Aortic sclerosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]

Aortic sclerosis commonly affects elderly population. Aortic sclerosis is defined based on transthoracic echocardiographic findings which include irregular leaflet thickening and focal valve thickening with associated increase in echogenicity.^[1][2][3][4]

Microscopic changes reveal lipoprotein accumulation, cellular infiltration and extracellular matrix formation that cause progressive thickening of the aortic valve.^[1]

Aortic sclerosis is non-obstructive degeneration of the aortic valve that presents predominantly in patients over 65 years of age who have risk factors for coronary artery disease. Because aortic sclerosis is associated with coronary artery disease risk factors, it is also associated with a significant increase in the risk of cardiovascular death, myocardial infarction even in the absence of hemodynamically significant left ventricular outflow tract obstruction.^[5][3][2]

The presence of aortic sclerosis has been suggested as a marker of increased cardiovascular risk, including increased mortality. However, it remains unclear whether aortic sclerosis is independently associated with risk or merely a marker of coexistent cardiovascular risk factors.^[4]

Calcification of the aortic valve is common among the elderly population and shares epidemiologic and histopathologic similarities to atherosclerosis.^[6] Progressive thickening and calcification of the aortic valve subsequently causes left ventricular stiffness resulting in left ventricular outflow tract obstruction, thereby leading to aortic stenosis.^[2] Prognostically, it is known that aortic stenosis is clearly associated with adverse cardiovascular outcomes; however, it is unclear whether aortic sclerosis independently increases the risk of cardiovascular events or progression of aortic sclerosis to aortic stenosis increases the risk, including mortality.^[2]

• Mostly asymptomatic
• Aortic sclerosis is an incidental echocardiographic finding

While a short mid-systolic murmur may be heard in aortic sclerosis, there is no fusion of the commisures and no significant obstruction to forward flow across the aortic valve. As a result, the S2 is normal in aortic sclerosis and the carotid upstroke is normal (i.e. pulsus parvus et tardus) is absent.

• Focal areas of valve thickening with associated increase in echogenicity is the hallmark of aortic sclerosis,^[1][2][3][4] as opposed to the diffuse thickening observed as a part of normal aging
• Aortic side of the valve in the center of the valve cusp is commonly affected
• Commissural areas are spared
• Irregular leaflet thickening
• Leaflet mobility is normal
• Valvular hemodynamic parameters are normal with a jet flow velocity of less than 2.5 m per sec across the valve

• Aortic sclerosis has been suggested as a marker of increased cardiovascular risk, including increased mortality.^[1][7] Therefore, risk factor reduction among this patient population is reasonable although no definitive study has demonstrated reduction in aortic sclerosis progression achieved with aggressive management of hypertension and dyslipidemia

• Patients with isolated aortic valve disease rarely experience embolic events, therefore, according to the 2008 ACCP guidelines no antithrombotic therapy is required for the prevention of calcific microemboli.^[8]

• According to the 2008 ACC/AHA guidelines,^[9] no antibiotic prophylaxis is recommended for patients with aortic sclerosis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]

Calcific aortic valve disease includes both aortic sclerosis and aortic stenosis.^[1]

In patients with calcific aortic valve disease, microscopic examination reveals lipoprotein accumulation,^[2] macrophage and T-cellular infiltration,^[3] basement membrane disruption and extracellular matrix formation that lead to progressive thickening of the aortic valve.^[4][5][1]

• Otto et al,^[5] demonstrated the following histological characteristics observed in patients with aortic sclerosis:

1. Subendothelial thickening on the aortic side of the leaflet, between the basement membrane and elastic lamina
2. Presence of large amounts of intracellular and extracellular neutral lipids and fine, stippled mineralization
3. Disruption of the basement membrane overlying the lesion
4. Regions of the fibrosa adjacent to these lesions were characterized by thickening and by protein, lipid, and calcium accumulation

• Aortic sclerosis is non-obstructive degeneration of the aortic valve developed consequently to calcification of the aortic valve and macrophage accumulation which is dependent on the synthesis of osteopontin protein.^[6]

• Disturbances in mineral metabolism such as higher serum phosphate concentration has shown to contribute to the development of aortic sclerosis.^[7][8]

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]

Aortic sclerosis is non-obstructive degeneration of the aortic valve that presents predominantly in patients over 65 years of age who have risk factors for coronary artery disease. Because aortic sclerosis is associated with coronary artery disease risk factors, it is also associated with a significant increase in the risk of cardiovascular death, myocardial infarction even in the absence of hemodynamically significant left ventricular outflow tract obstruction.^[1][2][3]

Aortic sclerosis commonly affects those aged 65 years and over.^[4][3][2][1]

In a large cohort study of 5,201 patients,^[2] aortic sclerosis was present in ~37% patients > 75 years of age while aortic stenosis was seen only in 2.6% of patients > 75 years of age.^[5] Aortic sclerosis was even more common in another study of 425 patients with a mean age of 68 +/- 15 years who presented to an emergency room with chest pain. The rate of aortic sclerosis in this study was 49%.^[6]

Although less frequent, aortic sclerosis can be observed in middle-aged patients, and the risk of aortic sclerosis increases as the age in such a cohort increases.^[7][8]

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]

Aortic sclerosis is non-obstructive degeneration of the aortic valve that presents predominantly in patients over 65 years of age who have risk factors for coronary artery disease. Because aortic sclerosis is associated with coronary artery disease risk factors, it is also associated with a significant increase in the risk of cardiovascular death, myocardial infarction even in the absence of hemodynamically significant left ventricular outflow tract obstruction. However, it remains unclear whether aortic sclerosis is independently associated with risk or merely a marker of coexistent cardiovascular risk factors.^[1]

• Independent clinical factors that is associated with increased incidence of aortic sclerosis include:

• Age (twofold increased risk for each 10-year increase in age)^[2][3]
• Male gender (twofold excess risk)^[2][3]
• Present smoking (35% increase in risk)^[2][3][4]
• History of hypertension (20% increase in risk)^[2][3] with subsequent left ventricular hypertrophy ^[5]
• Height^[2][3]
• Elevated lipoprotein(a) and elevated low density lipoprotein cholesterol levels^{[2][3][6][7][8][4]}
• End-stage renal disease on maintenance dialysis.^[9][10]
• Metabolic syndrome and diabetes mellitus^[11]

• The MESA study quantified aortic valve calcification by serial computed tomographic images from 5,880 participants aged 45 to 84 years reported an 1.7% per year incidence rate of aortic valve calcification which increased significantly with age.^[3]

• In addition to the presence of traditional risk factors for coronary artery disease such as hypertension,^[5] diabetes,^[11] hyperlipidemia^[6][7][8] and smoking, the presence of multiple calcium deposits in the mitral annulus, aortic valve or aortic root have been shown to be a predictor of coronary artery disease among elderly patients with aortic sclerosis.^{[12][2][13][14][15]}

• The Heart and Soul study evaluated 814 outpatients with established coronary heart disease and no evidence of aortic stenosis, to examine the association of aortic sclerosis with subsequent cardiovascular events. At baseline, 40% of the enrolled subjects had aortic sclerosis. During 4-year follow-up, a significant number of patients with aortic sclerosis experienced myocardial infarction in comparison to patients without aortic sclerosis: 10% versus 5% (HR 1.8; 95%CI,1.1-3.1; P=0.02). Additionally, the association between aortic sclerosis and MI appeared to differ by statin use (P=0.15 for interaction). Thus, the study concluded aortic sclerosis was independently associated with a 2.4-fold increased rate of subsequent MI. Furthermore, administration of statins attenuated the risk of future MI in patients with aortic sclerosis.^[16]

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]

Calcification of the aortic valve is common among the elderly population and shares epidemiologic and histopathologic similarities to atherosclerosis.^[1] Progressive thickening and calcification of the aortic valve subsequently causes left ventricular stiffness resulting in left ventricular outflow tract obstruction, thereby leading to aortic stenosis.^[2] Prognostically, it is known that aortic stenosis is clearly associated with adverse cardiovascular outcomes; however, it is unclear whether aortic sclerosis independently increases the risk of cardiovascular events or progression of aortic sclerosis to aortic stenosis increases the risk, including mortality.^[2]

• Echocardiographic indicators of progression of aortic sclerosis to aortic stenosis include:

• Restricted leaflet mobility
• Increased echogenicity suggestive of increase leaflet calcification
• Increase in jet flow velocity across the valve

• Based on a database study from 1987 to 1993, that evaluated 2131 cases of aortic valve thickening with minimum 1-year echocardiographic follow-up, reported the development of aortic stenosis in 15.9% cases, of which 10.5% developed mild AS, 2.9% had moderate AS and 2.5% had severe AS. Thus, this study demonstrated the prevalence of benign aortic valve thickening with the progression to significant aortic stenosis.^[3][4]

• Another large population-based cohort reported an ~9% of subjects with aortic sclerosis progressed to aortic stenosis over a 5-year echocardiographic follow-up. Additionally, no association was observed between C-reactive protein levels and the presence of calcific aortic-valve disease or incidental aortic stenosis. However, if C-reactive protein was present it was a poor predictor of subclinical calcific aortic-valve disease.^[5]

Spontaneous calcific embolization has been associated with calcific aortic valve disease;^[6] however, Boon et al^[7] and Kizer et al^[8], demonstrated no significant increase in the risk of stroke in aortic sclerosis patients with or without aortic stenosis.^[2]

• Prognostically, it is known that aortic stenosis is clearly associated with adverse cardiovascular outcomes; however, it is unclear whether aortic sclerosis independently increases the risk of cardiovascular events or progression of aortic sclerosis to aortic stenosis increases the risk, including mortality.^[2] One of the possible explanation, could be that aortic sclerosis serves as a inflammatory marker for coronary artery disease;^{[9][10][11][12]} however, Novaro et al demonstrated no association between C-reactive protein levels and the presence of calcific aortic-valve disease or incidental aortic stenosis.^[5]

• Population-based prospective study, evaluated baseline echocardiograms obtained from 5621 men and women 65 years of age or older, off which 70% had normal aortic valve, 29% had aortic sclerosis without outflow obstruction and only 2% had aortic stenosis. During a mean 5-year follow-up, a stepwise significant increase in mortality was observed in patients with increasing aortic-valve abnormality. Thus, the study concluded an ~50% increase in the risk of death from cardiovascular causes and the risk of myocardial infarction in patients with aortic sclerosis, even in the absence of hemodynamically significant obstruction of left ventricular outflow.^[2]

• Similar association between aortic sclerosis and the incidence of new coronary events were reported in multiple prospective studies^[13][14] and was independent of co-existing cardiovascular disease or traditional cardiovascular risk factors.^[15]

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