Clinical Editor's Corner: Kern

A Brief Review of Hemodynamics for Structural Interventions Part 1: Mitral Regurgitation

Morton Kern, MD, MSCAI, FACC, FAHA
Clinical Editor; Chief of Medicine
Long Beach VA Medical Center
Long Beach, California;
Associate Chief Cardiology, 
University of California, Irvine Medical Center, Orange, California

Morton Kern, MD, MSCAI, FACC, FAHA
Clinical Editor; Chief of Medicine
Long Beach VA Medical Center
Long Beach, California;
Associate Chief Cardiology, 
University of California, Irvine Medical Center, Orange, California

Correction to Figure 1: Figure 1 is incorrectly labeled in the print version, where the two papillary muscles should be labeled as “anterolateral” (instead of the incorrectly shown posterolateral) and “posteromedial” (instead of the incorrectly shown anteriomedial). CLD thanks Dr. Jason Rogers for alerting us to this error in the original figure. It is corrected online.


Mitral Valve Anatomy

As we are now deep into an era where structural heart interventional procedures are becoming routine, our fellows mentioned that a review of basic hemodynamics and interpretation of pressure waveforms would be helpful. With this in mind, let’s briefly review hemodynamics that might be seen during MitraClip (Abbott Vascular) implantation for mitral regurgitation (MR). In Part 2, to follow in the next issue of CLD, we will review the hemodynamics of balloon valvuloplasty for mitral stenosis (MS).

Mitral valve function and hemodynamics are determined by the coordinated operation of the two valve leaflets, and the subvalvular components1, which include the restraining chordae tendinae and attached papillary muscles that are influenced by the function and anatomy (e.g., dilation) of the left ventricle (Figure 1). Figure 2 shows the cross-sectional computed tomography (CT) anatomy of the left atrium (LA) and portion of the left ventricle (LV). The pressure waves in the LA are determined by three inputs and outflows:  1) the pulmonary vein flow as inputs; 2) the transmitral valve outflow; and 3) the LV backflow or resistance to LA outflow. The net result of pressure waves in the LA (and any other chamber) is also the result of the overall compliance or stiffness of the LA as plotted by the pressure/volume curves (Figure 2, lower right). A low compliance LA (i.e., stiff chamber) has a steeper pressure-volume (P-V) curve (upper curve), which means that a small change in flow can produce a big change in pressure and vice versa for a high compliance LA (i.e., compliant or easily expandable stiffness) (lower curve).

Normal Mitral Valve Hemodynamics

The famous Charles Wiggers diagram (Figure 3) describes normal cardiac pressures over the cardiac cycle corresponding to the electrocardiogram (ECG) (top of Figure 3). The LA pressure waveform normally demonstrates three waves representing three phases of the cycle: atrial systole (‘a’), ventricular contraction generating the ‘c’ wave, and the atrial filling ‘v’ wave. Clinically, in the cath lab, we often superimpose the pulmonary capillary wedge (PCW) (or LA) pressure over the simultaneous LV pressure tracing to assess mitral valve hemodynamics, either regurgitation or stenosis. As a reminder, the left ventricular end diastolic pressure (LVEDP) occurs at the end of ‘a’ wave and can be marked by a line from the ECG ‘r’ wave (Figure 3, right side, dotted line). Notably, because the LVEDP includes atrial contraction rather than only passive filling, in certain states, it can significantly exceed the PCW or mean LA pressure.

The ‘v’ Wave and MR

The size of the ‘v’ wave is the result of pressure, flow and the compliance of the LA. For example, a non-compliant LA after a cardiac operation, infection, or from an infiltrative myopathic process can produce a large ‘v’ wave even for normal filling. In cases where the mitral valve leaflets, chordae, or papillary muscle fail, the high pressure in the LV is transmitted into the LA, resulting in a large ‘v’ wave. A low compliance LA has a steeper P-V curve (upper curve on Figure 2) than a high compliance curve (lower curve) and therefore, because of the unknown variable of compliance, a large ‘v’ wave alone is of limited value in the prediction of MR.2

On physical exam, MR is usually detected by loud, holosystolic murmur and by transthoracic or transesophageal echocardiography3 (Figure 4), where a large, eccentric MR high velocity jet (arrow) into the LA can be visualized. Hemodynamically, severe MR is often associated with large ‘v’ waves (Figure 4, right side). Note on this tracing that there is a ‘c’ wave, but no ‘a’ wave, as the patient is in atrial fibrillation. The simultaneous right atrial pressure (RA) has no significant ‘v’ wave, indicating little if any tricuspid regurgitation or very high RA chamber compliance. The pullback of the LA pressure catheter across the atrial septum at the vertical line (*) showed matching of LA/RA pressures.

MR Leading to Pulmonary Hypertension

In patients with MR, the LV and LA pressure waveforms have different patterns depending on whether they occur in a compensated or decompensated patient (Figure 5).3 Acute, severe MR is generally associated with large ‘v’ waves, severely elevated LVEDP, and low peak LV systolic pressure, often with low forward cardiac output or cardiogenic shock. With progressive LV and LA dilation in compensated chronic MR, the peak ‘v’ wave and LVEDP remain relatively low. As LV systolic function deteriorates and LA compliance decreases in decompensated chronic MR, peak ‘v’ waves and LVEDP increase. After mitral valve surgery, there is generally a significant decrease in peak ‘v’ waves and mean LA pressures. The pattern of LA/LV waveforms are related to the LV contractile function and chamber compliances. Over time, as decompensation occurs, LA pressure, which is not elevated in the compensated severe MR setting, will begin to rise as a result of LV systolic or diastolic dysfunction, or reduced LA compliance. The processes that govern the development of pulmonary hypertension in MR are multifactorial.4 Chronic MR is believed to be one of the common initiating factors of pulmonary hypertension.

Reduction of MR With MitraClip and LA Pressure Changes

The percutaneous repair of MR using the MitraClip (Figure 6) is a remarkable advance5 and provides an unprecedented opportunity to observe the LA pressures as the regurgitant volume decreases. This information can help assess the success of the procedure and prognosticate about how patients will do over the long term. Gajjar et al6 demonstrated continuous LA pressure monitoring during MitraClip (Figure 7) using a new modification of the standard delivery system permitting measurement of pressure through the guide catheter. The ability to easily and reliably measure continuous LA pressure will likely improve the effectiveness and efficiency of the MitraClip procedure. Indeed, Kuwata et al7 reported on 50 patients having MitraClip repair with recording of continuous LA ‘v’ wave pressure (LAvP), LA mean pressure (LAmP), LV systolic pressure, and LV end-diastolic pressure (Figure 8A). In multivariate Cox regression analysis, increase of LAmP index, but not post-MitraClip ≥2 residual MR, was associated with rehospitalization due to heart failure (P=.007) and with New York Heart Association (NYHA) class III to IV (P=.005) in the follow-up period. An increase in LAmP was a predictive of worse clinical outcomes at short-term follow-up, independent from echocardiographic findings (Figure 8B).

MR Confounder: The Perivalvular Regurgitant Jet

‘V’ waves can result from high regurgitant flow across the mitral valve or flow around a recently implanted valve with a large perivalvular leak. The pressure waves look identical as the mechanisms are nearly identical. Nkomo et al8 present a beautiful demonstration of a large ‘v’ wave of a perivalvular leak (Figure 9). Four Amplatzer vascular plugs (Abbott Vascular) were deployed to close the posteromedial and anterolateral leaks. A marked reduction in paravalvular prosthetic MR with significant hemodynamic reduction of the large ‘v’ wave post procedure was seen. Percutaneous device closure is an effective procedure for the treatment of clinically significant paravalvular prosthetic regurgitation.

The Bottom Line

Careful inspection of the anticipated and characteristic pressure waves will confirm clinical impressions and echocardiographic findings. LA pressure waves are a function of the chamber compliance; a stiff LA can produce large ‘v’ waves without mitral regurgitant flow. Monitoring LA pressure during MitraClip procedures appears to be helpful in predicting outcomes.

I hope this review has been helpful. Stay tuned for Part 2 on mitral valvuloplasty hemodynamics in our next column.

Disclosures: Dr. Morton Kern reports he is a consultant for Abiomed, Abbott Vascular, Philips Volcano, ACIST Medical, Opsens Inc., and Heartflow Inc.


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  3. Matiasz R, Rigolin VH. 2017 focused update for management of patients with valvular heart disease: summary of new recommendations. J Am Heart Assoc. 2018; 7: e007596.
  4. Patel H, Desai M, Tuzcu EM, et al. Pulmonary hypertension in mitral regurgitation. J Am Heart Assoc. 2014; 3(4): e000748.
  5. Feldman T, Kar S, Rinaldi M, et al; EVEREST Investigators. Percutaneous mitral repair with the MitraClip system: safety and midterm durability in the initial EVEREST (Endovascular Valve Edge-to-Edge REpair Study) cohort. J Am Coll Cardiol. 2009 Aug 18; 54(8): 686-694.
  6. Gajjar M, Yadlapati A, Van Assche LMR, et al. Real-time continuous left atrial pressure monitoring during mitral valve repair using the MitraClip NT system: a feasibility study. JACC Cardiovasc Interv. 2017 Jul 24; 10(14): 1466-1467.
  7. Kuwata S, Taramasso M, Czopak A, et al. Continuous direct left atrial pressure intraprocedural measurement predicts clinical response following MitraClip therapy. J Am Coll Cardiol Intv. 2019; 12: 127-136.
  8. Nkomo VT, Pislaru SV, Sorajja P, Cabalka AK. Plugged!. J Am Coll Cardiol. 2013; 61(3): 356-356.