Ischemic Heart Disease (IHD)
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Transcript of Ischemic Heart Disease (IHD)
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ISCHEMIC HEART DISEASE
Akram Saleh MD, FRCPDirector of cardiology unit
Consultant Invasive Cardiologist
15-Oct-2012
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Ischemic Heart Disease (IHD)
When to suspect patient with IHD
Basic: coronary circulation
Myocardial oxygen supply and demands
Causes of IHD
Management
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Case presentation
A 65 Year old male, presented to outpatient clinic complaining of chest pain of 5 months duration.
What are the possible anatomical causes of chest pain?
The pain is retrosternal, compressive in nature, precipitated by wakening of 400 meter , relieved by rest, radiated to left shoulder, associated with sweating.
Patient is diabeticAnd smoker
On examination: Blood pressure:160/100. pulse rate: 88 bpmHeart auscultation : normalWHAT IS THE PROBLEB?What is abnormal physical findings?What to do? Investigations
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Coronary Anatomy
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Ischemic Heart Disease
demand
supply
1- Heart rate
2- Contractility
3- Wall tension
4- Muscle mass (wall thickness
1- Coronary flow (patency of coronary artery)
2- Hemoglobuline level
3- Myocardial oxygen extraction
4- Arterial oxygen saturation
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Causes of coronary artery disease
95% Atherosclerosis Risk factors:
5% Nonatherosclerosis
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Risk Factors for Cardiovascular DiseaseRisk Factors for Cardiovascular Disease
Modifiable Hypertension Smoking Hyperlipidaemia
Raised LDL-C Low HDL-C Raised triglycerides
Diabetes mellitus Dietary factors Lack of exercise Obesity Homocysteinemia Lipoprotein a Gout Thrombogenic factors: fibrinogen, factors V,VII Excess alcohol consumption
Non-modifiable Personal history
of CVD
Family history of CVD
Age: M>45, F>55
Gender M>F (Premenopausal)
Personality type A
Genetic factors: ACE gene
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Upregulation of endothelialadhesion molecules
Increased endothelial permeability
Migration of leucocytes into the artery wall
Leucocyte adhesion
Lipoprotein infiltration
Endothelial Dysfunction in Atherosclerosis
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Formation of foam cells
Adherence and entry of leucocytes
Activation of T cells
Migration of smooth muscle cells
Adherence and aggregation of platelets
Fatty Streak Formation in Atherosclerosis
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Formation of the fibrous cap
Accumulation ofmacrophages
Formation ofnecrotic core
Formation of the Complicated Atherosclerotic Plaque
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Characteristics of Unstable and Stable Plaque
Thin fibrous cap
Inflammatory cells
FewSMCs
Erodedendothelium
Activatedmacrophages
Thickfibrous cap
Lack ofinflammatory cells
Foam cells
Intactendothelium
MoreSMCs
Libby P. Circulation. 1995;91:2844-2850.
Unstable Stable
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AHA-Classification
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Gottdiener JS. In: ACCSAP 1997-98 by the ACC and AHA
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Clinical Manifestations of Atherosclerosis
Coronary heart disease Asymptomatic Angina pectoris, variant angina Myocardial infarction, Unstable angina Heart failure (HF) Arrhythmias Sudden cardiac death.
Asympt sudden death
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IHD-clinicopathological correlation
1- stable angina: stenosis > 70% luminal narrowing
2-variant angina: increase coronay tone
30% normal coronaries
3-unstable angina: rupture plaque
subocclusive thrombus
progress to myocardial infarction 15-30%
4-myocardial infarction: rupture plaque
occlusive thrombus
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Angina Chest Pain:
Clinical Diagnosis
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CAUSES OF ANGINA
Reduced Myocardial O2 Supply1-Coronary artery disease
2-Sever Anemia
Increased Myocardial O2 Demand1-Left Ventricular Hypertrophy:
hypertension
aortic stenosis
hypertrophic cardiomyopathy
2- Rapid Tachyarrhythmias
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Differential diagnosis of angina
1- Neuromuscular disorder
2- Respiratory disorders
3-Upper GI disorder
4- Psychological
5- Syndrome X:
Typical angina with normal coronary angio
? Increase tone or decrease coronary vasodilatation
excellent prognosis
antianginal therapy is rarely effective
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Case presentation
A50 year old male presented to emergency room complaining of sudden sever chest pain of 1 hour duration. It is retrosternal, compressive, and radited to left shoulder and arm.
Associated with sweating, nausea and vomiting
On examination: patient is anxious, in pain, sweaty.BP: 100/60. PULSE: 120 BPM, RR: 26/minChest: basal crepitations
What is the most likely diagnosispathophysiology
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Characteristics of Unstable( RUPTURE-PRONE PLAQUE) and Stable Plaque
Thin fibrous cap
Inflammatory cells
FewSMCs
Erodedendothelium
Activatedmacrophages
Thickfibrous cap
Lack ofinflammatory cells
Foam cells
Intactendothelium
MoreSMCs
Adapted with permission from Libby P. Circulation. 1995;91:2844-2850. Slide reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
Unstable Stable
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PATHOGENESIS OF ACS
Plaque rupture-----Platelet adhesion---activation---aggregation
THROMBOSIS
1- Primary hemostasis: Initiated by platelet
platelets adhesion, activation, and aggregation---platelet plug
2- Secondary hemostasis:
activation of the coagulation system---fibrin clot.
These two phases are dynamically interactive:
Platelet can provide a surface for coagulation enzymes
Thrombin is a potent platelet activator
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platelet
Gp 11B/111A
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Thank you
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Diagnosis of Myocardial Infarction
1-History2-ECG (Electrocardiogram): STMI and NSTMI Hyperacute T wave ST-segment elevation Q- wave T- inversion ST-segment depresion
normal ECG will not exclude MI3-Cardiac Marker: Troponin,CPK, myoglobulin,.. Troponin T,I: 4-6 Hr last 10-14 days CPK:4-6 Hr, peak 17-24hr, normal 72 hr MB(MM,BB) MB2/MB1 >1.5
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Regions of the Myocardium
InferiorII, III, aVF
LateralI, AVL, V5-V6
Anterior / SeptalV1-V4
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ST Elevation
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ST segment Elevation MI
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ST segment Elevation
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Acute Inferior Wall MI
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Acute Posterior Wall MI
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Stable angina-Diagnosis
History : angina pectoris is clinical diagnosis Physical exam Electrocardiogram: 12 ECG, 24 ECG Stress ECG : diagnostic and prognostic information Radioactive studies: thalium scan,.. Echocardiography CT Coronary angiography Serum lipid( LDL, HDL, TG), FBG,CBC Coronary angiography
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Imaging Techniques Used to Assess Atherosclerosis
Invasive techniques Coronary angiography Intravascular ultrasound (IVUS)
Non-invasive techniques Magnetic resonance imaging (MRI) Computed tomography (CT) Ultrasound (B-mode)
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Intravascular Ultrasound (IVUS) Showing Atheromatous Plaque
Reproduced from Circulation 2001;103:604–616, with permission from Lippincott Williams & Wilkins.
Angiogram IVUS
atheroma
normal vessel
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Coronary Angiographyof Stenotic Coronary Artery
6
Arrow indicates atherosclerosis (stenosis) of the coronary artery
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Management goals of stable angina
To To improve prognosisimprove prognosis (mortality reduction) (mortality reduction) Modification of risk factorsModification of risk factors AspirinAspirin Lipid-lowering therapyLipid-lowering therapy ACE-InhibitorACE-Inhibitor Revascularization procedures (PTCA, CABG)Revascularization procedures (PTCA, CABG)
To To decrease anginal symptomsdecrease anginal symptoms Medical treatmentMedical treatment
ACC/AHA Guidelines. J Am Cardiol. 1999;33:2092-2197.
ESC Guidelines. Eur Heart J. 1997;18:394-413.
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Treatment of stable angina
1- General measures
2- Medical therapy: Increase O2 supply
Decrease O2 demand
3-Revasularization: PCI (percutaneous coronary intervension)
CABG (coronary artery bypass grafting)
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TREATMENT OF STABLE ANGINAGeneral Measures
Correction of established risk factors( reversible)
weight reduction (ideal body weight)
Areobic exercise: improve functional capacity, well-being sensation
Treatment of: anemia, thyrotoxicosis, arrhythmias,..
4.
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MEDICAL THERAPY OF STABLE ANGINAPrognostic: Aspirin, Statines, ACEI
Symptomatic: Nitrate,B-,CA-blocker, (nicorandil, ranolazine, ivabradine)
INCREASE O2 Supply
1-Increase diastolic time: B-blocker
2-Decrease coronary tone: nitrate, ca-blocker
3-Decrease LV diastolic pressure: nitrate
4-Correct coronary stenosis: PCI, CABG
5-Increase O2 capacity of blood: transfusion if anemia
DECREASE O2 Demand
1-Decrease heart rate: B-blocker, ca-blocker
2-Decrease contractility: B-blocker, ca-blocker
3- Decrease wall tension (LV pressure and cavity radius): nitrate
4- metabolic: trimetazidine
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Treatment in practice
1-General measures
2-Aspirin
3-Nitrate: S/L, Oral, dermal
3-B-blocker
4-Statins: LDL>100 mg/dl( 70mg/dl)
5-Ca-blocker
6-Angio :PTCA,CABG
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New medical and invasive therapies for refractory angina
Inhibition of fatty acid metabolism: trimetazidine
Potassium channel activators: Nicorandil.
Ranolazine: interact with sodium channel
Ivabradine: SA inhibitor
Endothelin Receptor Blockers: bosentan ??
Testosteron: improve endoth dysfunction.
Enhanced external balloon counterpulsation
Spinal cord stimulation.
Laser revascularization, angiogenesis.
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Prognosis of stable angina
mortality/year
2% single vessel-------12% left main stem
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VARIANT ANGINA-PRINZMETAL ANGINA
Chest pain with ST-Segment elevationUsually at rest, Troponin: negativeFemale > male
Spasm of large epicardial coronary vessel during the attackVasospastic symptpms in other organs
Can cause arrhythmias and death
Treatment: CA-blocker, Nitrate
B-blocker is contraindicated
Prognosis: 5 year mortality < 5%