Assessment of severity

Background 

Aortic stenosis (AS) is a common condition, especially in the elderly with a prevalence of 3.5% in over 75 year olds and 18% in over 90 year olds. 75% of patients have coexisting coronary artery disease due to similar underlying pathological processes related to calcium deposition and atherosclerosis following endothelial cell infiltration.

50% of cases are due to a bicupsid valve, these tend to be seen in younger patients <60 years. The classic clinical triad of angina, dyspnoea and syncope are often not seen due to poor mobility for other reasons in an elderly cohort and this is something to be mindful of when anaesthetising patients for joint replacement surgery where an accurate assessment of exercise tolerance is very difficult. One study concerningly found that 50% of supposedly "asymptomatic" patients developed symptoms under dobutamine stress-testing [1] 

Causes

1. Calcific degeneration of a trileaflet valve (most common)
2. Rheumatic heart disease - generally in younger patients and often associated with concurrent mitral rheumatic disease. More likely to have commissural fusion with less severe calcification.
3. Bicuspid valve - seen in younger patients under the age of 60 years with possible concurrent coarctation of the aorta, aortic root dilatation and VSD. The RCC and LCC are the most likely to be fused

Concurrent conditions and associations

• Calcification of the intervalvular fibrosa and in to the mitral annulus
• Aortic dilatation either from primary aortopathy or chronically elevated pressure in the ascending aorta)
• Coronary artery disease present in 75%

Pathophysiology and Aortic Stenosis Progression

The 2014 ACC/AHA guidelines have classified AS progression into the following spectrum which can help to give insight into how the disease progresses over time:

As AS progresses the aortic valve area (AVA) becomes smaller and LV function initially has to become hyperdynamic to maintain stroke volume through the narrowed orifice. The LV becomes pressure overloaded with an increase in LVEDP and LVESP required to eject blood through the calcific aortic valve.

With further progression the LV becomes increasingly hypertrophied and diastolic dysfunction ensues as LVEDP rises. The reliance of left atrial “kick” increases from a normal baseline of 20% up to 40% and at this stage atrial fibrillation (with loss of the atrial kick) is poorly tolerated and can result in decompensated heart failure.

Myocardial oxygen demand increases due to the increase in workload being performed by the thickened ventricle. Eventually a tipping point is reached where LVEF% begins to fall. At this stage the ventricle is struggling to maintain stroke volume due to increased afterload and often a compensatory LV dilational cardiomyopathy develops and the LV wall can appear paradoxically thin.

If the disease progresses further (and no fatal episodes of heart failure or arrhythmia are encountered!) Then elevated LA pressure leads to pulmonary hypertension and eventual RV impairment.

Coronary Perfusion Pressure (CoPP) = Aortic diastolic pressure (ADP) - LVEDP 

Coronary perfusion pressure can fall if the gradient between aortic diastolic pressure (ADP) and LVEDP is not maintained. Exercise where myocardial oxygen demand increases can result in angina despite normal coronary arteries. [5]  Other causes of aortic diastolic pressure reduction such as a drop in SVR from induction of anaesthesia or neuraxial blockade can result in acute myocardial oxygen deficit and a spiral of haemodynamic collapse.

A difficult scenario can arise in patients with reduced EF% (for unrelated reasons) where the LV pressure generated is insufficient to fully open the AV and the AVA will appear small by measurement but surgical AVR or TAVI will be ineffective (pseudo aortic stenosis). This condition can be ruled out with dobutamine stress echo (Increased LVEF% results in an improvement in calculated AVA)

Perioperative Risk 

Aortic stenosis has been a long-feared condition by anaesthetists due to the perceived risk of haemodynamic collapse at induction or after placement of neuraxial blockade due to a drop in systemic vascular resistance (SVR).

Older studies did show that severe aortic stenosis is associated with MACE and perioperative mortality. The original Goldman risk index in 1977 estimated 13% vs 1.6% increased mortality risk compared to control patients but AS was later removed in the revised Lee version in 1999. 

Mortality has since reduced, likely due to increased detection and aggressive perioperative management strategies once identified together with more ubiquitous invasive monitoring. Quoted 30 day mortality is now in the region of 2-3% with severe AS vs 1.5% in patients undergoing major non-cardiac surgery.[3] A further 2014 case control study involving > 500 patients showed that while patients were are at increased risk of MACE, overall perioperative outcomes were not as severe as expected with no statistically significant difference in 30 day mortality between the severe AS group and a control group. [2] 

One area of anaesthetic practice where the presence of aortic stenosis can influence management is in the elderly hip fracture cohort. One study from 2016 showed that the presence of severe aortic stenosis resulted in increased mortality (14% vs 4%) and 1 year mortality (46.8% vs 14.1%) [4] Current opinion is that postponing urgent surgery in severe AS in patients who are asymptomatic is likely overly conservative. European guidelines state that if symptomatic then AVR or TAVI should be performed (or considered) prior to elective surgery (i.e. angina or exertional breathlessness) [8] 

Papers to Consider

1. Kertai et al (American Journal of Medicine 1991-2000) [108 patients] [9]  • Moderate AS (MG 25-49mmHg) = 11% risk of perioperative MI or death  • Severe AS (MG>50mmHg) = 30% risk of perioperative MI or death  • Odds ratio = 5.2  2. Tashiro et al (European Heart Journal 2000-2010) [256 cases vs 256 controls] [10]  • Included patients diagnosed with severe AS 12 months prior or 3 months after surgery  • Surgery defined as intermediate or high risk and requiring a GA  • Defined as MG >40mmHg or AVA by continuity equation of <1cm2 or PV of >4m/sec  • 256 patients identified who underwent surgery of which 45% had symptoms in the preceding months leading up to surgery  • Strong association with increased mortality at 1 year (18% vs 7% in controls)  • Death and MACE at 30 days was similar for asymptomatic patients vs controls (3.3% vs 2.7%)  • The strongest predictor for death in both groups was emergency surgery  • Perioperative mortality in AS and control groups was <5% in both groups undergoing elective surgery  • Study advises that symptomatic patients, those with Revised cardiac risk index >2 or reduced LVEF% should have AS treated prior to elective surgery  • New or worsened heart failure was more common in the AS group which could complicate and delay discharge

References

1. Redfors B, Pibarot P, Gillam LD, et al. Stress Testing in Asymptomatic Aortic Steno-sis. Circulation. 2017;135(20):1956-1976. 

2. Tashiro T, Pislaru SV, Blustin JM, et al. Perioperative risk of major non-cardiac surgery in pa-tients with severe aortic stenosis: a reappraisal in contemporary practice. Eur Heart J. 2014;35(35):2372-2381.  3. Agarwal S, Rajamanickam A, Bajaj NS, et al. Impact of aortic stenosis on postoperative outcomes after noncardiac surgeries. Circ Cardiovasc Qual Outcomes. 2013;6(2):193-200.  4. Keswani A, Lovy A, Khalid M, et al. The effect of aortic stenosis on elderly hip fracture out-comes: A case control study. Injury. 2016;47(2):413-418  5. Jane Brown, MBBS FANZCA, Nicholas J Morgan-Hughes, MBChB MRCP FRCA, Aortic stenosis and non-cardiac surgery, Continuing Education in Anaesthesia Critical Care & Pain, Volume 5, Issue 1, February 2005, Pages 1–4  6. Moura LM, Ramos SF, Pinto FJ, Barros IM, Rocha-Gonçalves F. Analysis of variability and repro-ducibility of echocardiography measurements in valvular aortic valve stenosis. Portuguese Jour-nal of Cardiology. 2011;30(1):25-33  7. Rusinaru D, Malaquin D, Maréchaux S, Debry N, Tribouilloy C. Relation of Dimensionless Index to Long-Term Outcome in Aortic Stenosis With Preserved LVEF. JACC Cardiovasc Imaging. 2015;8(7):766-775.  8. Helmut Baumgartner, Volkmar Falk, Jeroen J Bax, Michele De Bonis, Christian Hamm, Per Johan Holm, Bernard Iung, Patrizio Lancellotti, Emmanuel Lansac, Daniel Rodriguez Muñoz, Raphael Rosenhek, Johan Sjögren, Pilar Tornos Mas, Alec Vahanian, Thomas Walther, Olaf Wendler, Stephan Windecker, Jose Luis Zamorano, ESC Scientific Document Group, 2017 ESC/EACTS Guidelines for the management of valvular heart disease, European Heart Journal, Volume 38, Issue 36, 21 September 2017, Pages 2739–2791  9. Kertai MD, Bountioukos M, Boersma E, et al. Aortic stenosis: an underestimated risk factor for perioperative complications in patients undergoing noncardiac surgery. Am J Med. 2004;116(1):8-13  10. Tashiro T, Pislaru SV, Blustin JM, et al. Perioperative risk of major non-cardiac surgery in pa-tients with severe aortic stenosis: a reappraisal in contemporary practice. Eur Heart J. 2014;35(35):2372-2381