11.13.4 Other combinations

 Aortic insufficiency and mitral insufficiency

This combination is common. Aortic insufficiency is most often the major lesion, because AI represents high pressure volume overload (PAdiast), whereas MI represents low pressure volume overload (PRA). LV dilatation is a serious phenomenon leading to severe dysfunction, whereas LA dilatation is benign. On the other hand, MI may be secondary to LV dilatation on the AI (functional MI). The high total regurgitant fraction results in increased circulating volume and dilatative hypertrophy of the LV. Ventricular dysfunction is usually severe and the risk of failure after AVR + MVR is significant [2]. The increase in diastolic intraventricular pressure caused by AI leads to premature closure of the mitral valve if the valve is normal; this phenomenon, which reduces the impact of AI, does not occur if the mitral valve is also inadequate. The ideal haemodynamic conditions for each lesion are quite similar, regardless of the dominant lesion. Anterograde flow depends on peripheral resistance and increases when afterload is low.

Valves can be damaged by certain drugs that induce fibrosis and leaflet retraction, notably adriamycin, methysergide, ergotamine, pergolide and certain anorectics (fenfluramine, phentermine, aminorex, benfluorex). Valvular damage leads to insufficiency, most commonly of the aortic but also of the mitral valve, associated with tricuspid insufficiency.

Minimal valve insufficiency (grade I) is common in the normal population, especially from the age of 60. After the age of 65, the incidence in a normal Western population is 11% for the aortic valve, 48% for the mitral valve and > 75% for the tricuspid valve [4,5]. They are of no clinical significance and do not require prophylactic antibiotic treatment.

The detection of MI in a patient undergoing aortic valve replacement (AVR) raises the question of its severity and origin [3].

  • Severe structural MI: concomitant prosthesis or replacement is usually recommended.
  • Functional MI: if secondary to LV dilatation, MI tends to decrease with ventricular size after AVR, but if severe (30% of cases), it increases mortality from surgery. If it is moderate or moderate-to-severe, it increases the risk of postoperative ventricular failure. In moderate to severe secondary MI, simple reduction annuloplasty is an option if the surgical risk is low or moderate, as it does not increase perioperative morbidity and mortality [1]. In severe (class IIa) MI, surgery is recommended [4].

 

Hemodynamics in aortic and mitral insufficiency 
In terms of equivalent severity, AI is the most severe component.
Near-optimal conditions for both defects
High preload
High rate
Contractility preserved
Low SAR
Normal PAR

 

Aortic insufficiency and mitral stenosis

This combination imposes opposite preload conditions on the LV. It has the advantage of maintaining satisfactory left ventricular dimensions: in the absence of anterograde diastolic filling (mitral stenosis), the LV fills by aortic reflux and maintains an adequate volume. On the other hand, its dilatation is reduced by the small volume supplied by the mitral valve. The massive increase in stroke volume and pulse pressure typical of AI is absent.

The preoperative assessment and the clinical manifestations should make it possible to determine which lesion is the most haemodynamically significant; generally, this is mitral stenosis. On echocardiography, the size of the LV (small in mitral stenosis, enlarged in aortic regurgitation), the size of the LA (huge in mitral stenosis) and the Doppler flows through the two valves give a more relevant answer than the symptomatology, which is generally dominated by the proximal lesion, masking the importance of the distal lesion. However, the calculation of the mitral surface area using the half-pressure time (Pt1/2) is distorted by the simultaneous filling of the LV by the AI; only planimetry (in 3D if possible) allows an accurate measurement. The indication for surgery is generally based on the presence of pulmonary hypertension.
 
 
 
Hemodynamics sought in aortic insufficiency and mitral stenosis 
 In terms of equivalent severity, mitral stenosis predominates
High preload
Normal rate (avoid tachycardia)
Preserved contractility
Low SAR
Low PAR (frequent PHT)
 
 
 Aortic and mitral stenosis
 
Again, the haemodynamic effect of mitral stenosis dominates the picture as it is the first barrier to blood flow. The symptoms are dominated by pulmonary congestion and hypertension. The left ventricle is small, noncompliant and concentrically enlarged. Cardiac output is low, with no real possibility of increasing it; stroke volume is fixed and low. Aortic stenosis is therefore easily underestimated by measuring transvalvular systolic gradients (low flow/low gradient situation). 
 
Double stenosis is usually of rheumatic origin. In calcific degeneration, aortic stenosis dominates the picture; mitral stenosis is less significant. It is characterised by calcification of the mitral annulus and the base of the leaflets and is usually associated with a variable degree of MI. While double valve replacement is necessary in ARF, the situation is more complex in calcific degeneration. These are usually elderly patients for whom a double operation is too risky. It is usually possible to manage with AVR if the mitral valve has moderate or not very severe lesions. Temporary relief of mitral obstruction by percutaneous balloon commissurotomy is possible in ARF (but not in calcific disease), but this treatment is dangerous if the aortic obstruction is not removed first, because of the sudden increase in preload on a restrictive, poorly compliant LV, which will immediately become congested [7]. 
 
 
Hemodynamics sought in aortic and mitral stenosis 
 High preload
Low frequency
Preserved contractility
High SAR (because SV is fixed and low)
Low PAR (frequent PHT)
After ECC: stroke volume remains very limited
 
 
 Left-sided valve disease and tricuspid insufficiency
 
This combination indicates dilatation of the tricuspid annulus due to right-sided overload in the presence of significant pulmonary hypertension. If the TI is mild or moderate and the tricuspid valve is normal, the reduction in PHT with correction of the left-sided valve disease is sufficient to reduce tricuspid regurgitation. On the other hand, the presence of moderate to severe TI increases the long-term mortality of left-sided correction. Therefore, concomitant correction of left valve is preferred in the following situations [6]:
 
  • Severe and symptomatic TI;
  • Severe TI due to organic tricuspid pathology (ARF, prolapse, endocarditis, etc);
  • Moderate to severe TI with tricuspid annular dilatation (D > 4.0 cm on echo) and/or RV failure;
  • Moderate TI with annular dilatation, RV failure and/or severe PHT (class IIa).
 In these conditions, TI is a sign of progressive tricuspid disease, which will progressively worsen and worsen the patient's prognosis. It requires correction at the same time as surgery on the left valve (usually annuloplasty) [4].
 
 
Left-sided valve disease and tricuspid insufficiency 
Management is dominated by the constraints of left-sided valve disease and any right-sided ventricular failure.  
 
Indications for concomitant tricuspidoplasty
- Severe symptomatic TI (primary or secondary)
- Severe TI with tricuspid annular dilatation (symptomatic or not) 
- Moderate TI with annular dilatation, RV failure and/or severe PHT
 
 
 
 
© CHASSOT PG, BETTEX D, August 2011, last update November 2019

 

References

 

  1. CONTINHO GF, COREIRA PM, PANCAS R, et al. Management of moderate secondary mitral regurgitation at the time of aortic valve aurgery. Eur J Cardio-Thorac Surg 2013; 44:32-40
  2. GENTLES TL; FINUCANE AK, REMENYI B, et al. Ventricular before and after surgery for isolated and combined regurgitation in the young. Ann Thorac Surg 2015; 100:1383-9
  3. MALHOTRA A, RAMAKRISHNA H, GUTSCHE JT, et al. Options for incidental mitral regurgitation found during aortic valve surgery for aortic regurgitation: an evidence-based clinical update for the perioperative echocardiographer. J Cardiothorac Vasc Anesth 2016; 30:555-60
  4. NISHIMURA RA, OTTO CM, BONOW RO, et al. 2014 AHA/ACC Guideline for the management of patients with valvular     heart disease. Circulation 2014; 129:e521-e643 
  5. OH JK, SEWARD JB, TAJIK AJ. The echo manual. 3rd edition. Philadelphia, Lippincott Williams & Wilkins, 2006, 189-242
  6. TARAMASSO M, VANERMEN H, MAISANO F, et al. The growing clinical importance of secondary tricuspid regurgitation. J Am Coll Cardiol 2012; 59:703-10
  7. UNGER P, CLAVEL MA, LINDMAN BR, et al. Pathophysiology and management of multivalvular disease. Nat Rev Cardiol 2016; 13:429-40