11.6.3 Clinical manifestations

 

 Many years can pass without symptoms, while the MI causes LV enlargement, impaired contractility and volume overload in the LA, which gradually dilates [1]. When they do occur, the clinical manifestations are determined by the size of the regurgitant volume and the LV function: dyspnoea due to pulmonary venous pressure overload (backward failure), fatigue due to the drop in effective systemic flow (forward failure), palpitations due to arrhythmias. If the atrium is very dilated and very compliant, it protects the lungs from the effects of MI and congestion is not very marked; the patient's main symptom is systemic weakness. However, dilation of the atrium increases the risk of arrhythmia and atrial fibrillation, which is clinically manifested by palpitations. If the MI progresses rapidly (e.g. chord rupture), the LA must accommodate the regurgitant volume without having had time to dilate; pressure rises and congestion is significant, often leading to pulmonary oedema; dyspnoea dominates the clinical picture. Sometimes very asymmetric regurgitation, directed towards the pulmonary veins on one side only, can cause unilateral pulmonary oedema.

As patients gradually reduce their activity, they do not always complain of fatigue. The best criterion is to ask about the most vigorous activity they can do. Auscultation will reveal a constant high-pitched apical pansystolic murmur radiating in the direction of the MI jet, generally towards the left axillary region (Figure 11.72). In prolapse and rupture, the radiation may be different depending on the orientation of the MI. There is little correlation between the intensity of the murmur and the severity of the insufficiency [2]. As the regurgitant volume returns to the ventricle in diastole, the anterograde mitral flow is increased and accelerated, often resulting in a high-flow diastolic murmur. The pulse is rapid and hyperdynamic. The ECG shows evidence of left ventricular hypertrophy and wide P waves in DII, bifid in V1. A stress test such as the 6-minute walk or dobutamine stress echo often leads to reclassification of asymptomatic patients from stage C (asymptomatic, with or without ventricular dysfunction) to stage D (symptomatic). A reduction in LV size on dobutamine indicates some functional reserve and a good prognosis, in contrast to worsening symptoms and MI, which indicate a decompensated state [9].

Medical therapy is limited in organic MI; vasodilators are only beneficial in functional or ischaemic MI. Atrial fibrillation requires systemic anticoagulation (dicoumarin for INR 2-3) and ventricular failure requires treatment of heart failure [8]. The presence of a secondary MI is a poor prognostic factor, and worsening prognosis is directly proportional to the size of the mitral leak.

The prognosis of mitral insufficiency is determined by a number of factors [9].

• Factors associated with regurgitation
  • Severity of the MI;
  • Chords rupture, deformation of structures;
  • Multiple leaflet damage;
  • Secondary MI.
• Clinical factors:
  • Age;
  • Functional class, severity of symptoms;
  • Coronary artery disease;
  • Ventricular failure;
  • Delay in intervention relative to onset of decompensation.
• LV and LA related factors:
  • EF < 60%;
  • LV dilatation (telesystolic diameter > 4.0 cm);
  • LA dilatation (volume > 60 mL/m²).
• Haemodynamic factors:
  • Atrial fibrillation;
  • Pulmonary hypertension.

 

 Figure 11.72: Auscultation in mitral insufficiency. The murmur is pansystolic, soft and regular and radiates towards the axilla.

 Clinically, mitral insufficiency is divided into 4 progressive stages, analogous to those of ventricular insufficiency [8,9].

• Stage A: Presence of risk factors for the development of MI (e.g. Barlow's disease);
• Stage B: Presence of moderate MI with progressive factors;
• Stage C: severe asymptomatic MI;
  • C1: preserved ventricular function
  • C2: ventricular decompensation and/or remodelling;
• Stage D: severe symptomatic MI.

 Functional examination

Contractility deteriorates progressively under very favourable loading conditions: ejection fraction (EF), which is particularly dependent on afterload, is an ineffective predictor of postoperative function [7]. An EF of 0.6 is no guarantee of preserved function, and a value of 0.5 already indicates significant impairment of systolic performance [4,10]. An EF of 0.4 indicates severe dysfunction that is unlikely to be significantly improved by surgical correction [3,7].

LV telesystolic dimensions correlate best with function and postoperative survival [5]. A normal telesystolic volume (LV diameter < 2.5 cm/m² or < 4 cm) corresponds to good contractility and a good postoperative prognosis (mortality ≤ 1%), whereas a diameter > 3.0 cm/m² indicates significant ventricular dysfunction and no longer ensures functional recovery after surgical correction (operative mortality 5-6%) [5,6,7]. For example, after mitral valve surgery, the incidence of left ventricular dysfunction is 9% when the LV telesystolic diameter is < 3.7 cm and 33% when it is > 3.7 cm [11].

In summary, the clinical features of mitral insufficiency are as follows

 

Characteristics of mitral insufficiency

High preload (LV volume overload) Low afterload (MI leaks when PLV > P LA) LV dilatation (telediastolic diameter > 7 cm or > 4 cm/m2) Impaired systolic function despite preserved EF Criterion for LV dysfunction: telesystolic diameter > 4 cm (> 2.5 cm/m2) MI increases when : RAS ↑ , Vtd ↑ , contractility ↓ Systemic CO dependent on low SAR Intolerance to hypovolemia

 

 

 © CHASSOT PG, BETTEX D, August 2011, last update November 2019