Cardio Flashcards

Question

Acute HF Management

Answer 1

In general – Establish Diagnosis ASAP (guidelines say <2h after contact in ED) – Start with ABCs, IV O2 Monitor (IOM) – Focused history: dyspnea, fatigue, edema – Focused physical: congestion, valvular dz, perfusion – CBC, lytes, urea/Cr, gluc, BNP, Tn – ECG, CXR – Echo (w/in 48h) – Consult CCU/Cardiology – Consider potential etiologies or triggers for decompensation * Ischemia, HTN, Anemia, rapid afib, infection, med or diet non adherence, NSAIDs, PE, thyroid...

Answer 2

Establish etiology Practically: Hx/PE/labs + * Echocardiogram (r/o non-myocardial causes) * BNP: 2017 CCS recommends BNP if diagnosis unclear and for prognosis * Assess for CAD (very often coronary angiography) * CMRI for non ischemic etiologies Quantify degree of disability NYHA classification (I-IV) * Allows clinician to track progress * Becomes important for therapy considerations Risk factor modification & lifestyle interventions * Exercise (flexibility, aerobic, +/- resistance) * Salt restriction (<2-3g/d) à SODIUM-HF trial 2022 showed that strict salt restriction <2g/day did not improve HF related hospital visit or CV death * +/- fluid restriction (<2L/d) * Smoking cessation * EtOH avoidance * Discuss Driving Safety (see bonus slides) Treat HF-associated comorbidities (see later) Multidisciplinary care model Early advanced care planning discussions Interventional therapy considerations * ICD, CRT (see later) * Surgery / percutaneous treatment of functional MR (see later) * Revascularization in ICM Advanced HF * Really low EF, ++hospitalizations, NYHA IV, organ dysfunction, cardiac cachexia, high 1-year mortality, bad CPET performance... * May need: Mechanical circulatory support (eg) VAD, Transplant workup, or palliative care Once stabilized, reassess at least annually with clinical assessment + LVEF assessment

Answer 3

If choosing an option for revascularization for ischemic cardiomyopathy, CABG would likely lead to improved outcomes compared to PCI with the available evidence. However, optimizing medical therapy is paramount in ALL patients!

Answer 4

Guideline recommended pharmacotherapy for HFrEF “Backbone” of HFrEF therapy now QUADUPLE Tx * ARNI / ACEI/ARB * MRA * SGLT2i (even if not diabetic!) * BB [only start when euvolemic and hemodynamically stable] * Avoid CCBs with LVEF < 40% (amlodipine ok for HTN) * Do not start BBs on NYHA IV patients * ARNI initiation requires 36h “washout period” after ACEI use ARNI in clinical practice: Start ARNI: Hospitalized w new dx HFrEF Switch to ARNI if: - Hospitalized for HF on ACE/ARB - Symptomatic (NYHA2+) despite max ACE/ARB And CONSIDER : - Sinus rhythm and HR >70: Ivabradine - Recent HF hospitalization: Vericiguat* - Black pts on optimal GMT: Hydralazine/ISDN - Unable to take ACE/ARB/ARNI: Hydralazine/ISDN - Persistent symptoms despite Rx above or poor rate cntrl with AFIB: Digoxin Titrate drugs every 2-4 weeks over 3-6 mos then reassess: -If NYHA 1, LVEF >35, low risk: Continue current mgmt -If NYHA 1-4, LVEF ≤35 ambulatory: Check out Device therapy guidelines -If NYHA 3-4, high risk, advanced HF: Advanced care plan, palliation Refer for advanced HF therapy (LVAD etc)

Answer 5

* Beta blockers – Use bisoprolol, carvedilol or metoprolol SUCCINATE (extended release; not available in most of Canada) – NYHA IV patients should be stabilized prior to the initiation of a beta-blocker – Chronic beta-blocker should be continued in acute heart failure unless patient symptomatic from hypotension or bradycardia * Ivabradine – Acts on SINUS NODE to reduces heart rate in patients without reducing BP or contractility (need to be in SINUS RHYTHM) – Maximize dose of beta blocker first, use if hospitalized in last 12 months for CHF + HR > 70 * ACE/ARB/ARNI (Angiotensin receptor neprilysin inhibitor) – ARB should be used if patient intolerant to ACEI or develops angioedema (although angioedema can still occur with ARBs – rare). ARNI contraindicated if history of hereditary (familial) or idiopathic angioedema – When switching from ACE to ARNI, 36 hour washout period important to lower risk of angioedema. No washout required for ARB/ARNI switch * Vericiguat (Approved but not yet widely available in Canada) – Novel oral soluble guanylate cyclase stimulator, works by enhancing effects of NO – VICTORIA trial à NYHA II-IV HF (LVEF <45%) recent hospitalization or IV diuretic therapy * Primary outcome (CV death, HF hospitalization) reduced by 10% vs. placebo * Better for lower LVEFs * Well tolerated * More anemia in the vericiguat group

Answer 6

* Primary (low EF) vs. secondary prevention considerations * Primary prevention devices considered appropriate after: – 3m OMT – 3m post-revascularization – 40d after MI * Patients should have expected longevity > 1 year (or considerations for VAD, transplant) * Caution for patients with NYHA IV, not expected to improve - ICM, NYHA II-IV, LVEF ≤ 35% - ICM, NYHA I, LVEF ≤ 30% - NICM, NYHA II-III, LVEF ≤ 35%

Answer 7

1. Cardiac Arrest (VT-VF) 2.Sustained VT in the presence of significant structural heart disease 3. Sustained VT >48 h post MI or revascularization no reversible cause - give ICD ICD systems Transvenous: most common, lead through subclavian vein into RV, can pace and defib. Subcutaneous: devices sits in the axilla, lower risk of venous stenosis and endocarditis, shorter battery life, useful for younger patients. Does not pace!

Answer 8

- Cardiomyopathy à electromechanical V-V dyssynchrony - Dyssynchrony à lower SV/CO, more MR, higher filling pressures, worse functional status, more hospitalizations, more death - Dyssynchrony tends to correspond to abnormal QRSd on ECG - CRT paces RV and LV to ”Resynchronize” - Platform options – CRT-D (pacing + defibrillation), CRT-P (pacing only) - CRT has been shown to reduced HF symptoms, hospitalizations, death

Answer 9

Slam dunk (strong recommendation) * In Sinus Rhythm * Symptoms (NYHA II-II, ambulatory IV) * On GDMT * LVEF ≤ 35% * Typical LBBB * QRSd ≥ 130ms May respond (weak recommendation) * In Sinus rhythm * Symptoms (NYHA II-II, ambulatory IV) * On GDMT * LVEF ≤ 35% * Non-LBBB * QRSd ≥ 150ms Marginal candidates (weak recommendation) * Permanent AF * Patients who require chronic RV pacing + symptomatic HFrEF

Answer 10

“I NEED HELP!” Consider referral to heart failure specialist if: I - IV inotropes N - NYHA IIIB/V or persistently elevated BNP E - End organ dysfunction E - EF ≤ 35% D - Defib shocks H - Hospitalizations >1 E - Edema despite escalating diuretics L - Low systolic BP ≤ 90, tachycardia P - Progressive intolerance or down –titration of GDMT, Predicted mortality high risk in next 1 year

Answer 11

* Management principles are largely symptom-driven and rely on risk factor modification * Guideline-based recommendations: – BP control, based on HTN Canada guidelines – Loop diuretics to control symptoms of congestion – SGLT2i for all (even if not diabetic) to ↓ HF hospitalizations * new strong recommendation, 2022 – Consider candesartan *CHARM-Preserved trial –↓ HF hospitalizations but otherwise negative trial for MACE – Consider MRA * TOPCAT trial – overall negative trial for MACE; ↓HF hospitalizations but overall ‘all cause’ hospitalizations the same! MRA, ARB and ARNI to be “considered” to reduce HF hospitalization, particularly if LVEF on lower end of spectrum (i.e. LVEF 40-50%, 2B recommendation)

Answer 12

* ARNI and SGLT2i may reduce diuretic requirements when introduced – monitor carefully * CHF Exacerbation: Continuous infusion vs bolus furosemide? – Favour continuous infusion to more quickly achieve diuresis, but more studies needed given small and heterogenous studies (Cochrane review 2020) * Metolazone (TZD diuretic) is generally the second diuretic to be added to augment diuresis – Monitor for hypokalemia, hyponatremia, contraction alkalosis, renal function due to brisk diuresis associated with these agents used with Loop diuretics * Contraction metabolic alkalosis (low urine chloride, high urine sodium) can occur on high dose Loop / TZD diuretics = Consider adding ACETAZOLAMIDE – helps with alkalosis + RCT of IV acetazolamide 500 daily in addition to standard therapies for CHF exacerbation showed pts more likely to be ‘decongested’ in 72h (ADVOR trial, Mullens et al, NEJM 2022)

Answer 13

* Mostly, genetic variants that code for proteins of the sarcomere * Most common phenotype is asymmetric septal hypertrophy * Often associated with: – Dynamic LV outflow tract obstruction (LVOTO) – Systolic anterior motion (SAM) MV à eccentric MR – Papillary muscle abnormality * Causes - Chest pain, dyspnea, syncope, arrhythmia, stroke, HF, SCD * Broad management principles: – Family screening/genetics for 1st degree relatives – Avoid hypovolemia/low preload states – B-blockers: chest pain syndromes, LVOT Obstruction, SAM * Second line – CCBs, disopyramide – Interventions for refractory symptoms and LVOTO – septal myomectomy/ETOH ablation – Sports participation: ”shared decision making” in guidelines. -OAC for ANYONE with AF Consideration for ICD if: * Sustained VA or prior cardiac arrest (Class I) * FMHx of SCD, LV wall thickness >30 mm, unexplained syncope, apical aneurysm, LVEF <50% (Class IIa) * Extensive LGE on MRI or NSVT on Holter monitoring (Class IIb)

Answer 14

* An underfilled LV (decrease Preload) will cause the mitral valve to be close to the LVOT, causing worse obstruction * Increased afterload ”opens” the LVOT, increases ventricular volume, decreasing gradient/improves obstruction = reduced murmur * REDUCED murmur * Bradycardia (eg beta blockade) gives more diastolic filling time and increases ventricular volume, which improves obstruction = reduced murmur * Passive leg raise (↑venous return) – reduced murmur * Handgrip (↑ afterload)- reduced murmur * INCREASED MURMUR * Valsalva or standing up - ↓ venous return - increased murmur * Reduce afterload (ACEi) – increased murmur * Treatment involves adequate volume status, beta-blockers +/- disopyramide, avoiding afterload reducing agents (ACEi) and preload reducing agents (nitrate, diuretics)

Answer 15

* CA is usually a restrictive cardiomyopathy * Can be inherited or acquired * Most commonly – AL (cancer-associated) vs. ATTR (wild type vs. hereditary = slowly progressive more common to clinically present in older men) * Presents with HF (usually HFpEF), presyncope/syncope, atrial arrhythmia (Afib, sometimes Ventricular arrhythmias), bradyarrhythmia, higher rates of AS as well * Patients frequently also have extracardiac manifestations: – Autonomic dysfunction – Orthostatic hypotension – Gastroparesis – Sexual dysfunction – Sweating abnormalities – Neuropathy – Carpel tunnel syndrome – Renal insufficiency/Nephrotic syndrome Suspect if pts with HF and any one of: ”normotensive” LVH ”low flow, low gradient AS” w EF >40 Unexplained sensorimotor neuropathy / dysautonomia Bilateral Carpal Tunnel history

Answer 16

Evaluation involves * ECG – low voltage, pseudoinfarction pattern * Echo – LVH, diastolic dysfunction * +/- CMRI * BW – S/U PEP, serum free light chains à AL * Tc-99m-PYP scan à ATTR (both wild type + hereditary) * Genetic testing à hereditary ATTR * +/- biopsy Therapy * Very different from standard HF therapy * +++ diuretics * Cautious use / avoidance of - BB, CCB, ACEI/ARB, dig * OAC for AF (again, regardless of CHADS65) * ATTR- tafamidis or inotersen or patisiran +/- liver transplant * AL -chemotherapy +/- autologous stem cell transplant * ICD decisions difficult à EP problem

Answer 17

Transthoracic echocardiography is the initial diagnostic test for all valvular disease General AHA staging system similar for all valve disease * Stage A - “at risk” * Stage B - “progressive” * Stage C - ”severe disease, but asymptomatic” * Stage D -“severe disease, with symptoms” Severe disease matters most (and usually guides intervention) * Symptoms: angina, dyspnea, heart failure, syncope * Surrogate markers of impending badness (e.g. LV dilatation, pulmonary HTN, new Afib) * Repeat assessment (e.g. echo) q6-12m for severe valvular disease Valve type (bioprosthetic vs. mechanical) * For any patient whom VKA is contraindicated à bioprosthetic * Younger patients (<50y) à mechanical * Older patients (>65y) à bioprosthetic * Patients 50-65y à individualized decision making

Answer 18

Very few recommendations for medical therapy in valve disease (primarily an interventional disease) * Aortic stenosis - 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 - Treat HTN (preferably with ACE/ARB); symptomatic AR and/or LV systolic dysfunction + prohibitive surgical risk - GDMT with ACE/ARB or ARNI * Mitral stenosis - Anticoagulation (VKA) indicated if - prior embolic event OR LA thrombus OR AF; control tachycardia can help symptoms (AF or sinus tachycardia) * MR, TR - Treat HF as per standard guidelines; vasodilator therapy is NOT recommended for asymptomatic primary MR and normal LV function

Answer 19

Etiology: bicuspid (young ), rheumatic (developing countries), calcific (old) – Bicuspid AV associated with aortopathy *** * 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 <1.0 cm2

Answer 20

Class I indications for replacement*: * Severe, symptomatic AS * Severe, asymptomatic AS with LV dysfunction (LVEF <50%) * Severe, asymptomatic AS undergoing other CV surgery * Symptomatic low-flow, low gradient AS with LV dysfunction (LVEF<50%) * Symptomatic low-flow, low gradient AS with LVEF >50% (“paradoxical” low-flow, low-gradient aortic stenosis) – if AS most likely cause of symptoms *Options include surgical AVR (SAVR) or transcatheter aortic valve implantation (TAVI) – For SAVR, mechanical valve is recommended is age <50 and no contraindications for VKA, bioprosthetic valve recommended if age >65 or if contraindication to VKA; ages 50-65 engage in shared decision making – TAVI (/TAVR) – expanding indications in 2020 guidelines: * for intermediate, high, prohibitive surgical risk patients * age >80 or younger patients with life expectancy <10y * consider for patients ages 65-80* vs. SAVR – TAVI CONTRAINDICATED if comorbidities preclude benefit (palliative care recommended instead if life expectancy with reasonable QOL <1y) – All TAVI valves are bioprosthetic (and need endocarditis prophylaxis)

Answer 21

* Acute AR – Dissection – Endocarditis – Trauma – Prosthetic valve dysfunction * 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

Answer 22

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)

Answer 23

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 – Management considerations for AF and heart rate * MS does not like high HRs -loss of diastolic filling time * MS does not like AF - loss of atrial kick * Severe MS: – MV area ≤1.5 cm2 (very severe = ≤1 cm2) – Pulmonary artery systolic pressure >50mmHg – Diastolic pressure half time (PHT) >150 ms

Answer 24

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

Answer 25

* Acute MR – VERY unstable patients – 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 is the disease * Valve leaflet (MVP [myxomatous, fibroelastic deficiency], rheumatic) * Annulus (calcification) * Chordae (trauma, infection, idiopathic) * Papillary muscle (trauma) – SECONDARY (“functional”) à is the consequence * Dilated or ischemic cardiomyopathy -> leaflet tethering (being pulled towards the apex) + annular dilatation -> leaflet malcoaptation leading to regurgitation * Severe MR is defined using specific echocardiographic parameters that you should not need to know

Answer 26

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)

Answer 27

Update for Treatment of Secondary MR * “We recommend that maximally tolerated GDMT, including cardiac resynchronization therapy (CRT) and revascularization where appropriate, be implemented before consideration of percutaneous mitral valve repair (PMVR) for patients with HFrEF and severe FMR (Strong Recommendation, High-Quality Evidence). * We suggest that patients with symptomatic HF (HFrEF) despite maximal GDMT and severe mitral regurgitation be evaluated for PMVR (Weak Recommendation, Moderate-Quality Evidence). (CCS 2020 HF Update) AHA 2020 Guidelines à congruent with CCS * focus on GDMT * no class I indication for surgery/intervention for 2o MR

Answer 28

TR can be primary or secondary as well * Primary: lead-related, trauma, IE, rheumatic, carcinoid, CTDz, ... * Secondary: Pulm HTN-related, RV-related, RA-related Severe TR is defined using specific echocardiographic parameters that you should not need to know Class I indications for surgery: * Severe TR in patients undergoing left sided valve surgery Class IIa indications for surgery: * Addition of an annuloplasty ring for moderate or more TR at the time of left sided valve surgery * Severe primary or secondary TR if right sided heart failure and no pulmonary hypertension to reduce symptoms and risk of heart failure hospitalization

Answer 29

Mechanical Valves *** NO DOACs *** * Lifelong therapy with warfarin; add ASA if other antiplatelet indication * Goal INR varies with: type of valve, valve position, patient risk factors – *NEW* INR 1.5-2.0 ON-X valve (useful if INR monitoring/compliance issues, needs low dose ASA) – INR 2.5 (2-3)for current generation AVR and no other risk factors – INR 3.0 (2.5-3.5) for any MVR or old AVR (ball-in-cage) or AVR with risk factors (RF = AF, prior clot, LV dysfxn, hypercoagulable state) – Bridging for invasive procedures is reasonable when the INR is subtherapeutic based on an individualized assessment of thrombosis and bleeding (see perioperative medicine lecture) Bioprosthetic Valves * Lifelong therapy with ASA 75-100mg daily * Initial 3-6 months post-implantation – Surgical valve replacement à consider VKA (INR 2.5) in addition to ASA – TAVI à may consider DAPT (clopidogrel) or VKA (INR 2.5) if low risk bleed (ASA monotherapy likely safer per guideline text) * Bioprosthetic valve (within 3 months) + new onset AF - VKA

Answer 30

Often presents as a “tearing” or “ripping” pain radiating to the back. Risk factors include hypertension, vasculitis, valvular heart disease (esp. Bicuspid AV), drugs (cocaine), collagen disorders (Marfan, Ehlers-Danlos) Look for – focal neuro deficit – Pulse deficit/differential BP !!! CHECK BILATERAL BPs !!! – Enlarged aorta or mediastinum on CXR * CT scan is best first-line imaging modality – Others - MR, TEE

Answer 31

* Management – Preferentially use IV meds (easy on / easy off), in ICU setting with arterial line monitoring – BBs first line (or CCBs if BB contraindication/intolerance) à vasodilators (nitroprusside, ACEI) – Control HR * Target HR < 60-80 * IV labetalol good 1st line option (both HR and BP) – Control BP * DO NOT control BP before HR (hypotension à compensatory incr. HR à more shear stress) * Target BP <120 systolic (or to lowest BP that maintains adequate perfusion) – Control pain with as needed analgesics (will help with hemodynamics) – Further management depends on type of dissection (Stanford Classification – Type A or B) * Type A -dissection involves ascending aorta - refer for urgent surgical intervention * Type B - dissection does not involve ascending aorta medical management HR and BP control – Exception: if the type B dissection causes malperfusion (e.g. gut ischemia, leg ischemia), endovascular management will be necessary. Rupture is another rare indication for surgery

Answer 32

* *NEW* With aortic dilatation/aneurysm, perform transthoracic echocardiography at the time of diagnosis to assess aortic valve anatomy and function. Perform serial echocardiography yearly in Loeys-Dietz and Marfan, every 1- 3 years in degenerative or bicuspid aortic valve aortopathy. If age <50, MRI is first line test as serial tests will be required (so try and avoid CT to limit recurrent radiation) – Try to use same imaging modality serially If clinical features of connective tissue disease (Marfan, Loeys-Dietz, Ehlers-Danlos), family history of thoracic/peripheral/intracranial aneurysms, or onset age less than 60, refer for genetic testing – If gene positive, family members who are also positive should be screened with an echocardiogram – If no culprit gene identified, first degree relatives should be screened with an echocardiogram. Treat hypertension – Target: BP <140/90mmHg, lower may be better (AHA 2022 = 130/80 and CCS 2023 mention this but do not provide specifics) – Antihypertensive choice: * ACC/AHA and CCS recommend beta blocker followed by ARB for BP control (IIa recommendation) * Marfan: use a beta blocker or losartan (class I recommendation) regardless if the patient has HTN * Other recommendations: – Smoking cessation (class I) – Statins and/or antiplatelets if evidence of atherosclerosis (class IIa), statins may be considered for primary prevention if no atherosclerosis (class IIb) (see: Size criteria for operative management of asymptomatic aneurysm)

Answer 33

* Where to refer? – Generally planned, not complex, ascending aorta procedures can be done at a local cardiac centre – More complex patients should be managed with an Aortic Team (tertiary or quaternary centre) e.g. outpatient planned but complex like an arch replacement, or complex acute presentations like a Type B dissection with malperfusion * All patients with identified aortic disease, gene positive aortopathy or “at risk” for aortic disease are recommended to be referred to an Aortic Team – Rationale: the Aortic Team will help to optimize and monitor patients prior to any intervention, as well as monitor for complications post intervention

Answer 34

Screen all men >65-80 for AAA once with U/S [Canadian Task Force on Preventive Services 2017] * In those with asymptomatic AAA, smoking cessation is the only medical therapy proven to reduce risk of rupture – Recommendations for BP management (<140/90 CCS / <130/80 AHA), statin use (if atherosclerotic disease is reasonable, if no atherosclerosis can consider) and low dose aspirin if atherosclerotic disease present, are similar to thoracic aortic aneurysm – Avoid fluoroquinolones in patients with known aortopathy due to increased risk of rupture [FDA, 2018] * Surveillance recommendations (ultrasound first line, CT if ultrasound not adequate): – 3.0 to 3.9 cm: imaging every 3 years – 4.0 to 4.9 cm men, 4.0 to 4.4 cm women: imaging every 12 months – >5.0 cm men, >4.5 cm women: imaging every 6 months * Threshold for surgery (needs to balance risk of aneurysm rupture and risk of repair): – Men: 5.5 cm or more or <5.5 cm if symptoms attributable to AAA (class I) – Women: 5.0 cm or more or <5.0 cm if symptoms attributable to AAA (class I) – If rate of growth is greater than 0.5 cm in 6 months, AAA repair is reasonable class IIb) * Keep in mind other patient factors (e.g.) family history, connective tissue disorder, refer early to vascular surgery in these groups

Answer 35

* Inflammation of the pericardium * Characterized by at least 2 of: – Pleuritic chest pain – Friction rub – Diffuse ST-segment elevation +/- PR depression, without reciprocal ST-segment depression – Presence of new/worse pericardial effusion * Additional supporting evidence – Inflammatory markers (CRP) – Inflammation on CT, MR * Troponin can be (+): “Myo-pericarditis” – Myocardial involvement – Higher risk

Answer 36

Etiologies: most cases idiopathic, consider TB if risk factors – Vascular – post MI – Infectious - Coxsackie, echovirus, adenovirus, flu, parvo, TB, fungal ... – Toxin (drug)- procainamide, hydralazine, INH, minoxidil, dilantin – Autoimmune – RA, SLE ... – Metabolic - uremia, dialysis, hypothyroidism – Iatrogenic – Radiation, post CV Surg – Neoplastic - mesothelioma, breast/lung/melanoma mets, leukemia, lymphoma

Answer 37

Risk factors in pericarditis: * Immunocompromised * Trauma * Oral anticoagulation therapy * Myopericarditis (Troponin elevation) * Fever T>38oC * Subacute onset * Significant effusion (>20mm) or cardiac tamponade * Hemodynamic instability * Lack of improvement after 7d appropriate therapy

Answer 38

First episode: High dose NSAID 1-2 weeks (as needed until pain/CRP resolves) + Colchicine x3 months * Recurrence: High dose NSAID x2 weeks (as needed until pain/CRP resolves) + Colchicine x6 months * Post-MI Use ASA instead of NSAIDs (High dose = ASA 650 po QID) * Pregnancy – < 20 weeks - ASA (1st line), NSAIDs, Tylenol, pred – > 20 weeks - Tylenol, pred; [NO ASA or NSAIDs] – Breastfeeding - avoid ASA – NO colchicine * Steroids settle inflammation acutely but increase recurrence risk – avoid unless immune-mediated etiology or clearly non-responsive/contraindications to ASA/NSAIDs. – Should still give colchicine in addition – Use low doses (0.25-0.5mg/kg/d) – Strongly consider taper Other considerations: * GI protection * Exercise restriction * For advanced cases – IVIG vs. anakinra vs. azathioprine * Last line of defense - pericardiectomy

Answer 39

* Constriction = fibrous, non-compliant pericardium limits expansion of cardiac chambers – Rapid early filling of ventricles then abrupt cessation as they hit the “stretch limit” of pericardium à rapid Y descent, square root sign on cardiac cath – +ve Kussmaul’s sign and often no pulsus paradoxus * Tamponade = accumulation of fluid in pericardial space increases the intrapericardial pressure and overcomes intracardiac pressure leading to impaired filling – Pulsus paradoxus, blunted Y descent on JVP, Beck’s Triad (hypotension, distended JVP, muffled heart sounds)

Answer 40

* Constriction and tamponade are pericardial problems characterized by enhanced ventricular interdependence – Increased R heart filling = Reduced L heart filling * Patients with tamponade are often unstable * Patients with constriction normally present with heart failure * Patients with restriction have a myocardial problem that can resemble constriction but no ventricular interdependence Use history, clinical exam, and other clues to help differentiate

Answer 41

* General Population – pulse-based screening or rhythm-based screening at all routine health assessments in people >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

Answer 42

Major Considerations: * Always look for an etiology/precipitant (EtOH, drugs, withdrawal, ischemia, PE, valves, thyroid disease, OSA, infection, sleepdeprivation, acute pulmonary disease ... ) * Basic Workup for new AF: * Document rhythm * ECHO – assess LV size and function, LA size, valve .. * CBC, lytes (Ca, Mg), Cr, Coags, TSH for all * LFT before amiodarone prescription * A1C, FBG, Fasting lipid profile as part of comprehensive cardiac risk assessment * Always assess patient AF-related symptoms and quality of life (CCS-SAF), assess patients with AF for frailty, cog impairment,dementia, depression

Answer 43

Major Considerations cont’d: * Prevention = modifiable risk factor management * Achieve rate control with b- blocker, CCB, or digoxin * AF with pre-excitation (WPW): DC cardioversion (or procainamide) * Rhythm control preferred if QoL impaired (symptomatic despite rate control) or hemodynamically unstable (DC cardioversion)

Answer 44

* 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)

Answer 45

* Stage 3 CKD (eGFR >30) – A/C as usual * Stage 4 CKD (eGFR >15 <30) – A/C as usual – “Non randomized data supports the use of OAC for AF” – “The CCS recommends that a DOAC is preferred over VKA” – “Apixaban and rivaroxaban are approved for use with stage 4 CKD” * Stage 5 CKD (eGFR <15) : “ we suggest that such patients not routinely receive anticoagulation therapy or antiplatelet therapy for AF”

Answer 46

CHADS65 = 0 - Single Antiplatelet – “Consider” ASA + low dose rivaroxaban (2.5mg bid) per COMPASS trial to reduce CV mortality CHADS65 > 0 OAC only – Prefer DOAC > VKA (2a) AFIB + PCI (elective or ACS) -Individualize based upon thrombotic risk LOW RISK thrombotic events Elective PCI (no ACS) CHADS65 = 0 - DAPT – DAPT for 6-12 months per CCS 2018 Antiplatelet Guidelines for non-AF patients CHADS65 >0 “Dual Pathway” – SAPT with a P2Y inhibitor* + OAC for at least 1 month, up to 12 months after PCI, then OAC alone HIGH RISK thrombotic events or ACS with PCI CHADS65 = 0 à DAPT CHADS65 >0 à “Triple Therapy”x1-30d THEN “Dual Pathway Therapy” = clopidogrel + OAC up to 12 months post PCI THEN OAC only (2a) AFIB + ACS – NO PCI /stent Individualize based upon thrombotic risk CHADS65 = 0 DAPT = Dual Antiplatelet Therapy (ASA + P2Y inhibitor) CHADS65 > 0 - “Dual Pathway Therapy”: clopidogrel + OAC [apixaban1] for 1 to 12 months post ACS THEN OAC only

Answer 47

Core principles when considering PPM therapy * Pacemakers are class I therapy for: – Symptoms – Prevention of sudden death in asymptomatic patients * Other considerations – Allow for uptitration of GDMT with significant (usually mortality) benefit – Syncope (narrow indications) * So ... in general, those that get PPMs have symptoms related to some bradyarrhythmia OR high-grade conduction system disease with risk of death

Answer 48

Sinus Node Dysfunction à need symptoms * Sinus bradycardia, sinus pauses * Requirements for GDMT * Tachy-brady syndrome * Chronotropic incompetence Acquired AV Block - do not need symptoms * 2nd degree AVB Mobitz type 2 * 3rd degree AVB * High grade AVB * Permanent AF and symptomatic bradycardia * Symptomatic AVB (spontaneous or from required drug therapy) *If in doubt, a symptomatic patient with a bradycardic rhythm should prompt a consult from Cardiology/Electrophysiology

Answer 49

* NB. ESC makes it easier – “ implantation of permanent pacemaker is indicated with the same recommendations as the general population when AVB does not resolve within a waiting period of at least 5d post-MI” ACC/AHA explicit recommendations * Temporizing measures – Atropine administration reasonable – Temporary pacing for medically refractory symptoms or hemodynamic significance related to SND or AVB * Permanent pacemaker – Mobitz II AVB – High grade AVB – Alternating BBB – 3rd degree AVB * Class III recommendations – Transient AVB that resolves – New BBB or isolated fascicular block

Answer 50

* If unstable -> ACLS!! Defibrillation, ABCs, look for etiology (ischemia, long QT, etc.) * Electrical storm (≥3 episodes in 24h) – Beta Blocker, preferably non-selective – IV amiodarone – Consider sedation / anesthesia – Consult heart rhythm expert early – Treat acute HF, if present * If stable, sustained (>30 sec) VT – DC cardioversion vs. procainamide – Amiodarone IV 150mg then 900mg/24h infusion – Lidocaine * Polymorphic VT/VF – Normal QT à acute ischemia (ACS Tx and amio or lido) vs. no ischemia (amio) – Prolonged QT à IV Mg, overdrive pacing, non-selective BB, lidocaine if refractory

Answer 51

ICDs are indicated in the setting of sudden cardiac arrest and expected meaningful survival greater than 1 year, or recurrent ventricular arrhythmias not controlled with medical therapy. Brugada syndrome is an autosomal dominant mutation, most commonly in sodium channels (SCN5A in 20-30% ofpatients, but many more mutations exist). In an asymptomatic patient with only aninducible Type 1 pattern (i.e. no Brugada without provoking agent), no therapy is indicated. In an asymptomatic patient with a spontaneous Type 1 pattern (i.e. persistent, not induced), EP study can be considered for risk stratification. Aside from cardiac arrest, ICD also indicated for syncope presumed to be from a ventricular arrhythmia with Type 1 ECG. Quinidine is useful in the setting of recurrent ICD shocks. – CPVT involves a mutation in the ryanodine receptor. Bidirectional VT can be provoked by exercise, diagnosed bystress testing. Treatment is nadolol. ICD only indicated if sudden cardiac death.

Answer 52

Long QT syndrome involves mutations in potassium channels (LQTS1/2) and sodium channels (LQTS3). Various triggers (exercise=1, loud noises=2, sleep=3) and patterns. A QTc over 500 ms is long as needs explanation! Differential includes a bundle branch block (widens the QRS so would extend the QTc), drugs, electrolytes, medications, congenital. Beta blockade is recommended if QTc is 470 ms or more to reduce risk of ventricular arrhythmias. * Torsades occurs in the setting of QT prolongation is triggered by an “R-on-T” event, in which a premature ventricular contraction hits the T-wave, producing polymorphic VT. * Acute management involves stopping offending medications and correction of electrolytes (Target Mg = 1.0, K >4). Increasing the patient’s heart rate (shortens the QT interval and makes it less likely for a PVC to hit the QT) may be necessary, which can be achieved with temporary pacing (overdrive pacing) or isoproterenol (beta agonist). Lidocaine can be helpful as it does not lengthen, and actually may shorten, the QTc. * If the QT interval cannot be corrected, device therapy if often necessary (dual chamber ICD which can be used to pace the patient atrially at 80 bpm to prevent bradycardia/PVCs, and also act to treat polymorphic VT. * Why beta blockers if we are preventing bradycardia with overdrive pacing? They likely suppress ventricular ectopy, reducing the “R- on-T” likelihood and have been shown in studies to reduce the risk of cardiac arrest

Answer 53

1. Look for a “smoking gun” – AV dissociation à P waves marching, capture beats, fusion beats 2. Look at the axis, QRS polarity in aVR – NW axis, upright in aVR point towards VT 3. Does the QRS look like a typical bundle branch block? – Is there concordance in the precordial leads? – Is there RSr’ (atypical “bunny ears”) in V1 if RBBB-ish – Is there a Q wave in V6 if LBBB-ish 4. +/- Consider the width of the QRS Signs of VT : Absence of typical RBBB or LBBB morphology Extreme axis deviation (“northwest axis”): QRS positive in aVR and negative in I and aVF Very broad complexes > 160ms AV dissociation: P and QRS complexes at different rates P waves are often superimposed on QRS complexes and may be difficult to discern Capture beats: Occur when the sinoatrial node transiently “captures” the ventricles in the midst of AV dissociation, producing a QRS complex of normal duration Fusion beats: Occur when a sinus and ventricular beat coincide to produce a hybrid complex

Answer 54

PAD can manifest as intermittent claudication, chronic limb threatening ischemia or acute limb ischemia * Diagnosis: ABI or TBI test of choice to confirm diagnosis of PAD in patients with symptoms * Screening: adults age>50 with risk factors (smoking, diabetes), even if asymptomatic – No role for routine testing in asymptomatic individuals without risk factors – No role in also routinely screening for coronary artery disease/carotid artery disease unless they have symptoms of these conditions – Guideline doesn’t specify frequency of screening

Answer 55

* Management: – Smoking cessation : NRT, bupropion, varenicline, CBT – Exercise program, walking therapy, foot care, wound therapy – Diabetes management tight control may reduce MALE, including SGLT2i (↓MACE, no increased amputation risk) – Statins indicated à add on ezetimibe/PSCK9 inhibitor to target – Hypertension per Hypertension Canada, <140/90, ACEi/ARB first line therapy – Antithrombotic: indicated ONLY if symptomatic (i.e. not indicated if asymptomatic) * First line: ASA + low dose rivaroxaban 2.5 bid if high risk of ischemic events – high-risk comorbidities such as polyvascular disease, diabetes, history of heart failure, or renal insufficiency) and low bleeding risk * Otherwise SAPT (clopidogrel > aspirin) * Recommend against full dose anticoagulation + antiplatelet in stable chronic PAD

Answer 56

* Postural Orthostatic Tachycardia Syndrome (orthostatic tachycardia without orthostatic hypotension) – Orthostatic intolerance (sustained ↑ HR >30bpm supine within 10 mins of standing with no drop in BP 20/10) * Rule out 2o causes (hypovolemia, thyroid etc.) * Rule out systemic disease e.g. Ehlers Danlos, Autoimmune neuropathy... – Symptoms associated: palpitations, chest discomfort, lightheadedness, chronic fatigue, chronic pain, nausea * Workup – if diagnosis clear - do not need specialized cardiac testing. Recommend basic labs (CBC, electrolytes, Cr, TSH, am cortisol) * Non-Pharm management: exercise training, Na 10g/d, H2O 3-4 L /d, compression stockings waist high * Pharm management: Midodrine, fludrocortisone – Other weak recommendations: Ivabradine, Methyldopa, Clonidine

Answer 57

1. Systolic versus diastolic? –MR. ASS married MS. ARD 2. Right sided murmurs increase with inspiration 3. Left sided murmurs increase with expiration 4. Save your energy, and bundle your murmurs! – Increase venous return à leg raise/squat; decrease standing/Valsalva – Increase afterload - hand grip; decrease - amyl nitrate – AS/MS: louder with increased venous return & with decreased afterload – AR/MR: louder with increased venous return & increased afterload – HOCM/MVP (the opposite of AR/MR): louder with decreased venous return & decreased afterload

Answer 58

N.B. Cardiac arrest, VF or sustained VT are class I indications for ICD MAJOR (class IIa recommendations for ICD) Family history of SCD Spontaneous sustained VT UNEXPLAINED syncope Apical aneurysm LVEF 50% or less LV thickness ≥ 30mm (*positive predictive value low – most who die <30mm thickness) MINOR risk factors (class IIb recommendations for ICD) NSVT (on Holter) Extensive LGE on Holter