Worldwide perspective of valve disease

Heart

Volumn 83, Issue 6, 2000, Pages 721-725

  Soler Soler, Jordi ^a   Galve, Enrique ^a  

^a HOSPITAL UNIVERSITARI VALL D HEBRON   (Spain)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIBIOTIC AGENT; ERGOT ALKALOID; ERGOTAMINE; ERYTHROMYCIN; FENFLURAMINE; METHYSERGIDE; PENICILLIN DERIVATIVE; PHENTERMINE;

ACQUIRED IMMUNE DEFICIENCY SYNDROME; ANTIPHOSPHOLIPID SYNDROME; ARTICLE; ATHEROSCLEROSIS; DRUG INDUCED DISEASE; HUMAN; MIGRAINE; OBESITY; PRIORITY JOURNAL; RHEUMATIC DISEASE; STREPTOCOCCUS INFECTION; VALVULAR HEART DISEASE;

ANTIPHOSPHOLIPID SYNDROME; DEVELOPED COUNTRIES; DEVELOPING COUNTRIES; HEART VALVE DISEASES; HUMANS; RHEUMATIC HEART DISEASE;

EID: 0034129650     PISSN: 13556037     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (20)

1. Veasy LG, Wiedmeier SE, Orsmond GS, et al. Resurgence of acute rheumatic fever in the Intermountain area of the United States. N Engl J Med 1987;316:421-7. The paper reports an outbreak of acute rheumatic fever that occurred in 74 children during a 18 month period (from January 1985 to June 1986) at one centre in Salt Lake City. The children were predominantly white and from middle class families with above average incomes and ready access to medical care. There was no apparent increase in the incidence of streptococcal disease or other explanation for the major increase in rheumatic fever. In the previous 10 year period the average incidence had been six cases per year.
2. Narula J, Virmani R, Reddy KS, Tandon R, eds. Rheumatic fever. Armed Forces Institute of Pathology, Washington: American Registry of Pathology, 1999. This book is a comprehensive multidisciplinary review of the state of the art of rheumatic fever at the present time. The monograph comprises aspects such as history, epidemiology, microbiology of group A streptococci, clinical manifestations, the problem of the resurgence of rheumatic fever, treatment, and prevention (including the progress on the vaccine development).
3. World Health Organization. Rheumatic fever and rheumatic heart disease. WHO Technical Report Series no. 764. Geneva: WHO, 1988.
4. Arguedas A, Mohs E. Prevention of rheumatic fever in Costa Rica. J Pediatr 1992;121:569-72.
5. Dale JB. Group A streptococcal vaccines. Infect Dis Clin North Am 1999;13:227-43.
6. Passik CS, Ackermann DM, Pluth JR, et al. Temporal changes in the causes of aortic stenosis: a surgical pathologic study of 646 cases. Mayo Clin Proc 1987;62:119-23.
7. Stewart BF, Siscovick D, Lind BK, et al. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J Am Coll Cardiol 1997;29:630-4. Clinical factors associated with aortic sclerosis and stenosis were evaluated in older subjects (> 65 years of age) enrolled in the Cardiovascular Health Study. Independent clinical factors found to be associated with these types of degenerative valve disease were age, male sex, present smoking, and hypertension, while high Lp(a) and LDL cholesterol concentrations were other significant factors.
8. Boon A, Cheriex E, Lodder J, et al. Cardiac valve calcification: characteristics of patients with calcification of the mitral annulus or aortic valve. Heart 1997;78:472-4.
9. Wilmshurst PT, Stevenson RN, Griffiths, et al. A case-control investigation of the relation between hyperlipidemia and calcific aortic valve stenosis. Heart 1997;78:475-9. A case control study designed to evaluate the relation of hyperlipidaemia to calcific aortic valve stenosis. The presence of a stenosed tricuspid aortic valve was associated with a significant increase in total plasma cholesterol, while for bicuspid valves the degree of elevation was less and not significant.
10. Michaels AD, Lederman RJ, MacGregor JS, et al. Cardiovascular involvement in AIDS. Curr Probl Cardiol 1997;22:109-48.
11. Ribera E, Miro JM, Cortes E, et al. Influence of human immunodeficiency virus 1 infection and degree of immunosuppression in the clinical characteristics and outcome of infective endocarditis in intravenous drug users. Arch Intern Med 1998;158:2043-50.
12. Acierno LJ. Cardiac complications in acquired immunodeficiency syndrome (AIDS): a review. J Am Coll Cardiol 1989;13:1144-54. This review emphasises that the most common endocardial lesion seen in AIDS is non-bacterial thrombotic bacterial endocarditis (so-called marantic endocarditis). This type of involvement is probably due to the long-term wasting characteristics of AIDS.
13. Milei J, Grana D, Fernandez Alonso G, et al. Cardiac involvement in acquired immunodeficiency syndrome - a review to push action. The committee for the study of cardiac involvement in AIDS. Clin Cardiol 1998;21:465-72.
14. Redfield MM, Nicholson WJ, Edwards WD, et al. Valve disease associated with ergot alkaloid use. Echocardiographic and pathologic correlations. Ann Intern Med 1992;117:50-2. This is a report of the clinical, echocardiographic, and pathologic findings of five patients with valvar disease associated with long term ingestion of ergot alkaloids. Valvar disease was sufficiently symptomatic to necessitate valve replacement in all cases. Patients were identified because gross pathologic findings were unusually severe for rheumatic disease.
15. Connolly HM, Crary JL, McGoon MD, et al. Valvular heart disease associated with fenfluramine-phentermine. N Engl J Med 1997;337:581-8. Investigators at the Mayo Clinic describe 24 women in whom valvar heart disease developed after an average of 12 months of treatment with fenfluramine and phentermine. Eight women also had newly documented pulmonary hypertension. At the time of the report valve surgery was needed in five cases of the series. This paper was the first to arouse concern about this relation and prompted other studies that finally confirmed the association.
16. Khan MA, Herzog CA, St Peter JV, et al. The prevalence of cardiac valvular insufficiency assessed by transthoracic echocardiography in obese patients treated with appetite-suppressant drugs. N Engl J Med 1998;339:713-8. Echocardiograms from 257 obese patients that had taken or were taking fenfluramine, dexfenfluramine or phentermine were reviewed, and compared against 239 matched controls. A total of 1.3% of the controls and 22.7% of the patients met the case definition of valvar regurgitation (FDA criteria).
17. Jick H, Vasilakis C, Weinrauch LA, et al. A population-based study of appetite-suppressant drugs and the risk of cardiac valve regurgitation. N Engl J Med 1998;339:719-24.
18. Weissman NJ, Tighe JF, Gottdiener JS, et al, for the Sustained-Release Dexfenfluramine Study Group. An assessment of heart-valve abnormalities in obese patients taking dexfenfluramine, sustained-release dexfenfluramine. or placebo. N Engl J Med 1998;339:725-32. An echocardiogram was performed in 1072 patients who had participated in a randomised double blind trial comparing dexfenfluramine and placebo. Although the period of treatment was very short (only 72 days) and the recording was performed a median of one month after the discontinuation of treatment, the prevalence of either aortic or mitral regurgitation was significantly higher in those patients that had taken dexfenfluramine, although in most cases the valve insufficiency was considered as trace or mild.
19. Asherson RA, Cervera R. Antiphospholipid antibodies and the heart. Lessons and pitfalls for the cardiologist. Circulation 1991;84:920-3. Although an editorial, this article is also a good review which summarises the relations between antiphospholipid antibodies and cardiac disease with a very appropriate clinical sense. With respect to valvar involvement, clues to differentiating antiphospholipid lesions from infective endocarditis are provided.
20. Galve E, Ordi J, Barquinero J, et al. Valvular heart disease in the primary antiphospholipid syndrome. Ann Intern Med 1992;116:293-8. A series of 28 consecutive patients with primary antiphospholipid syndrome, and 28 age and sex matched healthy controls, studied by Doppler echocardiography. Valvar involvement was found in 38% of patients, lesions being of the regurgitant type (no stenoses were found), and appearing as irregular, localised valve thickening, not vegetative.