ABSTRACT
INDICATIONS FOR PREOPERATIVE REVASCULARIZATION: identical to stable CAD or unstable angina or NSTEMI or STEMI (g Chapter 2 - CAD)
BB - INDICATIONS: 1) Patient already treated with BB (Class I recommendation); 2) Intermediateor high-risk non-invasive stress test (IIb); 3) ≥ 3 RCRI risk factors (IIb); 4) Initiate in patients with a compelling long term indication (IIb)
STATINS - INDICATIONS: 1) Patient already on statin (I); 2) Initiate if undergoing vascular surgery (IIa); 3) Initiate in patients with clinical indications who are undergoing elevated-risk procedures (IIb)
ECG: Preoperative A CAD, arrhythmia, PAD, cerebrovascular disease or structural heart disease (except for low-risk procedures); Post-operative A A) Signs or symptoms suggestive of ischemia / MI / arrhythmia; B) Usefulness of routine screening in asymptomatic patient is uncertain (IIb)
POSTOPERATIVE TROPONIN: Indications A A) Signs or symptoms suggestive of ischemia or MI; B) Usefulness of routine screening in asymptomatic patient is uncertain (IIb)
DIAGNOSIS OF PERIOPERATIVE MYOCARDIAL INFARCTION: g Chapter 2 (Definition of MI) › Consider type 1 myocardial infarction (rupture of fragile plaque) or type 2 (O2 supply/ demand mismatch); Type 1 MI causes < 5% of troponin elevation postoperatively
DEFIBRILLATOR: Temporarily deactivate tachyarrhythmia therapies or apply a magnet during the operation › N.B.: a magnet applied to a defibrillator deactivates tachyarrhythmia therapies, but does not change the pacing mode to VOO or DOO; risk of inappropriate inhibition of pacing
SPECIFIC ENTITIES HCM: avoid dehydration / vasodilators / hypotension / beta-agonists SEVERE AORTIC STENOSIS › Asymptomatic: complete preoperative clinical reassessment with stress test; consider AVR before elective high-risk non-cardiac surgery; monitor intravascular volume; avoid tachycardia; avoid intraoperative hypotension (treat with phenylephrine) › Patient refusing AVR or not a candidate or requiring urgent surgery: operative mortality ≥ 10%; consider TAVI or balloon valvuloplasty if hemodynamically unstable
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POST-PCI SURGERY AND DUAL ANTIPLATELET THERAPY › Post-PTCA: wait 2-4 weeks (then operate under ASA) › Post-BMS: dual antiplatelet therapy for a minimum of 2-4 weeks (then operate under ASA) • Discontinue Clopidogrel 5-7 days preoperatively › Post-DES: dual antiplatelet therapy for a strict minimum of 3 to 6 months with new generation stents (consider bridging with IV tirofiban / eptifibatide / cangrelor if surgery required before this time) then operate under ASA
MECHANICAL VALVE PROSTHESIS
ATRIAL FIBRILLATION
THROMBOEMBOLIC DISEASE
High thromboembolic risk (annual risk > 10%)
• Mitral valve prosthesis • Old generation aortic valve prosthesis (cagedball; tilting-disk) • Stroke or TIA < 6 months
• CHADS 5 or 6 • Stroke or TIA < 3 months • Rheumatic disease
• Thromboembolism < 3 months • Severe thrombophilia (protein C or S or antithrombin deficiency; antiphospholipid antibodies; multiple anomalies)
• Stop Warfarin 5 days pre-op + Bridge with IV heparin or LMWH - Prosthetic Valve or AF A Enoxaparin 1 mg/kg bid or Dalteparin 100 IU/kg bid; Venous thromboembolism A Enoxaparin 1.5 mg/kg qd or Dalteparin 200 IU/kg qd • INR on the day before surgery (vitamin K 1 mg PO if INR > 1.5) • Stop IV Heparin 4-6 h pre-op; Last dose of LMWH 24 h pre-op (Enoxaparin 1 mg/kg or Dalteparin 100 IU/kg administered 24 h pre-op) • Resume Warfarin 12-24 h post-op if adequate hemostasis • Resume Heparin (without bolus) or LMWH 48-72 h post-op depending on hemostasis • Consider IVC filter in the presence of venous thromboembolism < 4 weeks
Moderate thromboembolic risk (annual risk 5-10%)
Bileaflet aortic valve prosthesis with ≥ 1 risk factor: AF • History of stroke or TIA • HTN • DM • Heart failure • > 75 years
CHADS 3 or 4
• Thromboembolism 3-12 months • Nonsevere thrombophilia: Leiden factor V or prothrombin mutation (heterozygous) • Active neoplasia
• Case-by-case decision for heparin bridge (thromboembolic risk versus perioperative bleeding risk)
Low thromboembolic risk (annual risk < 5%)
Bileaflet aortic valve prosthesis with no other risk factor
CHADS 0 to 2 (with no history of stroke or TIA)
Thromboembolism > 12 months (with no other risk factor)
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ASA: not recommended as part of routine primary prevention › ★ Antithrombotic Trialists’ Collaboration: marginal benefit of ASA for primary prevention (high NNT); bleeding risk › Consider ASA for primary prevention: in the presence of a low bleeding risk but high cardiovascular risk (subclinical atherosclerosis; multiple risk factors; family history of premature cardiovascular disease) (Class IIb recommendation; C)
Smoking Complete cessation
Dyslipidemia High dose statin; Target A ≥ 50% H LDL
HTN Target BP < 140/90 (< 140/85 in the presence of DM)
EVALUATION OF CARDIOVASCULAR RISK
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Antiplatelet therapy
ACE inhibitors As secondary prevention for all patients (especially when LVEF ≤ 40% or HTN or DM or CRF)
BB • LVEF ≤ 40%: Long term • Normal LVEF: can be stop 3 years after ACS • Antianginal: Long term
DM HbA1c < 7%
Physical exercise > 30 min moderate exercise 5 x per week
Obesity • BMI: 18.5 - 24.9 kg/m² • Waist: M < 102 cm and F < 88 cm
Healthy diet Healthy and balanced diet
Influenza vaccine Annually
Hormonal therapy; NSAID Avoid
INTERVENTION 1) Confirm that the patient is a smoker; 2) Strongly recommend smoking cessation; 3) Ask the patient whether he/she wants to stop smoking (if the patient refuses, suggest reducing consumption ± nicotine replacement therapy); 4) Establish a plan and a date for complete cessation; 5) Inform the patient’s friends and relatives; 6) Remove all objects related to smoking; 7) Cease all activities related to smoking; 8) Have a plan in the case of temptation / relapse; 9) Propose drug therapy; 10) Propose support by a smoking cessation center; 11) www.smokefree.gov ; 12) Ensure regular follow-up
Nicotine gum
Initially 1 gum every 1-2 h then decrease (maximum: 24 gums per day) • ≤ 24 cigarettes / day: 2 mg gum • ≥ 25 cigarettes / day: 4 mg gum
• 6-month abstinence rate: 19% • Adverse effects: Nausea; Oropharyngeal irritation
Transdermal nicotine patch
• < 10 cigarettes / day: 14 mg patch for 6 weeks then 7 mg patch for 4 weeks then stop • > 10 cigarettes / day: 21 mg patch for 6 weeks then 14 mg patch for 2 weeks then 7 mg patch for 2 weeks
• 6-month abstinence rate: 23% • Adverse effects: Local skin reaction; Nausea; Insomnia
Bupropion SR
• Inhibits dopamine and norepinephrine reuptake • Bupropion SR 150 mg PO daily for 3 days then bid for 12 weeks then stop • Start 10 days before smoking cessation • Can be combined with nicotine replacement therapy
• 6-month abstinence rate: 24% • Adverse effects: Decreased seizure threshold; Insomnia; Xerostomia; Nightmares
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Varenicline
• Partial agonist of acetylcholine nicotinic receptor • Varenicline 0.5 mg PO daily for 3 days then bid for 3 days then 1 mg bid for 11 weeks then stop • Start 1 to 2 weeks before smoking cessation • Can be combined with nicotine replacement therapy
Contraindicated in the case of pregnancy or breastfeeding or CRF or mental illness
VLDL: large nonatherogenic lipoproteins transporting TG from the liver; apoB100 LDL: atherogenic lipoproteins responsible for atherosclerosis; mainly contain cholesterol; apoB100 › Calculated LDL (mmol/L) = TC - HDL - (0.45 x TG) (valid if TG < 4.5 mmol/L) › Calculated LDL (mg/dL) = TC - HDL - (TG / 5) (valid if TG < 400 mg/dL) NON-HDL CHOLESTEROL (= TC - HDL): cholesterol contained in LDL - VLDL - IDL - Lp(a); predictive of cardiovascular risk
› ApoB: comprises LDL - VLDL - IDL - Lp(a) HDL: antiatherogenic properties; contains apolipoprotein ApoA1 HYPERTRIGLYCERIDEMIA: TG-enriched LDL A formation of smaller and denser LDL (due to modification by hepatic lipase) A dense, atherogenic LDL
› HyperTG: TG-enriched HDL (CTEP) AG recovery of HDL by the liver AH HDL › HyperTG: associated with metabolic syndrome (G TG; H HDL; dense, atherogenic LDL) › HyperTG: risk of pancreatitis (especially if TG > 10 mmol/L or > 885 mg/dL) LP(a): apolipoprotein(a) bound to a molecule of LDL; associated with an increased risk of cardiovascular events; plasma concentration is genetically determined
Apolipoprotein
Phospholipids
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• Male ≥ 40 years • Female ≥ 50 years (or postmenopausal) • DM • HTN • Smoking • BMI > 27 kg/m² • CRF - CrCl < 60 mL/min • Atherosclerosis
• Family history of premature CAD (M < 55 years; F < 65 years) • Family history of dyslipidemia • SLE - RA - Psoriatic arthritis - Ankylosing spondylitis - Inflammatory bowel disease • COPD • Erectile dysfunction • HIV (treated with antiretroviral agents) • Clinical features of familial dyslipidemia (xanthomas; xanthelasmas; arcus senilis)
HYPERTRIGLYCERIDEMIA: Obesity; DM; Alcohol; CRF; Hypothyroidism; Corticosteroids; Antipsychotics (Clozapine; Olanzapine); Nonselective BB; Thiazides; Cyclosporine; HIV protease inhibitors; Retinoic acid; Hormonal therapy; Sirolimus; Bile acid sequestrants
Familial hypercholesterolemia
• Arcus senilis • Xanthelasmas • Pathognomonic tendinous xanthomas (extensor tendons; MCP; Achilles tendon) • Premature CAD
Defective Apo B100 G LDL
• H Affinity for LDL-R receptor • Autosomal dominant
• Similar presentation to familial hyper-cholesterolemia
Familial LPL deficiency G TG
• Abnormal catabolism of chylomicrons and VLDL
Familial Apo-C-II deficiency G TG
• Apo-CII is the LPL activator
• Similar presentation to familial LPL deficiency
Familial dysbetalipoproteinemia
• Homozygote for ApoE2 (less effective binding to hepatic receptors) • Accumulation of remnant lipoproteins (IDL; remnant chylomicrons)
• Premature CAD • Tuberous xanthomas (elbows; knees) • Palmar xanthomas • Consider diagnosis: ApoB (g/L) / TC (mmol/L) ratio < 0.15
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Familial combined hyperlipidemia
• 1-2% of the population • Extremely heterogeneous • Interactions between multiple genes and environment • Hepatic overproduction of lipoproteins apo-B100 (associated with VLDL) • Defective LPL in 1/3 of patients (G TG)
• Xanthelasmas • Arcus senilis • Premature CAD • Dense, atherogenic LDL • Consider diagnosis: Apo B > 120 mg/dL + TG > 1.5 mmol/L + family history of premature CAD
Familial H HDL H HDL a) Apo A-I deficiency b) Tangier (CERP protein dysfunction) c) Familial LCAT deficiency
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