**5. Echocardiographic predictors in patients with severe aortic stenosis and preserved left ventricular systolic function**

Global LV function, assessed by conventional EF remains normal in most of AS patients. However, the long axis systolic function, assessed by M-mode echocardiography and/or tissue Doppler imaging (TDI) velocities, decreases even in patients with preserved EF. In AS patients with preserved EF, the longitudinal velocity, strain and strain rate are decreased and deteriorate further as AS become severe. These changes reflect that the LV myocardial dysfunction beginning at the subendocardium in early stages of AS and progress to midwall and to transmural contraction impairment in patients with severe AS. Recent studies have shown also that in patients with AS and preserved LV EF, the apical rotation and LV twist are increased and untwist is delayed compared to normals, as compensatory mechanisms for the increased intracavitary pressure overload and subendocardial ischaemia. Also, it was shown that these LV myocardial correlate with the severity of AS. However, these compensatory mechanisms are lost after the LV EF deterioration.

Strong evidence exists showing beneficial effect of AVR, not only in improving patients' symptoms but also in recovering, even partially, overall cardiac function. Improvement of LV ventricular function in these patients is interpreted on the basis of regression of myocardial hypertrophy, increased myocardial perfusion and hence overall cavity performance, at early and mid-term post-operative periods. While EF is the most popular measure of pre-operative LV systolic function in such patients, and surgical risk assessment it lacks representing subendocardial component of the LV function.

Severe aortic stenosis causes significant subendocardial dysfunction despite preserved ejection fraction. Aortic valve replacement surgery and removal of left ventricular afterload results in recovery of intrinsic subendocardial function within a week of surgery, well before mass regression and reverse remodeling. Such degree of pre-operative subendocardial disturbances may represent early changes that if ignored may substantiate and become irreversible. Thus, the presence of such abnormalities in symptomatic patients, even with normal ejection fraction, may suggest further evidence for a need for valve replacement in order to maintain overall integral ventricular function and to avoid potential clinical complications.

In patients with severe aortic stenosis and and maintained LV EF, the left ventricular twist is increased as compared with normal subjects suggesting a wall motion compensation for the reduced long axis motion in the aim to preserve LVEF. These motions alter towards normal values within six months of aortic valve replacement (Figure 3). These findings are growing evidence that on LV dysfunction and their improvement after AVR, even in asymptomatic patients, and may assist in identifying patients needing surgery before LV damage becomes irreversible.

Echocardiography in Severe Aortic Stenosis 31

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Fig. 3. Example of LV rotation and twist in control, pre AVR and post AVR. Purple line showing peak of apical rotation and green showing peak basal rotation. AVR, aortic valve replacement (Reproduced from *Lindqvist P et al.* Aortic valve replacement normalizes left ventricular twist function. Interact CardioVasc Thorac Surg 2011;12:701-706, doi:10.1510/icvts.2010.262303, with permission from the European Association for Cardio-Thoracic Surgery).

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Fig. 3. Example of LV rotation and twist in control, pre AVR and post AVR. Purple line showing peak of apical rotation and green showing peak basal rotation. AVR, aortic valve replacement (Reproduced from *Lindqvist P et al.* Aortic valve replacement normalizes left

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**3** 

*Australia* 

**Epiaortic Ultrasound Assessment of the** 

A considerable burden of cerebral embolism in association with cardiac surgery reflects dislodgement of aortic atheroma caused by manipulating the aorta during a surgical procedure (Barbut and Gold 1996; Van Zaane, Zuithoff et al. 2008; Whitley and Glas 2008; Yamaguchi, Adachi et al. 2009). It clearly makes logical sense to identify and attempt to avoid dislodgement of aortic atheroma. This strategy depends on two key elements; the accurate detection of atheroma in the aorta, and the surgeons ability to avoid or otherwise

In this chapter we will describe how epiaortic echocardiography is essential to the complete examination of the ascending aorta and aortic arch for the detection of atheroma, and what surgical options may be available for the avoidance or minimisation of aortic atheroma

Whilst clinical stroke is relatively infrequent in cardiac surgery (1-3%) (Calafiore, Di Mauro et al. 2002; Douglas and Spaniol 2009; Rosenberger, Shernan et al. 2008; Shroyer, Coombs et al. 2003), such events can be properly viewed as major cerebral injury. Subclinical brain injury on the other hand is not often clinically apparent but may be detected by subtle neurocognitive testing and this is frequently present (20-60%) (Hammon, Stump et al. 1997; Mahanna, Blumenthal et al. 1996; Zamvar, Williams et al. 2002). MRI studies post cardiac surgery similarly highlight a far higher frequency of cerebral embolic events then the clinical assessment of neurological status would suggest (Deslauriers, Saunders et al. 1996; Djaiani, Fedorko et al. 2004; Vanninen, Aikia et al. 1998). Brain injury may be caused by other factors related to cardiopulmonary bypass, systemic inflammatory response syndrome, tissue oedema, air embolism, post-operative hypotension, anaesthetic agents used, ischaemia and reperfusion injury, or alternative causes of embolism. Nevertheless, the *predominant cause* of embolic brain injury reflects surgical manipulation of the atheromatous aorta and thus offers

**1. Introduction** 

manipulation.

minimise manipulation of atheromatous disease.

**2. Background summary of the literature** 

the greatest prospect for changing outcome.

**2.1 Intraoperative cerebral embolism and brain dysfunction** 

**Thoracic Aorta in Cardiac Surgery** 

Alistair Royse1 and Colin Royse2

*2Pharmacology, The University of Melbourne,* 

*1Department of Surgery, and* 

 *The Royal Melbourne Hospital* 

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