Cardiology 2025 PDF

CARDIOLOGY November 30, 2024 Dr. Michael Ruiz www.internalmedicinereview.ca © Internal Medicine Review 2025  Guiding Principles Broad strokes: Help symptomatic patients feel better Help...

CARDIOLOGY November 30, 2024 Dr. Michael Ruiz www.internalmedicinereview.ca © Internal Medicine Review 2025  Guiding Principles Broad strokes: Help symptomatic patients feel better Help patients live longer Identify and treat risk factors Practice evidence-based medicine RC tips: Use Canadian Guidelines (CCS) when possible Do not worry about understanding advanced cardiovascular techniques (ablation, angiography, etc.) Be safe!  Outline ACS Acute Coronary Syndrome 1. Coronary artery disease CRT (D) Cardiac Resynchronization Therapy (with Defibrillator) vs. (Pacing only) vs. (P) 2. Heart failure / cardiomyopathy CCTA Coronary CT angiography 3. Valvular heart disease DAPT Dual Antiplatelet Therapy (ASA + clopidogrel or prasugrel or ticagrelor) EST Exercise Stress Test 4. Aortopathy METs Metabolic Equivalents 5. Pericardial disease DOACs Direct Oral Anticoagulants (ex apixaban, dabigatran, rivaroxaban) NSTEACS Non ST Elevation Acute Coronary Syndrome 6. Arrhythmias and implantable cardiac OAC Oral Anticoagulants (Includes VKA, DOAC) devices OMT Optimal Medical Therapy 7. Peripheral arterial disease POBA Plain Old Balloon Angioplasty PCI Percutaneous Coronary Intervention NB. ECGs and Cardiac Physical Exam will be VKA Vitamin K Antagonist (warfarin) self study online SAPT Single Antiplatelet Therapy (ASA OR Clopidogrel) SPECT Single photon emission computed tomography Coronary Artery Disease Key resources: CCS 2014 Guidelines – Diagnosis and management of stable ischemic heart disease ACC/AHA 2023 Guidelines – Chronic CAD  Coronary Artery Disease (CAD) Two major presentations: Chronic stable CAD 2014 CCS guidelines on stable ischemic heart disease 2023 ACC/AHA Guideline on Management of Patients with Chronic Coronary Disease Acute coronary syndromes Various CCS/ACC/AHA guidelines on ACS, antiplatelets  How Do Patients Present? Ischemic cascade – with increasing ischemic time: 1. Blood flow changes (can be seen on myocardial perfusion) 2. Diastolic, then systolic dysfunction (wall motion abnormalities) 3. ECG changes 4. Symptoms 5. Myocardial necrosis  Diagnostic Tests for CAD Functional STRESS: pick exercise whenever possible! Non-invasive stress tests: – Provides prognostic info: e.g. duration of exercise, METs – STRESS = exercise, – Not possible if physical limitations or contraindications drugs (inotropes, (e.g. critical aortic stenosis) vasodilators) – TEST = ECG, ECG+echo, TEST: consider functional imaging (e.g. nuclear) if: ECG+nuclear – Cannot accurately assess for ischemia on ECG LBBB, paced rhythm, preexcitation, significant ST changes at Structural rest à the ECG is not interpretable in these cases – RBBB interpretable generally – Coronary angiography – Need specific anatomic correlation (e.g. prior – CT coronary revascularization) angiography  Able to exercise and no contraindications? Principles of Non- YES NO Invasive ECG Normal à Exercise Stress TEST ECG Abnormal ECG normal or abnormal Testing NO LBBB or V- Paced LBBB or V paced LBBB or V rhythm rhythm No LBBB or V paced paced rhythm Rhythm Exercise Cardiac CT myocardial Exercise ECHO Vasodilator Vasodilator myocardial myocardial Angiography perfusion Image perfusion imaging perfusion imaging Dobutamine or vasodilator Adapted from 2014 echo CCS – Stable Ischemic Heart Disease  Absolute Contraindications to EST Acute MI (within 2 days) Mnemonic: Ongoing unstable angina I – Inflammation Uncontrolled hemodynamically-significant arrhythmia D – Dissection O – Ongoing angina Active endocarditis Symptomatic severe AS N – No consent O – Ongoing MI Decompensated heart failure T – Thrombosis Acute PE, pulmonary infarction, DVT S – Severe AS Acute myocarditis, pericarditis T – Technical issues Acute aortic dissection R – Rhythm E – Endocarditis Physical limitations S – Systolic dysfunction S – Slow  EST Results Positive Negative Equivocal Uninterpretable Maximal vs. submaximal test – Patient should reach 85% of age predicted maximum heart rate to rule out ischemia – (Max HR = 220 – age)  EST Results Positive test High risk features* – ≥ 1mm STE – Duke Treadmill Score -11 or less – ≥ 1 mm STD (horizontal or – 120, drop in BP >10, drop below baseline] – Ventricular arrhythmia 2013 AHA – Exercise standards for testing and training 2014 CCS – Stable Ischemic Heart Disease  Myocardial Perfusion Imaging Radioactive tracer (e.g. 99mTc) is used that distributes into myocardium proportionally with blood flow SPECT imaging detects decay of tracer Stress = exercise vs. pharmacologic (e.g. dipyridamole) – Pharmacologic stress based on coronary perfusion mismatch after vasodilation dipyridamole (aka Persantine) most commonly used for nuclear stress, less commonly adenosine Dobutamine used commonly for stress echocardiography – Diseased coronary vessels are already maximally dilated and develop perfusion mismatch – False negatives can be seen: Drug interactions with dipyridamole (caffeine, theophylline – hold before test!) Severe flow limiting triple vessel or left main disease (“balanced” ischemia so no perfusion mismatch detected) Consider as a potential first-line test if patient cannot complete ECG stress test Contraindications: active or severe asthma/COPD, as dipyridamole can cause bronchospasm – Reversal agent for dipyridamole is aminophylline Coronary CT Angiography (CCTA) NB. CCTA is not the same as a Coronary Artery Calcium (CAC) Score from CT. CAC scoring is recommended for further risk stratification of intermediate risk (FRS 10-19%) asymptomatic patients aged > 40 who are not candidates for statin based on other risk factors Can consider CAC scoring for low risk patients with family hx premature CV Dz and genetic dyslipidemia CAC score > 100 is basically a statin indicated condition; start therapy regardless of FRS  Coronary CT Angiography (CCTA) Procedure specifics: – Low dose CT with beta blockade +/- IV nitro given (HR target 65%) with asymmetric septal hypertrophy, septum up to 22 mm, with systolic anterior motion (SAM) and significant left ventricular outflow tract (LVOT) obstruction. Which of the following medical therapies is generally NOT indicated as first-line therapy for LVOT obstruction in HCM? A) Beta-blockers B) Non-dihydropyridine calcium channel blockers C) ACE inhibitors D) Maintaining hydration and stopping diuretics 48  Cardiomyopathy Guiding Principles 1) The etiology is an essential consideration à will heavily direct management and risk stratification (e.g. cardiac disease may be the first presentation for amyloid) 2) Most cardiomyopathy management plans include a significant component of HF treatment 3) Look for any other contributing comorbidities (OSA, smoking, DM, ETOH/drugs, iron-deficiency, arrhythmia, etc.)  HF Classification HF by EF: HFrEF (EF ≤ 40%) Ischemic CM r = reduced HFmEF (EF 41-49%) Valves m= mid-range HFpEF (EF ≥ 50%) p= preserved Non HF ischemic CM Rhythm Primary *applies mostly to HFrEF Muscle Congenital Secondary  Diagnostic approach All patients with heart failure (regardless of LVEF): ECG, echocardiogram, CBC, lytes, creatinine, ferritin, TSH, troponin, BNP, lipids, A1c Common etiologies: ischemic heart disease (perform ischemia testing if known CAD or risk factors), HTN/LVH, tachyarrhythmias, valvular disease – Non-invasive imaging to rule in/out CAD should be considered – Invasive (coronary angiography): Recommend if HF with angina / Ischemic symptoms, likely to be good candidates for revascularization Consider if: LVEF 30 mm, unexplained syncope, apical aneurysm, LVEF 40 – Sweating abnormalities Unexplained sensorimotor neuropathy – Neuropathy / dysautonomia – Carpel tunnel syndrome Bilateral Carpal Tunnel history – Renal insufficiency/Nephrotic syndrome CCS 2020 Evaluation and Management of Patients With Cardiac Amyloidosis  Cardiac Amyloidosis Evaluation involves Therapy (nuanced from standard HF therapy) ECG – low voltage, pseudoinfarction pattern Mainstay is diuretics (high doses, often Echo – LVH, diastolic dysfunction multiple) +/- CMRI Cautious use / avoidance of BB/CCB (reduce cardiac output, particularly if restrictive BW – S/U PEP, serum free light chains à AL physiology), ACEI/ARB (exacerbate Tc-99m-PYP scan à ATTR (both wild type + dysautonomia/orthostasis), and digoxin hereditary) (reduce inotropy) Genetic testing à hereditary ATTR OAC for AF (again, regardless of CHADS65) +/- biopsy ATTR à tafamidis or inotersen or patisiran +/- liver transplant AL à chemotherapy +/- autologous stem cell transplant CCS 2020 Evaluation and Management of Patients With Cardiac Amyloidosis ICD decisions difficult à EP problem  CCS 2023 Fitness to Drive Guidelines - HF Category Private Car Commercial Major updates from previous guidelines: Driver (Truck, Bus) Functional status (NYHA class) is NYHA I OK to drive LVEF ≧ 30% OK weighted higher than LVEF NYHA II OK to drive LVEF ≧ 30% OK For private driving, only significant NYHA III OK to drive NO DRIVING change is that patients with LVAD can Heart NYHA IV NO DRIVING NO DRIVING drive 2 months after implant if NYHA Failure 1–2 (previously disqualified) Home NO DRIVING NO DRIVING inotropes For commercial driving, LVEF LVAD 2 months after implant NO DRIVING threshold lowered from ≧ 35% to ≧ if NYHA 1-2 30% for NYHA I-II Heart 6 weeks after discharge 6 months post transplant + NYHA 1-2 + stable discharge + Recommendations for post heart immunosuppression + NYHA 1 + LVEF ≧ transplant commercial now requires followed annually 50% + followed annually LVEF ≧ 50% (previously 35%) CCS Fitness to Drive Guidelines 2023  MCQ #2 2025 A 35-year-old man with a family history of HCM is seen in evaluation for exertional dyspnea, chest pain, and syncope. Echocardiography reveals a hyperdynamic left ventricle (LVEF >65%) with asymmetric septal hypertrophy, septum up to 22 mm, with systolic anterior motion (SAM) and significant left ventricular outflow tract (LVOT) obstruction. Which of the following medical therapies is generally NOT indicated as first-line therapy for LVOT obstruction in HCM? A) Beta-blockers Answer: C. ACE inhibitors are generally avoided in HCM with LVOT obstruction, as they reduce B) Non-dihydropyridine calcium channel blockers afterload which can worsen outflow tract C) ACE inhibitors obstruction. Beta blockers and non-dihydropyridine CCBs reduce heart rate, which improves LV filling, D) Maintaining hydration and stopping diuretics and reduces inotropy, reducing contractility, both which reduce LVOT obstruction. Maintaining hydration and stopping diuretics will improve LV filling and reduce LVOT obstruction by increasing preload. 80  Valvular Heart Disease Key Resources: ACC/AHA 2020 Valve Guidelines CCS 2020 HF Update PHYSICAL EXAM – High Yield for Applied Scenarios – see BONUS SLIDES for info on distinguishing etiology of murmurs clinically.  MCQ #3 2025 A 22-year-old asymptomatic woman presents for a routine physical exam. She has no known medical history. There is a family history of sudden cardiac death in a cousin, which she does not know the details of. Auscultation reveals a 3/6 midsystolic click followed by a late systolic murmur, best heard at the apex. The click and murmur become earlier and softer with squatting. Which of the following murmurs is MOST likely? A) Aortic stenosis B) Mitral regurgitation C) Hypertrophic cardiomyopathy D) Mitral valve prolapse 82  Valve Disease - Guiding Principles Valves disease is a complicated topic – Know the physical exam findings (JAMA RCE/physical exam) – more resources at the end of this section – Know WHEN TO REFER for CONSIDERATION of intervention (Class I guidelines). Class II recommendations have been added for completeness, knowing the principles around these recommendations is helpful but it is unlikely you will need to know the specific numbers for Class II recommendations. – *Canadian guidelines are old (2004); ACC/AHA 2020 Valvular Heart Disease Guidelines more up to date and testable – Don’t need to know PV disease or much about TV intervention Valves management involves: Surveillance à duration changes based on risk and severity of pathology Pharmacotherapy à temporizes a mechanical problem, treats symptoms - NB. indications for endocarditis prophylaxis Surgery à effective, durable, generally more carries risk Catheter-based interventions à less durable, less data, usually less risk Valve Disease - Guiding Principles Transthoracic echocardiography is the initial diagnostic test for all valvular disease General AHA staging system similar for all valve disease Stage A à “at risk” Stage B à “progressive” Stage C à ”severe disease, but asymptomatic” Stage D à “severe disease, with symptoms” Severe disease matters most (and usually guides intervention) Symptoms: angina, dyspnea, heart failure, syncope à guides treatment Surrogate markers of impending badness (e.g. LV dilatation, pulmonary HTN, new Afib) Repeat assessment (e.g. echo) q6-12m for severe asymptomatic valvular disease Valve type (bioprosthetic vs. mechanical) For any patient whom VKA is contraindicated à bioprosthetic Younger patients (65y) à bioprosthetic Patients 50-65y à individualized decision making  Pharmacotherapy for VHD Very few recommendations for medical therapy in valve disease (primarily an interventional disease) Aortic stenosis à Treat HTN as per standard guidelines; treat lipids per guidelines for prevention of atherosclerosis (not to prevent hemodynamic progression of AS – no evidence for this); use ACEI/ARBs post-TAVI Aortic regurgitation à Treat HTN (preferably with ACE/ARB); symptomatic AR and/or LV systolic dysfunction + prohibitive surgical risk à GDMT with ACE/ARB or ARNI Mitral stenosis à Anticoagulation (VKA) indicated if à prior embolic event OR LA thrombus OR AF. Control tachycardia with betablocker/CCB can help symptoms (AF or sinus tachycardia) as this reduces the gradient through the valve MR, TR à Treat HF as per standard guidelines; vasodilator therapy is NOT recommended for asymptomatic primary MR and normal LV function ACC/AHA 2020 Valve  Aortic Stenosis Etiology: bicuspid (young), rheumatic (developing countries), calcific (old) – Bicuspid AV associated with aortopathy ***, heritable, screen 1st degree family members Prolonged asymptomatic period, then rapid deterioration with onset of symptoms (angina, syncope, HF) Patients with severe AS are often afterload dependent (caution with vasodilators/afterload reducers, e.g. ACEi) Severe AS Criteria (mostly from echo now): – Mean Gradient ≥40 mmHg – Max jet velocity ≥4 m/s – AVA 65%) to maintain cardiac output. These patients will have a LOW stroke (SV index 2000 in men, >1300 in women indicates severe). Dobutamine stress echo will NOT be helpful here as the ventricle is already squeezing well (LVEF is normal). Aortic Stenosis - Intervention AHA 2020 Valve Class I indications for replacement*: Severe, symptomatic AS Severe, asymptomatic AS with LV dysfunction (LVEF 80 or younger patients with life expectancy 4m/s). surgical risk To know someone with Asymptomatic, severe AS with low surgical risk and elevated BNP 3x upper severe AS is truly limit of normal asymptomatic can be a Asymptomatic, severe AS with low surgical risk and increase in aortic challenge. Stress testing or BNP can be helpful. velocity 0.3m/s or more per year Progressive increases in aortic velocity, or decreases Class IIb indications for replacement (can be considered): in LVEF while still in the Asymptomatic, severe AS with progressive decrease in LVEF to less than normal range, signal a 60% in at least 3 serial studies higher risk patient, hence these class II Moderate AS undergoing surgery for other indications recommendations.  Aortic Regurgitation Acute AR – Dissection – Endocarditis – Trauma – Prosthetic valve dysfunction Chronic AR (many, but remember these) – Primary aorta problems: dilatation (associated with autoimmune conditions, syphilis, Marfan, bicuspid, HTN, others …), dissection, trauma – Primary valve problems: degenerative (calcific), bicuspid, rheumatic, endocarditis, VSD Severe AR is defined using specific echocardiographic parameters that you should not need to know  Aortic Regurgitation - Intervention Class I indications for surgery*: Severe, symptomatic AR Severe, asymptomatic AR with LVEF ≤ 55%, if no other cause for LV dysfunction identified Severe, asymptomatic AR undergoing other CVSx *May require AVR + ascending aortic replacement if associated aortopathy (more info to come) AHA 2020 Valve  BONUS Read on own Aortic Regurgitation - Intervention Class IIa indications for surgery (reasonable): Aortic regurgitation causes a volume load on Asymptomatic, severe AR with LVEF >55%, if LV is the left ventricle. severely enlarged (cut off LV end systolic Systolic dysfunction is a dimension >50mm or indexed to body surface devastating consequence area >25mm/m2) of volume loading (which is why it is a class I Moderate AR undergoing other cardiac surgery recommendation to intervene). Volume loading also Class IIb indications for surgery (can be considered): causes LV dilation through remodeling, Asymptomatic, severe AR with LVEF >55% but hence why LV progressive decline in LVEF on three serial studies enlargement is included in class IIa and IIb to 55-60% or progressive increase in LV dilation indications for (LV end diastolic dimension >65mm) intervention. AHA 2020 Valve  Mitral Stenosis Etiology is almost all rheumatic (other – MAC, radiation, autoimmune … ) – Often associated with AF – OAC with VKA if i) rheumatic MS and AF; ii) rheumatic MS and prior embolic event; iii) rheumatic MS and LA thrombus (N.B. ii and iii do not require AFIB) INVICTUS trial: VKA vs. rivaroxaban in pts with rheumatic heart disease and AF à VKA had ↓ stroke/systemic embolism/MI/death (i.e. DOAC harmful in this setting!) NEJM 2022 – Management considerations for AF and heart rate MS does not like high HRs à loss of diastolic filling time MS does not like AF à loss of atrial kick Severe MS: – MV area ≤1.5 cm2 (very severe = ≤1 cm2) Echo criteria for severe MS in – Pulmonary artery systolic pressure >50mmHg guidelines… but we don’t think – Diastolic pressure half time (PHT) >150 ms you need to memorize! AHA 2014, 2017, 2020 Valve  Mitral Stenosis - Intervention 2 types of interventions – percutaneous vs. surgical Percutaneous mitral balloon commissurotomy (PMBC) indicated if (Class I): Severe, symptomatic MS + favourable valve anatomy + can be performed at a “Comprehensive Valve Centre” – CONTRAINDICATED if: i) LA thrombus (need preop TEE) ii) >moderate MR MV surgery (commissurotomy +/- repair OR replacement) indicated if (Class I): Severe, symptomatic MS + acceptable surgical risk + contraindicated/failed PMBC Severe MS and other cardiac surgery planned AHA 2014, 2017, 2020 Valve  BONUS Read on own Mitral Stenosis - Intervention Percutaneous mitral balloon commissurotomy (PMBC) is reasonable if (Class IIa)*: An obstructed – Asymptomatic, severe MS with pulmonary hypertension (PA systolic mitral valve leads pressure > 50mmHg by echocardiography or right heart catheterization) to LA dilation, atrial arrhythmias and pulmonary Percutaneous mitral balloon commissurotomy (PMBC) can be hypertension. considered if (Class IIb)*: – Asymptomatic, severe MS with new atrial fibrillation Therefore, think of pulmonary – Asymptomatic, severe MS with mean gradient >15 mmHg or wedge hypertension and pressure >25 mmHg with exercise atrial fibrillation – Highly symptomatic patients (NYHA III-IV) with severe MS with unfavourable as the “end anatomy or high risk for surgery (as a palliative attempt to try to relieve organ” effects of symptoms) mitral stenosis! *All recommendations require the PMBC be performed at a “Comprehensive Valve Centre”. PMBC remains contraindicated if LAA thrombus or moderate or more MR 97  Mitral Regurgitation Acute MR – VERY unstable patients (hypotensive, pulmonary edema, quiet murmur due to rapid pressure equalization – Ischemia à papillary muscle dysfunction – Chord rupture à patients with mitral valve prolapse may rupture a chord acutely, leading to a flailing mitral valve leaflet acute severe MR – Endocarditis – Trauma Chronic MR – PRIMARY (“degenerative”) à leaflet problem Valve leaflet (MVP [myxomatous, fibroelastic deficiency], rheumatic, endocarditis) Annulus (calcification) Chordae (trauma, infection, idiopathic) Papillary muscle (trauma) – SECONDARY (“functional”) à “around” the leaflet problem “Ventricular functional” e.g. dilated or ischemic cardiomyopathy à leaflet tethering (being pulled towards the apex) + annular dilatation à leaflet malcoaptation leading to regurgitation “Atrial functional” e.g. atrial fibrillation à atria enlarge à annulus dilates à leaflet malcoaptation leading to regurgitation Severe MR is defined using specific echocardiographic parameters that you should not need to know  Mitral Regurgitation - Intervention PRIMARY MR – “the goal of therapy is to correct MR before onset of LV systolic dysfunction” Class I indications for surgery (repair when possible vs. replacement) for PRIMARY MR: Severe, symptomatic 1o MR irrespective of LVEF Severe, asymptomatic 1o MR + LV systolic dysfunction (LVEF ≤ 60%, LVESD ≥ 40mm) AHA 2014, 2017, 2020 Valve  BONUS Read on own Mitral Regurgitation - Intervention Class IIa indications for for PRIMARY MR (reasonable): Asymptomatic patients with severe MR with preserved systolic function (LVEF ≥60%, LVESD 95% success and 65yrs – follow-up with ECG assessment if “irregularly irregular” Cardiac Implantable Electrical Device (PPM, ICD) – interrogate all high atrial rate episodes for possible AF Non-lacunar Embolic Stroke of Unknown Source – ”at least 24h of ambulatory ECG monitoring” Longer monitoring if AF is still suspected but not proven CCS 2020 AF Update  AF Etiology & Initial Investigations Major Guideline: CCS 2020 CCS – SAF Scale – Symptoms of AF Major Considerations: Class 0 Asymptomatic Always look for an etiology/precipitant Class I Minimal symptoms or 1 episode without syncope or CHF (EtOH, drugs, withdrawal, ischemia, PE, Class II Symptoms have minimal effect: valves, thyroid disease, OSA, infection, sleep - Mild awareness if in persistent/permanent AF deprivation, acute pulmonary disease … ) - Rare episodes (“less than a few per year”) in those Basic Workup for new AF: w/ paroxysmal AF. Document rhythm Class III Symptoms have moderate effect on QOL: ECHO – assess LV size and function, LA size, valve.. - Moderate awareness most days with CBC, lytes (Ca, Mg), Cr, Coags, TSH for all persistent/perm AF LFT before amiodarone prescription - More common episodes (”more than every few A1C, FBG, Fasting lipid profile as part of comprehensive months”) or more severe symptoms in pts with cardiac risk assessment paroxysmal AF Always assess patient AF-related symptoms and quality of life (CCS-SAF), assess patients Class IV Symptoms have severe effect on QOL: - Syncope due to AF and / or with AF for frailty, cog impairment, - CHF due to AF and / or dementia, depression - Unpleasant symptoms in pts with persistent/perm AF and / or - Frequent and highly symptomatic episodes in pts w CCS 2020 AF Update paroxysmal AF  AF: Prevention and Treatment Major Considerations cont’d: Prevention = modifiable risk factor management Achieve rate control with b-blocker, CCB, or digoxin AF with pre-excitation (WPW): àDC cardioversion (or procainamide) Rhythm control preferred if QoL impaired (symptomatic despite rate control), concurrent HF, or hemodynamically unstable (DC cardioversion) This cutoff of 130/80 Is not mentioned in the CCS text anywhere, only in this figure! We suggest just go with HTN CCS 2020 AF Update Canada guidelines for resting BP target. CCS 2020 AF Update  What about Atrial Flutter (AFL)? “It is recommended that patients with Atrial Flutter be stratified and treated in the same manner as patients with atrial fibrillation.” 128  Anticoagulation in AF/AFL DOACs are 1st line for almost everyone – VKA (i.e. warfarin) should be used instead of DOAC for valvular AF (CCS 2016, 2018 and 2020 definition): Mechanical heart valves Rheumatic mitral stenosis Moderate-severe non-rheumatic mitral stenosis – Warfarin should also be considered (class IIa) in patients with new onset AF ≤ 3 months post-valve replacement (surgical or percutaneous) FRAIL-AF (Circulation, 2023) looked at elderly (>75) frail patients with AF who were already on VKA and randomized to change to DOAC vs stay on VKA. Surprisingly, more bleeding was observed in those who were switched to DOAC (15.2%) compared to those who continued VKA (9.4%), trial stopped early. – Criticisms – small trial (n=1330), bleeding events were self reported and the primary outcome was driven by minor bleeding, not major bleeding. No formal guideline recommendations have incorporated this trial. – No difference in ischemic/embolic events – Take Away #1 – if elderly frail patient stable on VKA can continue – Take Away #2 – caution in extrapolating results of other RCTs to populations excluded from enrolment (frail elderly) CCS 2020 AF, CCS 2020 Valve  CCS 2020 AF Update ACC/AHA 2023 AF Update Anticoagulation in CKD/ESRD Calculate CrCl using Cockroft – Gault at baseline, and at REFERENCE: Dosing per manufacturer least annually: Apixaban Stage 3 CKD (eGFR >30) – A/C as usual – 5mg PO BID – 2.5 mg PO BID if 2/3: ≥80 years, ≤ 60kg, creatinine ≥133umol/L Stage 4 CKD (eGFR >15 75 years or eCrCl 30-49 mL/min – “The CCS recommends that a DOAC is preferred over VKA” Edoxaban – 60 mg PO daily – “Apixaban and rivaroxaban are approved for use – 30 mg PO daily if CrCL 30-50 mL/min, ≤ 60kg, or concomitant use of potent P-glycoprotein inhibitors with stage 4 CKD” Rivaroxaban Stage 5 CKD (eGFR 0 à OAC only – Prefer DOAC > VKA *STABLE CAD = no PCI or ACS in preceding 12 months CCS 2020 AF Update  (2a) AFIB + PCI (elective or ACS) Individualize based upon thrombotic risk LOW RISK thrombotic events HIGH RISK thrombotic events or Elective PCI (no ACS) ACS with PCI CHADS65 = 0 à DAPT CHADS65 = 0 à DAPT – DAPT for 6-12 months per CCS 2023 Antiplatelet Guidelines for non-AF patients, if high bleeding risk 1-3 mos DAPT CHADS65 >0 à “Dual Pathway” CHADS65 >0 à “Triple Therapy”x1-30d – SAPT with a P2Y inhibitor* + OAC for at THEN least 1 month, up to 12 months after PCI, “Dual Pathway Therapy” = clopidogrel + OAC up to 12 then OAC alone months post PCI THEN OAC only CCS 2023 Antiplatelet Guidelines says for PCI and need for OAC, dual pathway is recommended over triple therapy but specifies they receive 1 dose of ASA with PCI. Therefore it is as if they had “1 day of triple therapy.” If asked in an exam situation, minimizing triple therapy (1-30 days) or going straight to dual pathway would be guideline recommended durations. Talking with the interventionalist would also be an important step (i.e. how complex was the PCI). *P2Y inhibitor = Pick CLOPIDOGREL – lower bleeding risk CCS 2020 AF Update Who is HIGH RISK Post-Elective PCI? Mitigate bleeding risk: Avoid prasugrel/ticagrelor – that’s why they choose clopidogrel in guideline table Consider PPI Avoid other NSAIDs if VKA target INR 2-2.5 CCS 2020 AF Update  (2a) AFIB + ACS – NO PCI /stent Individualize based upon thrombotic risk CHADS65 = 0 à DAPT = Dual Antiplatelet Therapy (ASA + P2Y12 inhibitor) CHADS65 > 0 à “Dual Pathway Therapy”: clopidogrel + OAC [apixaban1] for 1 to 12 months post ACS THEN OAC only 1TIP – the only OAC studied after ACS without PCI is apixaban 5mg po bid. This is favoured in wording of guidelines for this scenario with clopidogrel. CCS 2020 AF Update  Prescribing notes – not all OAC the same dose in dual pathway and triple therapy: The OAC component of dual pathway regimens includes: normal dose edoxaban, apixaban, dabigatran BUT rivaroxaban only 15 mg PO daily (10 mg in patients with CrCl 30-50 mL/min). – A DOAC is preferred over warfarin, however if warfarin is to be used the lower end of the recommended INR target range is preferred. All patients should receive a loading dose of ASA 160 mg at the time of PCI (if previously ASA-naïve). The OAC component of triple therapy regimens includes: warfarin daily, rivaroxaban 2.5 mg PO BID, or apixaban 5 mg BID (reduced to 2.5 mg if they met two or more of the following dose reduction criteria: age > 80 years of age, weight < 60 kg, or Cr > 133 μmol/L). – A DOAC is preferred over warfarin, however if warfarin is to be used the recommended INR target is 2.0-2.5. All patients should receive a loading dose of ASA 160 mg at the time of PCI (if previously ASA-naïve). Thereafter, ASA may be discontinued as early as the day following PCI or it can be continued longer. The timing of when to discontinue ASA will depend on individual patient’s ischemic and bleeding risk. The dose of OAC beyond one year after PCI should be standard stroke prevention doses. A combination of an OAC and single antiplatelet therapy may be used only in highly selected patients with high-risk features for ischemic coronary outcomes, and who are also at low risk of bleeding CCS 2020 AF Update  CCS 2020 AF Update ACC/AHA 2023 AF Update AF – OAC in Special Populations Liver Disease We recommend that OAC not be routinely prescribed in Child-Pugh class C or liver disease associated with significant coagulopathy Cancer Individualize OAC treatment in pts with active cancer. Consider DOAC> VKA. Congenital Heart Disease OAC for most patients with AF and HCM OAC if CHADS65 risk factors Frail Elderly OAC for most frail elderly – individualizing recommendations if high risk bleed Thyrotoxicosis OAC for “most patients during acute thyrotoxicosis until euthyroid state is restored” Secondary Atrial Fibrillation No OAC (however, if suspected high recurrence risk consider OAC) =clearly provoked by transient/ *NEW* ACC/AHA 2023 AF Update: counsel patients about recurrence risk, arrange follow-up reversible risk factor such as sepsis, including thromboembolic risk stratification and surveillance of recurrence. The benefit of post non-cardiac surgery anticoagulation is uncertain Pregnancy No DOACs (cross placenta). Consider LMWH, Warfarin (Tri2-3) in unique circumstances (see OB (2021 CCS Pregnancy Heart Disease Med lecture for more details). Anticoag should be considered for pregnant women with AF and Update) (1) structural heart disease or (2) no structural heart disease but CHADS >=1 Atrial high rate episodes (AHRE) *NEW* ACC/AHA 2023 AF Update: >24h AHRE with CHA2DS2-VASc of 2+ (correlates to risk of (often represent subclinical atrial CHADS-65 of 1+) à OAC with shared decision making fibrillation detected by a pacemaker; 5 min-24 hours of AHRE with CHA2DS2-VASc of 3+ (correlates to risk of CHADS-65 of 2+) à could also be atrial tachycardia) OAC with shared decision making (based on novel data from ARTESIA trial (NEJM 2024)  Cardio- version of AF DOAC preferred “Recent stroke” is defined as stroke within the last 6 months CCS 2020 AF Update  MCQ #4 2025 Which of the following patients would be LEAST likely to benefit from an early rhythm control strategy for their atrial fibrillation? A) A 55-year-old woman with newly diagnosed paroxysmal atrial fibrillation and a severely reduced ejection fraction (LVEF 30%) B) A 68-year-old man with persistent atrial fibrillation, significant symptoms (NYHA Class III), and a history of multiple admissions for heart failure C) A 42-year-old man with recent-onset (within 1 year) paroxysmal atrial fibrillation and few comorbidities D) A 72-year-old woman with persistent atrial fibrillation over 5 years, well-controlled symptoms (NYHA Class I) on rate control, and a normal ejection fraction (LVEF)  Rate vs. Rhythm Control Until recently, we taught that for most patients rate = rhythm control (AFFIRM Trial) – Target resting HR