CSIM 1.64: Cardiovascular Disease 3 Flashcards
What are the types of ischaemia?
- Arterial ischaemia
- Capillary ischaemia
- Venous ischaemia
What are the aetiologies of arterial ischaemia
- Atheroma, thromboses and embolism
- Vasculitis (inflammation of blood vessels - these tend to thrombose)
- Hypertension (causing arteriolar changes)
- Spasm
What is Reynaud’s disease and which type of ischaemia is it likely to cause?
Vasospasms due to cold or emotional stress causing peripheral loss of flow
• Spasms arterial ischaemia
What increases susceptibility to arterial ischaemia?
- Lower adequacy of organ function and perfusion prior to ischaemia
- Single arterial supply as opposed to dual supply
- Sudden/fast onset as opposed to gradual (where collaterals have time to develop)
- Tissue susceptibility (brain and heart highly susceptible)
Which common clinical syndromes are caused by arterial ischaemia?
- Angina
- Hypertensive renal disease
- Claudication (brain infarct or gangrene)
- Ischaemic colitis
Describe capillary ischaemia and give some examples of the common syndromes caused by this.
Blocked or damaged capillaries leading to very localised ischaemia
• Frostbite
• Cryoglobulinaemia
• Disseminated intravascular coagulation
• Diabetic microangiopathy
What is a strangulated hernia, and what type of ischaemia does it lead to?
What other pathology of the gut can cause venous ischaemia?
Intestines herniate, which strangulates the venous return from this section of intestine. This causes retrograde pressure increase and flow cessation.
–> VENOUS ISCHAEMIA
Volvulus of the gut - a loop of gut twists around its mesenteric base, obstructing venous return
Describe chronic ischaemic cardiopathy
Myocyte atrophy and fibrosis following an infarct of the heart (silent or clinical). This results in myocardial degeneration and ultimately death by cardiac failure.
What is cardiac sudden death?
What causes it?
Unexpected death due to heart problems occurring
What is the alternative name for angina and what causes it?
Angor Pectoris
• Paroxysmal and recurrent chest discomfort caused by transient myocardial ISCHAEMIA which fails to induce necrosis
What are the types of angina?
Stable angina
• Atherosclerosis with 50% stenosis
• Occurs at rest
Unstable crescendo angina
• Progressively increasing frequency of pain with less effort
• Disruption of plaque with superimposed partial thrombus (type 6)
What are the ACUTE coronary syndromes?
Unstable crescendo angina:
• No elevation of biomarkers of myocardial necrosis
Non-ST-segment elevation MI (NSTEMI):
• Elevation of biomarkers of myocardial necrosis
• Q waves absent
• ST segment not elevated
• Due to partial-thickness MI
• Partial thrombotic occlusion over plaque
ST-segment elevation MI (STEMI): • Elevation of biomarkers of myocardial necrosis • Q waves present • ST segment elevated • Due to transmural MI • Complete thrombotic occlusion
IMG 156 and 157
What can be observed using imaging when looking for aspects of MI?
- Reduction of loss of tissue perfusion (using contrasts)
* Cardiac wall motion abnormalities
What are the patterns of pathogenesis of MI
Transmural MI
• 90%
• Affects the whole thickness of the myocardium
• Caused by a thrombosis over an unstable atheromatous plaque
Subendocardial MI
• 10%
• Multiple foci of necrosis found in the subendocardial layer
• Caused by diffuse atherosclerosis
Describe the macroscopic appearances of a heart infarct
4 hours (histological) • Wavy fibres at border 18 hours (histological) • Coagulation necrosis • Loss of cross striations • Polymorphonuclear infiltration 24 hours • Pallor of myocardium • Contraction bands and nuclear pyknosis histologically 72 hours • Pallor with hyperemia • Total loss of nuclei 7 days • Mononuclear infiltration • Central yellowing as fibrovascular response begins • Hyperemic border 21 days • Maximally yellow and soft • Prominent granulation tissue from fibrovascular reponse • Vascular margins 7 weeks • White fibrosis
IMG 158
How can MI be detected after 24 hours with immunohistochemistry?
By assessing C9 complement fraction
IMG 159
Describe where coronary arteries typically become occluded, and what each of these typically supplies.
Left coronary artery
OCCLUSION: Anterolateral MI (LAD & LCx)
LCA: Anterior descending (LAD)
OCCLUSION: Anteroseptal MI
• Anterior left ventricle
• Anterior 2/3 of the inter-ventricular septum
LCA: Left circumflex (LCx)
OCCLUSION: Lateral MI
• Lateral wall of left ventricle
Right coronary artery
OCCLUSION: POSTERIOR INF MI
• Posterior left ventricle
• Posterior 1/3 of inter-ventricular septum
IMG 160
What are the complications of MI?
Early phase complications 2-10 days • Reinfarction • Arrhythmia • Cardiac rupture • Acute ventricular aneurysm
Late phase complications 10+ days
• Chronic ventricular aneurysm
• Chronic cardiac failure
• Dressler syndrome
What is Dressler syndrome?
Pericarditis 2-10 months after an MI due to immunological pathogenesis. Indicated by elevated ESR.
What is the most common arrhythmia that results from MI?
• Ventricular fibrillation
What cardiac rupture can occur as an early phase complication post MI?
What does each result in?
Free wall rupture
• Haemopericardium
• Cardiac tamponade
Papillary muscle rupture
• Acute severe mitral regurgitation
Intra-ventricular septum rupture
• Left-to-right shunt
