Echo assessment of LV diastolic function

Assessing left ventricular diastolic function can get complicated. However, things were made a bit easier recently with the publication of some new joint ASE/EACVI guidelines on the echo evaluation of LV diastolic function. The guidelines are detailed (they're almost 40 pages long), but the principal take home message can be summarized as follows:

Echo diagnosis of LV diastolic dysfunction

The guidelines recommend measuring four key parameters to assess LV diastolic function:

Annular e' velocity

An abnormal e' velocity is indicated by a septal e' <7 cm/s, or a lateral e' <10 cm/s.

Average E/e' ratio

The authors recommend that an average E/e' ratio is used (rather than separate septal and lateral E/e' ratios), and that the average E/e' ratio is considered to be abnormal if it is >14. If an average can't be calculated, then a lateral E/e' >13, or a septal E/e' >15, is considered to be abnormal.

Left atrial volume index

The left atrial maximum volume index is abnormal if it is >34 mL/m2.

Peak tricuspid regurgitation velocity

This is abnormal if peak TR velocity is >2.8 m/s.

Judging whether LV diastolic function is normal or abnormal depends upon how many of the measured parameters are abnormal:

• If more than 50% of the measured variables are abnormal, then LV diastolic function is abnormal
• If less than 50% of the measured variables are abnormal, then LV diastolic function is normal
• If 50% of the measured variables are abnormal, then LV diastolic function is indeterminate

This method of using the majority of available parameters to make an overall judgement about LV diastolic function is useful, as it allows a conclusion to be made about diastolic function even if all four parameters aren't available.

The guidelines can be found by clicking here, and are well worth reading. As well as giving overall advice about the echo assessment of LV diastolic function, they also contain guidance on assessing diastolic function in specific situations (such as atrial fibrillation and hypertrophic cardiomyopathy).

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Making sense of S2, the second heart sound

In our blog a few days ago, we looked at the first heart sound and how it varies with different clinical conditions. In today's blog, we're going to take a look at S2, the second heart sound.

The second heart sound is made up of two components:

• A2, caused by aortic valve closure
• P2, caused by pulmonary valve closure.

In expiration, the A2 and P2 components are virtually indistinguishable (in adults) and are essentially heard as a single sound. However in inspiration, the increase in venous return to the right heart slightly delays right ventricular emptying, which in turn slightly delays P2. Thus in inspiration we hear normal physiological splitting of the second heart sound, with P2 occurring just after A2.

This physiological splitting of the second heart sound gets wider (and therefore easier to auscultate) if P2 occurs late - this happens in right bundle branch block (because of the later contraction of the right ventricle), and also in pulmonary stenosis (due to greater impedance to right ventricular emptying). As you might expect, splitting of the second heart sound also gets wider if A2 occurs early - this is seen with mitral regurgitation, and also in ventricular septal defect, because left ventricular emptying occurs more quickly.

The splitting of the second heart sound becomes reversed (i.e. A2 occurs after P2) if emptying of the left ventricle is delayed - as occurs in left bundle branch block or aortic stenosis. When reversed splitting occurs, it's easiest to hear in expiration.

Transesophageal echo showing a secundum ASD

Fixed splitting of the second heart sound occurs in the presence of an atrial septal defect. In this situation, pressure changes with respiration affect the right and left atria equally, and so we no longer see the delay in P2 that normally occurs during inspiration.

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Ten key facts about S1, the first heart sound

When we auscultate the heart, we normally hear the first (S1) and second (S2) heart sounds. Here are ten key facts about the first heart sound to be aware of when you're examining patients.

Factors that affect the intensity of the first heart sound (S1)

1. The first heart sound (S1) results from mitral and tricuspid valve closure.
2. Although S1 has two separate components (the mitral component and the tricuspid component), they occur so close together that they're normally heard as a single sound.
3. If the patient's circulation is hyperdynamic, S1 will be louder than usual.
4. Conversely, S1 will be quiet if the patient has a low cardiac output.
5. S1 is louder than normal in Wolff-Parkinson-White syndrome. Why? Because the short PR interval in WPW syndrome means that the mitral leaflets are still widely separated at the start of systole.
6. Conversely, S1 will be quiet in the PR interval is long. This is because the mitral valve leaflets have already started to close by the time that systole begins.
7. S1 is louder than normal in mitral stenosis, for the same reason as with a short PR interval - in mitral stenosis, the slow exit of blood from the left atrium through the narrowed mitral valve means that the ventricle is still filling with blood, and thus the mitral leaflets are still widely separated, at the start of systole.
8. In mitral stenosis, S1 can be so loud that it can be palpated at the apex. This is described as a 'tapping' apex beat, the palpable first heart sound in mitral stenosis.
9. S1 is quieter than normal in mitral regurgitation.
10. An S1 of variable intensity is heard with atrial fibrillation, ectopic beats and complete heart block.

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Ready for another heart failure subgroup? How about HFrecEF?

In the language of heart failure, we're familiar with the terms HFrEF (heart failure with a reduced ejection fraction), and HFpEF (heart failure with a preserved ejection fraction). More recently, we had a proposed new category of HFmrEF (heart failure with a mid-range ejection fraction, namely an LVEF of 40-49%). In fact we've already talked about HFmrEF in a recent blog post.

We now have another subgroup to consider - HFrecEF. This is heart failure with a recovered ejection fraction, and refers to those patients who have had a reduced ejection fraction in the past, but whose left ventricular ejection fraction (LVEF) has subsequently improved.

HFrecEF, a new subgroup in heart failure

More specifically, HFrecEF is defined when the patient's current LVEF is >40%, but has previously been documented to be ≤40%.

Why is the concept of HFrecEF gaining attention? It's because of a recent paper by Kalogeropoulos and colleagues, published in JAMA Cardiology. This paper looked at patients with HFrecEF in a retrospective cohort study, and found that the clinical course of patients with HFrecEF was different to those with HFrEF and HFpEF, with fewer clinical events such as deaths or hospitalizations during the study period.

Why does this matter? Well, if patients with HFrecEF are a distinct subgroup with different (better) clinical outcomes compared to those with HFrEF and HFpEF, then this may have an impact on the findings of heart failure trials more generally. The authors therefore propose that patients with HFrecEF may need to be considered as a separate group in future heart failure studies.

If you'd like to read the original paper, you can do so here:

Kalogeropoulos AP, et al. Characteristics and Outcomes of Adult Outpatients With Heart Failure and Improved or Recovered Ejection Fraction. JAMA Cardiol. doi:10.1001/jamacardio.2016.1325

Understanding LVH: Concentric versus eccentric hypertrophy

When we talk about left ventricular hypertrophy (LVH) in cardiac imaging, the terms concentric LVH and eccentric LVH are often used. However the word 'eccentric' sometimes causes confusion - it's important to realise that the word 'eccentric' does not mean 'asymmetric' in the context of LVH. So what is eccentric LVH, and how does it differ from concentric LVH?

Cardiac MRI showing severe concentric LVH

Concentric LVH is seen in situations where there is pressure overload of the left ventricle. Examples include hypertension and aortic stenosis. The heart adapts to pressure overload by adding new sarcomeres in parallel to existing sarcomeres. This leads to an increase in left ventricular wall thickness and left ventricular mass, but the cavity size remains normal.

Eccentric LVH, in contrast, occurs when there is volume overload of the left ventricle. This is seen with valvular regurgitation (aortic or mitral), or can occur as a result of cardiac remodelling in endurance athletes. In this situation, the heart adapts to volume overload by adding new sarcomeres in series with existing sarcomeres. The end result is an increase in left ventricular cavity size and an increase in left ventricular mass, but the wall thickness remains normal.

Concentric versus eccentric LVH

If you'd like to read more on this topic, check out these links:

Mihl C, et al. Cardiac remodelling: concentric versus eccentric hypertrophy in strength and endurance athletes. Neth Heart J 2008; 16: 129–133.

Marwick TH, et al. Recommendations on the use of echocardiography in adult hypertension: a report from the European Association of Cardiovascular Imaging (EACVI) and the American Society of Echocardiography (ASE). European Heart Journal – Cardiovascular Imaging 2015; 16: 577-605.

What's the best probe position to assess aortic stenosis severity?

When you're assessing aortic stenosis using echo, it's essential to make an accurate assessment of stenosis severity. One of the key indicators of severity is the peak flow velocity through the aortic valve (Vmax), as measured using continuous wave (CW) Doppler. Severe aortic stenosis is indicated by a peak velocity >4.0m/s. But where is the best probe position to measure this from?

CW measurement of aortic valve Vmax from the apical echo window

During transthoracic echo, CW Doppler measurements of aortic valve flow are most commonly made from the apical window, as in the image above. But is this always the best place to make this measurement?

In a 2015 paper by Thaden and colleagues, transthoracic echo studies were performed in 100 patients with severe aortic stenosis. The authors used CW Doppler to measure aortic valve Vmax from several different imaging windows during each patient's echo:

• Apical window
• Suprasternal notch
• Right supraclavicular window
• Right parasternal window

The authors then looked at where the highest value of Vmax was obtained. They found that the right parasternal window was the one where the highest Vmax was most often obtained (50% of cases), followed by the apical window (39% of cases).

The authors also found that if only the apical window was used, then in 23% of cases the Vmax was significantly underestimated (i.e. patients with severe aortic stenosis were misclassified as having moderate or even mild stenosis).

The take-home message from this study is that the sole use of the apical echo window to measure Vmax commonly leads to underestimation of the severity of aortic stenosis, and therefore that the echo assessment of aortic stenosis should include the use of multiple imaging windows (and in particular the routine use of the right parasternal window) to measure Vmax.

If you'd like to read the original paper, it can be accessed here:

Thaden JJ, et al. Doppler Imaging in Aortic Stenosis: The Importance of the Nonapical Imaging Windows to Determine Severity in a Contemporary Cohort. J Am Soc Echocardiogr 2015; 28: 780-785.

Myocardial crypts in hypertrophic cardiomyopathy

Over recent years there has been interest, and debate, about the significance of myocardial crypts seen on cardiac MRI scanning. Crypts (also known as clefts, crevices or fissures) are defined as an invagination of the myocardium that penetrates >50% of the myocardial thickness in diastole. An example is shown in the figure below: here there are two crypts in the inferior wall.

Two inferior wall myocardial crypts (arrowed)

To see this image as a cine CMR video, click on the video below to play it:

So are myocardial crypts significant? It has been suggested that they may represent a 'prephenotypic marker' of hypertrophic cardiomyopathy, based upon a 2012 paper in which crypts were  found with a high prevalence in genotype-positive (phenotype-negative) hypertrophic cardiomyopathy patients, but in none of a normal control group.

More recently, however, a study has shown that they are not uncommonly seen as an incidental finding in cardiac MRI studies, with an overall prevalence of 6.7%, although the prevalence is higher in patients with hypertrophic cardiomyopathy, myocarditis and hypertension.

So are myocardial crypts significant or not? The jury is still out, but for now the incidental finding of myocardial crypts, especially if multiple, should always prompt a careful review for any other imaging findings, clinical features or family history that might point towards a diagnosis of hypertrophic cardiomyopathy.

Maron MS, et al. Prevalence and Clinical Profile of Myocardial Crypts in Hypertrophic Cardiomyopathy. Circulation: Cardiovascular Imaging 2012; 5: 441-447.

Petryka J, et al. Prevalence of Inferobasal Myocardial Crypts Among Patients Referred for Cardiovascular Magnetic Resonance. Circulation: Cardiovascular Imaging 2014; 7: 259-264.