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Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19
© Borgis - New Medicine 3/2003, s. 37-39
Marzenna Zielinska1, Anna Ledakowicz1, Krzysztof Kaczmarek1, Andrzej Walczak2, Wlodzimierz Koniarek1
Is aortic valve sclerosis in the elderly related to coronary artery disease?
1 Department of Cardiology, Institute of Cardiology, Medical University of Lodz, Poland
Head: prof. Halina Bolinska-Soltysiak, MD, PhD
2 Department of Cardiovascular Surgery, Institute of Cardiology, Medical University of Lodz, Poland
Head: prof. Janusz Zaslonka, MD, PhD
Summary
Introduction: Aortic valve sclerosis (AS) is thought to be a degenerative process connected with ageing. Usually AS is asymptomatic and is revealed incidentally by echocardiography. The pathogenesis of AS remains unknown.
The aim of this study was an evaluation of the incidence of AS in patients with coronary artery disease (CAD), and an analysis of any relationship between AS and the risk factors of atherosclerosis and coronary angiography.
Material and methods: A group of 274 patients (167 men, 61%), aged 65-87 years old, hospitalised with a diagnosis of CAD was studied. The following atherosclerosis risk factors of CAD were analysed: age, sex, BMI, diabetes, arterial hypertension, current smoking, family history of CAD, and serum lipids. Each patient underwent transthoracal echocardiography (TTE), with a detailed evaluation of aortic valve morphology and function. All patients had coronary angiography.
According to the presence or absence of AS, patients were divided into groups: Group I (n=183, 63.5% men, 73.3±5.4 yrs) and Group II (n=121, 57.9% men, 71.6±4.6 yrs).
Results: None of the atherosclerotic risk factors was significantly more frequent in any group.
Coronary angiography revealed no relation between AS and CAD.
Analysis of any relation between AS and age revealed a positive correlation. The final regression model showed a high correlation between AS and age (r=0.91; r2=0.882; p=0.005).
Conclusions: 1. Aortic valve sclerosis in the elderly is not a marker for coronary artery atherosclerosis. 2. The pathomechanism of aortic valve sclerosis is probably different from that of coronary artery atherosclerosis. 3. Age is a unique independent risk factor for aortic valve sclerosis.
INTRODUCTION
Aortic valve sclerosis (AVS) is a calcifying disease of the aortic valve leaves, defined as a focal leaf thickening without significant obstruction to left ventricular outflow (1, 2). It occurs mainly in the elderly. Some studies suggest that AVS may be related to the presence of atherosclerosis risk factors (3, 4). Some authors connect AVS with the presence of coronary artery disease (CAD) (5, 6, 7). However, the relationship between AVS and CAD has not been clarified. The aim of this study was to determine the prevalence of AVS in patients with CAD symptoms and to identify clinical factors associated with degenerative aortic valve disease. The relation between aortic valve echocardiographic image and coronary angiography results was analysed.
METHODS
Study population
The study group, 274 patients, was selected from all consecutive patients with CAD symptoms, hospitalised in our Cardiology Department during the last two years. Inclusion criteria were, first, an age of 65 years old or more. Second, all patients suffered from CAD. Third, patients underwent transthoracal echocardiography (TTE) with a detailed evaluation of aortic valve, and fourth, had coronary angiography performed. The presence or absence of AVS in TTE divided the study population into two groups: Group I and Group II, respectively.
Clinical Data
The following atherosclerotic risk factors were analysed: age, sex, body mass index (BMI), diabetes (DM), arterial hypertension (HA), present smoker (PS), family history of CAD (FH), serum total cholesterol (TCH), serum LDL-cholesterol (LDL) and serum HDL-cholesterol (HDL).
Echocardiographic study
Detailed evaluation of the aortic valve morphology and function was obtained by 2D-echocardiographic imaging. The dimensions of the ventricles and atria were collected with M-Mode echocardiography, guided by 2D imaging. Ejection fraction (EF) was visually estimated and combined with calculated values. Doppler and Colour Doppler imaging was applied to evaluate valve stenoses or insufficiencies.
Coronary angiography
All patients underwent coronary angiography according to a standard protocol. Left ventriculography was not routinely performed. Coronary angiography was interpreted visually by each operator on site. Left main coronary artery disease was defined as ?50% stenosis in the artery. Stenoses ?70% were considered significant in all other coronary arteries.
Statistical Analysis
Continuous variables are expressed as mean±SD. Group comparisons used Student´s T-test or a ?2 test, as appropriate P=0.05 was considered to be statistically significant.
Correlation was calculated using multiple regression models. Values with P=0.05 were tested with multivariate modelling and added to the final models. The result of multiple regression is expressed with a regression equation, coefficient of correlation (R), coefficient of determination (R2), and P value.
RESULTS
Patient Characteristics
The study population, 247 patients, aged 65-87 years (72.35±5.42), 61% men, was divided into: Group I (183 patients, 56.2%) and Group II (121 patients, 43.8%). There were no significant differences in age (73.3±5.5 vs. 71.2±4.6) and sex (male: 63.6% vs. 57.9%) between the groups. Analysis of further clinical data and laboratory parameters present any significant dissimilarity (Table 1). Thus, none of the analysed atherosclerotic risk factors became statistically different in any group.
Table 1. Atherosclerosis risk factors.
 BMIDMHAPSFHTCHLDLHDL
Group I26.48 ? 4.6036.87%66.67%20.29%25.4%204.5 ? 46.9126.4 ? 37.750.1 ? 9.9
Group II26.69 ? 3.7133.87%63.80%19.17%28.3%211.6 ? 44.1133.9 ? 38.550.6 ? 14.0
PNSNSNSNSNSNSNSNS
The coronary angiography results were classified as no occlusion in coronary arteries, one-vessel disease or as multi-vessel disease (Table 2). There was a similar incidence of each coronary artery image in both study groups and no significant dissimilarities were revealed.
Table 2. Results of coronary angiography.
 No occlusion1-vessel diseaseMulti-vessel disease
Group I4%49.6%46.4%
Group II3.9%49%47.1%
 NSNSNS
Multiple Regression Models revealed that age is the unique parameter correlated with AS. The relation between the incidence of aortic valve sclerosis and age is shown in Figure 1. The regression results present a very strong positive correlation of AS incidence to age (R=0.91), high determination (R2=0.88) and significant P value (P=0.005). Inclusion of any other analysed variable did not improve the regression model results.
Fig. 1. Relation between incidence of aortic valve sclerosis and age groups.
DISCUSSION
The question whether AVS is a result of more generalised atherosclerosis or reflects a primary degenerative process, progressing with advancing age, remains still without answer. AVS occurs mainly in the elderly. We found that the prevalence of AV sclerosis increased significantly with age, consistent with the results of previous studies (2, 4, 7, 8).
Many studies have shown an association between AVS and atherosclerosis risk factors (e.g. hypertension, diabetes, and hyperlipidemia) (5, 6). Sometimes, AVS is called "a window” to diffuse atherosclerosis of the vascular system (3, 9, 10, 11). In our study we did not observe any such correlation. Both groups (with AVS and without AVS) were matched for the presence of hypertension, diabetes and hyperlipidemia or other atherosclerosis risk factors.
In our study, multivessel disease was observed equally often in both groups. The presence of AVS in an ECHO examination does not allow us to predict coronary angiography results. Our results are similar to the conclusion reached by Roger et al (12). They did not find age, sex, ejection fraction or the presence of CAD to be associated with the progres of AVS.
CONCLUSIONS
1. Aortic valve sclerosis in the elderly is not a marker of coronary artery atherosclerosis.
2. The pathomechanism of aortic valve sclerosis is probably different than coronary artery atherosclerosis.
3. The patient´s age is a unique independent risk factor of aortic valve sclerosis.
Piśmiennictwo
1. Robicsek F. et al.: Cause of degenerative disease of trileaflet aortic valve: review of subject and presentation of new theory. Ann. Thorac. Surg. 2002 Apr; 73:1346-54. 2. Tolstrup K. et al.: Aortic valve sclerosis, mitral annular calcium and aortic root sclerosis as a marker of atherosclerosis in men. Am. J. Cardiol. 2002 May; 89:1030-4. 3. Branch K.R. et al.: Aortic valve sclerosis as a marker of active atherosclerosis. Curr. Cardiol. Rep. 2002 Mar; 4:111-7. 4. Robicsek F. et al.: Aetiology of degenerative disease of the tri-leaflet aortic valve: a simple explanation for a complex problem. Z. Kardiol. 2001; 90, Suppl. 6:35-8. 5. Pohle K. et al.: Progression of aortic valve calcification: association with coronary atherosclerosis and cardiovascular risk factors. Circulation 2001 Oct 16; 104:1881-3. 6. Agmon Y. et al.: Aortic valve sclerosis and aortic atherosclerosis: different manifestations of the same disease? An insight from population-based study. J. Am. Coll. Cardiol. 2001 Sept; 38:837-34. 7. Carabello B.A.: Association of aortic-valve sclerosis with cardiovascular mortality and morbility in the elderly. Otto C.M. et al. N. Engl. J. Med. 1999 Jul 15; 341:142-7. 8. Croft L.B. et al.: Calcific aortic stenosis: new pathophysiologic insight and possible new medical therapy. Curr. Cardiol. Rep. 2003 Mar; 5:101-4. 9. Adler Y. et al.: Non-obstructive aortic valve calcium as a window to atherosclerosis of the aorta. Am. J. Cardiol. 2000 Jul 1; 86:68-71. 10. Wierzbicki A., Shetty C.: Aortic stenosis: an atherosclerosis disease? J. Heart Valve. Dis. 1999 Jul; 8:416-23. 11. Boon A. et al.: Cardiac valve calcification: characteristics of patients with calcification of the mitral annulus or aortic valve. Heart 1997 Nov; 78:472-4. 12. Roger V.L. et al.: Progression of aortic stenosis in adults: new appraisal using Doppler echocardiography. Am. Heart J. 1990; 119:331-338.
Adres do korespondencji:
kaczmarekk@poczta.fm

New Medicine 3/2003
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