06.1 pathology of ischaemic heart disease
TRANSCRIPT
The Pathology of Ischaemic Heart Disease
Ischaemic Heart Disease (IHD)Definition
Refers to structural and functional abnormalities of the heart as a consequence of an inadequate blood supply
(Most cases are due to coronary atherosclerosis)
Risk Factors for IHD(Same as for Atherosclerosis)
Hypertension Hyperlipidaemia Cigarette smoking Diabetes mellitus Sedentary lifestyle Obesity Stress
Causes of IHD other than Atherosclerosis
Congenital anomalies of coronary arteries Arteritides (inflammatory conditions) Coronary embolism Coronary ostial stenosis Trauma Others – Iatrogenic injury, dissection
Clinical Syndromes of IHD
Angina pectoris Myocardial infarction Sudden cardiac death Chronic ischaemic heart disease
Pathogenesis of IHD Fixed coronary obstruction due to
atherosclerosis with significant narrowing of lumen
Secondary disruption of the plaque leading to:
Occlusive thrombosis Platelet aggregation Arterial spasm
Angina PectorisDefinition
A clinical syndrome characterized by paroxysmal chest pain resulting from transient ischaemia, which falls short of inducing infarction (cellular necrosis)
Different clinical patterns are recognized
AnginaPathophysiology
Atherosclerosis of coronary arteries almost invariably present
No specific morphological changes present in myocardium
Different clinical patterns may have correlation to pathophysiologic changes
Myocardial Infarction (MI) General
Most important form of IHD & leading cause of death in industrialized nations
Difference in race (white vs blacks) is debatable Incidence increases with age Males > females (until menopause) Predisposing factors = Those of atherogenesis
Diagnosis of Acute MI
Typical symptoms ECG changes Laboratory investigations :
Hematological - ESR, WBCBiochemical - CK, AST, LD, Troponims
(Radiographic procedures)
Pathology of Myocardial Infarction
Two major morphologic types: Transmural - involving the whole
thickness of a wall Subendocardial
Features of Transmural Infarction
Almost always occurs in the LV Extends from subendocardium to
subepicardium Thrombotic occlusion of a major coronary
vessel almost invariably present Distribution of infarction uniform: extent
variable
Relation of Coronary Artery Lesion to Location of Infarction
LAD (40-50 %) - Anterior LV
- Anterior IV septum RCA (30-40 %) - Posterior LV
- Posterior IV septum LCX (15-20 %) - Lateral wall of LV
Subendocardial Infarction Affects only inner portion of myocardium May extend beyond perfusion territory of a
single coronary artery Often multifocal Stenosis of 3 vessels often present Total occlusion of large coronary artery does
not play a significant role in the pathogenesis May be a result of marked fall in BP
Macroscopic Changes in MI<12 hr. - Not visible on gross examination
12-24 hr. - Red-blue appearance
3-4 days - Area sharply defined; border
more distinct
7-10 days - Bright yellow area
3 weeks - Thinning of myocardium - fibrous tissue becomes apparent
6-8 weeks - Scar tissue well established-white
Histology of MI Necrotic myocytes
Attract acute inflammatory response
- predominantly neutrophils (2-4 days)
- increasing macrophages (4+ days)
Granulation tissue
Fibrous tissue
Major Complications of MI
Arrhythmias Cardiogenic shock Mural thrombosis ± thromboembolism Cardiac rupture (external or internal) Ventricular aneurysm
Sudden Cardiac Death (SCD)
Death occurring within 1 hour of onset of cardiac symptoms
Other causes besides IHD exist When due to IHD, sole abnormality is
coronary atherosclerosis Mechanism of SCD attributed to a lethal
arrhythmia Term NOT synonymous with early MI
CORONARY ARTERY ATHEROSCLEROSIS
Spasm
Platelet aggregation
OCCLUSIVE THROMBOSIS
Myocardial O2 demand
Other predisposing factors
ACUTE MYOCARDIAL ISCHEMIA
ACUTE MYOCARDIAL ANGINA PECTORIS
INFARCTION
HEALED INFARCT SUDDEN CARDIAC DEATH
Current Therapeutic Modalities for Reperfusion
Intracoronary thrombolytic therapy
- Streptokinase
- Other thrombolytics Percutaneous transluminal coronary
angioplasty (PTCA) ± Coronary artery stenting
Coronary artery bypass graft (CABG)