High Blood Pressure: the basics

Hypertension, or high blood pressure, increases the amount of work the heart has to do. It’s like going to the gym and lifting heavier weights. Just like when you lift heavier weights at the gym to get bigger biceps, when your heart beats against a higher pressure it compensates by getting thicker. However, this compensatory mechanism can actually weaken the heart over time making it harder to perfuse the heart with blood and over time increases your risk of heart failure, heart attack, and stroke.

Some of my patients tell me, “but I feel fine”. And that’s the thing- high blood pressure is a silent killer. You can have elevated blood pressure for many years and not even ‘feel’ it. That doesn’t mean it can’t cause serious harm and increase your risk of future heart attack or stroke.

Defining Hypertension (high blood pressure)

A ‘normal’ blood pressure is <120/80. That means both the systolic (top number) and diastolic (bottom number) need to be below 120 and 80, respectively. Some people have lower blood pressures and that can be completely normal. The short and skinny of it is that you want your blood pressure less than 120/80.

Below are the different stages of hypertension. How we treat blood pressure depends on your individual circumstances and medical history. It is based on robust data summarized in a the 2017 ACC/AHA (American College of Cardiology/American Heart Association) guidelines.

If you have a normal blood pressure reading (<120/80) that doesn’t mean you’re off the hook. You should still get a yearly blood pressure reading. Sometimes you just hit a certain age where your blood pressure starts to creep up a little bit. This is a good reminder that having high blood pressure, like many things in medicine, is both genetic predisposition as well as some behavioral and lifestyle choices that can impact it. Having high blood pressure doesn’t mean you did anything wrong. Some of my patients are the healthiest individuals I’ve ever met. Except that hypertension runs in their family. We will get into some behavioral and nutritional choices you can make to help bring down your blood pressure in another post.

Elevated blood pressure is 120-129/<80. Notice the different goals for the systolic and diastolic (i.e. top and bottom numbers). Essentially, if your bottom number goes above 80 you are considered hypertensive. But if your diastolic remains <80 but your systolic is 120-129 we generally recommend rechecking your blood pressure in 3-6 months. This doesn’t mean you need medications but it does mean that we want to ensure you don’t develop high blood pressure. It’s also another chance to make some positive lifestyle habits and nutritional choices that can pay off over time. As many of my patients can attest, one of my favorite sayings is that many of the choices we make today can pay off over time. Like building a strong retirement fund with a good interest rate. In contrast, ignoring high blood pressure is like having bad debt. Either way- the interest is going to compound. So it’s always better to know if you have high blood pressure than to ignore it.

Stage 1 hypertension is either a systolic between 130-139 or a diastolic between 80-89. This is where working with your physician is important. In patients at higher risk of heart disease, like those who already have clinical evidence of atherosclerotic cardiovascular disease (i.e. prior stroke, heart attack) we often will initiate both lifestyle modifications and treatment with blood pressure medications. If you are a low risk patient we can consider lifestyle modifications alone and rechecking your blood pressure in a few months. If lifestyle modifications do the trick and bring down your blood pressure we can avoid using medications. But if you are doing all the right things and your blood pressure won’t budge then you likely will require medications to lower your blood pressure. Regardless, patients with stage 1 hypertension should be reassessed in 1 month.

Stage 2 hypertension is either a systolic >140 or a diastolic >90. In these patients we often jump to use medications while also initiating lifestyle modifications because the degree that lifestyle modifications will impact your blood pressure likely won’t be enough. Just like how you wouldn’t ignore a leak under your sink you should also not ignore high blood pressure-both will cause damage over time. This is where talking with your physician is important because not all patients are alike. If you want to avoid using medications I certainly don’t think it’s unreasonable to hold off if you are right on the borderline of stage 1 and stage 2 of hypertension as long as we have a plan in place and you continue to follow up. However, a blood pressure of 142/88 for instance is very different than a blood pressure of 180/100. For latter blood pressure (i.e. 180/100) would likely require initiation of medications right away. All patients with stage 2 hypertension should be also reassessed in 1 month (just like those with stage 1 hypertension).

The more uncontrolled your blood pressure is and the greater the period of time that it remains uncontrolled the greater your risk of heart disease (e.g. heart attack, stroke). Just because you have high blood pressure doesn’t mean you will have a heart attack and just because we treat your high blood pressure doesn’t mean you won’t. It’s all about decreasing that intrinsic risk.

Why you should check your blood pressure at home

In my clinical practice I like when my patients take their blood pressure at home for a few reasons. First, if you’ve ever been to a doctor’s office you know it can be a little anxiety inducing. That’s why I never make drastic changes based on a single blood pressure reading. Some patients can have white coat hypertension– when the blood pressure readings at your doctor’s office are always elevated but when you take them at home they are normal. These patients don’t need to be treated for high blood pressure!

Second, you can only go the doctor’s office so many times. Taking your blood pressure at home gives us additional data points to use to estimate your average blood pressure. Generally, I care the most about the your blood pressure trend. Let’s look at two patients as an example. ‘Patient 1’ consistently gets systolic blood pressure readings in the 140-150’s but occasionally gets a systolic blood pressure of 118. ‘Patient 2’ on the other hand gets consistent systolic blood pressure readings in the 120’s but occasionally gets a systolic blood pressure reading in the 140’s. In both patients I won’t ignore the occasionally high or low reading but I care more about where your blood pressure average tends to be.

How to take your blood pressure at home

Type of blood pressure cuff

Generally, arm cuffs are better than wrist cuffs. However the most important thing is that you use an appropriately sized cuff. Using the wrong size blood pressure cuff can give you falsely high or falsely low readings (shown below).

If you want to be accurate, the American Heart Association recommends a cuff bladder width 40% of the arm circumference and a bladder length 80% of the arm circumference. Use the middle part of your arm to check the circumference (shown below).

How to actually measure your blood pressure

If you don’t like reading I made a short TikTok video explaining how to actually check your blood pressure (shown below). The following tips aren’t to torture you- they are so we get accurate readings. The important things to remember are:

Blood pressure cuff should be bare to skin (not over clothing)
Keep your arm supported (don’t elevate it in the air)
Keep your feet flat on the ground
Don’t cross your legs
30 minutes before taking your blood pressure do not smoke, drink caffeine, or exercise (life hack- take it first thing in the morning before your first cup of coffee or if you smoke before your first cigarette)
You can repeat the reading after waiting 5 minutes. I typically tell patients to take it once in the morning and once in the evening
WRITE DOWN YOUR READINGS IN YOUR PHONE OR NOTE PAD AND BRING THE READINGS TO YOUR NEXT DOCTOR’S VISIT

@marckatzmd
How to accurately take your blood pressure at home #Cardiology #Hypertension #Medicine #MedicineExplained #fyp #PepsiApplePieChallenge
♬ Roxanne – Instrumental – Califa Azul

Don’t forget to bring your readings to your next doctor’s appointment

Every day after work when I leave the hospital I put my hospital identification card in my car. That way I don’t have to remember to take it with me to work the next day. Because believe me there’s nothing worse than getting to work and having to turn around and drive home to pick up your ID badge. Similarly, remove road blocks from bringing your blood pressure readings to your next doctor’s appointment by putting the information directly into your phone. This way you don’t have to remember to bring the notepad you’ve been writing your blood pressure readings in. If you choose to do it the old fashioned way with pen and paper that is perfectly fine. Just remember to bring it to your next visit. Remember to document both the top and bottom number in addition to your heart rate. Lastly, please do not rely on your memory to serve as a blood pressure log. I want to know what blood pressure readings you are getting at home and not just that it was ‘high’ or ‘normal’.

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January 29, 2022April 6, 2022

Coronary CT for Cardiology Fellows

My notes on coronary computerized tomography (CT).

Anatomy

Coronary artery segmentation
Normal coronary course
Normal anatomy on CT
Common anomalous coronary arteries
Common anomalous coronary arteries

Classification of anomalous coronary arteries

Anomalies of:
1. Origin (>LCX from right coronary sinus most common)
2. Course
3. Intrinsic anatomy
4. 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 high negative 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

Right coronary artery originating from the left coronary sinus. RCA in red, Left main coronary artery yellow. The proximal RCA’s acute angle take off passes through the pulmonary trunk and aortic root causing moderate compression.
Myocardial bridging of the mid LAD

Pulmonary trunk level showing LMCA originating from pulmonary artery (red asterisk)
Aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
Again showing aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
Anomalous left coronary from the pulmonary artery (ALPACA or Balnd-White-Garland syndrome). Poor prognosis. Infant type worse as no time for collaterals and die within first year of life without surgical intervention. Adults can develop robust collaterals with giant tortuous vessels

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°

CTA plaque phenotype features
CTA plaque phenotype features
CAD-RADS scoring and modifiers

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

CACS of 0
CACS of 0. Minimal calcium in the aortic root and aortic valve

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

Extensive coronary calcifications (CACS 1832) in 97th age and sex matched percentile. Diffuse in D1 and dRCA, concentric in mRCA, and spotty at ostial LAD and LCX. Very high likelihood of CV events and high likelihood of obstructive CAD.
Bicuspid AV with aortic dilation, and non-obstructive mixed plaque with evidence of positive remodeling

pLAD, mLAD, dLAD in cross section
Obstructive CAD in LAD

Coronary Dissection

Linear low-density intraluminal image suggestive of focal dissection
Moderate ostial RCA stenosis. PRedominantly non-calcified eccentric lesion with low-attenuation core
Moderate ostial RCA stenosis. PRedominantly non-calcified eccentric lesion with low-attenuation core

LAD calcification

Calcified LAD with severe dLAD lesion
Severe focal, eccentric, predominantly non-calcified lesion in mid-to-distal LAD with low attenuation core, positive remodeling, and napkin ring sign

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

Diffuse calcification of D1 and CTO of LCX

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
Symptomatic
Other concurrent cardiac/aortic surgery

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-AS Download

LFLG-AS-when-is-it-severe Download

Bicuspid Aortic Valve

Bicuspid AV algorithm
Frequency of bicuspid anatomy
Bicuspid AV imaging surveillance guidelines

Surgical indications for dilated aortic root/ascending aorta

Aorta size	Indication	Class recomendation
≥ 5.5 cm	Risk factors for dissection (FH, growth rate >0.5cm/year, bicuspid AV)	I
> 5.0 cm	Risk factors and low surgical risk <4% (FH of dissection, growth 3-5mm/year, aortic coarctation, small stature)	IIa
> 5.0 cm	Low risk, experienced surgeon, expert center	IIa
> 4.5 cm	Bicuspid AV planning for surgical AVR for AS/AI	IIa

*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)
Abnormal function of any one of the structures may result in MR
Etiologies of chronic mitral regurgitation (MR)- acute and chronic
Pathophysiology of acute and chronic MR
Qualitative assessment of MR
MR algorithm

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

MR-in-Contemporary-Era_2018_JACC Download

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 (TEER) of severe MR
Semiquantitative parameters in MR
Quantitative measures for severe MR by PISA
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

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)

Non-invasive markers associated with SCD in MVP

Arrhythmic-MVP-Review_-JACC-2018 Download

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

Download

Invasive Hemodynamics Review

Hemodynamics Download

Classic Valvular Murmurs

Lesion	Timing	Quality	Radiation	Severity
AS	Crescendo-decrescendo Gap between S1, murmur, and S2	Harsh, noisy
MR	Holosystolic through S2 Starts with S1 through S2	Blowing, high pitched	Anterior 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 PVC	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

Prosthetic Valve Thrombosis

Urgent-surgery-compared-with-fibrinolytic-therapy-for-the-treatment-of-left-sided-prosthetic-heart-valve-thrombosis-a-systematic-review-and-meta-analysis-of-observational-studies Download

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

Recommendations-for-Evaluation-of-Prosthetic-Valves-With-Echocardiography-and-Doppler-Ultrasound Download

Heart Failure

Non-Ischemic Cardiomyopathy (NICM)

Spectrum-of-Restrictive-and-Infiltrative-Cardiomyopathies-1 Download

Spectrum-of-Restrictive-and-Infiltrative-Cardiomyopathies-2 Download

2022 AHA/ACC/HFSA Guidelines

2022-AHAACCHFSA-Guideline-for-the-Management-of-Heart-Failure-A-Report-of-the-American-College-of-CardiologyAmerican-Heart-Association-Joint-Committee-on-Clinical-Practice-Guidelines-Download

Abnormalities in Hepatic Vein Flow on Doppler

Hepatic-Vein-Flow_JACC-Review-Article Download

Amyloidosis

Diagnostic algorithm for diagnosis of amyloidosis

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

Treatment for ATTR amyloidosis

Cardiac-Amyloidosis-Evolving-Diagnosis-and-Management-A-Scientific-Statement-From-the-American-Heart-Association Download

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 measurable	No	Low
≤2.8 or not measurable	Yes	Intermediate
2.9-3.4	No	Intermediate
2.9-3.4	Yes	High
>3.4	Not required	High

Echo Findings in Pulmonary Hypertension (pHTN)

Ventricles	Pulmonary Artery	IVC, RA
RV/LV basal diameter ratio >1	RVOT acceleration time (AT) <105ms ±midsystolic notching	IVC >21mm, <50% inspiratory collapse with sniff (or <20% with quiet inspiration)
IVS flattening	Early diastolic PI velocity >2.2m/s	RA size >18cm2 at end-systole
	PA diameter >25mm

JACC_Rev0ew_Management-of-PAH_2015 Download

Chagas Cardiomyopathy

Chagas-Cardiomyopathy Download

Hypertrophic Cardiomyopathy (HCM)

Surgical options and complications	Septal myectomy –> LBBB Alcohol septal ablation —> RBBB
Dysopyramide	QT-prolongation
Physical exam maneuvers	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)

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

Managment-HCM Download

Coronary Artery Disease

Guidelines/Review Articles

HTN in CAD Download

ACCAHA-versus-ESC-guidelines-on-DAPT-2018 Download

2021-Chest-Pain-Guidelines Download

2022-non-statin-therapy Download

2021-Hypertriglyceridemia Guidelines Download

Chest Pain Case Report: who needs additional testing beyond ECG and troponin?Download

Triaging Down the 2021 Chest Pain Guidelines: case report review Download

Dissecting Into the 2021 Chest Pain Guidelines: non-cardiac chest pain Download

CABG (coronary artery bypass graft) Guidelines

CABG-guidelines Download

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:

Elevated troponin
Dynamic ST-changes
Recurrent angina
EF <40%
Recent PCI
Prior CABG
DM
Intermediate/high risk score (GRACE >140)

2014-AHAACC-Guideline-for-the-Management-of-Patients-With-Non–ST-Elevation-Acute-Coronary-Syndromes Download

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

Treatment	Indication
Entresto	HFrEF (≤40%) and NYHA II, III
Ivabridine	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	Sarcoid	IIa

CIR.0000000000000548 Download

Hypertension (HTN)

Type	Definition
Resistent HTN	≥130/80 on 3 meds for ≥ 1 month
Refractory HTN	Not adequately controlled on 5 meds
Pseudoresistent	White coat HTN
Masked	Normal in office, high at home

Genetics

Mutation	Associated Disease
Lamin A/C	Skeletal muscle dystrophies
Notch 1	Bicuspid AV, early AV calcification
T-box 5	Holt-Oram syndrome (abnormal thumbs, ASD, VSD, HCM, conduction disease)
FBN1	Fibrillin-1. 90% AD for Marfan syndrome
COL3A1	Collagen- Ehlers-Danlos syndrome

Long QT-Syndromes

Syndrome	Gene	Functional Effect	Association	Inheritance
LQTS 1	KCNQ1	⬇️ I_KS	Swimming	AD; AR, ~30-35%
LQTS 2	KCNH2	⬇️ I_KR	Startle	AD, ~25-30%
LQTS 3	SCN5A	⬆️ I_NA	Sleep	AD, ~5-10%
JLNS 1, 2	KCNQ1, KCNE1	⬇️ I_KR	Deafness	AR, 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

Murmur	Lesion	Location Best Heard
Fixed split S2	ASD
Single 2^nd 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 2^nd 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.

Electrophysiology (EP)

CRT Indications

2018 Guidelines for Bradycardia and Cardiac Conduction Delay

Antiarrhythmic Medications

Syndrome	Gene		Miscellaneous
ARVC	PKP-2	Plakophillin-2	Intracellular calcium signaling abnormality
ARVC	DSP	Desmoglein-2	Intracellular calcium signaling abnormality
ARVC	DSC2	Desmocollin-2	Intracellular calcium signaling abnormality
ARVC	JUP	Plakoglobin	Intracellular calcium signaling abnormality
Marfan	FBN1	Fibrillin-1	Associated with aortic aneurysm, dissection
Ehlers-Danlos	COL3A1	Collagen type 3, a1	Associated with aortic aneurysm, dissection
Loeys-Dietz	TGFB1, 2	Transforming growth factor	Associated with aortic aneurysm, dissection
CPVT1	RYR-2	Ryanodine receptor	AD (>70% of cases, intracellular Ca-signaling)
CPVT2	CASQ2	Calsequestrin	AR inheritence
LQTS1	KCNQ1	K current IKs	bb (nadalol > propanalol) ***Associated with SCD while swimming
LQTS2	KCNH2	K current IKr	K-supplementation (IIb rec)
LQTS3	SCN5A	alpha-unit of INa	±Mexilitine (IIb rec) GAIN of function mutation
Brugada	SCN5A		LOSS of function mutation
Hereditary PAH	BMPR-2	Bone morphogenic protein receptor	Associated with >70% of inherited pulmonary arterial HTN
DCM	Lamin A/C		± skeletal muscle dystrophy
T-box5			Holt-Oram (hand heart, ASD)
Notch 1			Bicuspid AV, premature AV calcification

Genetic mutations associated cardiac conditions

Supraventricular Tachycardia (SVT)

2019-ESC-SVT-Guidelines Download

2015-SVT-Guidelines Download

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

RVOT: later R-wave transition (≥V3)
LVOT: earlier R-wave transition, LBBB, inferior axis

Differentiating-LVOT-RVOT-VT-Origin Download

Management of PPM/ICD Infection

tldr-ICD-device-infection-guidelines Download

2.-Circulation-2010_Update-on-Cardiovascular-Implantable-Electronic-Device-Infections-and-Their-Management Download

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 Rhythm*, 13(2), 433-440. doi: 10.1016/j.hrthm.2015.09.029

2:1 AV Block

	AV node	HPS
Type of Block	Mobitz I >> Mobitz II	Mobitz II > Mobitz I
Conducted QRS	Narrow (unless preexisting BBB)	Wide (except intra-His block)
Escape rhythm	Reliable (narrow QRS)	Unreliable (wide QRS)
PR on conducted beats	Long	Normal
*Carotid sinus pressure	Block worsens	Blok improves
*Exercise/atropine	Improves block	Block worsens

Characteristics to identify site of block in 2:1 AVB

Stroke (CVA) Management

Blood Pressure

If tPA used: BP should be lowered <180/110 prior to tPA administration
After tPA: <180/105 for at least 24 hours post-tPA
No tPA: only treat if >220/120
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

Absolute	Relative
History of hemorrhagic stroke or stroke unknown origin	TIA in prior 6 months
CVA within previous 6 months	Oral anticoagulation
CNS neoplasm	Pregnancy or first post-partum week
Major trauma, surgery, or head injury in past 3 weeks	Non-compressible puncture site
Bleeding diathesis	Traumatic resuscitation
Active bleeding	Refractory HTN (sBP > 180)
	Advanced liver disease
	Infective endocarditis
	Active peptic ulcer

Pulmonary Embolism

Advanced-Management-of-Intermediate-and-High-Risk-Pulmonary-Embolism Download

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)

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

Complications Following D-TGA Surgical Correction: Atrial Switch

Supravalvular AS, pulmonic stenosis (AS), PPS (pulmonary artery stenosis)
Coronary stenosis at re-implantation site
Branch pulmonary artery stenosis
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

Past, present, and future of the arterial switch operation: historical review
Download

Biostats

Term	Definition	Example
Relative risk reduction (RRR)	Rate in treatment/rate in placebo	10%/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

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

Interpretation of SPECT/ CT Myocardial Perfusion Images: Common Artifacts and Quality Control Techniques Download

Occupational Dose Limits

1 Rem = 0.01 Sv (international standard unit)

Location	Rem	Sv
Whole body (organs)	5 Rem	0.05 Sv
Skin	50 Rem	0.5 Sv
Lens of eye	15 Rem	0.15 Sv
Pregnant workers (Over gestation period)	500 mRem	5 mSv
Fetus (non-occupational worker)	500 mRem	5 mSv
General public	100 mRem	1 mSv

Shielding

Alpha particles

Particle type	Shield requirement
Alpha particles	Sheet of paper
Beta particles	Plastic/clothing
Gamma rays	Inches/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

HTN with LVH
Difference in HR between rest and stress
Technical difficulties in image acquisition

November 24, 2020August 7, 2023

Most Commonly Used Tools Cardiologists Use For Palpitations

Palpitations are one of the most common reasons that I see patients in the inpatient and outpatient setting. Palpitations are abnormal the sensation of your heart beating. I explain them briefly in this TikTok video:

@marckatzmd
What are palpitations and other questions explained in greater detail on my 15min YouTube video #Cardiology #MedicalTikTok #Cardiologist #Palpitations
♬ original sound – Marc Katz, M.D.

Depending on the underlying diagnosis they can be completely benign or potentially life-threatening. I go into much greater detail in a much longer separate YouTube video here:

To understand the common tools we use to diagnose and treat palpitations you have to find out how frequently they occur. So let’s review the most common tools cardiologists use to evaluate palpitations.

If they’re happening right now- get an ECG! Sometimes an Apple Watch can even diagnose some abnormal heart rhythms like atrial fibrillation. But if palpitations are not happening when you get the ECG then you will not catch the rhythm. In the inpatient setting we often also use telemetry. This also underpins the importance of talking to patients to evaluate how frequent palpitations occur as different tools can be used for different durations of time. Sometimes even when we diagnose certain abnormal heart rhythms we use the next few tools to quantify the ectopic burden (how many extra beats are there) as this may influence treatment.

Holter Monitor: 24 – 48 hours

Holter monitors are 24-48 hour mini ECG’s, as depicted above. Patients wear them and document when they feel symptoms and we correlate the information we collect from the monitor. This can also help quantify how frequently someone is having a known abnormal heart rhythm to help guide other treatment choices.

ZioPatch Event monitor: 1 – 2 weeks

Event monitors are the next step up in duration. They can be worn for extended period of time, typically for 1-2 weeks. My favorite is the ZioPatch, shown above. It can be worn for weeks at a time (again, typically 1-2) and is small, goes on the chest, and records everything while being worn, and patients can even shower with this device. They click a button on the device to note when symptoms occur and then we go back to see what rhythm was happening at that time when we receive the report. It does not get transmitted in real time. Instead, as shown below, patients actually take it off at home and send it back to the company in the mail who then forward a report to the ordering physician.

The wireless future of medicine | zhiyaobme

Implantable Loop Recorder: up to 3 years

Lastly are implantable loop recorders (ILR). ILRs are less than 2 inches long and quite thin, as depicted below.ILRs are the only monitoring device that is actually implanted under the skin on the chest. They record everything and have up to a 3 year battery life! The ILR automatically records certain fast and slow rhythms but patients can also use an activator to save rhythms if they’re having symptoms. We often use these when the palpitations are infrequent or if we have a high suspicion of an underlying arrhythmia without a documented diagnosis that might change management. For example, I frequently use these in tandem with neurologists in stroke patients in whom we suspect but have not diagnosed atrial fibrillation (AF). If we see AF on an ILR then we would start a blood thinner but sometimes don’t want to treat empirically. The location these are placed is shown below and often can be safely removed.

Just like any test these tools aren’t perfect. First, patients can have palpitations a few days a week but for whatever reason don’t have any symptoms when wearing the monitor. Depending on the clinical scenario sometimes we will redo the test. Second, these monitors should not be ordered unless clearly indicated. If you were to place Holter monitors on 100 random individuals you are certain to find some abnormal heart rhythms that are completely benign. Thus ordering unnecessary cardiac monitoring for patients can lead to unnecessary follow up procedures, testing, and possible harm.

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