11.9.2 Pathophysiology

Aortic insufficiency (AI) represents a volume overload for the LV, which it compensates by increasing its end-diastolic volume. This increase in preload allows it to maintain an adequate stroke volume (Frank-Starling principle); in addition, tachycardia increases cardiac output. For the LV, the increase in wall tension due to dilatation is equivalent to an increase in afterload during protosystole; it induces eccentric hypertrophy. In contrast to mitral insufficiency (MI), where leakage into the LA keeps afterload low despite excess systolic volume, aortic insufficiency forces the LV to eject all its volume into the aorta, which is a high-pressure system. On the other hand, the upstream pressure of regurgitation is the aortic diastolic pressure (40-80 mmHg), which is much higher than the LA pressure in systole (5-10 mmHg). In AI, the SAR directly controls LV afterload in systole and the regurgitant fraction in diastole. Reducing SAR is therefore doubly important for LV function.
  • AI decreases when APdiast decreases;
  • LV ejection is improved when APsyst decreases.

Because it is both a volume and pressure overload, AI is less well tolerated than MI [4]. The amount of blood that regurgitates from the aorta to the LV depends on

  • The surface area of the orifice kept open in diastole (severe AI: > 0.3 cm2).
  • Duration of diastole: bradycardia increases the duration of diastole and therefore the volume of regurgitation.
  • The pressure gradient between the aorta and the LV in diastole: this depends on the pressure in the ascending aorta, the SAR and ventricular compliance; it is highest in protodiastole and decreases with increasing AI (rapid equilibration of aortic and intraventricular pressure).

Tachycardia shortens diastole and the volume regurgitated per cardiac cycle decreases. As a result, LV dilation is slowed. Bradycardia is a major hazard because of the overfilling of the LV during long diastole, when the AI pours a large amount of blood into the ventricle. The optimum rate is probably around 80-90 beats per minute. It is certainly dangerous to go below 60 beats per minute.

 Chronic aortic insufficiency

As ventricular dilatation increases wall stress (σ ), the LV will thicken and hypertrophy to keep this stress normal (Laplace's law: σ = (P · r) / 2h). This leads to eccentric or dilatory hypertrophy by serial replication of the sarcomeres and elongation of the fibres (Figure 11.128) [9].

Over time, myocardial fibrosis progresses; it is clearly visible on MRI and is doubly punishing: fibrotic myocardium no longer participates in contraction but reduces diastolic compliance. Laplace's law states that the larger the ventricle, the greater the wall stress required to develop the same systolic pressure. Chronic AI causes the greatest ventricular enlargement of all cardiopathies: ventricular mass can be impressive, reaching > 600 g (bovine heart). With regurgitation rates of up to 5-8 L/min, the LV is forced to deliver 10-12 L/min to maintain peripheral perfusion ! Exercise is relatively well tolerated because the SAR decreases and tachycardia shortens diastole: the regurgitant fraction decreases [7]. The usual indices of systolic function, such as ejection fraction, are generally within normal limits, but do not reflect the true contractility of the myocardium with maximum use of preload reserve. The telesystolic dimension of the LV (diameter > 2.5 cm/m2 ) is a more useful index for determining the patient's prognosis, as it is less dependent on preload [3]. The ratio of wall stress to telesystolic volume is the best predictor of functional recovery after AVR [10].

As long as systolic function is preserved, compliance is preserved; the dilated ventricle accommodates large volumes at still normal filling pressures; progressive volume overload has shifted the entire compliance curve to the right (Figure 11.129). However, the slope of the diastolic P/V relationship is straightened at high volumes; in acute failure the LV operates on the rising part of the curve, i.e. at high diastolic pressure. The pressure-volume diagram for AI also shows that the Emax-compliance-P/V loop triangle, the area of which represents the internal work of pressure (IWP), is of variable size. During the period of compensation, the ventricle expends more energy on the external work of ejection; this ratio is favourable for energy efficiency and O2 consumption . However, as dilation worsens, wall tension becomes excessive and the effective afterload of the LV increases; the IWP increases.

Fig11 128 en
 
Figure 11.128: Schematic representation of left ventricular remodelling in weaning aortic insufficiency. A: Normal heart. Laplace's law states that wall stress (σ ) is proportional to the pressure generated (P) and the radius of the cavity (r) and inversely proportional to its thickness (h). B: Severe aortic insufficiency. The left atrium is dilated, the LV undergoes severe dilatative hypertrophy, its wall is thickened and its cavity is very enlarged. Chronic AI results in the greatest dilatation of the LV.
 
Fig11 129 en
 
 Figure 11.129: Pressure-volume loop in chronic aortic insufficiency (AI). The compliance curve is shifted to the right because of the increase in diastolic volume due to the regurgitation that occurs at the diastolic pressure of the aorta, but its slope remains very flat because the LV is still flexible. The ejected volume is immense (SV) compared to its normal value (yellow) because AI causes the greatest ventricular dilatation seen in clinical practice (bovine heart). The work of pressure (light blue dotted triangle) is increased due to the high wall tension (dilatation) in protosystole. In acute AI, the LV volume is at the upper limit of normal but does not have time to expand; on the other hand, diastolic overfilling with normal compliance leads to a very significant increase in diastolic pressure; the PV loop is reduced but elevated.
 
 As long as the LV geometry is preserved, replacement of the defective valve allows good functional recovery, but when the LV becomes spherical, remodelling and functional damage are irreversible [2]. As a result, LV size at telesystole is the best predictor of ventricular performance after AVR. 
 
Over time, decompensation sets in: systolic function declines, the LV continues to dilate, its wall stress increases, its ejection fraction decreases and the regurgitant fraction increases. As compliance decreases, ventricular diastolic pressure rises and pulmonary venous stasis develops, first on exertion and then at rest. Ischaemia is a late sign and occurs by several mechanisms [1,8].
 
  • Increased O2 demand due to high wall tension;
  • Decreased O2 supply due to low aortic diastolic pressure and high intraventricular pressure (coronary perfusion pressure: CPP = PAdiast - PtdLV);
  • Contractile mass increases disproportionately to the development of the coronary capillary network. 
 
Ischaemia further impairs systolic performance, creating a vicious circle: ischaemia → ↑ systolic function → ↑ AI → ↑ Vtd → ↑ wall tension → ↓ coronary perfusion →  more ischaemia. 
 
 Acute aortic insufficiency
 
Acute AI occurs mainly in cases of endocarditis, A dissection or trauma. It causes a sudden volume overload: the normally compliant LV dilates a little, but not as much as in chronic cases. Diastolic pressure and wall stress increase abruptly because the end-diastolic volume corresponds to the rectified part of the compliance curve (see Figure 11.17). This is even more pronounced when AI occurs in concentric LVH with a thick wall and small cavity, as in a hypertensive patient.
 
The physiological compensation is an intense sympathetic stimulation causing hypercontractility and tachycardia: effective flow is maintained by increasing total systolic flow. Unfortunately, sympathetic stimulation also increases systemic resistance, exacerbating diastolic regurgitation. When the valve is virtually destroyed, aortic diastolic and LV end-diastolic pressures equalise. The pressure increase due to retrograde filling of the LV is so rapid that the mitral valve closes prematurely in diastole [5]. Occasionally, ventricular dilatation prevents the mitral valve from closing normally, leading to diastolic MI [6]. Myocardial ischaemia is common due to collapse of coronary perfusion pressure (CPP = PAdiast - PtdVG), subendocardial pressure and tachycardia.
 
Acute AI rapidly leads to cardiogenic shock requiring intensive management with inotropic support (dobutamine, milrinone-adrenaline) and vasodilatation (nitroprusside). β-blockers and intra-aortic balloon pump are contraindicated. AVR is urgently required.
 
 
Pathophysiology of aortic regurgitation 
AI increases LV Vtd; in diastole the ventricle is filled by the diastolic pressure of the aorta (40-80 mmHg). Wall stress is increased in the protocole, which represents an increase in effective afterload. AI is a volume and pressure overload. It induces large ventricular dilatation.
 
AI increases as SAR increases and decreases as SAR decreases. LV ejection is facilitated when its afterload is low because its dilation makes it very sensitive to systolic wall stress. The decrease in SAR is therefore doubly important:
- AI decreases when diastolic pressure falls.
- LV ejection is improved when systolic pressure falls.
 
The longer the diastole, the greater the regurgitant volume; tachycardia allows it to be broken down into smaller units, thereby reducing the regurgitant fraction and ventricular dilatation. Tachycardia is beneficial, whereas bradycardia is dangerous. Optimum rate: 80-90 beats/min.
 
AI induces eccentric hypertrophy. EF does not reflect true LV function; telesystolic dimensions are a better criterion. Function is reduced when Vts > 2.5 cm/m2.
 
Myocardial ischaemia develops late due to three phenomena:
- ↑ mVO2 on ↑ Wall stress
- ↑ DO2 by ↓ PAdiast and ↑ PtdLV
- Insufficient capillary development in relation to contractile mass
 
 
 
 
 
 
  © CHASSOT PG, BETTEX D, August 2011, last update November 2019

 

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