LVOT Obstruction

LVOT obstruction as a phenomenon is probably more common than we realise, especially after cardiac surgery and in individuals with an anatomical predisposition to obstruction. Haemodynamic changes seen in conditions such as sepsis and liver failure (which reduce afterload) combined with administration of inotropic drugs (to counteract the reduction in afterload) can lead to obstructive physiology.

LVOT Obstruction is diagnosed if doppler interrogation reveals a gradient of >30mmHg either at rest or following provocation. Severe LVOTO is diagnosed as gradient >50mmHg

LVOT Anatomy

The entire cardiac output must pass through the LVOT and therefore small changes to the size and shape can produce large haemodynamic consequences in certain individuals. Relational anatomy is important when considering possible sites of fistulation in endocarditis as well as the functional relationship to the AML (described in more detail later)

• The LVOT is 25mm in length with a shape that changes from near-circular (in diastole) to ovoid (in systole) through the cardiac cycle
• Posteromedial = formed by the intervalvular fibrosa with the adjoining AML
• Medial = membranous septum
• Anterolateral (half of the circumference) = Ventricular septum / LV wall

LVOT Obstruction Causes

Features of LVOTO can occur either at rest or when exposed to certain physiological stressors depending on disease severity. Note that even individuals with normal LVOT anatomy and function can exhibit signs of flow acceleration and obstruction with dobutamine therapy or other hyperdynamic states. Anatomical predisposing factors together with physiological stressors therefore need to be considered in unison when making the diagnosis.

Anatomical predisposition:

Genetic

1. Hypertrophic cardiomyopathy (Of which 74% exhibit LVOTO)
2. Infiltrative cardiac disease
1. Amyloidosis
2. Fabry disease
3. Friendrich’s ataxia
4. Sarcoidosis

Acquired

1. Concentric LVH
2. Eccentric LVH with predominant septal hypertrophy
3. Takotsubo cardiomyopathy (basal hyperkinesia compensating for apical akinesia)
4. RV dilatation (via ventricular interdependence with reduced LV preload)

Post-surgical

• “High-profile” MVR
• Malpositioned MVR with “struts” obstructing the LVOT
• Post AVR/TAVI (Immediate afterload reduction causes flow acceleration in the LVOT in individuals with very hypertrophic ventricles)

Fixed obstructions

• Subaortic stenosis e.g. from subaortic membrane. This should be strongly considered if there is flow acceleration present in the LVOT but no evidence of SAM. The membrane usually originates from the mitral subvalvular apparatus
• Bicuspid aortic valve (pathological calcification can also occur in the LVOT obstructing flow)
• Coarctation of the aorta - note this is not obstruction of the LVOT but at the origin of the left subclavian. Physiological disturbances are similar though.

LVOT Obstruction Physiology

• Either at rest or in patients with a physiological precipitant for LVOTO the gradient is elevated
• Increased LVOT velocity causes a venturi effect pulling the AML into the LVOT. This results in:
• Worsened LVOT obstruction due to the AML physically obstructing blood flow
• Physiological mitral regurgitation (the MV cannot coapt properly if the AML is being pulled into the LVOT
• Reduced cardiac output eventually ensues starting a vicious cycle where preload into the LV eventually drops, exacerbating the LVOTO.

Physiological Precipitants

1. Inotrope infusion - especially dobutamine where the combination of venodilation (and reduced preload), tachycardia and increased inotropy all serve to precipitate LVOTO.
2. Exercise - Exercise stress echo can be used to diagnose the condition when gradients are normal at rest. LVOTO is typically worse just after stopping exercise when preload is at it’s lowest and the LVOT diameter is narrowest
3. Reduced preload - from any cause e.g. bleeding
4. Reduced afterload - Nitrate administration was shown to reduce cardiac output by 60% in one study and is likely to be the most important contributor to dynamic LVOTO. Maintenance of afterload is of utmost important in order to reduce the outflow gradient from the LV into the aorta.

Diagnostic Criteria

• LVH or strain pattern may be seen on ECG although in most individuals ECG is normal
• Measure LVOT gradient using PWD, 30mmHg = LVOTO present, 50mmHg = severe LVOTO
• Provocation testing using valsalva in the first instance (Gradient > 50mmHg on provocation is diagnostic)
• GTN is not routinely recommended as it is poorly tolerated and doesn’t mimic exercise physiology well
• Dobutamine also not recommended due to being poorly tolerated
• Exercise testing is the next best mode of provocation if valsalva fails to ellicit a response

Clinical features:

• Ejection systolic murmur made louder on valsalva (as flow acceleration increases)
• Mitral regurgitation murmur (if SAM is also present, which it usually is)
• Haemodynamic instability especially during stress or exertion
• “Spike and dome” appearance of the arterial pressure trace
• Sudden collapse (especially just after easing exercise)

Echo Features:

• Increased velocity in the LVOT:
• Aliasing seen on colour flow doppler can help locate the obstruction
• Use PWD and move from the apex to the base of the LV (obstruction may be seen at multiple levels in some individuals)
• Use CWD if gradients are very high (>50mmHg)
• Abnormalities of the AML
• Elongation of the AML > 18mm with anterior dispalcement
• Abnormalities of the papillary muscles (displaced anteriorly)
• Abnormalities of the chordae (elongated or associated with subaortic membranes)
• Presence of SAM - Typically occurs late in systole. SAM can be provoked and worsens as LVOT velocities increase. A venturi effect in the LVOT pulls the SAM anteriorly creating a vicious cycle
• Hypertrophy of the ventricle
• Coexistent HCM or severe LVH
• Presence of other cardiomyopathy (amyloidosis etc…)

Management strategies

Perioperative and ICU management of patients with LVOTO can be challenging due to non-intuitive responses to standard haemodynamic interventions. There should be a low threshold for TTE or TOE-guided management given the usual treatments (Inotrope infusion, fluid administration etc…) can potentially worsen the condition. The following management goals should be considered:

Preload

Maintain or aim for “high preload”. The main goal is not to let the LV become underfilled resulting in a reduction in LVEDV. This reduction can lead to the LVOT area narrowing as the hypertrophied walls of the LVOT push inwards. This worsens flow acceleration through the narrowed orifice creating a vicious cycle.

Contractility

Aim to minimise additional contractility beyond what is necessary. Hyperdynamic states such as sepsis can exacerbate LVOTO as can excessively high noradrenaline or adrenaline infusions where increased flow velocities created by increased contractility worsen SAM and LVOTO.

Aim to keep heart rate “low-normal”. Atrial arrhthythmias such as AF can often precipitate circulatory collapse and should be treated aggressively. Maximising the diastolic filling time helps to maximise LVEDV keeping the LVOT open and also has a secondary benefit of maximising coronary perfusion pressure in a hypertrophied ventricle.

Afterload

Afterload should be maintained in order to reduce the gradient from the LV into the aorta during systole. The LV in patients with HCM is by definition hypertrophied and therefore maintaining an adequate CoPP (via maintained afterload) is of critical importance to maximise diastolic filling. Drugs such as metaraminol, phenylephirine and vasopressin should be considered first-line as contractility is usually not a problem.

Brockenbrough-Braunwald-Morrow [3]

This phenomenon is a niche piece of cariothoracic esoterica which is unlikely to ever be of clinical utility but does explain the physiology of LVOTO quite eloquently.

After a premature ectopic is seen on the ECG a characteristic post PVC arterial waveform is then seen which has a smaller pulse pressure and reduced overall pressure. If you are able to simultaneously measure the LV pressure trace (via a wire in the cath lab) the corresponding LV pressure peak will be considerably higher than those preceding it.

This is caused by:

1. Time between the PVC and the next systole results in an increase in LVEDP
2. Increased LVEDP = Increased contractility (via Starling’s Law)
3. Increased contractility = Increased LVSP = Increased LVOTO
4. Final result = Decreased pulse pressure with overall reduced peak pressure of the arterial waveform in the beat following the PVC.

The abnormal beat can be seen at 6 seconds in on the graph below:

Surgical Management

Surgical myomectomy (Morrow’s procedure)

Surgery remains the standard of care for selected patients who have LVOT obstruction refractory to medical therapy. This procedure involves meticulous “shaving” of the septal myocardium in order to increase the LVOT diameter leaving 5-8mm of myocardium behind. The operative success rate is in excess of 90%.

The risks include:

• Sternotomy
• CPB
• Iatrogenic VSD formation.
• PPM post-procedure (3-5%) Due to close proximity to AV node

Percutaneous septal ablation

This is achieved with 3mls of 96% of alcohol targeted at specific endocardial vessels resulting in targeted myocardial necrosis. The results are favourable with LVOT gradient reduction in 90% of patients in specialist centres.

The risks include:

• AV Block requiring PPM (5-30% - Figures overall are reducing, possibly with enhanced imaging techniques allowing for more targeted therapy)
• Death (1-2%)
• Ventricular septal defect
• Pericardial effusion / tamponade

Created 11/1/2024 - Dr Sean Edwards [sean.edwards1@nhs.net]

References

1. Slama, Michel; Tribouilloy, Christophe; Maizel, Julien. Left ventricular outflow tract obstruction in ICU patients. Current Opinion in Critical Care 22(3):p 260-266, June 2016
2. https://www.escardio.org/Councils/Council-on-Cardiovascular-Genomics/Cardiovascular-Genomics-Insight/Volume-1/how-to-measure-intraventricular-obstruction-in-hypertrophic-cardiomyopathy
3. Lasam G. Brockenbrough-Braunwald-Morrow Sign: An Evaluative Hemodynamic Maneuver for Left Ventricular Outflow Tract Obstruction. Cardiol Res. 2018 Jun;9(3):180-182
4. https://www.lhch.nhs.uk/left-ventricular-outflow-tract-obstruction
5. https://www.escardio.org/Councils/Council-on-Cardiovascular-Genomics/Cardiovascular-Genomics-Insight/Volume-1/how-to-measure-intraventricular-obstruction-in-hypertrophic-cardiomyopathy