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oscar,m jolobe, retired geriatrician manchester medical society, c/o john rhyalnds university library, oxford road, manchester M13 9PP
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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 |
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Habib U Rehman, Clinical Assistant Professor Regina Qu
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Ramaraj et al, in their article on degenerative aortic stenosis recommend antibiotic prophylaxis for infective endocarditis in all patients with aortic stenosis (1). This advice is not in accordance with the most recent guidelines by the American Heart association on prevention of infective endocarditis (2). According to these guidelines, antibiotic prophylaxis is indicated only for certain cardiac conditions with the highest risk of infective endocardits. These include prosthetic heart valves or prosthetic material used for cardiac valve repair, previous infective endocarditis, unrepaired cyanotic congenital heart disease (CHD), completely repaired congenital heart defect with prosthetic material, or CHD with residual defect at bthe site or adjacent to the site of a prosthetic patch, and cardiac transplant patients who develop cardiav valvulopathy. These guidelines are based on the results of latest research which indicate: 1- Few cases of infective endocarditis would be preventable with antibiotic prophylaxis, even with 100% effectiveness assumed (3). 2- Most patients with endocarditis on a known cardiac lesion do not get the disease as a consequence of a dental or medical procedure. Thus in one study, endocarditis developed within 30 days of a procedure in only 25 (12.7%) of 197 patients who had had heart disease. 9 out of 10 patients with heart disease contracted endocarditis in some other way (4). The current guidelines are evidence-based as opposed to the previous guidelines which were at best based only on consensus opinion of experts, case studies or standards of care. Thus antibiotic prophylaxis is no longer recommended for any other form of CHD, except for the conditions listed above References: (1)Ramaraj R, Sorrell V. Degenerative aortic stenosis. BMJ 2008; 336: 550-5. (2)Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee. American Heart Association Council on Cardiovascular Disease in the Young. American Heart Association Council on Clinical Cardiology. American Heart Association Council on Cardiovascular Surgery and Anesthesia. Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis. Circulation 2007; 116:1736-54. (3)Strom BL, Abrutyn E, Berlin JA, Kinman JL, Feldman RS, Stolley PD, et al. Dental and Cardiac Risk Factors for Infective Endocarditis: A Population-Based, Case-Control Study. Ann Intern Med 1998; 129: 761-9. (4)van der Meer JTM, van Wijk W. Lancet 1992; 339: 135-9. Competing interests: None declared |
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ahmed shokry beshr, Consultant physician and Nephrologist Royal Shrewsbury HOSPITAL
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Dear Sir I am surprised that the author of this clinical review failed to mention the important role in the pathogenesis and progression of degenerative aortic stenosis played by chronic kidney disease especially at stage 4&5 and going through renal replacemet therapy and the association of uraemic toxins mainly high serum calcium and /or phosphate and their ratios in these group of patients. It is well established that rapid deterioration of aortic valve can progree from normal valve to severe stenosis in very short time and in severe cases in less than one year. Competing interests: None declared |
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Thato Mabote, Specialty Registrar Year 2 Diana Princess of Wales Hospital, Grimsby,DN33 2BA, Thato Mabote
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The prognosis of asymptomatic but severe AS is generally regarded as excellent(1,2). The risk of sudden death without preceding symptoms, although reported as rare(1,3), remains a concern. Furthermore, pulmonary hypertension can complicate longstanding severe AS thereby increasing the morbidity and risk of sudden death(4,5). The use of beta blockers may potentially be beneficial in this setting(5). Beta blockers have been shown in the experimental model(6) to slow the heart rate leading to improvement of LV filling and unloading of the pulmonary circulation, thereby lowering the PA pressure. The timing of surgery is crucial.AVR can be performed at a 2% to 3% operative mortality with an 85% age-corrected 10-year survival(2,7). Pre- operative myocardial damage leading to post AVR congestive cardiac failure has been shown to a be a poor prognostic indicator(8). Finally, in asymptomatic patients, severe valvular calcification coupled with a rapid increase in aortic jet velocity predicts a very poor prognosis(4). Rapid progression of the disease in such patients is alarming, with 80% requiring AVR or dying in 4 years(4).Observational data in a study by Pai et al(9)indicates that the natural history of asymptomatic AS is not benign and that survival is dramatically improved by AVR. Should a stronger case for early AVR be made in severe asymtomatic AS since it has been shown that ealier operative intervention infers a better post AVR long term survival rate(8)? References 1) Ramaraj R,Sorrell V.Degenerative aortic stenosis.BMJ 2008; 336: 550-555 2) Carabello BA.Timing of Valve Replacement in Aortic Stenosis. Circulation. 1997;95:2241-2243 3) Rosenhek R,Binder T et al.Predictors of Outcome in Severe, Asymptomatic Aortic Stenosis. NEJM;343:611-617 4) Kapoor N,Varadarajan P,Pai R.Echocardiographic predictors of pulmonary hypertension in patients with severe aortic stenosisEuropean Journal of Echocardiography. 2008;9(1):31-33 5) McHenry MM, Rice J, Matlof HJ, Flamm MD Jr. Pulmonary hypertension and sudden death in aortic stenosis. Br Heart J.1979;41:463–7. 6) O'Blenes SB, Fischer S et al. Hemodynamic unloading leads to regression of pulmonary vascular disease in rats. J Thorac Cardiovasc Surg.2001;122:634–5. 7) Lindblom D, Lindblom U, Qvist J, Lundstrom H. Long-term relative survival rates after heart valve replacement. J Am Coll Cardiol.1990;15:566-573. 8) Lund O. Preoperative risk evaluation and stratification of long-term survival after valve replacement for aortic stenosis. Reasons for earlier operative intervention. Circulation. 1990 Jul;82(1):124-39. 9) Pai RG, Kapoor N, B RC, Varadarajan P.Malignant natural history of asymptomatic severe aortic stenosis: benefit of aortic valve replacement. Annals of Thoracic Surgery. 2006;82:2116-22 Competing interests: None declared |
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Cesar Augusto Guevara-Cuellar, Professor University of Santiago de Cali Palmira, Carlos A. Pineda-Cañar
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Although there is controversy that statins could to retard the progression of aortic stenosis, perhaps this option is not useful in all types of these patients. The RAAVE study (Rosuvastatin Affecting Aortic Valve Endothelium) demonstrated that patients with high levels of cholesterol and aortic stenosis had lower rate of progression compared with patients with normal levels (1). This study suggests that lipid lowering therapy could be a first option in this subset of patients. 1.Moura LM, Ramos SF, Zamorano JL, Barros IM, Azevedo LF, Rocha-Gonçalves F et al. Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis. J Am Coll Cardiol. 2007 ;49:554-61. Competing interests: None declared |
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