Cardio Flashcards
How Do CAD 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
Non-invasive stress tests:
– STRESS = exercise,
drugs (inotropes,
vasodilators)
– TEST = ECG, ECG+echo,
ECG+nuclear
STRESS: pick exercise whenever possible!
– Provides prognostic info: e.g. duration of exercise, METs
– Not possible if physical limitations or contraindications
(e.g. critical aortic stenosis)
- TEST: consider functional imaging (e.g. nuclear) if:
– Cannot accurately assess for ischemia on ECG - LBBB, paced rhythm, preexcitation, significant ST changes at
rest à the ECG is not interpretable in these cases
– RBBB interpretable generally
– Need specific anatomic correlation (e.g. prior
revascularization)
Structural
– Coronary angiography
– CT coronary
angiography
Absolute Contraindications to EST
- Acute MI (within 2 days)
- Ongoing unstable angina
- Uncontrolled hemodynamically-significant
arrhythmia - Active endocarditis
- Symptomatic severe AS
- Decompensated heart failure
- Acute PE, pulmonary infarction, DVT
- Acute myocarditis, pericarditis
- Acute aortic dissection
- Physical limitations
EST Results
Positive test
– ≥ 1mm STE
– ≥ 1 mm STD (horizontal or
downsloping)
High risk features*
– Duke Treadmill Score -11 or less
– <5 METs achieved
– Low threshold angina / ischemia
– STE
– Severe STD ≥ 2mm
– Ischemia on ≥ 5 leads
– Ischemia ≥ 3 mins into recovery
– Abnormal BP response [failure to
achieve SBP>120, drop in BP >10,
drop below baseline]
– Ventricular arrhythmia
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 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 <60), breath hold
Indications:
– Diagnosis of CAD for low to intermediate pre-test prob patients
– Risk stratification in patients with stable CAD
Contraindications:
– ACS
– Severe structural heart disease (AS or HCM)
– Usual CT precautions: Contrast Allergy, Renal Failure, Pregnancy
Treatment of Chronic Stable CAD
General Principles
- Treat symptoms with medical therapy first
- Consider revascularization if refractory symptoms, high risk structural disease (e.g. LM
disease), LV dysfunction, severe MR
Optimal Medical Therapy (OMT) is non-inferior to revascularization (PCI/CABG) for
patients with Stable CAD
- ALL patients with CAD:
– Commence medical treatment for CAD
– Aspirin + statin for evidence of coronary atheroscerosis regardless of the
modality of diagnosis
– Clopidogrel can be used as SAPT if ASA intolerant
Antianginal (symptomatic benefit):
– Beta blockers: reduce HR/contractility, indicated
for most patients*
– CCBs: reduce HR/contractility (non- dihydropyridine, beware if LVEF<40%), reduce
preload (dihydropyridine)
– Nitrates: venodilate, reduce LVEDP
– Others: ranolazine (calcium modulator that
reduces angina, just so you’re aware of but use in
Canada is rare)
Disease modifying therapies:
– ACE inhibitors: HTN, T2DM, LVEF <40%, CKD, can
be considered for all for vascular protection
– Beta blockers: LVEF<40%
* *If no previous MI and LVEF >50 = use of BB therapy
does not ↓ MACE, in absence of other indication for
BB (eg for control of HTN or rapid afib) – ACC/AHA
2023
– CAD + DM: SGLT2i or GLP1RA
– Hypertension, dyslipidemia, diabetes management
Revascularization - PCI vs. CABG
In general, invasive angiography
should be considered for:
- High risk features on non- invasive testing
- Medically refractory
symptoms
In general PCI is less invasive and useful to
treat symptoms. CABG preferred if:
* L main disease (>50% occlusion)
* Multivessel disease with diabetes
* Multivessel disease with LV
dysfunction/CHF
For MCQs:
* Conflicting stroke data
* Less repeat revascularization with CABG
* Survival with CABG in highly select
scenarios
* “Team-based decision” beyond scope of
GIM
Immediate Medical Management of ACS
The ACS “cocktail”
* Antiplatelet: ASA + 2nd agent (ticagrelor, clopidogrel, prasugrel)
– Loading doses à ASA (160 mg CHEWED), Ticagrelor (180 mg), Prasugrel (60mg) Clopidogrel
(300-600 mg)
* Ticagrelor C/I if previous intracranial hemorrhage, prasugrel C/I if ANY prior TIA/Stroke
* If thrombolysis à ASA + Clopidogrel (NO TICAGRELOR OR PRASUGREL)
– Maintenance doses à ASA (81 mg OD), Ticagrelor (90 mg q12h), Clopidogrel (75 mg OD)
Anticoagulation: UFH or LMWH or Fondaparinux
– Continued for 48 hours until discharge or 8 days, stop if revascularized
Antianginals: beta-blocker, cautious administration, within 24 hours for stable
patients.
Reperfusion Therapy – STEMI
Principle: achieve coronary patency in ALL
patients presenting <24h from symptom
onset, or with ongoing symptoms
- Options:
– Primary PCI
– Fibrinolysis/pharmaco-invasive (“drip & ship”) - Primary PCI > fibrinolysis:
– if timely - PCI capable hospital à FMC-to-balloon time <90 min
- Non-PCI capable hospital à FMC-to-balloon time <120 min
FMC = First Medical Contact à ER triage if walk-in, or EMS arrival if 911
– if later presentation (12-24h of symptom onset)
– if cardiogenic shock
- Fibrinolysis indicated if PCI is not readily available (>120min)
- Pharmaco-invasive strategy superior to rescue PCI: Drip (give lysis)
then ship (send immediately to PCI centre for angiogram/PCI
within 3-24 hours)
– If fibrinolysis à should be administered within 30 minutes of FMC
– If Fibrinolysis à PCI should occur within 24 hr.
– Timing of fibrinolysis à the earlier, the better, but can be given up to
24h after onset of chest pain w STE
The Second Antiplatelet… CCS 2023
Ticagrelor preferred (conditional)
– vs clopidogrel greater efficacy, no
increased bleeding risk
If patient is High bleeding risk
– DAPT for 1-3 months non-inferior to
longer durations
* “practice point” – if stepdown to SAPT
choose P2Yinhibitor over ASA
* Step-down to SAPT should incorporate
cardiologist – (eg) avoid if high risk PCI or
hx stent thrombosis
CCS 2023 Pearls… ACS à CABG
If you strongly suspect CABG will be required, can withhold P2Yi prior to Angiogram
even if expected delay >24h post ACS
- Stopping P2Yi prior to CABG
– Limited evidence… “multidisc team” to decide, hold 2-7d pre-op - Suggest hold Ticagrelor 2-3 days rather than 5-7d [weak, conditional]
- Postop Antiplatelet Regimen
– Off-pump – favour DAPT, with ASA + ticagrelor/prasugrel over ASA + Clopidogrel
– On-pump – favor SAPT
– AFIB? – consider OAC monotherapy
The Second Antiplatelet… Nuances
Ticagrelor is contraindicated if history of:
– intracranial hemorrhage
– active pathological bleeding
– moderate-severe hepatic impairment
– combinations with CYP34A inhibitors (ketoconazole, clarithromycin, ritonavir)
– Should consider avoiding in patients with evidence of heart block or bradycardia.
– Dose: 180mg load then 90 mg bid x 12 months then 60mg bid thereafter
- Prasugrel is contraindicated if:
– active bleeding
– prior TIA/stroke [even ISCHEMIC stroke]
– hypersensitivity reaction – Dose: 60mg load then 10mg daily (reduce to 5mg if <60kg) - Ticagrelor & Prasugrel have NOT been adequately evaluated in the setting of
fibrinolysis in STEMI à Use clopidogrel pre-PCI
Reperfusion Therapy - NSTE-ACS
Timing & risk stratification are the major differences vs. STEMI
1. Risk stratify using clinical judgment + risk scores (TIMI, GRACE)
- Do not memorize these, but understand what factors involved
- Int/high risk patients: early invasive strategy (angiogram within
48hr)
- Early invasive reduces risk of rehospitalization for ACS but NO
mortality benefit - Low risk patients and/or unclear diagnosis: non-invasive testing
(often with functional imaging) reasonable to determine
benefit of invasive strategy
PCI options
- Plain-Old-Balloon-Angioplasty (POBA)
– Rare - Bare metal stent (BMS) – rarely used
– Endothelialize quickly = lower risk of stent thrombosis after 4+ weeks
– But…higher risk of re-stenosis - Drug eluting stent (DES) – standard of care
– Elute anti-proliferative agents
– Lower rates of restenosis vs. BMS = can be used in smaller vessels, CABG grafts
– But…take longer to endothelialize - Drug coated balloon (DCB)
– Expand a blood vessel and deliver antiproliferative agents (e.g. Paclitaxel) without delivering
a stent
– Useful for in-stent restenosis (ISR), bifurcating/branch lesions, buying time for definitive
treatment
Stents and DAPT Durations(without AF)
POST ACS (STEMI or NSTEMI/UA): Aim for 12 months of DAPT
– ACS DAPT= ASA + Ticagrelor 90 BID or Prasugrel 10 OD (preferred over ASA+Clop)
* NEW CCS 2023: If High Risk of Bleeding with PCI post ACS, can de-escalate to SAPT after 1-3 months
of DAPT OR de-escalate from a more potent second antiplatelet (i.e. change from ASA+ticagrelor to
ASA+clopidogrel)
* Reassess bleeding at 1 year.
– If HIGH RISK bleed: SAPT ASA 81 or Clopidogrel 75
– If LOW RISK bleed: Continue DAPT - Good evidence for up to 3 years (DAPT trial)
DAPT After 12 months: Suggest ASA + one of:
* Ticagrelor (60 mg po bid) (reduced dose, not standard dose)
* Clopidogrel (75 mg po daily)
* Prasugrel (10mg po daily) (weaker recommendation that others for extended therapy)
Non-ACS situations (ELECTIVE PCI)
* High Risk of Bleeding: Elective PCI DAPT = ASA 81+ Clopidogrel 75
– BMS = DAPT for 1 month then SAPT with ASA 81 or Clopidogrel 75 indefinitely
– DES = DAPT for 3 months then SAPT with ASA 81 or Clopidogrel 75 indefinitely
* Not at high risk of bleeding: DAPT for 6 months, then reassess
– If High Risk thrombotic events: extend DAPT up to 3 yrs
– If not at high risk of thrombosis or if now at high risk bleeding: SAPT (ASA or Clop)
CCS 2023 Antiplatelet Guideline:AFIB + Antiplatelets
- Antiplatelet and anticoagulation (i.e. patient on OAC for atrial
fibrillation)
– Dual pathway (clopidogrel+OAC) recommended over previous
strategy of triple therapy for 1-30 days in most patients (but the small
text says they need to receive 1 dose of ASA at PCI time, so it is like
they only received 1 dose of triple therapy)
– OAC monotherapy preferred over OAC+aspirin in stable CAD (from the
AFIRE trial which showed rivaroxaban+ASA had more bleeding with no
reduction on ischemic events compared to rivaroxaban alone)
Complex PCI
Complex PCI = patient that you would be less willing to do a shorter duration/less potent regiment of DAPT.
Just need 1:
* Left main
* 3 vessels
* 3 lesions
* 3 stents
* >60mm stent
* Bifurcation stents
* Bypass graft PCI
* Atherectomy, CTO
procedure
Periop Mgmt - Stents and DAPT
Elective Non-Cardiac Surgery
* BMS – Delay surgery for at least 1 month post PCI
* DES – Delay surgery for at least 3 months post PCI
Semi-Urgent Non-Cardiac Surgery
* BMS – Delay surgery for at least 1 month post PCI*
* DES – Delay surgery for at least 1 month post PCI*
*weak recommendation, low quality evidence – individualize as semi-urgent sx usually can’t be delayed 1 month
Pre-Op
* Hold Clopidogrel and Ticagrelor 5-7d preoperatively
– 5-7 days if neuraxial anesthesia or very high risk bleeding, speak to anesthetist and surgeon
* Hold prasugrel 7-10d preoperatively
* Continue ASA perioperatively “whenever possible”
Post-Op
- Restart DAPT post-op as soon as deemed safe by surgical team
Post-MI Complications
- Heart failure
- Arrhythmias
– Tachy: Atrial, ventricular
– Brady: Heart block (esp. inferior MI) - Mechanical complications
– Papillary muscle dysfunction and acute MR
– Ventricular septal rupture
– Free wall rupture
– RV infarction (esp. inferior) - Pericarditis
– Post MI pericarditis = Early (5d) vs. delayed [Dressler syndrome] (2-8wks)
– Fever, pleuritic chest pain, pericardial rub and/or pleural effusion; Rx is
high dose ASA + colchicine
Chronic Management/Risk factors
Initiate BEFORE Discharge
* High potency statin
* ACEi, BB
* Identify +/- optimize diabetes
* Influenza vaccine
* Smoking Cessation Therapy [see Resp Lecture BONUS slides]
* Cardiovascular Rehab
* Driving restrictions [NEW! CCS 2023 Guidelines]
Diagnostic approach Cardiomyopathies
& Heart Failure
All patients with heart failure (regardless of LVEF): ECG,echocardiogram, CBC, lytes, creatinine, ferritin, TSH, troponin, BNP
- 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 <35, at risk of CAD, irrespective of angina, likely good candidates for
revascularization
* Consider if: systolic HF and non-invasive coronary perfusion testing consistent with high
risk
Diagnostic approach Cardiomyopathies
& Heart Failure- continued
Less common etiologies (i.e. non-ischemic):
* Familial dilated cardiomyopathy
* Genetic (HCM, ARVC, hemochromatosis)
* Drugs /toxins (alcohol, cocaine,
chemotherapy)
* Pregnancy (Postpartum cardiomyopathy)
* Inflammatory (myocarditis, sarcoid)
* Endocrine (pheochromocytoma, Cushing)
* Nutritional (thiamine deficiency / beriberi,
selenium deficiency)
* Infiltrative (amyloid, Fabry)
Workup for non ischemic cardiomyopathy
– Good History
* Testing directed by history (eg) genetics if family
history
– Cardiac MRI for most with non-ischemic
cardiomyopathy
(If available)
* To help rule out infiltrative, ARVC
Acute HF Management
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…
Long-term Management of HFrEF
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
Revascularization and ischemic cardiomyopathy
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!
HFrEF Pharmacotherapy
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)
Important HF Medication Considerations
- 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
ICDs in HF
- 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%
ICDs for 2o prevention
- Cardiac Arrest (VT-VF)
2.Sustained VT in the presence of significant structural heart disease - 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!
Cardiac Resynchronization Therapy (CRT)- general principles
- 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
CRT Indications
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
When Should We Worry About HFrEF Patients?
“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
HF with Preserved EF (HFpEF)
- 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)
Diuretics in Heart Failure
- 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)
Hypertrophic Cardiomyopathy- dx and tx
- 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)
HCM-Principles for physical exam
- 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)
Cardiac Amyloidosis
- 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
Cardiac Amyloidosis- dx and tx
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
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 - “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
Pharmacotherapy for VHD
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
Aortic Stenosis
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
Aortic Stenosis - Intervention
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)
Aortic Regurgitation
- 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
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)
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
– 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
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
Mitral Regurgitation
- 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
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)
Mitral Regurgitation - Intervention (part 2)
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
Tricuspid Regurgitation
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
Antithrombotic Therapy After Valve Replacement
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
Thoracic Aortic Dissection- presentation
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
Thoracic Aortic Dissection- management
- 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
Thoracic Aortopathy/Aortic Aneurysm
-
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)
The Aortic Team- when to refer?
- 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
Abdominal Aortic Aneurysm Pearls
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
Acute Pericarditis- presentation
- 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
Acute Pericarditis-Etiology
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
When to Admit Pericarditis
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
Treatment of Acute Pericarditis
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
Pericardial Constriction and Tamponade
- 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)
Constriction vs. Tamponade vs. Restriction
- 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
Screening for Atrial Fibrillation (AF)
- 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
AF Etiology & Initial Investigations
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
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):
DC cardioversion (or
procainamide) - Rhythm control preferred if QoL
impaired (symptomatic despite
rate control) or hemodynamically
unstable (DC cardioversion)
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)
Anticoagulation in CKD/ESRD for those with AF
- 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”
Niche scenarios of when to use OAC/DAPT in patients
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
Bradyarrhythmia & Pacing (core principles)
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
Pacemakers (Summary of Indications)
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
Pacemakers after Myocardial Infarction
- 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
Ventricular Arrhythmias
- 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
Channelopathies and ventricular arrhythmias
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.
Long QT syndrome
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
Tips to Help Differentiate VTfrom SVT w/ Aberrancy
- Look for a “smoking gun”
– AV dissociation à P waves marching, capture beats,
fusion beats - Look at the axis, QRS polarity in aVR
– NW axis, upright in aVR point towards VT - 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 - +/- 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
Peripheral Arterial Disease- Dx and Screening
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
Peripheral Arterial Disease Management
- 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
Postural Orthostatic Tachycardia Syndrome (POTS)
- 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
Tips for Tackling Murmurs
- Systolic versus diastolic?
–MR. ASS married MS. ARD - Right sided murmurs increase with inspiration
- Left sided murmurs increase with expiration
- 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
Risk Factors for Sudden Death in HCM:
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
