In 1877, German anatomist Ludwig Stieda made the early observation of striated muscle fibers extending into the walls of pulmonary veins (PVs), a finding that puzzled early anatomists because veins typically feature smooth muscle. A whopping 121 years passed and clinicians didn’t know what to make of them (Stieda, 1877, as cited in Hassink et al., 2003).

Fast forward to 1998, and Haïssaguerre’s Bordeaux team proved those same fibers fire the beats that trigger atrial fibrillation. This discovery changed the way cardiac sonographers and cardiologists approach cardiac ablations and the Doppler assessment of the pulmonary veins on echocardiography (Haïssaguerre et al., 1998).

Here is the anatomy that made it all possible; most people (about 60% to 70%) have four pulmonary veins with two from each lung. The remaining population may have three or five, which are benign anatomical variations that do not affect health or function.

Standard Pulmonary Vein Anatomy

Each pulmonary vein drains oxygen-rich blood from a specific region of the lungs to the left atrium:

• Right superior pulmonary vein – drains the upper and middle lobes of the right lung.

• Right inferior pulmonary vein – drains the lower lobe of the right lung.

• Left superior pulmonary vein – drains the upper lobe and lingula (“the tongue”) of the left lung.

• Left inferior pulmonary vein – drains the lower lobe of the left lung.

Pulmonary Veins in Atrial Fibrillation and Ablation

Haïssaguerre's Bordeaux team ran a study in 1998 that changed how we treat AFib today. They studied 45 patients with AFib that wasn't responding to medication. Using multiple mapping catheters, they traced exactly where each abnormal heartbeat started. What they found surprised everyone: the ectopic beats weren't coming from the atrium at all. They were firing from inside the pulmonary veins themselves (Haïssaguerre et al., 1998).

The pulmonary veins became the new target overnight.

Atrial fibrillation (AFib) often originates in the pulmonary veins or their junction with the left atrium. Among these, the left superior pulmonary vein is most commonly implicated in triggering arrhythmia.

You just learned the century-long history behind pulmonary veins and atrial fibrillation. But how do we assess the pulmonary veins with echocardiography, and what do the waveforms tell us in significant cases of mitral regurgitation?

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Today, atrial fibrillation is commonly treated with a catheter ablation. This procedure uses heat (radiofrequency) or cold (cryoablation) to create tiny scars around the pulmonary vein ostia in the left atrium, thereby blocking abnormal electrical signals.

The goal of PVI is to reduce AFib symptoms such as palpitations, shortness of breath, and fatigue, especially when medications and other interventions have failed. By electrically isolating the pulmonary veins, the procedure can significantly improve rhythm control and quality of life. But how are these veins assessed with with echo?

Pulmonary Veins in Echocardiography

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Most sonographers wait until the end of the year to scramble for CME credits. We built a program that keeps you on track instead.

Every September, ten new activities are ready for you. Each one blends current guidelines, new research, and real cases, so you are staying sharp, not just staying certified. Complete the activity, pass a short quiz, and your credit is filed to SDMS automatically. No certificate to save or upload yourself.

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— The Echo Journal Team

Initial considerations included the size of the cusps and sinus number, along with adjectives to explain the appearance of the valve. This approach was scattered and concerning for a valvular abnormality that affects about 2% of the general population.

In 2007, the whole approach to evaluating and describing bicuspid aortic valves changed; Dr. Hans-Hinrich Sievers and Dr. Claudia Schmidtke studied 304 surgical specimens over a 5 year period at one clinical site and published their approach in the Journal of Thoracic and Cardiovascular Surgery.

The clinical utility of this discovery provides a reproducible and formalized framework. Whether you are a cardiac sonographer or a cardiovascular surgeon, this language is universally understood to plan for valve assessment, replacement, and repair.

With the evolution of transcatheter aortic valve replacement (TAVR), explanation of raphe calcification and annular geometry is increasingly important for clinical teams for proper device selection and research on procedural outcomes.

So how did this research in Germany manifest across the world? Let’s dive in…

Key Considerations

These three characteristics are evaluated as part of the Sievers classification system across multiple cardiovascular imaging modalities.

1. The spatial position of the raphes

2. The number of raphes

3. The functional status of the valve

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The Three Types of Bicuspid Aortic Valve: Sievers Classification

The Sievers classification remains the standard system for describing bicuspid aortic valve (BAV) morphology. Sievers and Schmidtke’s conclusions outlined the following types of BAV in a more organized approach for sonographers, physicians, and other allied healthcare professionals in the continuum of care.

Type 0 — No Raphe
A true bicuspid valve with two functional cusps and no raphe. This is the least common morphology, present in 7% of specimens Sievers assessed (Sievers and Schmidtke; Scalia).

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Tomorrow at 11am EST, our CME program officially opens! Ten new activities, built around current guidelines, new research, and real cases, ready for you to complete from home on your own schedule.

Pass the quiz, and your credit is filed to SDMS automatically. No certificate to save or upload yourself, and no more scrambling for credits at the end of the year.

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Happy echoing!

-The Echo Journal Team

Up to 90% of cardiac sonographers develop a work-related musculoskeletal disorder, and it can start within your first six months.

One in five sonographers who develop symptoms end up with a career-ending injury.

In this article, you’ll learn the setup, grip, and recovery habits the ASE recommends to protect your neck, shoulders, and wrists while scanning, plus the early warning signs you should never wave off as “just part of the job.” You’ll also get language for the conversation with your department when the real problem is the schedule, not your technique.

Introduction

A work-related musculoskeletal disorder, or WRMSD, is an injury to the muscles, tendons, nerves, or joints caused by the physical demands of your job, not a single accident. For cardiac sonographers, that means prolonged transducer pressure, repetitive motion, and sustained postures every single study.

Per the ASE’s newly published guideline, WRMSDs affect up to 90% of cardiovascular sonographers during their careers. Symptom rates start at 15% within six months on the job, climbing to 45% by three years and 72% by ten. This isn’t a retirement-age problem. It starts almost immediately.

It’s not just personal, either. Sonographer injury shrinks lab capacity and adds to an already strained workforce. The ASE now frames WRMSD prevention as shared responsibility, but this article focuses on what’s in your hands: protecting your body, and knowing when the problem is bigger than your technique.

Fix Your Setup Before You Touch the Probe

Most strain starts with distance, not effort. Reaching, not scanning itself, is what loads the shoulder and spine. Before each exam, work through your setup in this order:

• Bring everything close. Patient, table, and system positioned as close together as possible, minimizing reach in every direction.

• Adjust your chair first. Forearms roughly horizontal with elbows near 90 degrees, feet flat on the floor or a footrest, knees roughly level with your hips.

• Recline slightly. About 10 to 20 degrees back, with the seatback supporting your lower back, keeps your spine neutral instead of rounding forward.

• Position the monitor at or slightly below eye level, at least 24 inches away, with a slight backward tilt, so your neck stays neutral instead of craned or rotated.

• Keep your scanning arm relaxed and close to your body, shoulder neutral. When extended reach can’t be avoided, use an arm support or bolster to carry that load instead of your shoulder.

Common Positioning Mistakes to Avoid

The ASE guideline calls out four setup errors that show up in almost every ergonomic assessment:

• Patient positioned too far away. Forces forward trunk flexion, shoulder abduction beyond 30 degrees, and misaligned hips.

• Monitor too high or off to the side. Causes neck craning, extension, and head rotation, even when the rest of your body is positioned well.

• Controls or keyboard out of reach. Leads to overreaching and extended wrists, often while your trunk is already flexed forward.

• Sitting too low relative to the table. Puts your wrists into extension and rounds your shoulders and back to compensate.

Optimal positioning fixes all four at once: upright seated posture, minimal reach in any direction, and the monitor aligned at eye level. If you catch yourself twisting, craning, or reaching mid-study, treat that as a cue to stop and readjust rather than push through it.

Fix Your Grip

A common novice error is wrapping the fingers fully around the transducer handle, like gripping a hammer. It feels stable, but it locks the wrist into a strained position that the ASE specifically flags as a WRMSD contributor.

The recommended technique, called the standard grip, holds the probe lightly with the fingertips and thumb opposing the fingers. This preserves dexterity and keeps the wrist neutral in most imaging windows.

A few windows call for a modified grip:

• Subcostal views typically use an overhand grip, with the index finger pressing the top of the probe for downward pressure.

• Apical views in left-handed sonographers often require an underhand grip, flipping the probe in the hand.

• Parasternal and suprasternal views generally keep the standard grip regardless of handedness.

Handedness Isn’t Fixed

Only about 10% of people are left-handed, but left-handed scanning has a real ergonomic upside: it keeps you closer to the chest wall and reduces forward reach. The tradeoff is more shoulder abduction, which raises rotator cuff risk.

Right-handed scanning means reaching across the patient’s torso, which often forces trunk flexion and wrist flexion, especially with larger patients.

The ASE guideline names ambidextrous scanning as a legitimate long-term strategy. It distributes load across both arms and protects your ability to keep working if one arm gets injured. It takes deliberate practice to build, and most sonographers never train for it, but it’s worth knowing it’s an option, not just a party trick.

Build Recovery Into Your Day

None of the setup advice above works if you never get a break from it. The ASE recommends:

• Microbreaks during exams. Even briefly releasing the transducer and relaxing your hand reduces sustained muscle contraction.

• A daily warm-up and midshift stretch, 3 to 5 minutes, targeting the upper body.

• Regular strength training, which supports spinal stability and reduces susceptibility to strain injury.

• At least 30 minutes of moderate activity most days of the week.

These don’t replace good ergonomics. They’re what makes good ergonomics sustainable over a 20 or 30 year career instead of a 5 year one. Want the specific stretches and routine? We built the complete guide in the link below.

The ASE guideline is direct about this: these symptoms are routinely normalized as “part of the job,” which delays intervention until the injury is harder to reverse. Report early. Get evaluated early. It’s the single highest-leverage thing you can do for your own longevity in this field.

When the Problem Isn’t Your Technique

Good ergonomics only goes so far when the schedule itself is the hazard, and that part isn’t on you to fix alone.

Here’s the gap worth knowing: the Intersocietal Accreditation Commission requires a minimum annual study volume to maintain accreditation, but it sets no maximum daily workload. That ceiling, if it exists at all, is set locally, by your department.

The ASE guideline also names portable and inpatient studies as higher ergonomic risk than lab-based exams, due to immobile beds, poor acoustic windows, and no room to adjust equipment. It explicitly recommends institutions minimize non-essential portable imaging when patients are stable enough to come to the lab instead.

If your week is stacked with back-to-back portables and no built-in recovery time, that’s not a personal failing. It’s a scheduling problem the ASE guideline names directly, and it’s a reasonable thing to raise.

If you do raise it, you don’t have to argue from how you feel alone. The guideline puts a number on the tradeoff: a single WRMSD injury costs an institution between $28,000 and $54,000 in direct and indirect costs, with severe cases exceeding $700,000. Compare that to $800 to $2,500 for an ergonomic scanning chair, or $4,000 to $12,000 for a height-adjustable exam table. That’s the math to bring into the room, not just the fatigue.

Key Takeaways

• WRMSDs affect up to 90% of cardiac sonographers, with symptom rates of 15% by six months, 45% by three years, and 72% by ten years on the job

• One in five sonographers who develop symptoms suffer a career-ending injury

• Minimize reach by keeping patient, table, and system close together, adjust your chair first, and keep elbows near 90 degrees with a neutral shoulder

• Watch for the four common setup mistakes: patient too far away, monitor too high, controls out of reach, and sitting too low

• Use a fingertip grip with opposing thumb, not a full-hand “hammer grip,” to protect the wrist

• Ambidextrous scanning is a legitimate long-term strategy for distributing strain and protecting career longevity

• Build microbreaks, daily warm-ups, and regular strength and cardio training into your routine

• Report early symptoms (tingling, reduced grip strength, recurring pain) instead of normalizing them

• Workload and scheduling are named risk factors, not a personal failing. Portable and inpatient studies carry higher risk, and there’s no accreditation-mandated daily maximum

• A single WRMSD injury can cost $28,000 to $54,000 or more, versus a few thousand dollars for ergonomic equipment. That’s useful context for a conversation with your department

References

Davis, Ashlee, et al. “Guidelines for the Prevention of Work-Related Musculoskeletal Disorders for Cardiac Sonographers: Recommendations from the American Society of Echocardiography.” Journal of the American Society of Echocardiography, vol. 39, no. 8, Aug. 2026, pp. 699-716, https://doi.org/10.1016/j.echo.2026.04.018.

Pike, Ian, et al. “The Prevalence of Musculoskeletal Disorders Among Diagnostic Medical Sonographers.” Journal of Diagnostic Medical Sonography, vol. 13, no. 5, 1997, pp. 219-227, https://doi.org/10.1177/875647939701300501.

This publication is for educational purposes only and does not constitute medical advice. By subscribing, you agree to our Terms of Use, Privacy Policy, and Disclaimer.

A year-long Mayo Clinic study just tested whether daily stretching actually helps, and tracked exactly what it did and didn’t change.

Upper extremity disability scores were roughly cut in half. Low back pain told a messier story.

This week: the real results of that study, the specific 15-minute routine it tested, a faster 5-minute alternative for the days you can’t spare that, and where the evidence draws a hard line on what stretching can’t do for you.

Your body responds to a system: your setup, your workload, and your recovery. This is the recovery piece. Here's what pulling on that one lever did, on its own, over a full year.

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Mitral valve prolapse (MVP) and mitral valve flail sit on the same spectrum of degenerative mitral disease, and reports use the two terms interchangeably more often than they should. The 2D imaging planes, probe movements, and the measurements taken help determine which abnormality we are actually dealing with.

This issue covers the imaging planes where the diagnosis is actually valid, the key features that separate the two at the bedside, and the color Doppler trap that talks clinical teams out of severe mitral regurgitation.

Introduction

Mitral valve prolapse is an issue with tissue, catchy right? The leaflet body or tips displace more than 2 mm past the mitral annular plane during systole but the leaflets still meet. A background of myxomatous or fibroelastic changes are common in MVP.

A flail mitral valve is a mechanical failure. The subvalvular apparatus gives way, the leaflet tip reverses and points into the left atrium, and coaptation is lost at the affected segment.

That distinction matters most at the bedside. Ling and colleagues followed 229 Mayo Clinic patients with isolated mitral regurgitation from a flail mitral leaflet and found excess mortality and high morbidity even under medical management, with surgery nearly unavoidable within ten years of diagnosis.

The posterior mitral leaflet was involved in 187 of those 229 patients, so you should know how to scrutinize the posterior leaflet. Calling a flail leaflet prolapse in your report is an error you don’t want to make and directly affects the referral pathway.

Echo Evaluation

Get the imaging plane right before you call anything

The 2 mm criterion applies to the parasternal long axis and the apical long axis only. The mitral annulus is saddle shaped, and its lowest points sit anterolaterally and posteromedially, which is exactly where the apical four chamber view cuts through it. On TTE, the parasternal long axis is the gold standard view.

Normal leaflets can appear to cross the annular plane in the four chamber view. This is pseudoprolapse, and it is the most common false positive in the field. The ASE comprehensive transthoracic examination guideline defines these planes precisely, and following them is not optional here.

Watch the leaflet tip, not the leaflet body

Here is where I slow down.

In prolapse the leaflet body bulges up toward the atrium, but follow it out to the very tip and you’ll see the tip is still angling toward the ventricle, still touching its partner. That contact point is the whole thing.

Flail is the opposite. The tip itself flips up and points back into the atrium, and the leaflets stop touching at that segment entirely.

The part nobody tells you in school is that you cannot always reliably see this in real time, especially when images are suboptimal or the patient has tachycardia. At 90-120 beats a minute the tip does its thing in about two frames.

Freeze the various loops and scroll through systole one frame at a time; you can even snap a still frame image when it is clear and in view.

I’ve talked myself out of a flail more than once by watching it play at normal speed and deciding it looked like a significant prolapse.

Hunt for the ruptured chord

A ruptured chord appears as a thin, highly mobile linear echodensity whipping into the left atrium, still tethered to the flail segment. It is a short-lived target on the screen, so set the machine up for it before you go looking.

• Narrow the sector and reduce depth to boost frame rate

• Set the focus at or just below the area of interest

• Sweep off axis through multiple views rather than holding one clean plane

The finding is considerably easier to appreciate on transesophageal imaging. The more you can define on TTE, though, the better coordinated the downstream care plan.

Localize the segment

Sweep the parasternal long axis from medial to lateral, take the short axis at the mitral leaflet level, and rotate through the apical views.

P2 is the most common flail segment, but the surgeon plans the repair around which scallop failed. A report that says “flail posterior leaflet” is less useful than one that says “suspected flail P2.”

Read the jet direction as an anatomic clue

Flail drives the jet away from the affected leaflet. A flail posterior leaflet produces an anteriorly directed jet that hugs the anterior atrial wall. A flail anterior leaflet produces a posteriorly directed jet.

If the jet direction and the segment you identified do not agree, one of the two is wrong. Go back and resolve it before the study leaves your station.

The habit that costs you the grade

Wall-impinging jets look smaller than they are. An eccentric jet that hugs the atrial wall loses energy and pulls less surrounding blood than a free central jet of identical severity, so color jet area systematically underestimates it. ASE lists flail leaflet as a specific sign of severe mitral regurgitation, which means your pretest probability is already high. Do not let a small-looking color jet talk you out of it.

Quantify anyway

Vena contracta width, PISA-derived effective regurgitant orifice area, and regurgitant volume are what carry the grade. Systolic flow reversal in the pulmonary veins is a strong supportive sign of severe regurgitation, and unlike color area it is not fooled by jet eccentricity.

One caution on PISA: the method assumes a hemispherical flow convergence zone, and an eccentric wall-constrained jet violates that assumption. Treat a single PISA number with appropriate suspicion and integrate parameters rather than trusting one.

Finish with the chamber evidence

Size the left ventricle and assess systolic function. Dilation with eccentric hypertrophy points to chronic volume overload and compensation, while a normal-sized, hyperdynamic ventricle suggests an acute event. Bear in mind that a normal EF in chronic MR may already reflect impaired contractility.

Then measure the left atrium: chronic regurgitation dilates it over time, whereas an acute jet meets a small, non-compliant chamber and drives pressure straight back into the pulmonary circulation.

Finally, look to the right heart. Assess right atrial area, right ventricular size and systolic function, and estimate pulmonary pressures: chronic pressure transmission remodels the right heart, but in acute severe MR pulmonary pressures may be markedly elevated before the right ventricle has had time to dilate.

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Key Takeaways

• Apply the 2 mm criterion in the parasternal or apical long axis only. Four chamber pseudoprolapse is the most common false positive in the field.

• Tip direction separates prolapse from flail. Frame-step through end systole instead of judging on real-time playback.

• Set up for the ruptured chord before you hunt for it: narrow sector, reduced depth, focus at the level of interest, off-axis sweeps.

• Name the scallop, not just the leaflet. The surgeon plans the repair around which segment failed.

• Jet direction points away from the flail segment. Use it to cross-check your anatomy before you finish the study.

• Wall-impinging jets underestimate severity on color area. Quantify with vena contracta, EROA, regurgitant volume, and pulmonary venous flow.

• Chamber size tells you the timeline. Dilated chambers mean chronic, small and hyperdynamic means acute.

References

Ling, Lieng H., et al. “Clinical Outcome of Mitral Regurgitation Due to Flail Leaflet.” New England Journal of Medicine, vol. 335, no. 19, 1996, pp. 1417–1423. DOI:10.1056/NEJM199611073351902.

Mitchell, Carol, et al. “Guidelines for Performing a Comprehensive Transthoracic Echocardiographic Examination in Adults: Recommendations from the American Society of Echocardiography.” Journal of the American Society of Echocardiography, vol. 32, no. 1, 2019, pp. 1–64. DOI:10.1016/j.echo.2018.06.004.

Zoghbi, William A., et al. “Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation.” Journal of the American Society of Echocardiography, vol. 30, no. 4, 2017, pp. 303–371. DOI:10.1016/j.echo.2017.01.007.

This publication is for educational purposes only and does not constitute medical advice. By subscribing, you agree to our Terms of Use, Privacy Policy, and Disclaimer.

The parasternal long axis view is our first look at cardiac structures and, oftentimes, we are multitasking at this stage of the protocol (i.e. explaining the exam to the patient, asking questions about their symptoms, and making small talk to ensure they are comfortable).

Gross biventricular function appeared unremarkable on 2D at the start of this exam and there was no evidence of pericardial effusion, calcific valves, or prolapse. Our guard was down and we start to get into ~flow state~ before things take a turn.

This echocardiogram was ordered for PVCs, which affects 3-20% of the general population, according to an article posted by the American Journal of Medicine in 2022 (Klewer et al, 2022).

We often assume a normal echocardiogram study when we see “PVCs”, right? Well… we were wrong this time.

A zoomed view of the mitral valve with a sweeping probe motion caught this on 2D before color Doppler was even used.

Here is the thing about this referral indication: “PVCs”

This is an electrophysiological abnormality that was confirmed by electrocardiogram. An echocardiogram was then ordered to assess any mechanical abnormalities that may be contributing.

Echocardiogram protocols exist for this very reason; cardiac sonographers can make mistakes because we are human (hopefully). Images are systematized for the sonographer and the interpreting physician.

A baseline protocol is established based on site-specific preferences and each abnormality that is seen will require a different subset of images for accurate quantification.

This abnormality was recognized early in the protocol resulting in a consistent and complete evaluation of structure, function, and flow.

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The maneuver most likely to catch it isn’t the one you were trained on first, it came out of a 2019 drug shortage.

And for patients who can’t safely stand, a gentler version catches what Valsalva alone would miss entirely.

Introduction

For the full workup on LVOT obstruction, views, spectral Doppler, gradient interpretation, see “Mastering LVOT Obstruction Assessment: A Step-by-Step Approach.” This piece is narrower: two provocative maneuvers you can add to that workup tomorrow, and how to pick the right one for your patient.

Squat-to-Stand: For Patients Who Can Do It

Valsalva has long been the default way to provoke a hidden gradient. But it’s effort-dependent and hard to standardize. Even a goal-directed protocol leaves a lot up to the patient, according to a 2018 study in the Journal of the American Society of Echocardiography. When amyl nitrite became scarce nationwide in 2019, Mayo Clinic’s echo lab needed a physiologic alternative. What they landed on outperformed Valsalva:

1. Obtain the resting LVOT velocity/gradient first.

2. Have the patient squat, allowing preload to increase.

3. Then have them rapidly stand.

4. You won’t be able to keep the transducer on the chest through that transition, so let it go and get back to the apical five-chamber view as fast as possible once they’re upright.

5. If the first attempt is technically inadequate or does not produce a clear response, repeat the maneuver rather than treating the first attempt as definitive.

6. Record the highest reproducible LVOT velocity/gradient associated with the maneuver.

Repeat as needed to get a technically adequate, reproducible peak gradient.

Squatting increases both preload and afterload, which tends to shrink or erase the gradient. Standing reverses both abruptly, and that combination is exactly what provokes obstruction, according to a 2012 review in Advances in Physiology Education.

A 2022 Mayo Clinic study put numbers to that difference:

• Latent obstruction: 36.1% with squat-to-stand versus 18.3% with Valsalva

• Severe latent obstruction: 25.2% versus 2.8%

• Median provoked gradient: 55 mmHg versus 29 mmHg

Sitting Maneuver: For Patients Who Can’t

Repetitive squatting isn’t realistic for a lot of your patients: balance issues, fall risk, and joint limitations, especially in an older population. A 2023 study in the Journal of Cardiology tested a gentler alternative built for exactly this group. After your routine resting images, have the patient move straight from supine or left lateral decubitus into an upright sitting position, no standing required. Capture the Doppler trace once they’re upright.

That study evaluated 33 non-HCM patients, average age 74:

• 61% had latent obstruction, defined there as a provoked gradient of 30 mmHg or higher

• 75% of those cases were caught only by the sitting maneuver, Valsalva missed them entirely

That 30 mmHg figure is a diagnostic cutoff for latent obstruction, not the same as the treatment threshold below.

Why It’s Worth Doing Tomorrow

A resting or provoked gradient of 50 mmHg or higher is the threshold that shifts the conversation toward septal reduction therapy in symptomatic patients, per the 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline. Whichever maneuver fits your patient, standing or sitting, don’t let Valsalva alone be the reason that gradient goes undetected.

Key Takeaways

• Squat-to-stand outperforms Valsalva for unmasking latent and severe LVOT obstruction, but requires the patient to squat and stand safely

• Get the resting gradient first, then squat, then stand rapidly. You’ll lose transducer contact during the transition, so reacquire the apical window fast and record the highest reproducible gradient

• For patients who can’t stand safely, the sitting maneuver (supine or decubitus straight to upright sitting) is a validated, better-tolerated alternative, and outperformed Valsalva in an older cohort

• A provoked gradient at or above 50 mmHg changes the clinical conversation, don’t let technique or patient mobility be the reason it goes undetected

References

Kumar, Suwen, et al. “Standardized Goal-Directed Valsalva Maneuver for Assessment of Inducible Left Ventricular Outflow Tract Obstruction in Hypertrophic Cardiomyopathy.” Journal of the American Society of Echocardiography, vol. 31, no. 7, 2018, pp. 791-798. doi:10.1016/j.echo.2018.01.022.

Ommen, Steve R., et al. “2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy.” Journal of the American College of Cardiology, vol. 83, no. 23, 2024, pp. 2324-2405. doi:10.1016/j.jacc.2024.02.014.

Peng, Lillian T., et al. “Repetitive Squat-to-Stand Provocation of Dynamic Left Ventricular Outflow Tract Obstruction in Hypertrophic Cardiomyopathy.” Journal of the American Society of Echocardiography, vol. 35, no. 3, 2022, pp. 323-326. doi:10.1016/j.echo.2021.10.016.

Salazar, Sergio A., et al. “On Systolic Murmurs and Cardiovascular Physiological Maneuvers.” Advances in Physiology Education, vol. 36, no. 4, 2012, pp. 251-256. doi:10.1152/advan.00128.2011.

Sekine, Ayako, et al. “Sitting Maneuver to Uncover Latent Left Ventricular Outflow Tract Obstruction in Patients Without Hypertrophic Cardiomyopathy.” Journal of Cardiology, vol. 83, no. 6, 2024, pp. 401-406. doi:10.1016/j.jjcc.2023.11.006.

This publication is for educational purposes only and does not constitute medical advice. By subscribing, you agree to our Terms of Use, Privacy Policy, and Disclaimer.

But a few millimeters of separation on echo can turn a routine report into a red flag for sudden cardiac death.

It has its own name, its own Doppler signature, and a nickname borrowed from a 19th-century military helmet.

In this article you will learn to identify mitral annular disjunction, measure it correctly, and recognize the imaging markers, including the Pickelhaube sign, that separate a benign variant from genuine arrhythmic risk. By the end, you will know when to look twice.

Introduction

Mitral annular disjunction (MAD) is a separation between the hinge point of the posterior mitral leaflet and the top of the left ventricular myocardium. Normally these structures are fused. In MAD, the atrial wall and leaflet attach several millimeters above the true annulus, leaving a gap that is most visible in systole.

Two phenotypes matter:

• True-MAD: atrial displacement of the posterior leaflet in both diastole and systole

• Pseudo-MAD: apparent displacement in systole only, and the more common of the two

Take a look at the example below. Can you tell which phenotype is being shown before you keep reading?

How often MAD shows up depends heavily on what you are looking with:

• General population: pooled prevalence of 8.7%

• MVP or Barlow’s disease: pooled prevalence of 30.1%

• Structurally normal hearts on CT: disjunction seen in 96%, median height just 3 mm

That last number is not a sign that everyone has pathologic MAD. Small, localized disjunction is a common anatomic variant. What actually tracks with arrhythmia is larger disjunction that wraps around the P2 scallop and coexists with myxomatous MVP.

Most patients with MAD are asymptomatic and found incidentally during a routine MVP workup. A minority present with palpitations, presyncope, or ventricular arrhythmia. In severe cases, MAD has been identified at autopsy in young, otherwise healthy patients after sudden cardiac arrest.

Echocardiography is the first-line imaging tool for any patient with known or suspected MVP, which makes it your first opportunity to catch MAD. It is less sensitive than cardiac MRI, but it is fast, available, and can be paired with tissue Doppler to pick up the arrhythmic risk markers described later in this article.

Echo Evaluation

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Your CME cycle ends this year and you’re short. Again.

So you go find credits. The cheapest ones that count. A module here, a lecture there, or a talk from someone who hasn’t held a probe in fifteen years. You click through it at 9pm, pass the quiz, and save the certificate somewhere on your desktop.

It counted, but you didn’t learn anything.

That’s the problem. Not the credits… the time. After a full day of scanning, nobody has an evening left for CME that doesn’t teach them anything.

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That answer lives in anatomy, not in a pressure half-time measurement.

In this lesson, you will walk the aortic valve from annulus to sinotubular junction, map every mechanism of AR onto the classification surgeons actually use, and learn why an eccentric jet hugging the anterior mitral leaflet is telling you something a central jet never will.

Trace-to-mild aortic regurgitation can be found in up to 15% of routine echocardiograms, the sonographer’s role transitions from simple detection to strategic quantification.

Accurate identification of the 0.5% who progress to moderate-to-severe AR is a clinical imperative, given that untreated severe AR more than doubles a patient’s mortality risk.

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Introduction

The aortic valve is made of three semilunar cusps attached to the aortic wall, and those attachments form part of the sinuses of Valsalva. The highest points of attachment at the commissures define the sinotubular junction. The lowest point of attachment where the aortic leaflets dip into the left ventricular outflow tract is called the nadir of the cusps, defining the annular plane.

The coaptation zone of the leaflets, called the lunulae, is fairly uniform in thickness. The exception is a slightly more fibrous area at the anatomic midpoint of each cusp known as the nodules of Arantius. On echocardiography, this portion of the leaflet can appear more echogenic even though it is normal.

Here is the concept that makes everything downstream easier: the aortic valve is a functional unit, not three isolated flaps. Annulus, cusps, sinuses, and sinotubular junction work together. Dilate any one of them and coaptation fails, even when the cusps themselves are perfectly normal.

Where Aortic Regurgitation Comes From

Given that anatomy, AR results from disease of the aortic leaflets, the aortic root, or both, in each case producing valve malcoaptation. The 2017 ASE recommendations for evaluating native valvular regurgitation organize the causes this way.

Bicuspid valves deserve a separate mention because you will see them constantly. All combinations of conjoined cusps can be identified on TTE, and visualizing the raphe is the key to classifying the type. Because stress is concentrated on the typically larger conjoined cusp, these valves can become stenotic, regurgitant, or both. AR may also appear secondary to the associated aortic dilatation rather than from the cusps at all. ASE reports TTE sensitivity up to 92 percent and specificity up to 96 percent for detecting bicuspid anatomy.

The Repair-Oriented Classification

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The left ventricle compensates for years, then stops, and the difference between those two states shows up on your images long before it shows up in the patient.

Image acquisition is where most of our training goes, and it should be. But it means we rarely learn how our role changes across the stages of a disease, or how that changes outcomes.

Today we’re connecting the echo findings to the disease course, so you can scan, report, and explain AR with more precision to your colleagues and patients.

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Chronic Aortic Regurgitation

When there is retrograde flow of blood from the ascending aorta back into the left ventricle, the ventricle gets confused due to the additional volume that it was trying to pump out.

Mild aortic regurgitation may never upset the left ventricle, but when severity approaches moderate and severe ranges, the effects are monitored and quantified (meaning with numbers), with echocardiography.

As the volume of aortic regurgitation increases, the left ventricular preload increases. Well, what is preload? It is, the force (volume of blood) applied to a system (the left ventricle) before its primary operation (systolic ejection).

The left ventricle is filling with the normal volume from the left atrium + the volume from aortic regurgitation = increase in end-diastolic volume.

Need to Know: The Frank-Starling law states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end-diastolic volume), when all other factors remain constant.

The ventricle eventually dilates and thickens, and that added compliance lets it hold the extra volume without raising filling pressures. This is why chronic aortic regurgitation stays quiet for years.

Eventually wall stress outruns the hypertrophy compensating for it. Contractility falls, ejection fraction drops, and LVEDP rises, leading to heart failure symptoms. The graphic below displays a compensated LV (successfully managing stress by changing shape).

This is why ejection fraction is a lagging indicator and LVESD (left ventricular end-systolic dimension) is often looked at in cases of aortic regurgitation.

Recognizing Heart Failure

Heart failure means the heart can no longer move enough blood to meet the body’s demands. Onset is usually gradual, though it can come on abruptly.

Watch for:

• Breathing: dyspnea on exertion or when supine, wheezing, and a persistent cough (sometimes productive of white or blood-tinged sputum)

• Fluid retention: swelling in the legs, ankles, feet, or abdomen, plus sudden weight gain

• Circulatory strain: fatigue, weakness, reduced exercise tolerance, and palpitations or an irregular rhythm

Acute Aortic Regurgitation

Acute aortic regurgitation is a cardiovascular emergency characterized by sudden left ventricular volume overload, most commonly caused by infective endocarditis, acute aortic dissection, blunt chest trauma, or iatrogenic injury such as complications from a transcatheter aortic valve replacement (TAVR).

The Cascade of Acute AR

1. Sudden aortic regurgitant volume into a normal-sized left ventricle: no time for remodeling, so LV dimensions are normal or mildly increased.

2. LVEDP rises rapidly. The pressure-volume curve is steep because the ventricle has not dilated to accommodate. LVEDP = diastolic BP − 4(AR end-diastolic velocity)²

3. Aortic and LV diastolic pressures equalize early. On CW Doppler the AR signal shows a steep deceleration slope and a short pressure half-time, typically under 200ms. The jet may not occupy all of diastole.

4. Premature mitral valve closure. M-mode across the mitral valve shows leaflet closure before the onset of QRS. This is the classic acute sign and it correlates with markedly elevated LVEDP.

5. Diastolic mitral regurgitation once LVEDP exceeds LA pressure. Color Doppler shows a diastolic MR jet.

6. Restrictive mitral inflow with short E deceleration time and blunted or absent A wave. The A wave disappears because of the high pressure resistance from the LV.

7. Low forward stroke volume, tachycardia, elevated PA pressures, pulmonary edema. EF is often “normal” while cardiac output is failing.

How do we assess Aortic Regurgitation with Echocardiography?

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A 2024 analysis of over 124 million US health records found atrial fibrillation in 3.89% of adults, and that number keeps climbing.

Every one of those patients still needs an accurate read on their left ventricular filling pressure.

The problem: the diastolic function algorithm you were trained on assumes a rhythm most of these patients don’t have.

In this article, you’ll learn why the standard E/A based approach falls apart in atrial fibrillation, which echo parameters actually hold up when there’s no organized atrial contraction, and how the newly updated 2025 ASE algorithm helps you reach a defensible conclusion instead of an indeterminate one

Introduction

Atrial fibrillation (AFib) is the most common sustained arrhythmia in the echo lab. It replaces coordinated atrial contraction with disorganized, chaotic electrical activity. A 2024 analysis of more than 124 million US health records found AFib in 3.89% of adults, roughly 4.8 million diagnosed patients, with prevalence rising sharply with age (Oltman et al.).

AFib and diastolic dysfunction travel together often. AFib is present, often undetected, in 15% to 41% of patients with heart failure with preserved ejection fraction (HFpEF), and a history of AFib raises the pretest probability for HFpEF in a symptomatic patient (Nagueh et al., “2025 Update”).

That overlap is why assessing filling pressure matters here. It’s also exactly where your usual approach breaks down, since AFib strips away the organized atrial contraction the standard algorithm depends on.

One limitation to know upfront: you cannot assign a Grade 1, 2, or 3 in AFib the way you can in sinus rhythm. Grading depends on the E/A ratio, and there is no A wave to generate one. The 2025 ASE algorithm classifies filling pressure as normal, elevated, or indeterminate instead, which is what this article walks through.

This builds directly on the sinus rhythm walkthrough. If you missed it, thats a better place to start.

Echo Evaluation

Why the Standard Algorithm Doesn’t Apply

The general diastolic function algorithm you use for most patients leans heavily on the E/A ratio, mitral A duration, and left atrial volume index (LAVi). None of that holds up in AFib.

• No A wave: Without organized atrial contraction, there is no true late diastolic filling velocity to capture. E/A ratio and A duration are not applicable, not just harder to measure.

• Beat to beat variability: Cycle length changes constantly, and any single cardiac cycle can give a misleading number in either direction.

• LAVi is confounded: Left atrial enlargement is common in AFib independent of filling pressure. The 2025 ASE guidelines specifically exclude AFib patients from the LAVi based structural criteria used in the general algorithm.

If you catch yourself hunting for the A wave on a mitral inflow tracing in a patient with AFib, stop. It isn't hiding in the signal. It physiologically doesn't exist.

Fixing the Acquisition

Before you get to which parameters to trust, fix how you acquire them.

• Average multiple cycles. Record several cardiac cycles and select the ones reflecting the patient’s average heart rate, not the fastest or slowest outliers.

• Watch beat to beat variability itself. Patients with less variability in mitral inflow from beat to beat tend to have higher filling pressures. A monotonous, unchanging pattern despite an irregular rhythm is a clue worth noting.

• Use dual Doppler probes when available. For E/e’ and other timing dependent ratios, simultaneous single beat recording of flow and tissue Doppler velocities is more accurate than averaging separate beats (Nagueh et al., “2025 Update”).

The Parameters That Hold Up

The 2025 ASE update identifies seven echocardiographic measurements with a validated association with elevated LV filling pressure in AFib.

Here’s the honest caveat: a multicenter study of 148 AFib patients tested these parameters against invasive filling pressure measurements and found that no single one was strong enough on its own to be recommended as a stand-alone marker (Khan et al.). That’s why current guidance is explicitly multiparametric.

The 2025 Decision Algorithm

The updated ASE algorithm scores four primary variables:

1. Mitral E velocity ≥ 100 cm/s

2. Septal E/e’ ratio > 11

3. TR velocity > 2.8 m/s or PASP > 35 mm Hg

4. Deceleration time ≤ 160 ms

If none or only one is present, filling pressure is normal. If three or more are present, filling pressure is elevated. If exactly two are present, move to a secondary tier:

• LA reservoir strain (LARS) < 18%

• Pulmonary vein S/D ratio < 1

• Body mass index > 30 kg/m²

None of those present means normal filling pressure, one present is indeterminate, and two or three present means elevated filling pressure (Nagueh et al., “2025 Update”).

This algorithm has moderate accuracy, not the sharper discrimination you get in a patient in normal sinus rhythm. Indeterminate cases will happen. That’s a real limitation of the data, not a technique failure on your part.

Common Mistakes

• Forcing an E/A ratio. It isn’t a measurement problem you can solve with a better angle. The physiology needed to generate an A wave isn’t present.

• Trusting a single beat. Cycle length variability makes one measurement unreliable. Average multiple cycles reflecting the mean heart rate.

• Reporting LAVi as if the patient were in sinus rhythm. An enlarged left atrium in AFib does not carry the same filling pressure implication it does in a structurally normal heart in sinus rhythm.

• Anchoring on one abnormal parameter. No single AFib specific measurement is validated as a stand-alone marker. Use the multiparametric algorithm instead.

Key Takeaways

• AFib eliminates the A wave, so E/A ratio, A duration, and the general diastolic function algorithm do not apply.

• You cannot assign a Grade 1, 2, or 3 in AFib. The algorithm classifies filling pressure as normal, elevated, or indeterminate only.

• Average multiple cardiac cycles reflecting the average heart rate. A single beat can mislead in either direction.

• Seven parameters (deceleration time, peak E acceleration rate, IVRT, pulmonary vein deceleration time, E/Vp, septal E/e’, TR velocity) are validated in AFib, but none works reliably alone.

• The 2025 ASE algorithm scores four primary criteria, with a secondary tier (LARS, pulmonary vein S/D, BMI) for indeterminate cases.

• LAVi should not be used as a structural filling pressure marker in AFib the way it is in sinus rhythm.

• AFib is present, often undetected, in 15% to 41% of HFpEF patients, which is exactly why getting this assessment right matters clinically

References

Khan, Faraz H., et al. “Evaluation of Left Ventricular Filling Pressure by Echocardiography in Patients with Atrial Fibrillation.” Echo Research & Practice, vol. 11, 2024, article 14. https://doi.org/10.1186/s44156-024-00048-x

Nagueh, Sherif F., et al. “Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography and for Heart Failure with Preserved Ejection Fraction Diagnosis: An Update from the American Society of Echocardiography.” Journal of the American Society of Echocardiography, vol. 38, no. 7, July 2025, pp. 537-569. https://doi.org/10.1016/j.echo.2025.03.011

Oltman, Connor G., et al. “Prevalence, Management, and Comorbidities of Adults with Atrial Fibrillation in the United States, 2019 to 2023.” JACC: Advances, vol. 3, no. 11, Nov. 2024, article 101330. https://doi.org/10.1016/j.jacadv.2024.101330

This publication is for educational purposes only and does not constitute medical advice. By subscribing, you agree to our Terms of Use, Privacy Policy, and Disclaimer.

Three variables. One algorithm. This is how the ASE says you should grade every diastology study.

Left atrial strain isn’t a bonus measurement anymore. It’s built into the primary pathway.

If you’ve been reading along, some of this will look familiar. We’re still getting questions on how the diastology guidelines actually work, and it’s not as hard as it seems once you see it for what it is: a short, structured decision tree built on measurements you’re already acquiring. Here’s the full breakdown, from diagnosing dysfunction to estimating LA pressure to connecting the grade to a HFpEF diagnosis, all in one place you can bookmark and use every time you need it.

Introduction

Diastolic function describes how well the left ventricle relaxes and fills with blood between heartbeats. When the ventricle stiffens or relaxes poorly, filling pressures rise and the left atrium remodels, often while the ejection fraction on your report looks completely normal. That combination, a normal EF with elevated filling pressures, is how a large share of heart failure with preserved ejection fraction (HFpEF) cases present.

Echocardiography is the frontline tool for making this call. Cardiac catheterization can measure filling pressures directly, but it’s invasive, and a well-performed diastology study can answer the same clinical question noninvasively in most patients.

Per the American Society of Echocardiography’s current guideline, the main algorithm estimates left atrial pressure (LAP) and assigns a grade using three core measurements you already acquire on a standard study.

Echo Evaluation

Step 1: Determine if LAP Is Normal or Elevated

This is the main algorithm, and it runs on three variables you’re already measuring.

Work through these three:

• All three normal: LAP is normal.

• All three abnormal: LAP is elevated.

• Mixed results: move to supplemental parameters before you call it.

A mixed result is not a dead end. Work through the supplemental parameters below before defaulting to an indeterminate call.

Supplemental parameters, used when the primary three disagree:

• None of these present: LAP is likely normal.

• Any of these present: LAP is elevated.

One nuance: when e′ is reduced but E/e′ and PASP are both normal, check E/A. If E/A is ≤0.8, LAP is normal, this is the pattern that becomes grade 1 in step 2, and if the patient is symptomatic despite it, that’s your cue for diastolic exercise echo. If E/A is >0.8 instead, don’t stop there, move to the supplemental parameters above before concluding LAP is normal.

Step 2: The Whole Grade Comes Down to Two Questions

Once you know whether LAP is normal or elevated, assigning the specific grade is this simple:

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This case did not stay in the textbook. A 35-year-old female patient presented with shortness of breath, and the TEE told a story most valves never will.

What Makes a Valve Unicuspid

A normal aortic valve has three leaflets meeting at three commissures. A unicuspid valve has one, fused together during fetal development into a single, often eccentric opening. It is rare, present in only about 0.02% of the general population (Cleveland Clinic).

There are two forms:

• Acommissural, the more severe type. No true commissures form. The leaflets fuse around a small central pinhole. Usually presents in infancy.

• Unicommissural, the more common type in adults. One commissure attaches to the aortic wall, leaving a slit-like opening some describe as a fish mouth. Often stays silent until the 20s or 30s.

This case was unicommissural, the type you are more likely to catch in an adult echo lab.

Why TEE, Not TTE

Diagnosing a unicuspid valve on TTE is genuinely hard.

Sensitivity and specificity for identifying unicuspid morphology (Chu et al.):

• TTE: 27% sensitivity, 50% specificity

• TEE: 75% sensitivity, 86% specificity

On mid-esophageal short axis, this valve showed the classic tell:

• A small, eccentric, posteriorly displaced orifice, in place of the familiar triangular trileaflet opening

• Single commissure oriented between the non-coronary and left coronary cusp positions, with fusion spanning the right coronary cusp

• The opposite leaflet edge doming into the orifice during systole

Calcification and image quality can still fool you. Unicuspid and bicuspid valves can look similar once heavy calcification obscures the leaflet edges. TEE narrows the diagnostic gap, but it does not close it completely.

Grading the Stenosis, and Why the Gradients Undersold It

The valve was interrogated using the continuity equation, per the joint ASE and EACVI recommendations (Baumgartner et al.).

• By aortic valve area: severe stenosis

• By mean gradient and peak velocity alone: closer to moderate

That gap makes sense given the setting. Gradients across a stenotic valve are flow dependent, and general anesthesia lowers cardiac output and transvalvular flow. A reduced flow state can make a genuinely severe valve look more moderate on velocity and gradient alone, exactly the discordant grading pattern the ASE and EACVI guidance flags.

Valve area, which is less flow dependent, carried the diagnosis here. This valve was severe by area, in a patient decades younger than the typical calcific aortic stenosis population.

Why This Patient Went to the Ross Procedure

A young patient facing aortic valve replacement has an unappealing set of options:

• Mechanical valve: durable, but lifelong anticoagulation

• Bioprosthetic valve: no anticoagulation, but degenerates faster in younger patients, often meaning a second surgery within a decade or two

The Ross procedure sidesteps both problems. The patient’s own pulmonary valve moves into the aortic position as a living autograft, and a pulmonary homograft replaces it in the lower pressure right side of the heart.

Unicuspid morphology used to raise questions about whether these patients did as well after Ross surgery as their bicuspid counterparts. A 2023 study of 286 Ross patients found (Gofus et al.):

• Unicuspid valves made up 39% of the cohort, the second most common indication behind bicuspid disease

• No worse perioperative or midterm outcomes compared to other valve morphologies

• No autograft reintervention in the unicuspid subgroup

Final Thoughts

A unicuspid aortic valve is not something most of us see often, but when we do, it tends to show up early and mean business. This valve never had a fair shot at lasting into middle age, and a low-flow TEE nearly told a softer story than the one underneath it. Recognizing it, grading it by the right parameter, and getting the patient to the right surgical conversation made the difference between one operation and a lifetime of chasing the wrong one.

If you have a case worth sharing, send it my way. This series runs on them.

References

Baumgartner, Helmut, et al. “Recommendations on the Echocardiographic Assessment of Aortic Valve Stenosis: A Focused Update from the European Association of Cardiovascular Imaging and the American Society of Echocardiography.” Journal of the American Society of Echocardiography, vol. 30, no. 4, Apr. 2017, pp. 372-392, https://doi.org/10.1016/j.echo.2017.02.009.

Chu, Justina W., et al. “Diagnosis of Congenital Unicuspid Aortic Valve in Adult Population: The Value and Limitation of Transesophageal Echocardiography.” Echocardiography, vol. 27, no. 9, Oct. 2010, pp. 1107-1112, https://doi.org/10.1111/j.1540-8175.2010.01209.x.

Cleveland Clinic. “Unicuspid Aortic Valve: Causes and Treatment.” Cleveland Clinic, 25 Mar. 2024, my.clevelandclinic.org/health/diseases/unicuspid-aortic-valve.

Gofus, Jan, et al. “Unicuspid Aortic Valve in Patients Undergoing the Ross Procedure.” The Annals of Thoracic Surgery, vol. 115, no. 3, Mar. 2023, pp. 626-631, https://doi.org/10.1016/j.athoracsur.2022.03.061.

Otto, Catherine M., et al. “2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease.” Circulation, vol. 143, no. 5, 2 Feb. 2021, https://doi.org/10.1161/cir.0000000000000923.

This publication is for educational purposes only and does not constitute medical advice. By subscribing, you agree to our Terms of Use, Privacy Policy, and Disclaimer.

LA volume index can sit comfortably inside normal limits for years while filling pressures climb quietly in the background.

By the time the atrium dilates enough for you to flag it in your apical volumes, the disease already has a head start.

There’s a strain parameter sitting in your speckle-tracking software right now that catches this dysfunction long before volume ever does. In this lesson, you’ll learn how to acquire and measure left atrial reservoir strain (LASr), which gating approach the 2025 ASE/EACVI consensus statement actually recommends, and the specific cutoff values that separate a reassuring study from one that needs a second look.

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Introduction

Speckle tracking echocardiography works by following speckles, the natural patterns of ultrasound backscatter within myocardial tissue, frame by frame through the cardiac cycle. As those speckles move, the software calculates how much the underlying muscle is deforming. That deformation is strain.

You already use this principle on the left ventricle every time you report global longitudinal strain (GLS). Apply the same logic to the left atrium and you get atrial strain, which breaks down into three distinct phases across a single cardiac cycle.

The Three Phasic Components of the LA

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It began with a bat, a submarine hunt, and a scrap metal factory floor.

None of the people responsible for the discoveries that made your machine possible had ever heard of a mitral valve.

In this lesson, you’ll trace the 450-year relay race of biology, physics, and wartime engineering that had to happen before anyone could watch a heart valve move in real time, and why the machine sitting next to you at work still runs on the exact same principle those discoveries uncovered.

Introduction

Ask most people when echocardiography was invented and you’ll get one answer: 1953, Lund, Sweden, Inge Edler and Carl Hellmuth Hertz. That’s true, and it’s the date every textbook leads with. But it’s also the last stop on a much longer trip. The physics that let Edler and Hertz see a heart wall move didn’t come from medicine at all. It came from a naturalist studying bats, a pair of brothers studying crystals, a physicist hunting submarines, and an engineer looking for cracks in steel.

Every one of them was solving a problem that had nothing to do with cardiology, and every one of them left behind a piece of the puzzle that eventually became your transducer, your pulse-echo principle, and your gain settings. Understanding that lineage isn’t just trivia. It’s a reminder that the tool in your hand is built on centuries of borrowed ideas, and that the physics you learned in your registry review didn’t start with ultrasound. It started with sound.

The Timeline

1513 — Leonardo da Vinci. Da Vinci’s anatomical sketches include the earliest known depiction of a bicuspid aortic valve, centuries before anyone understood its clinical significance.

1799 — Lazzaro Spallanzani. The Italian naturalist demonstrated that bats navigate in complete darkness using reflected sound rather than sight, the first documented evidence of echolocation and, in hindsight, the conceptual seed of every pulse-echo technology that followed.

1880 — Pierre and Jacques Curie. The Curie brothers discovered piezoelectricity: certain crystals generate an electrical charge when compressed, and deform when a charge is applied to them. That reversible relationship is the physical basis for every ultrasound transducer built since.

1886 — Sir William Osler. Osler documented a bicuspid aortic valve in roughly one percent of 800 consecutive autopsies, one of the earliest attempts to quantify how common the finding really was, decades before anyone could see it in a living patient.

1915 — Paul Langevin. Working from the Curies’ piezoelectric effect, Langevin developed the technology that became SONAR, using ultrasonic pulses to detect submarines during the First World War. This was the first practical, large-scale use of reflected ultrasound to “see” something invisible to the eye.

1937 — Sergei Sokolov. Sokolov adapted pulse-echo ultrasound to detect flaws hidden inside solid metal, an industrial application that, decades later, is what Edler and Hertz actually borrowed equipment from to examine the heart.

1953 — Inge Edler and Carl Hellmuth Hertz. A cardiologist and a physicist in Lund, Sweden borrowed an industrial ultrasonic reflectoscope, the same category of device used to inspect metal for flaws, and pointed it at a human chest instead. The first M-mode recording of a beating heart was made that October, and echocardiography as a clinical discipline was born.

1969 — Nils-Rune Lundström. Just across town from Edler, this Lund pediatric cardiologist showed that the technique wasn’t limited to adult mitral valve disease. Working with children suspected of congenital heart defects, he used ultrasound to diagnose conditions like cor triatriatum and Ebstein’s anomaly, presenting his findings at the First World Congress of Ultrasonic Diagnostics in Medicine in Vienna, and going on to publish some of the earliest pediatric echocardiographic reference values. Echocardiography’s leap from “a way to look at one adult valve” to “a way to evaluate an entire congenital heart” starts here.

Why This Still Matters at the Bedside

This isn’t just a fun piece of trivia to drop at journal club. The physics that Spallanzani, the Curies, Langevin, and Sokolov worked out are still running underneath every study you scan today.

Clinical Pearl

Every time you adjust transmit frequency, you’re working with the same piezoelectric crystal principle the Curies described in 1880: compress or shock the crystal, and it produces or receives ultrasonic energy.

Every time you adjust time-gain compensation to correct for attenuation, you’re compensating for the same signal loss that Sokolov’s industrial flaw detectors had to account for when reading returning echoes from inside solid metal.

The pulse-echo principle, send a wave out, measure how long it takes to come back, is the exact same logic Langevin used to detect a submarine and Edler and Hertz used to detect a mitral valve.

None of this changes how you scan tomorrow morning. But it explains why the physics section of your registry review keeps circling back to concepts that seem to have nothing to do with the heart. They didn’t start with the heart. Cardiology borrowed this technology from naval warfare and industrial inspection, and it only became a diagnostic tool because two people in Sweden were curious enough to ask whether a device meant for finding cracks in steel could find something useful in a chest instead.

Key Takeaways

• Echocardiography’s technical roots predate cardiology entirely: bat biology (1799), crystal physics (1880), naval SONAR (1915), and industrial flaw detection (1937) all came before the first clinical cardiac ultrasound in 1953.

• The piezoelectric effect discovered by the Curie brothers in 1880 is still the operating principle behind every modern transducer.

• Edler and Hertz’s breakthrough in Lund, Sweden came from repurposing an industrial ultrasonic reflectoscope, not from a device built for medicine.

• Nils-Rune Lundström, working in the same city just over a decade later, extended M-mode echo from adult mitral valve disease into pediatric congenital heart disease, laying groundwork for modern pediatric echo.

• The physics you review for your boards, attenuation, pulse-echo timing, transducer frequency, traces directly back to these non-medical origins.

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References

Fraser, Alan G., et al. “A Concise History of Echocardiography: Timeline, Pioneers, and Landmark Publications.” European Heart Journal - Cardiovascular Imaging, vol. 23, no. 9, 2022, pp. 1130-1143, doi:10.1093/ehjci/jeac111.

Edler, Inge, and Carl Hellmuth Hertz. “The Use of Ultrasonic Reflectoscope for the Continuous Recording of the Movements of Heart Walls.” Clinical Physiology and Functional Imaging, vol. 24, no. 3, 2004, pp. 118-136, doi:10.1111/j.1475-097X.2004.00539.x.

Feigenbaum, Harvey. “Evolution of Echocardiography.” Circulation, vol. 93, no. 7, 1996, pp. 1321-1327, doi:10.1161/01.CIR.93.7.1321.

Lundström, Nils-Rune. “Clinical Applications of Echocardiography in Infants and Children I: Investigation of Infants and Children Without Heart Disease.” Acta Paediatrica, vol. 63, no. 1, 1974, pp. 23-32, doi:10.1111/j.1651-2227.1974.tb04345.x.

Losanno, Teodoro, et al. “Bicuspid Aortic Valve: The Most Frequent and Not So Benign Congenital Heart Disease.” IJC Heart & Vasculature, vol. 51, 2024, doi:10.1016/j.ijcha.2024.101377.

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The spectral waveform is your confirmation step, the sign that tells you your color impression holds up or that something doesn’t add up.

Miss it, and a severe leak can slip through looking moderate.

Color Doppler gives you your grade. Spectral Doppler confirms it. This article walks the CW and PW signs that back up a severity call across all four valves, where each one is reliable, and the one situation where spectral stops confirming and starts leading.

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It’s the most common tumor found inside the human heart, and on a screen it can look a lot like something you already scan past every week.

About one in five of these tumors turn up on the wrong side of the heart entirely.

And when one lands in the right atrium, it can choke blood flow through the tricuspid valve badly enough to fake a valve disease that was never actually there.

In this lesson, you’ll learn exactly how to identify a right atrial myxoma on TTE and TEE, how color Doppler exposes the pseudostenosis these tumors create, and the specific features that separate a myxoma from thrombus, vegetation, and papillary fibroelastoma.

Introduction

A cardiac myxoma is a benign tumor that grows from multipotent mesenchymal cells nestled in the subendocardium, forming a soft, gelatinous mass usually attached to the heart wall by a stalk. In absolute terms it’s rare — primary cardiac tumors overall occur in only 0.0017% to 0.19% of the population based on autopsy series, according to a 2023 Journal of Clinical Medicine study on left atrial tumor outcomes. But among primary cardiac tumors, the myxoma dominates the field: it’s the single most common type, accounting for roughly 30% to 50% of all primary cardiac neoplasms, per a 2025 Journal of Cardiovascular and Thoracic Research surgical outcomes study.

Location matters here. About 75% of myxomas grow in the left atrium, but 15% to 20% show up in the right atrium instead, with a small remainder found in the ventricles. Most patients are diagnosed between their 40s and 60s. Across all myxomas, which are predominantly left-sided, women are affected roughly twice as often as men, though right atrial myxomas specifically do not carry that same female skew.

Myxomas cause trouble in three overlapping ways: obstructive symptoms from mechanically blocking blood flow, embolic events when a fragment breaks free, and constitutional symptoms like fever, weight loss, and fatigue that can mimic infection or malignancy. A right atrial myxoma has its own personality here. Instead of the systemic emboli you’d worry about with a left atrial mass, an RA myxoma fragment embolizes to the lungs, and its obstructive physiology mimics tricuspid stenosis rather than mitral stenosis. This is exactly why echocardiography carries the diagnosis. It’s fast, it’s already in your hands, and it shows you location, mobility, attachment, and hemodynamic consequence in real time, before anyone reaches for cross-sectional imaging.

Echo Evaluation

Views That Matter Most

• Subcostal 4-chamber view deserves to go first, not last. It images the interatrial septum perpendicular to the ultrasound beam, which is exactly what you need to confirm a myxoma’s classic attachment point near the fossa ovalis without the septal dropout that plagues the apical window.

• RV-focused apical 4-chamber view for overall mass size, shape, and its relationship to the tricuspid valve.

• Parasternal long-axis (RV inflow) and short-axis at the aortic valve level to confirm tricuspid involvement and rule out extension into the RV outflow tract.

• TEE, when available, using the mid-esophageal 4-chamber and bicaval views, gives you the clearest look at the stalk itself and confirms septal attachment with far less artifact than TTE.

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