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Ischaemic Heart Disease

Yusra Pintaningrum
Dept. of Cardiology & Vascular Medicine

NTB General Hospital,


Faculty of Medicine, Mataram University

Clinical Manifestation of IHD


Silent Ischemia/asymptomatic
Stable Angina

Acute Coronary Syndrome (NonSTEMI/UA and STEMI)


Arrhythmias Heart Failure Sudden Death

Epidemiology
MI occurs every 2 mins in UK Account for 100,000 deaths annually Cardiovascular death accounts for 40% all deaths under the age 75 yrs Major cause of cardiac arrest

Survival to discharge of all rhythm cardiac arrests is 10.7%

Mechanisms of ischaemia
Ischaemia disturbance in myocardial oxygen supply and demand Impaired coronary artery blood flow
Atherosclerosis Coronary artery spasm Dissection Tachycardia shortened diastole

Impaired oxygen delivery


Hypoxia Anaemia

Increased cardiac work

Pain patterns with myocardial ischemia


Usual distribution of pain with myocardial ischemia Less common sites of pain with myocardial ischemia

Right side

Jaw

Epigastrium

Back

Atherosclerosis

Pathology of atherosclerosis
Lipid laden macrophages form fatty streak

This allows lipids to deposit in the arterial wall


Smooth muscle cells, cholesterol and lymphocytes also join the plaque Eventually a fibrous cap forms around the whole structure causing a narrowing

Causes ischaemia by three mechanisms


Platelet aggregation can form clots emboli Plaque rupture

Progressive stenosis

Anatomy
1. Aorta
2. Right Coronary Artery 3. Left Anterior Descending Artery 4. Circumflex Coronary Artery

5. Left main stem

Circumflex artery obstruction


Lateral infarction
ECG changes leads I, AVL and V4-V6 20% cases

Left anterior descending obstruction


Anterior infarction
ECG changes V1-V4 50% cases most likely to cause left ventricular dysfunction

Right coronary artery obstruction


Inferior infarction ECG changes in II, III & AVF 30% cases - often causes bradyarrythmias

Posterior myocardial infarction


Usually right coronary artery but may be circumflex
ST depression in anterior leads Dominant R wave is actually a Q wave

Risk Factors
Fixed
Age

Modifiable
Smoking

Male sex
Menopause Family history

Hypertension
Hyperlipidaemia Obesity

Diabetes

Alcohol
Sedentary lifestyle

Stable angina
Myocardial ischaemia without muscle necrosis Caused by
Fixed stenosis Coronary artery spasm Other disease hypoxia, valvular disease

History
Exercise related, pressing precordial chest pain, can radiate to jaw and left arm, often relieved by nitrates. Can also manifest as breathlessness

Stable angina
Investigations
ECG
Often normal or non specific changes such as T wave inversion, can show ST depression reflecting ischaemia

Exercise ECG
ECG changes related to exertion particularly ST depression, dysrhythmias, hypotension

Stable Angina Management


Lifestyle modification
Stop smoking Good diabetic control Cut down alcohol Lose weight reduces myocardial work

Symptom control
Nitrates dilate coronary arteries
Rest

Stable angina Management


Drug therapy
Antihypertensives
Statins help prevent plaque rupture, LDL Aspirin antiplatelet

Beta blockers
Antagonists of adrenaline & noradrenaline Reduced contractility and heart rate

Calcium antagonist
Vasodilation (especially dihydropyidines) Prolongation of action potential, antidysrrythmic

Stable angina Management


Coronary revascularisation
Angina post myocardial infarction Unstable angina

Severe IHD
Stable angina uncontrolled by medication

Acute Coronary Syndrome


History
Site Left sided/central chest pain Onset sudden, can occur at rest Character dull, burning, sense of doom Radiation jaw, left arm, neck Associated factors sweating, nausea, vomiting, breathlessness, palpitations Timing >20mins, unrelieved by rest Exacerbating/ relieving factors Severity Like normal angina but much worse Risk factors

Pain patterns with myocardial ischemia


Usual distribution of pain with myocardial ischemia Less common sites of pain with myocardial ischemia

Right side

Jaw

Epigastrium

Back

PATHOPHYSIOLOGY

Goals of Treatment
Reduce Infarct size Reduce Mortality Prevention of Unfavorable Clinical Events
Recurrent Myocardial infarction Congestive heart failure Sudden death Avoid complication

Safety

Arrhythmias

Repeat Intervention
Satler L. SCAI-ACC I2 Summit 2008

MANAGEMENT OF UA/ NSTEMI

MANAGEMENT STEMI

Symptom Call to Prehospital Recognition Medical System

ED

CCU

Cath Lab

Delay in initiation of Pharmacologic Reperfusion

PELAYANAN KEGAWATAN JANTUNG KORONER


Hospital fibrinolysis : Door-to-Needle within 30 min

Not PCI capable

Onset of symptoms of STEMI

9-1-1 EMS Dispatch

EMS on-scene
Encourage 12-lead ECGs Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min

EMS Triage Plan


PCI capable

Goals
Patient 5 min after symptom onset EMS on Dispatch scene 1 min

EMS transport
EMS transport:EMS-to-Balloon within 90 min

Within Prehospital fibrinolysis : Patient self-transport:Hospital Door-to-Balloon within 90 min 8 min EMS-to-Handle within 30 min

Total ischemic time: Within 120 min*


*Golden Hour = First 60 minutes

Investigations
ECG - initially hyperacute T waves, then ST elevation, then T wave inversion then Q waves Chest x-ray Bloods FBC, U&Es, LFTs, Glucose, Cardiac enzymes

? Echo
CCU monitored bed

Indications for reperfusion


ST elevation >0.2 in 2 adjacent chest leads ST elevation >0.1 in 2 adjacent limb leads Dominant R waves and ST depression in V1-V3 (posterior infarct) New LBBB

Reperfusion Therapy
Percutaneous Coronary Intervention
Used for STEMI as these suggest full thickness infarction Should be done in <90mins

Method: Occluded vessel identified, guidewire passed, balloon inserted, stent inserted
Advantages
Culprit artery re-opened to normal calibre
Lower risk of major bleeding

Reperfusion Therapy
Thrombolysis
Advantages easy to perform, can be done quickly
Disadvantages
Inability to achieve reperfusion in all cases
Risk of inducing bleeding Cannot detect success of reperfusion

Contraindications
Recent CVA or previous haemorrhagic stroke Recent surgery

Active bleeding

Secondary prevention
Low Molecular Weight Heparin 1mg/kg OD Aspirin Clopidogrel Beta blocker usually Bisoprolol ACE inhibitor Glycoprotein IIb/IIIa inhibitor Statin Cardiac rehabilitation

CABG
Usually reserved for severe triple vessel disease not amenable to PCI Two forms
Vein grafts leg saphenous veins, quick to apply, annual failure 8% Arterial grafts more technically difficult, better long term survival, uses internal mammary artery

1% mortality if elective Prior to surgery optimise diabetes, do pulmonary function tests and vein mapping

Complications
Sudden death P- pump failure R- rupture of papillary muscle or septum E- embolism A- aneurysm and arrhythmias

D- Dresslers syndrome

Immediate - Dysrhythmias
Ventricular tachycardia/fibrillation usually respond well to resuscitation Sinus tachycardia heart failure or anxiety Sinus bradycardia early change particularly with inferior infarcts can treat with atropine Atrial fibrillation poor prognosis as indicates myocardial damage Complete heart block
Inferior MI usually resolves alone
Anterior MI bad prognosis, may need pacemaker

Heart failure
Left ventricular dysfunction can lead to hypotension, pulmonary oedema and renal impairment Treatment diuretics, nitrates, ACE inhibitor, later a beta blocker Cardiogenic shock very poor prognosis

Other complications
Pericarditis 48hrs after full thickness MI, widespread ST elevation Septal rupture acute haemodynamic deterioration, pansystolic murmur, treatment is surgery (2-5 days) Ruptured papillary muscle causes mitral prolapse (hours days) Left ventricular aneurysm persistent ST elevation Mural thrombus secondary to poor LV contraction Dresslers syndrome self limiting autoimmune pericarditis 2-3 weeks post MI

Post MI counselling
Explain medications and their use 2 months off work and avoid heavy labour Avoid sex for one month

Build up exercise gently


Stop smoking Reduce alcohol Avoid driving for 4-6 weeks Avoid flying for 2 months

THANK YOU

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