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Marc Katz MD

Advice for medical trainees, cardiology, & everything in between

High Yield Board Review Notes for Cardiovascular Disease Fellowship

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The following are iterative notes that I take while studying for my general cardiology, echocardiography, and nuclear cardiology board exams. Making them public so I can access them on the go and help out anyone else looking for similar information.


Valvular Heart Disease

Aortic Insufficiency/Regurgitation (AI/AR)

Severe AI, indications for surgery

  1. Asymptomatic: EF ≤55%
  2. Asymptomatic: EF >55% + LVESD >50mm or LVESDi >25mm/m2
  3. Asymptomatic: EF >55% with progressive decline in EF to low-normal (55-60%) with LVEDd >65mm
  4. Symptomatic
  5. Other concurrent cardiac/aortic surgery

  • Severe AI surgical indications
  • Accurate measurements
  • Severe AI via echo
  • Chronic sever eaortic regurgitation (AI/AR) symptom progression
  • Severe AI: survival and LV function
  • Severe AI: survival and NYHA class

Aortic Stenosis

  • Prostehtic AV algorithm

Low-Flow Low-Gradient AS (LF-LG AS)

  • LFLG algorithm 2

Bicuspid Aortic Valve

  • Bicuspid AV algorithm
  • Frequency of bicuspid anatomy
  • Screening guidelines
  • Bicuspid AV imaging surveillance guidelines
  • Bicuspid aortic valve surgical intervention guideline recomendations

Surgical indications for dilated aortic root/ascending aorta

Aorta sizeIndicationClass recomendation
≥ 5.5 cmRisk factors for dissection (FH, growth rate >0.5cm/year, bicuspid AV)I
> 5.0 cmRisk factors and low surgical risk <4% (FH of dissection, growth 3-5mm/year, aortic coarctation, small stature)IIa
> 5.0 cmLow risk, experienced surgeon, expert centerIIa
> 4.5 cmBicuspid AV planning for surgical AVR for AS/AIIIa

*Aortic root measured at sinus of Valsalva

ACC Guideline: Aortic Surgery for Bicuspid AV

Mitral Regurgitation

  • Simplified asymptomatic severe primary MR algorithm
  • Primary mitral regurgitation (MR) algorithm
  • Qualitative and quantitative MR by echocardiography (TTE)
  • Mitral valve anatomy
  • Etiologies of chronic mitral regurgitation (MR)- acute and chronic
  • Pathophysiology of acute and chronic MR
  • Qualitative assessment of MR
  • Clinical workflow for diagnosis and management of MR
  • MR algorithm
  • Qualitative and quantitative MR by echocardiography (TTE)
  • Medical therapy for chronic MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Transcatheter edge-to-edge repair (TEER) for severe primary MR

Mitral valve prolapse and flail

Carpentier Classification of MR

  • Type 1: normal leaflet mobility (primary: endocarditis, perforation, clefts; secondary: dilated annulus)
  • Type 2: excessive leaflet mobility (prolapse, flail)
  • Type 3: restricted leaflet motion
    • 3a: in systole and diastole (Fibrosis of subvalvular apparatus: rheumatic, radiation, drug-induced injury, inflammatory conditions)
    • 3b: only in systole (Leaflet or chordal tethering: ICM, NICM causing LV dilation)

Mitral Valve Regurgitation Review Article

Chronic MR Algorithms

  • Qualitative and Quantitative Assessment of MR severity by echo
  • Recommended Treatment of severe secondary MR
  • Severe MR Algorithm
  • Recommended Treatment of severe secondary MR
  • Algorithm for Eligibility of Transcatheter Edge-to-Edge Repair (TTER) in severe MR
  • Semiquantitative parameters in MR
  • Quantitative measures for severe MR by PISA png
  • Pulsed Doppler Volumetric Quantification of severe MR
  • Indications for exercise stress testing in MR
  • Routine monitoring of MR via echo
  • MR treatment algorithm

Indications for TTE, TEE in MR

  1. Initial evaluation if suspicious for MV disease or MVP
  2. Initial evaluation of known ur suspected MR
  3. Annual evaluation in severe MR
  4. Reevaluation of MR with change in clinical status
  5. TEE to determine mechanism of MR and suitability of valve repair
  6. *Inappropriate: routine evaluation of MVP with (1) no or mild MR and (2) no change in clinical status

Mitral Valve Prolapse (MVP)

Arrhythmic MVP

  • Non-invasive markers associated with sudden cardiac death (SCD) despite not having severe MR
  • High density of PVCs, inferior TWI, spiked systolic high-velocity signal on echo (Pickelhaube sign), myocardial/papillary scar on MRI
  • Pickelhaube sign: peak systolic lateral mitral annular velocity ≥16 cm/s. More likely to have malignant arrythmia in those with myxomatous bileaflet MVP (‘B’ in image below)
Non-invasive markers associated with SCD in MVP

Acute Severe MR

  • Rapid equalization of pressure across LA/LV may only cause a short, unimpressive murmur (may only appear as mild MR)
  • *Suspect in acute heart failure with normal LV systolic function
  • *Suspect in decreased LVOT VTI despite hyperdynamic LV EF (suggestive of low forward flow- consistent with severe MR)

Mitral Stenosis

  • Stages of mitral stenosis (MS)
  • Stages of mitral stenosis (MS)
  • Wilkins Score for rheumatic mitral stenosis (MS)
  • Mitral stenosis (MS) pressure half-time
  • Mitral stenosis (MS) pressure half-time 2
  • Mitral stenosis (MS) mean gradient (MG)
  • Mitral stenosis (MS) PISA
  • Continuity equation for mitral stenosis (MS)
  • Mitral valve area via LHC
  • Gorlin formula: mitral valve area via LHC
Typical appearance of rheumatic mitral stenosis

2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease


Invasive Hemodynamics Review


Classic Valvular Murmurs

LesionTimingQualityRadiationSeverity
ASCrescendo-decrescendo

Gap between S1, murmur, and S2
Harsh, noisy
MRHolosystolic through S2

Starts with S1 through S2
Blowing, high pitchedAnterior prolapse/flail: axilla, left intrascapular area

Posterior: anteriorly along aortic outflow in left parasternal area (can be confused with SEM)
Weak correlation between intensity and severity

S3: increase in diastolic flow across MV orifice during rapid filling phase  

Increased P2 intensity: pHTN   Enlarged, displaced LV impulse: LV dilation
Post PVCMR changes little: high gradient between LA/LV in SR and post-PVC*AS murmur increases post-PVC as SV after PVC is greater (more flow)  
MVPEarly, mid-systolic click ➡️ systolic murmur±High pitched, ‘whoop’ sound Maneuvers on click and murmur:
– ⬇️ LV volume/preload (Valsalva, squat to stand): murmur/click occur earlier in systole
– ⬆️ LV afterload (squatting): murmur/click occur later in systole
Severe MVP: holosystolic murmur 
Differentiating AS from MR

Prosthetic Valves

Prosthetic Aortic Valves

Pressure recovery: due to small aorta causing falsely elevated mean gradient readings and thus low AVA

Prosthetic Valve Thrombosis

Prosthetic Valve Guidelines from JASE (Journal of American Society of Echocardiography)


Heart Failure

Non-Ischemic Cardiomyopathy (NICM)

2022 AHA/ACC/HFSA Guidelines

Abnormalities in Hepatic Vein Flow on Doppler

Amyloidosis

Diagnostic algorithm for diagnosis of amyloidosis

Figure 2.
99mTechnetium-pyrophosphate imaging for transthyretin cardiac amyloidosis

Treatment for ATTR amyloidosis

Medical therapies for amyloid

  • Tafamadis: amyloidosis but not NYHA IV
  • Patisiran: for ‘papa’- familial amyloid neuropathy

Pulmonary Hypertension (pHTN)

Peak TR jet velocity (m/s)Presence of other echo ‘PH Signs’TTE probability of pHTN
≤2.8 or not measurableNoLow
≤2.8 or not measurableYesIntermediate
2.9-3.4NoIntermediate
2.9-3.4YesHigh
>3.4Not requiredHigh

Echo Findings in Pulmonary Hypertension (pHTN)

VentriclesPulmonary ArteryIVC, RA
RV/LV basal diameter ratio >1RVOT acceleration time (AT) <105ms ±midsystolic notchingIVC >21mm, <50% inspiratory collapse with sniff (or <20% with quiet inspiration)
IVS flatteningEarly diastolic PI velocity >2.2m/sRA size >18cm2 at end-systole
PA diameter >25mm

Chagas Cardiomyopathy

Hypertrophic Cardiomyopathy (HCM)

Surgical options and complicationsSeptal myectomy –> LBBB
Alcohol septal ablation —> RBBB
DysopyramideQT-prolongation
Physical exam maneuversLouder murmur with Valsalva (decreased preload)Softer murmur with hand grip
High risk features for SCD1. First degree relative SCD
2. IVSd ≥30mm (IIa indication: ICD for primary prevention)
3. Unexplained syncope in past 6 months
4. LV apical aneurysm
5. EF <50%
6. NSVT: children (IIa), adults (IIb)
7. Extensive LGE on CMR (IIb)
8. Exercise induced NSVT or abnormal BP response to (drop ≥20mmHg) + high risk features (IIa- it is IIb if no high risk features)
HCM family screening in 1st degree relatives

Echo following septal myectomy for HCM with edge-to-edge (Alfieri) repair of the mitral valve

  • Anterior and posterior leaflets are sutured together in the mid portion giving the typical appearance of a double-orifice mitral valve
  • The color jet that can be seen on the septal wall represents flow from a coronary-LV fistula, a common benign finding after septal myectomy procedures
  • May lead to functional mitral stenosis (MS) requiring surgical interventions following edge-to-edge repair

Coronary Artery Disease

Guidelines/Review Articles

CABG (coronary artery bypass graft) Guidelines

UA/NSTEMI

  • TIMI risk score for UA/NSTEMI: predicts all-cause mortality, new/recurrent MI, severe recurrent ischemia requiring urgent revascularization through 14 days
  • GRACE score for UA/NSTEMI: predicts in-hospital mortality and death or MI
  • Risk stratification into ischemia guided, immediate invasive

NSTEMI: Early invasive strategy (within 24 hours) if:

  1. Elevated troponin
  2. Dynamic ST-changes
  3. Recurrent angina
  4. EF <40%
  5. Recent PCI
  6. Prior CABG
  7. DM
  8. Intermediate/high risk score (GRACE >140)

ACS Medications and Anti-Platelet Agents

NTg and PDE5i interaction

  • NTg contraindicated 24 hours of last use of sildenafil (Viagra, Revatio)
  • NTg cointraindicated 48 hours of last use of tadalafil (Cialis)

Coronary Microvascular Dysfunction

  • Coronary flow reserve (CFR) <2.5 indicative of microvascular disease in the absence of obstructive epicardial CAD
  • Treatment: ± beta blockers, CCB but not definitive guideline

Coronary Flow Reserve

  • iFR ≤0.89 or FFR <0.8

STEMI

  • RCA vs. LCX: STE III >II indicates RCA

Spontaneous Coronary Artery Dissection

  • Risk factors: fibromuscular dysplasia (FMD), postpartum status, multiparity, connective tissue disorders, systemic inflammatory conditions, and hormonal therapy
  • FMD screening: screen for extracoronary disease from brain to pelvis with CTA or contrast-enhanced MRA for aneurysms, dissections, and other areas of FMD
  • Renal aneurysms: treat when >2cm
  • Renal stenosis: balloon angioplasty > stenting. Stent reserved for procedural complications (i.e. dissection)


General Cardiology

Guideline Indications

TreatmentIndication
EntrestoHFrEF (≤40%) and NYHA II, III
IvabridineHFrEF (≤35%) at max tolerated dose of bb in SR with HR ≥70bpm
IV iron sucrose or ferric carboxymaltoseNYHA II, III and at least 1 of the following: 1. Ferritin <100 ng/mL2. Ferritin 100-299 ng/mL but iron sat <20%
PatisiranFamilial amyloid neuropathy
ICD, primary prevention1. EF ≤35%, NYHA II, III due to N/ICM
2. EF ≤30%, NYHA I, II, III
CRT indications1. LBBB with QRS ≥150 msec
2. EF ≤35%
3. NYHA II, III or ambulatory type IV
4. Already on GDMT
(LOE A for NYHA class III, IV and LOE B for NYHA class II)

ICD Indications

EFNYHAEtiologyClass Indication
≤35%II-IIIN/ICMI
≤35%INICMIIb
≤30%IICMI
≤40%Inducible VT/VF on EPSICMI
>55%Inducible VT/VF on EPS with extensive scarring on PET/MRIBrugadaIIb
>55%Inducible VT/VF on EPS with extensive scarring on PET/MRISarcoidIIa

Hypertension (HTN)

TypeDefinition
Resistent HTN≥130/80 on 3 meds for ≥ 1 month
Refractory HTNNot adequately controlled on 5 meds
PseudoresistentWhite coat HTN
MaskedNormal in office, high at home

Genetics

MutationAssociated Disease
Lamin A/CSkeletal muscle dystrophies
Notch 1Bicuspid AV, early AV calcification
T-box 5Holt-Oram syndrome (abnormal thumbs, ASD, VSD, HCM, conduction disease)
FBN1Fibrillin-1. 90% AD for Marfan syndrome
COL3A1Collagen- Ehlers-Danlos syndrome

Long QT-Syndromes

SyndromeGeneFunctional EffectAssociationInheritance
LQTS 1KCNQ1⬇️ IKSSwimmingAD; AR, ~30-35%
LQTS 2KCNH2⬇️ IKRStartleAD, ~25-30%
LQTS 3SCN5A⬆️ INASleepAD, ~5-10%
JLNS 1, 2KCNQ1, KCNE1⬇️ IKRDeafnessAR, very rare

Genetic Screening

  • Start with index family member with unknown or uncertain patterns (athletes with LVH or apical hypertrophy)
  • Idiopathic dilated cardiomyopathy without known mutation in family: first degree relatives TTE q3-5 years

Physical Exam

MurmurLesionLocation Best Heard
Fixed split S2ASD 
Single 2nd heart soundTOF 
Absent A2AS 
Absent P2Pulmonary stenosis 
Loud P2pHTN 
Worsens with ValsalvaHOCM (decreased preload) 
Diastolic murmur?Subaortic membrane 
Early systolic clickBicuspid AV (stiff but mobile)Left 2nd IC space, apex
Mid-systolic clickMVPLeft lower sternal border
Diastolic opening snapMS (and diastolic rumble)Left lower sternal border in LLD position

JVD Physical Exam Findings

DiagnosisJVD Finding
Constrictive pericarditisProminent Y descent, ±prominent X descent
TamponadeProminent X descent, absent Y descent
RV infarctionAbsent X and Y descent
VT, CHBVariable size A-waves (‘cannon A-wave’)

Vascular Diseases

Abdominal Aortic Aneurysm (AAA)

Society for Vascular Surgery recommendations, surveillance intervals for asymptomatic AAA:

  1. >2.5 cm but <3.0 cm, rescreen after 10 years
  2. 3.0-3.9, repeat imaging every 3 years
  3. 4.0-4.9, repeat imaging in 12 months
  4. 5.0-5.4, repeat imaging in 6 months

Indications for elective repair of an asymptomatic AAA include:

  1. >2.5 cm but ≤5.5 cm
  2. rapid expansion
  3. AAA associated with peripheral arterial aneurysms or peripheral artery disease.

May-Thurner Syndrome

PathophysiologyAnatomical variant: right common iliac artery overlies and compresses the left common iliac vein against lumbar spine
Risk factorsLeft lower DVT
Scoliosis
Female sex
OCP use or recent pregnancy
Left lower extremity swelling in absence of DVT
Clinical presentationYoung adult woman with left leg swelling and DVT
Diagnostic testMagnetic resonance venography of the pelvis
References
1. Peters M, Syed RK, Katz M, et al. May-Thurner syndrome: a not so uncommon cause of a common condition. Proc (Bayl Univ Med Cent) 2012;25:231-3.
2. Baglin T, Gray E, Greaves M, et al.; British Committee for Standards in Haematology. Clinical guidelines for testing for heritable thrombophilia. Br J Haematol 2010;149:209-20.
3. Society for Vascular Medicine. Five Things Physicians and Patients Should Question (Choosing Wisely website). 2015. Available at: http://www.choosingwisely.org/wp-content/uploads/2015/02/SVM-Choosing-Wisely-List.pdf. Accessed 03/22/2019.
May-Thurner Syndrome

Electrophysiology (EP)

CRT Indications

Antiarrhythmic Medications

*DFT: defibrillator threshold
SyndromeGeneMiscellaneous
ARVCPKP-2Plakophillin-2Intracellular calcium signaling abnormality
ARVCDSPDesmoglein-2Intracellular calcium signaling abnormality
ARVCDSC2Desmocollin-2Intracellular calcium signaling abnormality
ARVCJUPPlakoglobinIntracellular calcium signaling abnormality
MarfanFBN1Fibrillin-1Associated with aortic aneurysm, dissection
Ehlers-DanlosCOL3A1Collagen type 3, a1Associated with aortic aneurysm, dissection
Loeys-DietzTGFB1, 2Transforming growth factorAssociated with aortic aneurysm, dissection
CPVT1RYR-2Ryanodine receptorAD (>70% of cases, intracellular Ca-signaling)
CPVT2CASQ2CalsequestrinAR inheritence
LQTS1KCNQ1K current IKsbb (nadalol > propanalol)
***Associated with SCD while swimming
LQTS2KCNH2K current IKrK-supplementation (IIb rec)
LQTS3SCN5Aalpha-unit of INa±Mexilitine (IIb rec)
GAIN of function mutation
BrugadaSCN5ALOSS of function mutation
Hereditary PAHBMPR-2Bone morphogenic protein receptorAssociated with >70% of inherited pulmonary arterial HTN
DCMLamin A/C± skeletal muscle dystrophy
T-box5Holt-Oram (hand heart, ASD)
Notch 1Bicuspid AV, premature AV calcification
Genetic mutations associated cardiac conditions
Cardiac Genetics Chart

Supraventricular Tachycardia (SVT)

  • Focal AT- ongoing treatment options

Early Afterdepolarization (EAD) and Delayed Afterdepolarization (DAD)

Localizing VT Origin: LVOT vs. RVOT

  • Step 1: V1
    • LBBB: anterior to posterior- RVOT
    • RBBB: posterior to anterior- LVOT
  • Step 2: concordance
    • Positive: originates near base
    • Negative: originates near apex
  • LVOT VT
  • RVOT VT
  • RVOT: later R-wave transition (≥V3)
  • LVOT: earlier R-wave transition, LBBB, inferior axis

Bidirectional Ventricular Tachycardia (aka CPVT or catecholaminergic polymorphic VT)

  • Also known as Familial polymorphic VT
  • Inheritance: RyR2 gene mutation is AD, CASQ2 gene mutation is AR
  • Treatment: Nadolol (non-selective β1 and β2 agonist)
  • Dose: 0.8 mg/kg of nadolol ~ 1 mg/kg of metoprolol SR
  • Flecainide also used (ask EP)
Source: Leren, I., Saberniak, J., Majid, E., Haland, T., Edvardsen, T., & Haugaa, K. (2016). Nadolol decreases the incidence and severity of ventricular arrhythmias during exercise stress testing compared with β1-selective β-blockers in patients with catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm13(2), 433-440. doi: 10.1016/j.hrthm.2015.09.029

2:1 AV Block

AV nodeHPS
Type of BlockMobitz I >> Mobitz IIMobitz II > Mobitz I
Conducted QRSNarrow (unless preexisting BBB)Wide (except intra-His block)
Escape rhythmReliable (narrow QRS)Unreliable (wide QRS)
PR on conducted beatsLongNormal
*Carotid sinus pressure Block worsensBlok improves
*Exercise/atropineImproves blockBlock worsens
Characteristics to identify site of block in 2:1 AVB

Stroke (CVA) Management

Blood Pressure

  1. If tPA used: BP should be lowered <180/110 prior to tPA administration
  2. After tPA: <180/105 for at least 24 hours post-tPA
  3. No tPA: only treat if >220/120
  4. Can treat if no tPA plus other reason to treat (Aortic dissection, pre/eclampsia, unstable CAD, acute HF)

CHA2DS2-VASc

  • 2 points: age ≥ 75 years and history of stroke/TIA/thromboembolism

Contraindications (CI) to tPA

AbsoluteRelative
History of hemorrhagic stroke or stroke unknown originTIA in prior 6 months
CVA within previous 6 monthsOral anticoagulation
CNS neoplasmPregnancy or first post-partum week
Major trauma, surgery, or head injury in past 3 weeksNon-compressible puncture site
Bleeding diathesisTraumatic resuscitation
Active bleedingRefractory HTN (sBP > 180)
Advanced liver disease
Infective endocarditis
Active peptic ulcer

Pulmonary Embolism


Cardiac Oncology

  • Dexrazoxane: prevent anthracycline-induced cardiotoxocity
  • Anthracycline cardiotoxicity: risk if >250mg/m2

Congenital Heart Disease (CHD)

D-Loop Transposition of the Great Arteries (D-TGA)

  • Atrio-ventricular concordance and ventricular arterial discordance
  • 2nd most common cyanotic congenital lesion (#1 is ToF)
  • Associated defects: VSD (~40%), pulmonic stenosis (PS), coronary artery anomalies
  • D-TGA anatomy
  • D-TGA Surgical Corrections
  • D-TGA surgical correction complications
  • Complications of arterial switch
  • Event free survival following atrial switch
  • Apical 4 chamber view showing anterior transposed aortic valve with posterior pulmonary valve behind it

Complications Following D-TGA Surgical Correction: Arterial Switch (Mustard/Senning Procedure)

  1. Arrhythmia: sinus node dysfunction, frequent SVT
  2. Systemic RV: 25% develop heart failure in their 30’s
  3. Tricuspid regurgitation (TR): functional due to annular dilation

Complications Following D-TGA Surgical Correction: Atrial Switch

  1. Supravalvular AS, pulmonic stenosis (AS), PPS (pulmonary artery stenosis)
  2. Coronary stenosis at re-implantation site
  3. Branch pulmonary artery stenosis
  4. Neo-aortic dilation and AI

L-TDA (or congenitally corrected-TGA)

  • Double-discordance (RA to LV to PA, LA to RV to aortia)
  • Non-cyanotic
  • Treat severe TR like severe MR in normal patients
  • Complications: TR, RV dysfunction, CHB (complete heart block)
  • L-TDA (ccTGA)
  • Complications of L-TGA


Biostats

TermDefinitionExample
Relative risk reduction (RRR)Rate in treatment/rate in placebo10%/20%=0.5
Absolute risk reduction (ARR)(Rate in placebo)-(rate in treatment)20%-10%=10% or 0.1
Number needed to treat (NNT)1/(ARR)1/(0.1)=10 so treat 10 patients over 2 years to prevent 1 event
Example: over a 2 year period therapy A has an event rate of 10% and placebo has an event rate of 20%

Echocardiography

Physics

Speed of sound propagation through tissue: 1540 m/s

Mitral Valve Leaflets on TEE

MV Leaflets on TEE

Stress Testing

Duke Treadmill Score= minutes of exercise – (5 x mm of ST-depression) – (4 x anginal index)

  • Anginal index: 0 for no angina, 1 for non-limiting angina, 2 for having to stop exercise due to angina
  • Positive score is good. Possible to get a negative score
  • Score ≤ -11 is high risk (79% survival at 5 years), -10 to +4 is medium risk (95% survival at 5 years) ≥5 is low risk (99% 5 year survival)
  • Consider LHC for high risk patients (≤ -11)

Nuclear Cardiology

Occupational Dose Limits

1 Rem = 0.01 Sv (international standard unit)

LocationRemSv
Whole body (organs)5 Rem0.05 Sv
Skin50 Rem0.5 Sv
Lens of eye15 Rem0.15 Sv
Pregnant workers
(Over gestation period)
500 mRem5 mSv
Fetus
(non-occupational worker)
500 mRem5 mSv
General public100 mRem1 mSv

Shielding

Alpha particles

Particle typeShield requirement
Alpha particlesSheet of paper
Beta particlesPlastic/clothing
Gamma raysInches/feet of concrete or lead

Common artifacts

  • LBBB: anterior septum (occurs least frequently with NM stress)

Abnormal TID (~1.36, exercise ≥1.29) with normal perfusion: special considerations

  1. HTN with LVH
  2. Difference in HR between rest and stress
  3. Technical difficulties in image acquisition

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