbetween 80 and 90 (or below)

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Diabetes

• heart problems are the leading causeof death with diabetes

• case of non-insulin-dependentdiabetes also known as Type IIdiabetes

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High blood cholesterol

• cholesterol is a fat-like substancecarried by blood

• liver produces all of the cholesterolto form cell membranes and to makecertain hormones

• Extra cholesterol -meats, eggs,andother similar products

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obesity and overweight

• increased total cholesterol levels,high blood pressure, and anincreased risk of coronary artery

disease• Developing other risk factors for

heart disease:

- high blood pressure

- high blood cholesterol

-diabetes

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Smoking

• smoking increases the risk of lungcancer

• increases the risk of heart diseaseand peripheral vascular disease

• increases the risk of stroke in peoplewho already have high bloodpressure.

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Angina Pectoris

aetiology, morphology,pathogenesis of stable

angina

WHAT IS

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WHAT ISSTABLE

ANGINA ???

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WHEN IT WILL

HAPPEN???

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WHICH PART THAT

 YOU WILL FEEL PAIN???

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FOR HOW LONG ???

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ETIOLOGY 

ü Coronary heart disease

ü Abnormal heart rhythms

ü Anemia

ü Coronary artery spasm

ü Heart failure

ü

Heart valve diseaseü Hyperthyroidism

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ü Cold weather 

ü Exercise

ü Emotional stress

ü Large meals

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PATHOGENESIS

Ø Your heart muscle is working all the time, so itneeds a constant supply of oxygen. This oxygenis provided by the coronary arteries, which carryblood.

Ø When the heart muscle has to work harder, itneeds more oxygen. Symptoms of angina occur 

when the coronary arteries are narrowed or blocked by hardening of the arteries(atherosclerosis), or by a blood clot.

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Angina Pectoris

Symptoms andComplications of Stable

Angina

Muhammad Hafiz bin Mohamad Radzi

10-2-165

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Common Symptoms

v tightness, heavy pressure, orsqueezing or crushing chest pain

Ø Occurs after activity or stress

Ø Lasts an average of 1 - 15 minutes

Ø Is relieved with rest or a medicinecalled nitro l cerin

Symptoms

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• Other symptoms

v feeling of indigestion or heartburn

v Dizziness or light-headedness

v Nausea, vomiting, and sweating

v Palpitations

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Cardiac arrhythmias

v Ventricular tachycardia

v Heart block

v Atrial fibrillation

v Congestive heart failure

Complications

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• Mitral regurgitation

v Pericarditis

v Pulmonary embolism

v Shock

v Stroke

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• Sudden death

v Ventricular fibrillation

v Ventricular aneurysm

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Angina Pectoris

aetiology, morphology,pathogenesis of unstable

angina

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Ø Heart does not get enough bloodflow and 0xygen ~ Heart Attack

Ø Acute Coronary Syndrome, norelease of the enzyme andbiomarkers of myocardial necrosis

Ø Braunwald Classification:Ø Class I : Less 2 months without rest

pain

Ø Class II : Next 48 hours + rest pain

Definitions

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Etiology & pathogenesis

Ø Characteristic:Ø High frequency of pain

Ø Precipitated by progressively less exertion

Ø Episodes tend to be more intense and

 – longer lasting than stable angina

Ø Pathogenesis:Ø Associated with plaque disruption + superimposed

partial thrombosis + distal embolization of thethrombus + vasospasm

F f i l

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Factors of etiology

Ø Factors of etiologyØ Supply-demand mismatch

Ø Plaque disruption or rupture

Ø  ThrombosisØ Vasoconstriction

Ø Cyclical flow

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Angina Pectoris

clinical features, fate orcomplications of unstable

angina

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Clinical Features, Fate and Complication of Unstable Angina

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Focused History &Physicalexamination

•  There is chest pain in the :-substernal lesion orepigastrium radiating to neck-left shoulder and left arm.

• There is severe discomfort orpain.

• Anginal equivalents likedyspnoea and epigastricdiscomfort are also frequentlypresent.

• There is diaphoresis (increasedsweating), pale skin, sinustachycardia, third and fourthheart sound, basilar rales orcrepts, sometime hypotension.

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•Angina starting within the past 2 months and

becoming more severe.

•Limiting their physical activity.

•Suddenly becoming more frequent, severe, or 

longer-lasting or being brought on by less exertion

than before.

•Occurring at rest with no obvious exertion or stress.

Some say these symptoms may wake you up.

•Not responding to rest or nitroglycerin.

•Have other than common symptom is chest pain or 

pressure symptoms like shortness of breath, nausea,and back or jaw pain (for woman).

PatientsComplaints:

ECG of unstable angina

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ECG of unstable angina

• There is ST segment depression

•Rarely there is transient ST segment

elevation

• There may be T inversions

•Any new ST segment changes like

depression of even 0.05 mV may denote

increasing severity.

•New deep T wave inversions (more than 0.3

mV) may be significant, but usually T wave

changes are nonspecific.

Cardiac biomarkers for

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•CK-MB and troponin (highly specific) are elevated

in MI and associated with increased risk of death.

•New cardiac markers are C-reactive protein, BNP

(B type nitriuretic peptide, CD-40 ligand etc.

Cardiac biomarkers forunstable angina

Fate of Unstable angina

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Fate of Unstable angina

Prognostic indicators

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Prognostic indicators

• Of note, studies have shown that the

following are significant

prognosticators for poor outcome:

• Ongoing congestive heart failure

• Presence/history of poor left

ventricular ejection fraction (LVEF)

Risk factors for coronary artery

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y ydisease include:

• Diabetes

• Family history of early coronary heartdisease -- a close relative such as asibling or parent had heart diseasebefore age 55 (in a man) or beforeage 65 (in a woman)

• High blood pressure

• High LDL cholesterol

Low HDL cholesterol

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Angina Pectoris

aetiology, morphology,

pathogenesis of variant

angina

Mohd Ridwan Shahputra bin

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What is variant angina?

• Prinzmetal• A form of chest pain, pressure, or

tightness (angina)• Extremely rare• N.B; the American cardiologist Dr.

Myron Prinzmetal• A form of unstable angina

• No identifiabletrigger

• Occur in clusters

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CoronaryVasospasm

Atherosclerosis

Injury to liningof artery

NervousSystem /

Muscle Tissue

Causes

Acetylcholine

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Acetylcholine

ParasympatheticNervous System

DirectMechanism

Dilatation of Coronary

Arteries

inducesvasoconstriction of vascular smooth

muscle cells

stimulatesendothelial cellsto produce NO

Mechanism

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Mechanism

Defect inendothelial Nitric

Oxide(NO)synthetase

enzyme

Reduced NO

Contraction of coronary vascular

smooth muscle

Endothelialfunction

abnormalities

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Risk factor

• Substance abuse

• Traditional cardiovascular risk factors

Exercise• Alcohol withdrawal

• Hyperventilation

• Hypertension

• Diets high in salt and saturated fats

Obesity• Diabetes

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Angina Pectoris

clinical features, fate orcomplications of variant

angina

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Clinical features•

Occurs at rest• Last for 5-30 mins( between 12 – 8 AM )• Painful headache & Raynaud’s

phenomenon• Elevation of ST segment ( must be

detected during attack, suggestingprovocative method)

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Fate

• Generally good prognosis

• Needs follow-up by doctors

• Treated with Calcium channel blockerand nitrates(vasodilators)

• In coronary blockade, angioplasty maybe considered.

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Complications

• During pain, Arrhythmia mayoccur( vent. Tachycardia, vent.fibrillations, heart block)

• Treatment of arrhythmia may causemedication reaction & intolerance.

• For angioplastic patient; plaque

recurrence, infection, medicationreaction.

i i

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Angina Pectoris

differences between eachtype of angina and

treatment

e

rences e ween ypesf A i

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ypof Angina

Points of differences Stable (typical) Unstable

(pre-infarct)

Variant(Prinzmetal’s)

State Most common form More severe,frequent and lastlonger

 Temporary suddennarrowing

Precipitated by 1. Exertion orphysical activity

2. emotional stress

(increase demand)

1. Less effort

2. even occurs atrest

1. Rest, awakenspatient from sleep

2. unrelated tophysical activity

Relieved by 1. Rest (to decreasedemand)

2. vasodilators (torelieve vasospasm)

1. Blood thinners(antiplatelet drugs)

2. Statins

1. vasodilators

2. calcium channelblockers

Coronary angiogram75% or more of atherosclerotic

narrowing

Non-occlusivecoronary thrombi

Near normal tosevere

atheroscleroticnarrowing

ECG analysis Depression of STsegment

1. ST segmentdepression

2. Rarely STsegment elevation

Elevation STsegment

Causes Fissuring ordisruption of the Coronary arterydisease due to Coronary vasospasm

M di i

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Medications

S i l d

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Surgical procedures

Angioplasty stentCoronary artery bypass graft

P ti

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Preventions

R f

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References

• PubMed Health : Stable angina, available from :http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001247/  [assessed at 4th April 2012]

• PubMed Health : Unstable angina, available from :http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH000125 0/ 

[assessed at 4th April 2012]

• PubMed Health : Variant angina, available from :http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH000121 2/ [assessed at 4th April 2012]

• Module 11 Semester 4 2011-2012 Year 2, TheCardiovascular System, Faculty of Medicine-AlexandriaUniversity : Heart Diseases, Ischaemic Heart Diseases(IHD), Classification of Ischaemic Heart Diseases, AnginaPectoris, page 208-210 [cited at 5th April 2012]

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 Thank you