Ischemic Heart Disease
- Non atherosclerotic angina
– AS, AR, HOCM
– Thyrotoxicosis
– Anemia - Monckeberg calcified medial sclerosis: benign condition involving the tunica media of arteries (muscular layer) in older patients
- Basic science: 3 types of troponin (C,I,T)
– C: binds to calcium
– I: inhibits interaction with actin and myosin
– T: binds to tropomyosin
– Troponin is specific (rules out MI) - Coronary circulation is
– Dependent on oxygen demand. High demand –> adenosine is released –> vasodilation
– Autoregulated within a range of BP - AV node is supplied by PDA
SA node is supplied by a branch from RCA 60% of the time
RBBB in anterior MI = occlusion prior to S1 - If typical sxs but ECG and troponin normal, next step is to do exercise test after the patient stabilizes with medical treatment.
- Most specific feature in MI? presence of Q waves
- GISSI I: Streptokinase provides mortality benefit in acute MI.
- GISSI II: No difference between SK and alteplase. Also no difference between heparin and no heparin. SK + heparin caused more bleeding.
- ISIS II: Aspirin + SK > SK or aspirin alone > no treatment
- Omega 3 FA *fish oil) reduces all cause mortality in CAD by 20%. Vitamin E has no benefit. Ezetimibe lowers LDL but no data regarding mortality.
- DIGAMI: IV insulin followed by 3 months of sub/c insulin improves mortality in MI (aggressive glycaemic control)
– probably in patients <70 yo with no previous MI and not on insulin - Post MI VT: Holter adds little to management
- MADIT trial: propylactic ICD in ischemic cardiomyopathy EF <30% reduces SCD
– But increased events of HF in ICD group due to unknown reason
– AHA/ACC recommendations: prophylactic ICD is indicated in
i) Non ischemic cardiomyopathy, post MI ICM with EF <35%, NYHA class II/III with expected survival > 1 year (level I, class A)
ii) Post MI ICM with EF <30%, NYHA class I with expecte survival > 1 year (level I, class B) - Driving post MI
– 1 month with thrombolytics/CABG
– 1 week with PTCA
Congestive HF
- basic science: BNP is released from ventricular myocardium due to stretch; function is opposite to angiotensin (vasodilation, increased GFR and diuresis)
– Synthesis is increased by presence of stress hormones (thyroid, glucocorticoid & AT II) - Treatment: start with ACEi first then slowly uptitrate Beta-blocker
- Digoxin has no added benefit in NSR
- Digoxin level can be measured by drawing blood 6 hours after the last dose (DigoX – SiX)
- High output cardiac failure in megaloblastic anemia: rx with blood transfusion !
- Drugs that cause water retention
– NSAIDs/celecoxib
– Glitazones
– OCP
Arrhythmias
- SVT in pregnancy: beta blocker is first line over calcium channel blocker, but avoid it in first trimester
- Avoid verapamil in VF/VT
Flecainide: used with care as can precipitate incessant VT
Adenosine is okay - Cardiac resynchronization indications
– Low EF <30%
– Wide QRS (LBBB)
– NYHA class III and above
3L: low EF, LBBB, low functionality of heart - ICD implantation indications
– Prophylactically in poor EF post MI (<35%)
– History of cardiac arrest with VF/VT
– Syndromes eg long QT, Brugada, ARVD - Thromboembolic risk in AF remains for 6 weeks, so the need for anticoagulation for at least 6 weeks.
Valvular diseases
- Annulus calcification of mitral valve is incidental finding and cause no symptoms.
- OS in MS will remain in AF if the valve can still open.
- Bicuspid aortic valve: calcify with aging
– Congenital, sporadic
– Systolic click - Most important prognostic factor in AS is LV function
– Other: severity of valvular calcification - Absolute indication for surgery in AS = symptomatology
– others: AS + HF (poor EF), AS + surgery in heart - Dilated LV: think AR
Other valvular diseases except MS have LV hypertrophy (small LV) - Austin flint murmur
– Can be indistinguishable from MS diastolic murmur
– Due to partial closure of mitral valve in AR
– DOES NOT predict AR severity - A.myxoma
– Mid-diastolic click (tumour plop)
– 1/3 asymptomatic, 1/3 emboli, 1/3 inflammation
– LA dilatation due to obstruction
– Carney complex: A.myxoma + skin pigmentation + endocrine abns - Poor prognostic factors in HOCM
– History of syncope
– Family history of SCD
– ECG non sustained VT
– Echo LV thickness > 3cm (most important)
– Exercise drop in BP
Physical examination
- Reversed splitting of S2
– A2 delayed: LBBB, severe AS
– P2 earlier: PDA, WPW type B - Loud S1: MS, PAC, tachycardia
Congenital HD
- Most common is VSD
- Most of congenital HB have unknown causes (not due to the presence of anti Ro)
- Turner’s syndrome
– COA is classical cause of hypertension, but the MOST COMMON is still essential hypertension - Differential cyanosis
– PDA + COA
– PDA + Eisemenger (reversal diminishes the loudness of the machinery murmur)
Hypertension and dyslipidemia
- Hypertension in young
<90th percentile: normal BP
90-95th: preHTN
95-99th: HTN stage I
>99th: HTN stage 2 - Most common cause is renal parenchymal (glomerulonephritis)
- Basic science:
– HDL gets cholesterol from peripheral tissues via ABCA1
– The cholesterol is esterified by LCAT
– The cholesteryl-ester is transferred to VLDL in exchange of its TG by CETP (CETP also transfers cholesterol from LDL to VLDL in exchange of its TG) –> this causes VLDL to become small dense LDL.
– TG is unstable, so is degrade by lipase, forming small dense HDL & LDL.
– The HDL is free to collect cholesterol again.
– The small dense LDL is what contributes to atherosclerosis. - Abetalipoproteinemia: 3A
– Acanthocytes (spur cells)
– Affects retina (retinitis pigmentosa)
– Affects neurons (neurodegeneration BUT IQ is normal) - Dyslipidemia:
– Type I: chylomicron (LPL defect)
– Type II: LDL
IIa: LDL (LDL receptor problem)
IIb: LDL + VLDL (LDL receptor problem + increased apoB)
– Type III: IDL (apoE2 defect)
– Type IV and V: VLDL (TG) (increased production) - Target cholesterol level
Total: <4 mmol/L
LDL: <2 mmol/L
TG: <2 mmol/L
HDL: >1 mmol/L
Others:
- Types of pericarditis: HPS FC
Hemorrhagic, purulent, serous, fibrinous, constrictive - In venous ulcer, before applying compression stocking, check ABI first to rule out arterial insufficiency. Arterial insuf is c/i for compression stocking
- Hemachromatosis genetic
– Homozygous C282Y/C282Y
– heterozygous C282Y/H63D
– Homozygous H63D/H63D has lower risk than the heterozygote - Sub/c nodules in rheumatic fever is NON TENDER and soft
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