My notes on coronary computerized tomography (CT).
Anatomy
Classification of anomalous coronary arteries
Anomalies of:
Origin (>LCX from right coronary sinus most common)
Course
Intrinsic anatomy
Termination
Hemodynamic consequence: non/significant
Coronary fistula
Complete myocardial bridging (>LAD most common)
Association with higher risk of sudden cardiac death (SCD)
Normal Anatomy
A normal CTCA has a highnegative predictive value (98– 100%) for excluding CAD
Indications for CTCA:
Low-to-intermediate risk patients with acute chest pain and non-diagnostic ECG and serum biomarkers
Low-to-intermediate probability of CAD and unable to exercise or with inconclusive functional test results
Malignant Anatomy: associated with chest pain, myocardial ischemia, or sudden cardiac death
RCA arising from left sinus
Left main coronary artery (LMCA) arising from right coronary sinus
LMCA arising from the pulmonary artery
RCA arising from left side- generally better prognosis
Ischemic Cardiomyopathy (ICM)
High risk calcification features associated with higher event rates:
Low attenuation plaque: <30 Hounsfield units
Positive remodeling: lesion with vessel area >10% larger than a proximal normal reference site (remodeling index >1.1)
Napkin-ring sign: low-attenuation core surrounded by a rim-like area of higher attenuation (but less than 130 HU)
Spotty calcification: <3 mm length calcifications comprising <90°
Coronary artery calcium score (CACS) of 0
Asymptomatic, independent of Framingham risk score: very low risk of events (0.10% per year), safety window of at least 5 years
No benefit from aspirin for primary prevention
Patients with abnormal lipid profile but CACS 0 have little benefit from statin
Stable symptomatic patients with low-to-intermediate pretest likelihood of CAD, a CACS 0 can safely exclude flow-limiting coronary disease
Abnormal coronary artery calcium score (CACS)
Symptomatic patients with CACS> 400 are at high risk of events (>2% per year), independent of risk factors and functional tests.
CACS>1000, even if normal stress testing, have significantly higher risk of major adverse events
Coronary Dissection
LAD calcification
CTO of LCX with RCA collaterals in patient with discordant normal SPECT but abnormal ECG stress (2mm ST-depressions) sent for CTCA to evaluate coronary anatomy
A quick reference guide for diagnostic ECG criteria with examples. Will continue to update regularly.
P-Wave Abnormalities
Right atrial enlargement (RAE)
2 things help me remember RAE. First, the normal P-wave on an ECG typically represents the left atrium because the right atrium is typically smaller and it’s electrical current is typically hidden in the left atrium’s electrical signal. Second, the SA node sits in the right atrium. So when the right atrium gets enlarged we start to see it on the ECG. The P-wave gets BIGGER! I think of it similar to what we see in left ventricular hypertrophy. Typically, in a normal QRS complex we only see the left ventricle because it’s size and electrical signal is so much larger than the right atrium (similar to our atria). However, in LVH the left ventricle gets even larger. So the electrical signal it puts out is even bigger too. This is just like what happens in RAE. The right atrium is able to be seen in the P-wave which manifests with TALL P-waves. Thus, the diagnostic criterion are:
Inferior lead P-waves: >2.5 mm in height (tall positive P-wave because the SA node is superior in the heart so the electrical signal in the inferior leads, the direction the electrical impulse goes toward, will be larger in size)
>1.5mm in V1, V2
Clinically can be seen in RVH, COPD, pHTN > CHD >>tricuspid stenosis
Left atrial enlargement (LAE)
Back to our discussion about P-waves. In normal physiology the SA node in the right atrium fires and then the signal has to travel all the way over the left atrium. We already know that on normal ECG’s that the P-wave represents the left atrium. Thus, if the left atrium gets enlarged you will see LONGER P-waves because it will take more time for that signal to reach the entirety of the left atrium. Or at least that’s how I remember it in my head. Thus, for LAE think “1 box deep, 1 box wide”. If you can fit 1 small box inside the negatively deflected P-wave you should be thinking about LAE. The diagnostic criterion are:
Terminal portion V1 > 1mm deep, >40ms duration
Inferior leads: notched P-wave > 120ms
Biatrial enlargement (BAE)
You can also have both diagnostic criterion met for both left and right atrial enlargement. In these cases we simply call it biatrial enlargement. Here’s a quick and dirty reference for atrial enlargement:
Ventricular Hypertrophy
Left Ventricular Hypertrophy (LVH)
There are a LOT of criterion for LVH but the most frequent ones that I use in clinical practice are:
aVL >11 (Sokolow-Lyon ‘stand alone‘ criteria)
Cornell Criteria: R wave in avL + S wave in V3 > 28mm in men/> 20mm in women (Easy way to remember: CorneLL has 2 L’s, aVL has 1 L. Add them together to remember you use lead V3)
Sokolow-Lyon Criteria: S wave in V1 + R wave in V5 or V6 > 35mm
Delayed intrinsicoid deflection in V5, V6 >50ms (interestingly this is the only non-voltage criteria for LVH)
LVH can also have a ‘strain pattern’ with T-wave inversions (TWI) as seen in the ECG below.
Right Ventricular Hypertrophy (RVH)
RAD: mean QRS axis ≥ 100 degrees
Secondary ST-T segment changes (STD, TWI) in right precordial leads
(R/S ratio in V1 > R/S ratio in V5, V6) or (R/S ration in V6 <1) or (R wave > 7mm in V1)
Clinically, Posterior MI can mimic RVH
Factors that favor RVH diagnosis: concomitant RAD, TWI in V1-V2
Factors that favor posterior MI: presence of inferior Q-waves
Combined Ventricular Hypertrophy
Exists when criteria for both isoloated LVH) and RVH are met
Should be suspected when criteria for LVH is present but QRS axis is > 90 degrees or criteria for right atrial enlargement exist
R/S ratio approximately equal to 1 in both V3 and V4 (Kutz-Wachtel phenomenon)
Intraventricular Conduction
Left Bundle Branch Block (LBBB)
QRS ≥120 ms
Terminal S-wave in V1 (late forces of QRS should be negative)
I, aVL, V5, V6: Broad notched or slurred R-wave. Occasional RS pattern in V5, V6 may be attributed to displaced transition of QRS complex)
No Q-waves in I, V5, V6 but in aVL a narrow Q-wave may be present without myocardial pathology
Delayed onset of intrinsicoid deflection >60 ms from beginning of QRS to peak of R-wave in V5, V6 but normal in V1-V3 when small initial R-wave can be discerned
Left Anterior Fascicular Block (LAFB)
LAD (QRS axis between -45 to -90 degrees) and mean QRS duration < 120 ms
qR complexes in I, aVL
rS complexes in II, III, aVF
Prolonged R wave peak time in aVL > 45ms (from beginning of QRS complex to peak of R wave)
*Absence of other causes of marked LAD such as inferior MI or LVH
Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left anterior fascicle supplies fibers to the anterior and lateral walls of the left ventricle. The above criteria of left anterior fascicular block do not apply to patients with congenital heart disease in whom left-axis deviation is present in infancy.
Left Posterior Fascicular Block (LPFB)
RAD (QRS axis 90 to 180 degrees in adults) with mean QRS duration < 120 ms
rS complexes in leads I and aVL
qR complexes in leads II, III and aVF
*Absence of other causes of right axis deviation including lateral MI, dextrocardia, or RVH
Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left posterior fascicle is shorter and thicker than the left anterior, and receives dual blood supply from both the left and right coronary arteries. Multivessel coronary artery disease is the most common cause of left posterior fascicular block.
Right Bundle Branch Block (RBBB)
QRS ≥ 120 ms
V1, V2: RSR’ with secondary R-wave usually wider than initial R-wave
Minority of patients may have a wide and often notched R wave pattern in lead V1 and/or V2
S wave duration > than R wave or > 40 ms in leads I and V6
Normal R peak time in leads V5 and V6 but > 50 ms in lead V1
Of the above criteria, the first 3 should be present to make the diagnosis. When a pure dominant R wave with or without a notch is present in V1, the 4th criteria should be satisfied
Incomplete Right Bundle Branch Block (iRBBB)
Same criteria for RBBB but QRS < 120ms but > 100ms
Non-specific inter-ventricular conduction delay
QRS ≥ 110 ms
Specific criteria for RBBB, LBBB not met
Quick and dirty reference to compare LBBB and RBBB:
Atrial Rhythms
Sinus Rhythm
In medical school we are taught this incorrectly. The correct way to tell that a P-wave is of sinus origin is that they are:
Upright in the inferior leads (remember the sinus node is in the right atrium so the electrical wave will go from the top down and thus be positive inferiorly)
Biphasic in V1
Axis between 0 to 75 degrees (i.e. upright in the inferior leads)
The number of P-waves before every QRS complex is irrelevant. You can have sinus rhythm but be in complete heart block. Or have sinus rhythm but have second degree type I or type II heart block. Generally however they should have the same morphology. A single P-wave with a different morphology can indicate a premature atrial complex (PAC) but if you have multiple different P-wave morphologies then you might be dealing with wandering atrial pacemaker (WAP) or multifocal atrial tachycardia (MAT). I think of WAP and MAT as the same rhythm across a spectrum ranging from a normal heart rate (WAP) to a fast heart rate (MAT).
Sinus Arrhythmia
Diagnostic criteria:
Normal P wave axis (0 to 75 degrees; i.e. upright in leads I and II)
P-P interval varies by > 10% or 0.16 seconds
tl;dr normal sinus P-waves (as above) but P-P interval varies by >10% or 160ms (4 little boxes). ECG intervals can vary with respiration but they shouldn’t vary by more than 10%. Often incidental without major clinical significance
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
Asymptomatic: EF ≤55%
Asymptomatic: EF >55% + LVESD >50mm or LVESDi >25mm/m2
Asymptomatic: EF >55% with progressive decline in EF to low-normal (55-60%) with LVEDd >65mm
Initial evaluation if suspicious for MV disease or MVP
Initial evaluation of known ur suspected MR
Annual evaluation in severe MR
Reevaluation of MR with change in clinical status
TEE to determine mechanism of MR and suitability of valve repair
*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)
MR 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)
MVP
Early, 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
Prosthetic Valves
Prosthetic Aortic Valves
Pressure recovery: due to small aorta causing falsely elevated mean gradient readings and thus low AVA
Louder murmur with Valsalva (decreased preload)Softer murmur with hand grip
High risk features for SCD
1. 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)
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
TIMI risk score for UA/NSTEMI: predicts all-cause mortality, new/recurrent MI, severe recurrent ischemia requiring urgent revascularization through 14 days
FMD screening: screen for extracoronary disease from brain to pelvis with CTA or contrast-enhanced MRA for aneurysms, dissections, and other areas of FMD
HFrEF (≤35%) at max tolerated dose of bb in SR with HR ≥70bpm
IV iron sucrose or ferric carboxymaltose
NYHA II, III and at least 1 of the following: 1. Ferritin <100 ng/mL2. Ferritin 100-299 ng/mL but iron sat <20%
Patisiran
Familial amyloid neuropathy
ICD, primary prevention
1. EF ≤35%, NYHA II, III due to N/ICM 2. EF ≤30%, NYHA I, II, III
CRT indications
1. 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
EF
NYHA
Etiology
Class Indication
≤35%
II-III
N/ICM
I
≤35%
I
NICM
IIb
≤30%
I
ICM
I
≤40%
Inducible VT/VF on EPS
ICM
I
>55%
Inducible VT/VF on EPS with extensive scarring on PET/MRI
Brugada
IIb
>55%
Inducible VT/VF on EPS with extensive scarring on PET/MRI
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
Murmur
Lesion
Location Best Heard
Fixed split S2
ASD
Single 2nd heart sound
TOF
Absent A2
AS
Absent P2
Pulmonary stenosis
Loud P2
pHTN
Worsens with Valsalva
HOCM (decreased preload)
Diastolic murmur?
Subaortic membrane
Early systolic click
Bicuspid AV (stiff but mobile)
Left 2nd IC space, apex
Mid-systolic click
MVP
Left lower sternal border
Diastolic opening snap
MS (and diastolic rumble)
Left lower sternal border in LLD position
JVD Physical Exam Findings
Diagnosis
JVD Finding
Constrictive pericarditis
Prominent Y descent, ±prominent X descent
Tamponade
Prominent X descent, absent Y descent
RV infarction
Absent X and Y descent
VT, CHB
Variable size A-waves (‘cannon A-wave’)
Vascular Diseases
Abdominal Aortic Aneurysm (AAA)
Society for Vascular Surgery recommendations, surveillance intervals for asymptomatic AAA:
>2.5 cm but <3.0 cm, rescreen after 10 years
3.0-3.9, repeat imaging every 3 years
4.0-4.9, repeat imaging in 12 months
5.0-5.4, repeat imaging in 6 months
Indications for elective repair of an asymptomatic AAA include:
>2.5 cm but ≤5.5 cm
rapid expansion
AAA associated with peripheral arterial aneurysms or peripheral artery disease.
May-Thurner Syndrome
Pathophysiology
Anatomical variant: right common iliac artery overlies and compresses the left common iliac vein against lumbar spine
Risk factors
Left lower DVT Scoliosis Female sex OCP use or recent pregnancy Left lower extremity swelling in absence of DVT
Clinical presentation
Young adult woman with left leg swelling and DVT
Diagnostic test
Magnetic 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.
LBBB: anterior septum (occurs least frequently with NM stress)
Abnormal TID (~1.36, exercise ≥1.29) with normal perfusion: special considerations
HTN with LVH
Difference in HR between rest and stress
Technical difficulties in image acquisition
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