Original article Relationship between aortic valve calcification and aortic atherosclerosis: a transoesophageal echocardiography study

Abstract

Introduction:
Clinical and laboratory data provide an increasing amount of information regarding the common aetiopathogenetic background of acquired heart defects with calcification and arterial atherosclerosis.
Aim:
To evaluate the relationship between presence and severity of calcifications of the aortic semilunar valves and the intensity of atherosclerotic lesions in the aorta and aortic stiffness (AS).
Methods:
The study group comprised 80 subjects (49 males and 31 females) aged 72.2 (±8.0) years with an aortic valve defect found on echocardiography. Patients were divided into two subgroups depending on the severity of valvular disease. Subgroup I comprised 42 patients with small valvular lesions (0 - absence of calcification of the valve, or + - trivial valvular calcifications, possible to find on detailed evaluation of the valve). Subgroup II consisted of 38 patients with intense calcifications (++ - large, easily found valve calcifications, +++ - massive calcifications affecting leaflet mobility). All patients underwent transoesophageal echocardiography to evaluate atherosclerotic lesions in the aorta. The assessment included the following: location of the lesions in the aorta, intimal thickness, presence of calcifications and mobile parts of plaques and possible associated thrombi. Aortic stiffness was also measured using the formula: AS=log (SBP/DBP)/Aomax-Aomin)/Aomin.
Results:
Atherosclerotic plaques were more frequent in patients with more prominent calcifications of the aortic valve (19 vs 10 patients, p <0.05). Intimal thickness was larger in patients with more pronounced valve calcifications (3.9±0.8 mm vs 2.2+0.6 mm, p <0.05). Presence of calcifications in the aortic wall was also more frequent in patients from group II, as they were found in 10 subjects compared to only 3 cases in group I. Mobile plaque parts were observed in 3 patients from group II; also thrombi were found in 3 individuals from this group. Patients with more prominent calcifications of the aortic valve had decreased aortic wall elasticity (AS 5.5±1.2 cm vs 3.4±0.9 cm, p <0.05).
Conclusions:
Severity of aortic valve calcification indicates simultaneous changes in the thoracic aorta. Stiffness of the aortic wall is greater in patients with a more pronounced defect of the aortic valve. Prevalence of atherosclerosis risk factors is increased in patients with aortic valve defect, enhanced atherosclerosis and rigidity of the aorta. Defect of the aortic valve and increased aortic rigidity may be different manifestations of atherosclerosis.