Natriuretic peptides in the management of aortic stenosis

Bergler‐Klein, Jutta

doi:10.1007/s11886-009-0014-z

Cited by 26 publications

(15 citation statements)

References 52 publications

(72 reference statements)

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“…Increased LV wall stress has been proposed as a stimulus for the release of Natriuretic peptide in aortic stenosis. 4 Majority of the symptomatic patients in this study had normal diastolic function or an impaired relaxation pattern rather than more severe diastolic dysfunction.…”

Section: Discussionmentioning

confidence: 81%

“…Its release is stimulated by an increase in ventricular wall stress. 4 in patients with AS, NT-proBNP rise in correlation with severity and functional status as assessed by the New York Heart Association (NYHA) classification. 5 The present study was aimed to use the NT-pro-BNP to correlate symptoms of AS with NT-proBNP level and to find out the correlation of NT-proBNP level with LV functions.…”

Section: Introductionmentioning

confidence: 99%

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N-Terminal Pro–brain Natriuretic Peptide (Nt-Probnp) as a Biochemical Marker for Assessing Severity of Aortic Stenosis

Singh¹,

Sharma²

2016

jemds

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

N-Terminal Pro–brain Natriuretic Peptide (Nt-Probnp) as a Biochemical Marker for Assessing Severity of Aortic Stenosis

Singh¹,

Sharma²

2016

jemds

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“…7 Serum levels of BNP increase in patients with asymptomatic aortic stenosis shortly before the onset of signs and symptoms, and higher levels correlate with the severity of the signs and symptoms. 7,28 Patients with a serum baseline BNP greater than 130 pg/mL are likely to become symptomatic within 6 months, and BNP greater than 550 pg/mL is predictive of a poor outcome. 28 …”

Section: Diagnosis and Diagnostic Studiesmentioning

confidence: 99%

“…7,28 Patients with a serum baseline BNP greater than 130 pg/mL are likely to become symptomatic within 6 months, and BNP greater than 550 pg/mL is predictive of a poor outcome. 28 …”

Section: Diagnosis and Diagnostic Studiesmentioning

confidence: 99%

Aortic Stenosis: Pathophysiology, Diagnosis, and Medical Management of Nonsurgical Patients

Cary

Pearce²

2013

Critical Care Nurse

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A ortic stenosis is caused by narrowing of the orifice of the aortic valve and leads to obstruction of left ventricular outflow. This stenosis is rare in persons less than 50 years old.1 Calcification of the aortic valve is the most common cause of aortic stenosis in adults in industrialized countries and affects more than 4% of North American and Europeans more than 75 years old.2 In a study 3 of 338 North American patients with severe asymptomatic aortic stenosis, the mean age was 71 (SD, 15) years. Aortic stenosis was also associated with higher morbidity and mortality rates than were diseases involving other cardiac valves. 4 For example, in a study 5 of 161 patients, patients with moderate and

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“…These findings suggest that patients with asymptomatic severe aortic stenosis with elevated or serially rising natriuretic peptide levels should be monitored more closely for symptom development or deterioration of LV function, at which point prompt surgical intervention may need to be considered. 42 However, the precise cut points at which intervention should be considered remain to be defined.…”

Section: Shah Asymptomatic Severe Aortic Stenosis 121mentioning

confidence: 99%

Severe Aortic Stenosis Should Not Be Operated on Before Symptom Onset

Shah

2012

Circulation

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A ortic valve stenosis resulting from calcific thickening of a previously normal 3-cusp aortic valve or a congenitally bicuspid aortic valve is a common clinical condition in developed countries, and its prevalence is continuing to increase with aging of the population. 1,2 In the Cardiovascular Health Study, which involved 5201 men and women Ͼ65 years of age, the prevalence of aortic stenosis was 1.3% in subjects 65 to 75 years of age, 2.4% in subjects 75 to 85 years of age, and 4% in subjects Ͼ85 years of age. 3 The precise mechanisms involved in the pathophysiology of aortic stenosis and its progression are incompletely understood, but advancing age and atherosclerosis-related risk factors have been implicated in the process. 4 In fact, atherosclerotic coronary artery disease is present in nearly 50% of patients with aortic stenosis. 5 Studies of valve pathology have suggested a potential role for dyslipidemia, inflammation, and angiogenesis in the process, but pharmacological therapies using statins to reduce dyslipidemia and associated inflammatory processes have yielded inconsistent but largely negative results in terms of reducing the rate of progression of aortic stenosis. 6 -10 Thus, in the absence of specific and effective disease-modifying medical therapies, surgical aortic valve replacement has been and continues to be the cornerstone of management of severe aortic stenosis. There is general agreement among physicians and surgeons that when severe aortic stenosis is accompanied by 1 or more symptoms, such as chest pain, syncope or near syncope, resuscitated sudden death, shortness of breath, fatigue, effort intolerance, or left ventricular (LV) dysfunction, aortic valve replacement is recommended because of well-established dismal outcome (Ϸ50% mortality within 3 years) in unoperated symptomatic cases and overall excellent surgical outcomes with relatively low perioperative mortality and morbidity even among octogenarians [11][12][13][14][15] (Figures 1 and 2). Thus, despite the absence of data from a randomized clinical trial, symptomatic severe aortic stenosis is considered a class 1 indication for surgery by various professional organizations. 16,17 In some, particularly elderly patients, timely surgical aortic valve replacement is not considered because symptoms are mistakenly attributed to comorbid conditions, or the severity of underlying aortic stenosis is underestimated by traditional indices such as aortic valve gradient and peak velocity; this is particularly the case in patients with lowflow, low-gradient with depressed LV ejection fraction but is also true with a recently recognized variant associated with paradoxical low-flow, low-gradient severe aortic stenosis despite normal LV ejection fraction. 18 -20 Response by Carabello on p 125In the past few years, less invasive nonsurgical transcutaneous transfemoral (and to a lesser extent, transapical) techniques (such as transcatheter aortic valve implantation) for implanting a new bioprosthetic aortic valve inside a diseased

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Natriuretic peptides in the management of aortic stenosis

Cited by 26 publications

References 52 publications

N-Terminal Pro–brain Natriuretic Peptide (Nt-Probnp) as a Biochemical Marker for Assessing Severity of Aortic Stenosis

N-Terminal Pro–brain Natriuretic Peptide (Nt-Probnp) as a Biochemical Marker for Assessing Severity of Aortic Stenosis

Aortic Stenosis: Pathophysiology, Diagnosis, and Medical Management of Nonsurgical Patients

Severe Aortic Stenosis Should Not Be Operated on Before Symptom Onset

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