Diabetes and hypercholesterolemia among patients with calcific aortic stenosis

Deutscher, Sigismond; Rockette, Howard E.; Krishnaswami, Venkataraman

doi:10.1016/0021-9681(84)90108-5

Cited by 113 publications

(51 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[13][14][15][16][17] Because the present study was conducted at a single tertiary-care medical center on the east coast of the United States, it is possible that there were biases with regard to the sample population. For example, there were only 3 Asian patients in the present study.…”

Section: Discussionmentioning

confidence: 99%

Bone Formation and Inflammation in Cardiac Valves

et al. 2001

View full text Add to dashboard Cite

Background-For nearly a century, the mechanical failure of calcified heart valves was attributed to a passive degenerative process. Recently, several case reports described bone formation in surgically excised heart valves and suggested an unexpected process of tissue repair. Methods and Results-We studied the prevalence and pathology of heterotopic ossification in 347 surgically excised heart valves (256 aortic, 91 mitral) in 324 consecutive patients (182 men, 142 women; mean age 68 years) who underwent cardiac valve replacement surgery between 1994 and 1998. The valves were examined microscopically to determine the prevalence and features of bone formation and remodeling. Two hundred eighty-eight valves (83%) had dystrophic calcification. Mature lamellar bone with hematopoietic elements and active bone remodeling were present in 36 valves (13%) with dystrophic calcification. Endochondral bone formation, similar to that seen in normal fracture repair, was identified in 4 valves. Microfractures were present in 92% of all valves with ossification. Neoangiogenesis was found in all valves with ossification. Bone morphogenetic proteins 2 and 4 (BMP 2/4), potent osteogenic morphogens, were expressed by myofibroblasts and preosteoblasts in areas adjacent to B-and T-lymphocyte infiltration in valves where ossification was identified. Mast cells were present in calcified and ossified valves and were especially prominent in atheromatous regions. Conclusions-Heterotopic

show abstract

Section: Discussionmentioning

confidence: 99%

Bone Formation and Inflammation in Cardiac Valves

et al. 2001

View full text Add to dashboard Cite

show abstract

“…[11][12][13][14][15][16] In addition, the presence of ACE and angiotensin II, which cannot be found in normal valve tissue, has been demonstrated in sclerotic aortic valves, 17 which suggests a potential role for the renin-angiotensin system in aortic valve lesion pathogenesis. ACE also is found in atherosclerotic lesions, 18 and angiotensin II, with its proinflammatory effects, is assumed to contribute to the atherosclerotic process.…”

Section: See P 1180mentioning

confidence: 99%

Statins but Not Angiotensin-Converting Enzyme Inhibitors Delay Progression of Aortic Stenosis

et al. 2004

View full text Add to dashboard Cite

Background— Recently, statins and angiotensin-converting enzyme inhibitors (ACEIs) have been shown to slow aortic valve calcium accumulation. Although several studies also suggest that statins may reduce the hemodynamic progression of aortic stenosis (AS), no data are available for ACEIs or the combination of both. Methods and Results— A total of 211 consecutive patients (aged 70±10 years, 104 females) with native AS, defined by a peak velocity >2.5 m/s (valve area 0.84±0.23 cm 2 , mean gradient 42±19 mm Hg), with normal left ventricular function and no other significant valvular lesion who were examined between 2000 and 2002 and who had 2 echocardiograms separated by at least 6 months were included. Of these, 102 patients were treated with ACEIs, 50 patients received statins, and 32 patients received both. Hemodynamic progression of AS was assessed and related to medical treatment. Annualized increase in peak aortic jet velocity for the entire study group was 0.32±0.44 m · s −1 · y −1 . Progression was significantly lower in patients treated with statins (0.10±0.41 m · s −1 · y −1 ) than in those who were not (0.39±0.42 m · s −1 · y −1 ; P <0.0001). This effect was observed both in mild-to-moderate and severe AS. ACEI use, however, did not significantly affect hemodynamic progression ( P =0.29). Furthermore, ACEIs had no additional effect on AS progression when given in combination with statins (0.11±0.42 versus 0.08±0.43 m · s −1 · y −1 for combination versus statin only; P =0.81). Cholesterol levels did not correlate with hemodynamic progression either in the group receiving statins or in the group that did not. Conclusions— ACEIs do not appear to slow AS progression. However, statins significantly reduce the hemodynamic progression of both mild-to-moderate and severe AS, an effect that may not be related to cholesterol lowering.

show abstract

“…3 Other significant associated factors include height, high lipoprotein (LP) (a) level, high low-density lipoprotein (LDL) level, and diabetes mellitus. 4,5 Secondary hyperthyroidism, Paget's disease, as well as elevated creatinine and calcium are also linked to progression of valve calcification. 6 …”

Section: Introductionmentioning

confidence: 99%

Aortic sclerosis—a marker of coronary atherosclerosis

Prasad

Bhalodkar

2004

Clinical Cardiology

View full text Add to dashboard Cite

Summary: Aortic valve sclerosis is defined as calcification and thickening of a trileaflet aortic valve in the absence of obstruction of ventricular outflow. Its frequency increases with age, making it a major geriatric problem. Of adults aged > 65 years, 21-29% exhibit aortic valve sclerosis. Incidence of aortic sclerosis increases with age, male gender, smoking, hypertension, high lipoprotein (Lp) (a), high low-density lipoprotein (LDL), and diabetes mellitus. Aortic valves affected by aortic sclerosis contain a higher amount of oxidized LDL cholesterol and show increased expression of metalloproteinases. Clinically, it can be suspected in the presence of soft ejection systolic murmur at the aortic area, normal split of the second heart sound, and normal volume carotid pulse, but it can be best detected by echocardiography. Aortic sclerosis may be accompanied by mitral annulus calcification up to 50% of cases. It is associated with an increase of approximately 50% in the risk of death from cardiovascular causes and the risk of myocardial infarction. The mechanism by which aortic sclerosis contributes to or is associated with increased cardiovascular risk is not known. Aortic sclerosis is associated with systemic endothelial dysfunction, and a small percentage of cases may progress to aortic stenosis. Lowering of LDL cholesterol by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have been shown to decrease progression of aortic valve calcification. Aortic sclerosis is not a mere benign finding. Once diagnosis of aortic sclerosis has been made, it should be considered a potential marker of coexisting coronary disease. Aggressive management of modifiable risk factors, especially LDL cholesterol lowering, may slow progression of the disease.

show abstract

Diabetes and hypercholesterolemia among patients with calcific aortic stenosis

Cited by 113 publications

References 11 publications

Bone Formation and Inflammation in Cardiac Valves

Bone Formation and Inflammation in Cardiac Valves

Statins but Not Angiotensin-Converting Enzyme Inhibitors Delay Progression of Aortic Stenosis

Aortic sclerosis—a marker of coronary atherosclerosis

Contact Info

Product

Resources

About