Clinical Editor's Corner: Kern

A Brief Review of Hemodynamics for Structural Interventions Part 2: Mitral Stenosis

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
mortonkern2007@gmail.com

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
mortonkern2007@gmail.com

Last month1, we reviewed the hemodynamics of mitral regurgitation and the changes seen with the mitral clip percutaneous repair on the left atrial pressure waves. In Part 2 of our brief hemodynamic review for structural heart interventions, we will focus on mitral stenosis and mitral balloon valvuloplasty.

The Stenotic Mitral Valve: Anatomy and Function

The stenotic mitral valve is characterized by thickened leaflets with reduced excursion. In the case of rheumatic mitral stenosis (MS), this thickening, calcification, and shortening can extend to involve the subvalvular apparatus (Figure 1). In the elderly, a very calcific, narrowed mitral annulus with extension into the base of the mitral valve leaflets can produce stenosis without as much impairment of the leaflet tip motion. Rare congenital causes of MS also include congenital parachute mitral valve, in which the leaflets attach to a single papillary muscle.

To recap the associated hemodynamic principles, the pressure waves in the left atrium (LA) are determined by 1) the pulmonary vein flow entering the LA from the lungs; 2) the transmitral valve outflow into the LV; and 3) the left ventricular (LV) back pressure or flow, producing resistance to LA outflow. Pressure waves in the LA (and any other chamber) are also the net result of the chamber (LA) stiffness. A low-compliance LA (i.e., stiff chamber) has a steeper P-V curve, which means that a small change in flow can produce a big change in pressure, and vice versa for a compliant or easily expandable LA chamber.2 Rheumatic heart disease affects LA stiffness as well as the anatomic valve-related structures.

Transvalvular Mitral Hemodynamics and Clinical Presentations

For MS, increased LA pressure raises the pulmonary venous and capillary pressures, resulting in exertional dyspnea. A transvalvular pressure gradient is a function of the flow and can be calculated by Doppler flow velocity (V) as ΔP=4V2. Thus, a doubling the velocity quadruples the pressure gradient. Exacerbating conditions for MS include tachycardia, pregnancy, hyperthyroidism, anemia, infection, and atrial fibrillation, and all of these conditions have one feature in common: an increased heart rate with reduced diastolic filling time. With tachycardia, diastole shortens more than systole, so that at any given stroke volume, the pressure gradient increases faster than the flow velocity. In atrial fibrillation, the irregular rhythm and loss of the atrial contraction further reduces the cardiac output by about 20%, a reduction independent of the increased resistance to transvalvular flow. The combination of reduced flow with high LA pressures ultimately brings about the onset of symptoms.3 The severity of MS is summarized in Table 1.

The percutaneous balloon valvuloplasty approach to mitral stenosis is the preferred treatment if subvalvular disease, calcification, thickening, and mobility of the valve leaflets is moderate or less (using a Wilkin’s score4<11), mitral valve regurgitation is no greater than mild, and thrombus is not present in the left atrium. Table 2 provides scores with recommendations from the American College of Cardiology/American Heart Association (ACC/AHA) for percutaneous balloon mitral valvuloplasty (PBMV). The results of PBMV are equal or superior to surgical commissurotomy. The rate of success and complications correlates strongly with experience; both the success and avoidance of complications are predicated in part on appreciating subtleties of hemodynamics during the screening and intra-procedure phases of management.5

Hemodynamics of MS Before and After Balloon Valvuloplasty

In general, the stenotic mitral valve area (MVA) can be measured in several ways (Figure 2).6 With confidence in the echocardiographic data, patients may be suitable for balloon valvuloplasty to open the stenotic valve and permit adequate cardiac output, and keep pulmonary hypertension at bay. At times, with equivocal data, exercise hemodynamics in the cath lab may be necessary. For best pressure and gradient data, use direct LA pressure from a transseptal approach rather than the pulmonary capillary wedge pressure (Figure 3). However, when pulmonary capillary wedge pressure is low and normal, it provides an effective first-line tool to screen for significant mitral valve gradients.

Percutaneous Mitral Balloon Valvuloplasty (PBMV) Hemodynamics

PBMV results in a gradient decrease of 50% or more, and a valve area increase to 1.5 cm2, the definition of success in the majority of the literature. In ideal valve anatomy, the mitral valve area will typically increase to 1.8 cm2 or more. Examples of the hemodynamic changes occurring in the pressure wave forms for a patient with MS before and after mitral balloon valvuloplasty are shown on Figure 4.

Figure 5 demonstrates the results of PBMV in young patient with low Wilkins scores with reduction of the mitral gradient after a single balloon inflation. Although occasionally seen, caution in achieving complete resolution of a residual gradient should be used to avoid producing severe mitral insufficiency. In fact, the absence of a gradient after PBMV more commonly correlates with severe mitral insufficiency. The hemodynamics of this example suggest a competent valve; in fact, no mitral regurgitation was detected by echocardiography. It is worth noting that there is often a characteristic minimal peri-commissural leak seen with successful PBMV.

The typical step-wise Inoue balloon (Toray) technique for PBMV involves assessing a maximal balloon size using the patient’s height; inflations usually begin with a balloon size several millimeters smaller (Figure 6). After each inflation, hemodynamics are reviewed for reduction of gradient and induction of any new mitral regurgitation. This is done by a combination of echocardiography (transesophageal or intracardiac echo, and occasionally, by transthoracic echo) and hemodynamics. A decrease in gradient of at least 50% and particularly an increase in mitral insufficiency by one grade should signal the operators to stop. Figure 7 shows this stepwise dilatation technique with an unfortunate result. The initial tracing (Figure 7, left panel) is consistent with severe mitral stenosis in a severely symptomatic woman. After initial inflation the gradient is significantly reduced (Figure 7, middle panel), but the operators continued to attempt to achieve a lower residual gradient. The next inflation with a 1 mm-larger balloon resulted in abolition of the gradient, but produced a giant ‘v’ wave to 70 mmHg (Figure 7, right panel), consistent with severe iatrogenic mitral insufficiency. At surgery to repair the torn valve, a commissure split was the predominant mechanism. The patient did well after emergency mitral valve replacement.

The Bottom Line

Mitral stenosis is relatively uncommon in the United States, but still plagues many developing areas of the globe. Prior to PBMV, the patient should have a thorough physical examination and graphics of the chest x-ray, electrocardiogram (ECG), and detailed 2D and 3D echocardiography. Should conflicting data between clinical presentation and graphic data of stenosis severity appear, exercise hemodynamic studies may be needed before proceeding to PBMV. Attention to the pressure gradient reduction during PBMV should guide the operators to achieve a satisfactory result with a reduced gradient, but a competent valve. Remember, sometimes the enemy of good is better.

As with our other presentations, I hope the hemodynamic review and waveform interpretation becomes a routine part of your structural heart disease interventional program. 

References
  1. Kern MJ. A brief review of hemodynamics for structural interventions part 1: mitral regurgitation. Cath Lab Digest. 2019 Apr; 27(4): 4-10.
  2. Kern MJ, Goldstein JG, Lim MJ (ed). Hemodynamic Rounds: Interpretation of cardiac pathophysiology from pressure waveform analysis. 4th ed. New York, New York: Wiley-Liss; 2017.
  3. Nishimura RA, Otto CM, Bonow RO, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Jun 10; 63(22): 2438-2488. doi: 10.1016/j.jacc.2014.02.537.
  4. Wilkins GT, Weyman AE, Abascal VM, et al. Percutaneous balloon dilatation of the mitral valve: an analysis of echocardiographic variables related to outcome and the mechanism of dilatation. Br Heart J. 1988; 60(4): 299-308.
  5. Ben Farhat M, Ayari M, Maatouk F, et al. Percutaneous balloon versus surgical closed and open mitral commissurotomy: seven-year follow-up results of a randomized trial. Circulation. 1998; 97(3): 245-250.
  6. Fredman CS, Pearson AC, Labovitz AJ, Kern MJ. Comparison of hemodynamic pressure half-time method and Gorlin formula with Doppler and echocardiographic determinations of mitral valve area in patients with combined MS and regurgitation. Am Heart J. 1990 Jan; 119(1): 121-129.
  7. American College of Cardiology/American Heart Association Task Force on Practice Guidelines; Society of Cardiovascular Anesthesiologists; Society for Cardiovascular Angiography and Interventions; Society of Thoracic Surgeons, Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2006 Aug 1;48(3):e1-e148.