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.
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)
|
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
|
- 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).
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
|
References
- 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
- 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
- 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
- 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
- OH JK, SEWARD JB, TAJIK AJ. The echo manual. 3rd edition. Philadelphia, Lippincott Williams & Wilkins, 2006, 189-242
- TARAMASSO M, VANERMEN H, MAISANO F, et al. The growing clinical importance of secondary tricuspid regurgitation. J Am Coll Cardiol 2012; 59:703-10
- UNGER P, CLAVEL MA, LINDMAN BR, et al. Pathophysiology and management of multivalvular disease. Nat Rev Cardiol 2016; 13:429-40