This chapter reviews LV hypertrophy and associated LV outflow tract obstruction. In settings where consultative echocardiography is available, PoCUS should not be used to definitively evaluate and define this condition. However, identifying obvious pathology and understanding the treatment implications may help generalists manage these patients when consultative services are unavailable.
Mild to moderate LV-wall thickening or hypertrophy (LVH) is relatively common, and identifying it often does not impact medical-decision making. It usually occurs as an adaptation to reduce wall tension in response to chronic hypertension or aortic stenosis. The LV also thickens with age, acromegaly, hyperthyroidism, amyloidosis, genetic storage diseases, or isolated hypertrophic cardiomyopathy (HCM). HCM is a cardiac-specific genetic disorder often inherited in an autosomal dominant fashion, so immediate family members are at high risk.
In the PLAX view, LV wall thickness is typically measured in the plane parallel to and just apical to the mitral valve during end-diastole. Most sources consider thicknesses >12 mm abnormal. However, PoCUS is often performed quickly and under suboptimal conditions. In this setting, it is easy to mistakenly include the cordae tendonae, mitral valve, pericardium, or the membranous interventricular septum in the measurement and overestimate LV thickness. Therefore, it’s reasonable to avoid routinely taking fine measurements of LV wall thickness. Instead, the more practical approach is to look for gross LV hypertrophy where the LV wall appears thicker than 1.5 to 2cm.
Image 5.1 Comparing parasternal long-axis views with normal LV wall thickness grossly less than 1.5cm (A) with LV hypertrophy with end-diastolic wall thickness grossly >1.5cm (B). These images with different depths are scaled for comparison.
Image 5.2 Subcostal 4-chamber (A) and subcostal short-axis (B) views of gross LVH.
Just as LVH is an adaptation that helps with systolic function, it does so at the expense of diastolic function as it requires more filling pressure to stretch out the LV wall. Therefore, LVH is associated with heart failure with preserved EF and may present with heart failure, syncope, tachyarrhythmias, or coronary ischemia. Severe LVH is associated with LV outflow tract (LVOT) obstruction, where an intraventricular pressure gradient forms as the mitral valve moves anteriorly towards the proximal interventricular septum during systole. It is essential to understand that this LVOT obstruction worsens when the LV is too empty (low preload, low afterload) or squeezes extra hard (high contractility). LVOT obstruction increases LV hypertrophy and oxygen demand, can induce mitral regurgitation, and ultimately limits cardiac output.
Image 5.3 LV outflow traction obstruction associated with severe LVH visualized with color Doppler as increased flow velocity occurs between the proximal interventricular septum and the anterior leaflet of the mitral valve.
Evaluating specifically for LVOT obstruction is outside the scope of most performing PoCUS. However, by identifying severe LVH, PoCUS can increase suspicion of possible LVOT obstruction and extra vulnerability to underfilled, hyper-contractile, tachycardic states. Patients with a significant LVOT obstruction can deteriorate when they receive strong beta-adrenergic agonists like epinephrine/adrenaline, dobutamine, or dopamine. They respond better to pure vasopressors like phenylephrine to improve vascular tone. Intravenous fluids may improve LV filling as well. Lastly, tachyarrhythmias are particularly difficult for patients with LVOT obstruction to tolerate and should be recognized and addressed immediately.1–3
Patients with severe LVH should have a consultative echocardiogram and ECG testing/monitoring if available. Outpatient treatment of LVOT obstruction includes continuous beta-blocker therapy.4 If atrial fibrillation or atrial flutter is present, then thromboembolic prophylaxis plus agents and interventions to maintain sinus rhythm should be considered. In high-resource settings, implanted cardiac defibrillators and advanced surgical and medical therapies may also be available. Patients without a systemic disorder to explain their LV hypertrophy should be educated on the possible familial nature of isolated hypertrophic cardiomyopathy, and their immediate family members should be screened.5