Degenerative aortic stenosis

The symptomatic phase is crucial to the subsequent evolution of aortic stenosis(AS) not only because, without aortic valve replacement, all symptomatic patients experience subsequent clinical deterioration, but also because only patients who have reached the symptomatic phase are eligible for aortic valve replacement(1). Accordingly, the clinical identification of AS as the underlying cause of symptoms such as syncope, angina, and breathlessness opens up all avenues, including the one leading to eventual valve replacement. For clinical evaluation to be most effective, the routine "work up" of patients who present with syncope, angina, and suspected heart failure ought to include all the clinical manouvres known to augment the intensity of the systolic murmur of AS.

These include auscultation, not only in the second right intercostal space(the so-called aortic area), but also at the lower left sternal edge and at the cardiac apex, with the patient sitting up, breath held in expiration(2). Auscultation at the cardiac apex might also elicit the murmur of mitral regurgitation, which may emerge as a secondary feature when severe AS is complicated by heart failure(3). The caveat here is that co-existence of atrial fibrillation(AF) might mislead the clinician into attributing the mitral systolic murmur solely to disease originating in the mitral valve instead of recognising it as a by-product of severe AS(4). The role of co-existing hypertension is even more complex. In the first place, given the fact that hypertension is a more widely recognised risk factor for AF, there is a risk of discounting the possibility of AS when hypertension, AF, and a systolic murmur co-exist. Secondly, over and above the afterload imposed on the left ventricle by valve obstruction, hypertension, which is prevalent in 35% to 45% of patients with aortic stenosis, imposes the additional afterload of elevated systemic vascular resistance(5). Thirdly, the presence of AS may itself affect the optimal treatment of hypertension(5). Other issues that need to be considered include evaluation of co-morbidities such as haematological "alarm" features of severe AS, exemplified by AS-related iron deficiency anaemia, when the latter is attributable to chronic gastrointestinal bleeding resulting from AS-related acquired von Willebrand syndrome(6).

References

(1) Ramaraj R., Sorrell VL Degenerative aortic stenosis British Medical Journal 2008:336:550-5

(2) Thibault GE., DeSanctis RW., Buckley MJ Aortic stenosis in The Practice of Cardiology 1989 volume 1, Second Edition Editors: Eagle KA., Haber E., DeSanctis RW., Austen WG Chapter 19, pages 701-22 Little, Brown and Co Boston/Toronto

(3) Morgan DJR., Hall RJC Occult aortic stenosis as a cause of intractable heart failure British Medical Journal 1979:1:784-7

(4) Rispler S., Rinkevich D., Markiewicz W., Reisner SA Missed diagnosis of severe symptomatic aortic stenosis American Journal of Cradiology 1995:76:728-30

(5) Otto C Valvular aortic stenosis Disease severity and timing of intervention Journal of the American College of Cardiology 2006:47:2141-51

(6) Vincintelli A., Suses S., Le Tourneau T et al Acquired von Willebrand syndrome in aortic stenosis New England Journal,of Medicine 2003:349:343-9

Competing interests: None declared