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The Pathology of Acute Myocardial Infarction Patrick J Gallagher MD PhD Centre for Medical Education University of Bristol

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Page 1: 05 Gallagher

The Pathology of Acute Myocardial Infarction

Patrick J Gallagher MD PhD

Centre for Medical Education

University of Bristol

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Scope of Presentation

• Incidence, classification and treatment of acute myocardial infarction

• The classical pathology of acute myocardial infarction

• The contemporary pathology of acute myocardial infarction

• Post operative myocardial infarction: Recent pathophysiological advances

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Classification of Acute Myocardial Infarction

• Clinical/physiological classification on basis of ventricular function

• Biochemical confirmation from troponin estimations

• ECG classification on basis of ST segment changes into NSTEMIs and STEMIs

• Pathological distinction between transmural and subendocardial infarcts

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Incidence of Acute Myocardial Infarction

• A small increase both STEMIs and NSTEMIs in the late 1990s

• A progressive and sustained decrease in incidence of STEMIs subsequently

• Progressive reduction in acute mortality

• Progressive increase in prevalence of cardiac failure

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Age- and Sex-Adjusted Incidence Rates of Acute Myocardial Infarction, 1999 to 2008.

Yeh RW et al. N Engl J Med 2010;362:2155-2165.

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Classical Appearances

• Confluent area of clearly defined coagulative necrosis

• Surrounding zone of hyperaemia

• Coronary artery thrombosis

• Adherent mural thrombus

• Myocardial rupture with PEA arrest

• Now rarely seen except in out of hospital deaths after “missed” myocardial infarcts

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Myocardial Reperfusion

• Early and successful myocardial reperfusion with thrombolytic drugs or primary cardiac intervention (PCI) is the ideal management strategy for AMI

• In the short and long term the pattern of cardiac pathology is very different to conventional textbook descriptions

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Current Appearances

• Successful reperfusion associated with haemorrhage into infarcted tissue

• Spotty ill defined areas of necrosis

• Incidence of mural thrombus and rupture much reduced

• Small residual thrombi after thrombolysis

• Stents in situ after percutaneous interventions

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Reperfusion Injury

• Prompt restoration of coronary blood flow preserves myocardium

• Histological changes include haemorrhage, contraction band necrosis, endothelial swelling and vascular plugging

• In a small proportion of cases reperfusion is associated with paradoxical death of myocytes, so called lethal reperfusion injury

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Myocardial Infarction after Surgery

• The infarcts are often small and usually close to an area of healed infarction

• Coronary thrombosis is rare

• Critical ischaemia is the result of tachycardia and coronary narrowing

• The infarcts are usually haemorrhagic, possibly because of reperfusion when heart rate declines

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Ischaemia after Vascular Surgery

• 185 patients, 70% male, mean age 66yrs

• 66 had transient ischaemic events with ST segment depression

• 12 (6.5%) had a myocardial infarct

• Mean duration of ischaemia was 225 mins. Most had a post operative tachycardia

• All infarcts were non Q wave/NSTEMIs, diagnosed biochemically

Landesberg et al JACC 2001;37:1839-45

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PeriOperative Ischaemic Evaluation (POISE study)

• 8351 patients, 190 centres, 23 countries

• Four post operative cardiac biomarkers and a range of clinical, ECG and imaging

• 415 (5.0%) had a perioperative MI

• Only 34.7% had ischaemic symptoms, only 12.3% had Q waves

• 30 day mortality 11.6% in those with MIs but 2.2% in remainder Devereaux et al Annals of Internal Medicine 2011;154:523

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Risk Factors for Perioperative MI

• Post operative increase heart rate

• History of stroke

• Major vascular or orthopaedic surgery

• Creatinine > 175µmol/l

• Increasing age

• Emergency or urgent surgery

• Serious bleeding (≥ 2 units transfused)

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Myocardial Infarction after Surgery

• The infarcts are often small and usually close to an area of healed infarction

• Coronary thrombosis is rare

• Critical ischaemia is the result of tachycardia and coronary narrowing

• The infarcts are usually haemorrhagic, possibly because of reperfusion when heart rate declines

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Summary Points

• New treatments have improved the survival after myocardial infarction

• These are associated with a range of new pathological changes

• All pathologists must be able to identify and evaluate coronary stents

• Post operative myocardial infarction must be identified both clinically and at autopsy