Topic summary Gems Flashcards
Three forms of atherosclerotic plaques
Ruptured atheromatous plaque: Large lipid pool, thin fibrous plaque that ruptures with adherent clot
Fibrous plaque: Calcium depoition and burried cap. More stable as has thick cap and small lipid pool
Superficial erosion: Acculuation of proteoglycan with focally denuded endothelium + adherant thrombus
Location of lesion by ECG changes: Septal
V1, V2 : LAD
Location of lesion by ECG changes: Anterior
V3, V4: LAD
Location of lesion by ECG changes: Anteroseptal
V1-4, LAD
Location of lesion by ECG changes: Anterolateral
V3,4,5,6 I aVL with reciprocal II, III, aVF Left anterior decendin, left circ or obtuse marginal
Location of lesion by ECG changes: Extensive anterior
V1-6 with I and aVL with reciprocal II, III, aVF
Left main CA
Location of lesion by ECG changes: inferior
II, III, aVF and reciprocal in I and aVL
Right coronary or R circ.
Location of lesion by ECG changes: lateral
I, aVL V5 V6 reciprocal in II, III, aVF
L Circumflex or obtuse marginal
Location of lesion by ECG changes: Posterior
V7-9 with reciprocal V1-4 Posterior descending (Branch of RCA or left circuflex)
Location of lesion by ECG changes: Right ventricular
II, III, aVF, V1, V3, V4 reciprocal in I and aVL
Right coronary
Framingham risk score: highest risk parameter
Age: 13 points as a maximum. With each decade of life the risk of vascular disease doubles.
Highest modifiable risk factor was total cholestrol specifically >280 in young people (20-39), smoker age 20-39 also risk of 8 points. Cholestrols importance decreases with age. E.g by 70-79 over 280 only worth 1 point
Smoking impact of MI
Incidence of MI increased x6 in F and x3 in M who smoke at least 20 cigs/day compared to non-smokers
Interheart study: highest modifiable risk factor (2004)
Abdominal obesity 61x risk increase, followed by smoker: 44 x
High Risk Patients (risk>15% in next 5 years) - treat with full preventative strategy!
• Patients with known coronary artery disease
• Patients with vascular disease (eg. Legs)
• Patients with other high risk conditions
o Age >60 with diabetes
o Diabetes and microalbuminuria
o Moderate or severe CKD
o Familial hypercholesterolaemia
o SBP >180, DBP >110
o Total cholesterol >7.5mmHg
Lipid Targets
o TC <4
o LDL <2 in high risk patients
o HDL >1
o TG<1.5
Lipid Targets
o TC <4
o LDL <2 in high risk patients
o HDL >1
o TG<1.5
Cardiac ladder of change in atherosclerosis
Normal –> perfusion abnormality on cardiac stress nuclear–> diastolic dysfunction on echo –> regional systolic dysfunction on ECHO –> ischemic ECG changes –> Angina pectoris
‘Good quality stress test’
adequate workload and 85% max heart rate reached
Contraindications: Recent ACS, uncontrolled arrythmia, severe AS, heart failure (decompensated), PE, dissection
Best predictor of outcome in exercise stress testing
<5METs (i.e. poor exercise capacity –> unable to exert to 5 or more metabolic equivalents)
Invasive angiography: meaning of fractional flow reserve
Measures pressure drop across a lesion: FFR <0.8 needs stent or alteration, >0.8 normal
Proven benefit of survival of CABGs in which 3 groups
left main disease
2 or 3 vessel CAD with prox. LAD
3 vessel CAD with impaired proximal LAD
Medication with clear benefit in stable angina
aspirin
Types of myocardial infarction
Type 1: spontaneous, likely related to atheroscleprosis
Typce 2: MI secondary to demand ischemia
Type 3: MI resulting in death without biomarkers available
Type 4a: MI related to PCI
Type 4 b: MI related to stent thrombosis
Tpe 5: MI related to CABG
Cardiac biomarkers and peak times: first through last
Myoglobin, CK, Troponin, LDH
NSTEMI management
• Aspirin to all
• DAPT if confirmed intermediate to high risk NSTEACS - continue for 12/12
• Don’t give P2Y12 inhibitor if possibility of emergency CABGs
• Anticoagulation
• Unfractionated heparin or Enoxaparin if confirmed intermediate to high risk NSTEACS
• Glycoprotein IIb/IIIa Inhibitors
• At time of PCI if high risk clinical and angiographic characteristics
Bivalirudin - alternative to glycoprotein IIb/IIIa inhibition and heparin (if likely high risk bleeding)
Glycoprotein IIb/IIIa inhibitors
abciximab, eptifibatide, tirofibran last two have lower affinity to the glycoprotein than abciximab
Abciximab MOA
By competing with fibrinogen and von Willebrand factor (vWF) for GP IIb/IIIa binding, GP IIb/IIIa antagonists interfere with platelet cross-linking and platelet-derived thrombus formation. Therefore agents blocking the GP IIb/IIIa receptor are very potent platelet inhibitors.
Algorithm for statin therapy
Is the LDL >4.9 mmol ? yes no (FH or not)
If no to >4.9 then evaluate risk. If >10% risk-statin, if 5-10% assessment further with CAC or lipoprotein-a level, if <5%, no statin
If >10% and commenced - recheck at 6 weeks. Hi intesity statin for >20% risk + LDL remaining >2.5
Moderate if 10-20
Statins are contraindicated in which patient group?
pregnant women
Secondary prevention post NSTEMI
• Statin - initiate and continue indefinitely
• Beta Blocker - initiate in patients with reduced LV function <40%
ACEI/ARB - initiate in those with CCF, LV dysfunction, DM, anterior MI or co-existant hypertension
STEMI: Patient presents within 60 minutes of pain
Access to cath within 60 mins: percutaneous cornoary intervention, if not Fibrinolysis
STEMI with symptom onset 1-3 hours before presentation
within 90mins available: PCI if not Fibrinolysis
STEMI with symptom onset 3-12 hours:
PCI avaialable withint 90 mins onsite or 2 hours offsite: PCI if yes, Lysis if no
Inidcation for rescue PCI
Fibrinolysis and no reperfusion iwthin 90 mins –> PCI within 12 hours.
STEMI >24 hours of symptoms
No benefit of intervention
Best outcome PCI candidates
present within 3 hours and 1 year mortality RR increases by 7.5 % every 30 minute delay
Contraindications to fibrinolysis
♣ active bleeding,
♣ significant closed head or facial trauma within 3/12,
♣ suspected aortic dissection, any prior ICH,
♣ ischaemic stroke w/in 3/12,
♣ known structural cerebral vascular lesion,
♣ known intracranial neoplasm
♣ Active bleeding or bleeding diathesis
Indications for implantable cardiac device post STEMI
Use if:
• LVEF ≤ 30% at least 40d post MI
LVEF ≤ 35%, cardiomyopathy (ischaemic/non-ischaemic), NYHA II/III, at least 40d post MI
Management of cardiogenic shock in STEMI
Most have extensive disease: L main or triple vessel. Treat as previously explained: however avoid bBlockers or any negative ionotrope. Arrythmia treated wtih amiodarone. Nor-adrenaline is useful as vasopressor support.
Timing of in stent thrombus and risk of DAPT
o BMS - Highest risk of stent thrombosis within 6 weeks post stent insertion
DES - High risk of stent thrombosis ongoing for 1 year post stent insertion
Causes of Pericarditis
Infectious Idiopathic Malignancy Autoimmune Metabolic (Uraemia)
MIAMI
Diagnostic criteria for pericarditis
Typical chest pain
Pericardial rub
ST changes on ECG
New pericardial effusion
2 criteria needed
Management of pericarditis
Depends on the cause (malignancy, bacterial etc.)
High risk patients (Fever, tamponade, immunosuppression) - admit
Low risk–> home
Avoid strenuous exercise
Colchicine + NSAIDs
Colchicine can reduce recurrence
Constrictive pericarditis: causes, physiology and presentation
Idiopathic, viral, post surgical, post radiation
Ventricular interdependance: negative intrathoracic pressure generated by inspiration doesn’t augment filling pressures to right heart
Early diastolic filling: Filling restricted due to pericardial fibrosis - fast filling first 1/3 of diastole, then slows
X and Y descent are prominent on JVP
Kussmal’s sign: paradoxical increase in JVP during inspiration
Pulsus paradoxus
Echo is diagnostic
Cardiac Tamponade: Presentation, Physiology
Becks triad: hypotension, soft heart sounds and JVP distension
Increased ventricular interdependance: Shifting of interventricular septum toward L during inspiration and R in expiration due to changes in intrathoracic pressure
Progressive decrease in venous return: Cardiac volume reduced due to compressive effusion: therefor as the ventricle contracts and creates a potential space, diastolic filling occurs. Total venous return falls.
Prominant X descent and absent Y descent
