11.1.1 Prevalence and risks

Prevalence

The prevalence of heart valve disease in the general population in Europe is approximately 2.5% [9]. This rises to 13% in people aged > 75 years [6]. Valvular heart disease is a major factor in perioperative mortality. In cardiac surgery, the average mortality for valve replacement (1-2% for aortic stenosis and 2-4% for mitral regurgitation) is two to three times higher than for coronary artery bypass grafting (0.5-2%) [10]. Mortality increases with age: valve replacement for aortic stenosis, for example, increases mortality by 1.5% for every 10 years after the age of 60 [6]. In non-cardiac surgery, the presence of moderate aortic stenosis multiplies the surgical risk by a factor of three, and severe stenosis by a factor of five, regardless of the patient's risk category or the number of associated risk factors [4,5].

Chronic valvulopathy develops slowly: it generally takes 10-30 years to reach full clinical manifestation and cardiac decompensation, during which time there is no parallel between the severity of symptoms and the degree of cardiac dysfunction. Acute valvulopathy is rare (10% of cases). These are usually sudden failures that abruptlly and severely compromise haemodynamics: ischaemic rupture of a mitral leaflet, rupture of the chordae tendineae (Barlow's disease), or infectious destruction of the aortic or mitral valve. The occurrence of arrhythmias such as paroxysmal atrial fibrillation (AF) can cause clinical decompensation due to lack of end-diastolic filling and exaggerated acceleration of the base rhythm. Although they may remain stationary, valvulopathies never heal spontaneously; only surgery offers a chance of recovery. And even then ! In fact, the valvular disease is replaced by another pathological situation: with a repair, the valve is repaired but abnormal; with a prosthesis, it depends on anticoagulation and the limited life of the implanted material.

At rest, blood flow in the ventricles is physiologically laminar and therefore quiet. The presence of a vortex indicates pathological acceleration: valvular stenosis, regurgitation from a high-pressure cavity to a low-pressure cavity, localised turbulence in the vicinity of sclerosis or simple cardiac erethism. The vortices of these eddies produce murmurs audible to the stethoscope and abnormalities visible on Doppler echocardiography. Normal heart valves can accommodate flow rates 5 to 7 times greater than the baseline, so the stenosis must be severe to become symptomatic at rest.

By analogy with heart failure, the clinical severity of valvular heart disease is divided into four stages [8].

• A: At risk; asymptomatic patients with simple risk factors.
• B: Progressive valve disease; asymptomatic patients with mild or moderate valve pathology.
• C: Severe but asymptomatic valvular disease; criteria of severity (stage IV) present on echocardiography, angio-CT or catheterisation.
  • C1: LV and RV function still compensated.
  • C2: left and/or right ventricular decompensation.
• D: Severe and symptomatic valvulopathy.

The presence or absence of symptoms is often difficult to determine because of the slow onset of the disease and the interference of multiple comorbidities. On the other hand, some patients are not very active and do not complain of any limitation in their activity because it is very low, especially in the frail elderly.

Risk assessment for heart valve surgery combines various factors such as the patient's physiological status, comorbidities and the specifics of each procedure. It measures the risk of mortality and major morbidity resulting in serious sequelae (in percent) [8].

• Low risk (< 4%): Satisfactory status, no comorbidity, simple operation.
• Intermediate risk (4-8%): moderate clinical status, presence of a major comorbidity (ventricular dysfunction, pulmonary hypertension, COPD, renal failure, cancer, etc.), intermediate-risk surgery.
• High risk (8-20%): fragile clinical status, presence of 2 organic comorbidities, high risk surgery.
• Prohibitive risk (≥ 25% at 30 days, > 50% at 1 year): very poor clinical status, low life expectancy, numerous major comorbidities, high-risk surgery.

Over the last decade, valve surgery has evolved along three distinct trends.

• The ageing population has pushed back the age limit for valve repair or replacement, particularly in the aortic position.
• Improvements in surgical outcomes have led to the indication for surgery being given earlier in the course of the disease, allowing patients to be operated on when they are in a better clinical condition.
• Endovascular replacement or grafting techniques have entered clinical use and are becoming effective options in intermediate and high-risk cases; they offer the possibility of using less burdensome anaesthetic techniques (fast-track) or proceeding under sedation-analgesia (see Chapter 10 Anaesthesia for TAVI).

 Medical treatment

Unfortunately, there is little alternative to surgery as there is no medical treatment for heart valve disease. Neither statins nor biphosphonates slow the progression of aortic stenosis. Converting enzyme inhibitors (CEIs) and angiotensin receptor blockers (ARBs) are only indicated for the treatment of hypertension as a major co-morbidity [7]. In aortic regurgitation, nifedipine and ACE inhibitors reduce regurgitant volume but do not alter disease progression. In mitral stenosis, beta-blockers prolong diastole and allow better filling of the LV. If the LV is failing due to aortic or mitral valve disease, pharmacological treatment of heart failure is necessary, but again without any effect on disease progression. Improving ventricular function can only reduce mitral regurgitation if it is secondary to LV dilatation [2].

Lifelong anticoagulation with an anti-vitamin K agent is required in patients with mechanical prostheses, but only for the first 3 months in those with bioprostheses. The new oral anticoagulants (NACOs) can be prescribed for atrial fibrillation in patients with aortic stenosis, mitral regurgitation and aortic regurgitation, but are contraindicated in patients with mitral stenosis or mechanical prostheses [1,3].

Finally, antibiotic therapy is central to the treatment of endocarditis, but infection prophylaxis is only recommended in certain high-risk situations (septic surgery, dental procedures involving invasion of the gingival mucosa) and in certain patients: prosthetic valve wearers, history of endocarditis, transplant patients, patients with congenital heart disease (cyanotic conditions, wear of prosthetic material in the first 6 months, residual defects around prosthetic material) [8].

Preamble to Chapter 11

Although stenosis and regurgitation are not always found in their pure form in clinical practice - it is often a case of valvular disease with a predominance of one or the other - their separate description provides a better understanding of the pathophysiology of each entity, its compensatory mechanisms and the signs that indicate its decompensation. These concepts are essential for distinguishing the main constraints within a complex haemodynamic system, as they determine the behaviour of the patient and the therapeutic attitudes of the practitioner, who must prioritise his interventions.

The anaesthetic management of patients with valvular heart disease is highly dependent on the pathophysiology of the disease. In cardiac surgery, on the other hand, it is important to understand the indications and surgical technique in order to adapt to the constraints of valve correction. For these reasons, this chapter places particular emphasis on two points:

• Cardiological nosology and the mechanisms of each valvulopathy;
• Surgical data and techniques.

Once these two areas have been clarified, the choice of anaesthetic technique becomes a matter of course. What's more, the cardiac anaesthetist's knowledge of cardiology and surgery, combined with his echocardiographic skills, make him an indispensable partner in the therapeutic decisions taken in the operating theatre. As part of a cardiac team, their day-to-day work is far more interesting and rewarding than that of a simple sleeper.

Too much information, however, kills information and paralyses decisions. To facilitate patient management, particularly for non-cardiac surgery patients, a summary has been added in a separate document (Appendix B); this describes in a simplified way the anaesthetic recommendations for each valve disease. Table 11.16 (valve stenosis) and Table 11.17 (valve insufficiency) summarise these recommendations.

As a routine imaging modality in the operating theatre, transesophageal echocardiography (TEE) will be used as the main source of visualisation of valvular pathology. The echocardiographic examination of valves and their pathology is described in detail in Chapter 26 (TEE 2^nd part), from which many of the figures have been taken.

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

References

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10 STS - Society of Thoracic Surgeons National Cardiac Surgery Database, 2017. https://www.sts.org/site/defaut/files/documents/ ACSD_ExecutiveSummary2017Harvest4_RevisedReport.pdf