Interrelations Between Arterial Stiffness, Target Organ Damage, and Cardiovascular Disease Outcomes

Background Excess transmission of pressure pulsatility caused by increased arterial stiffness may incur microcirculatory damage in end organs (target organ damage [TOD] ) and, in turn, elevate risk for cardiovascular disease ( CVD ) events. Methods and Results We related arterial stiffness measures...

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Vydané v:Journal of the American Heart Association Ročník 8; číslo 14; s. e012141
Hlavní autori: Vasan, Ramachandran S., Short, Meghan I., Niiranen, Teemu J., Xanthakis, Vanessa, DeCarli, Charles, Cheng, Susan, Seshadri, Sudha, Mitchell, Gary F.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England John Wiley and Sons Inc 16.07.2019
Wiley
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ISSN:2047-9980, 2047-9980
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Abstract Background Excess transmission of pressure pulsatility caused by increased arterial stiffness may incur microcirculatory damage in end organs (target organ damage [TOD] ) and, in turn, elevate risk for cardiovascular disease ( CVD ) events. Methods and Results We related arterial stiffness measures (carotid-femoral pulse wave velocity, mean arterial pressure, central pulse pressure) to the prevalence and incidence of TOD (defined as albuminuria and/or echocardiographic left ventricular hypertrophy) in up to 6203 Framingham Study participants (mean age 50±15 years, 54% women). We then related presence of TOD to incident CVD in multivariable Cox regression models without and with adjustment for arterial stiffness measures. Cross-sectionally, greater arterial stiffness was associated with a higher prevalence of TOD (adjusted odds ratios ranging from 1.23 to 1.54 per SD increment in arterial stiffness measure, P<0.01). Prospectively, increased carotid-femoral pulse wave velocity was associated with incident albuminuria (odds ratio per SD 1.28, 95% CI, 1.02-1.61; P<0.05), whereas higher mean arterial pressure and central pulse pressure were associated with incident left ventricular hypertrophy (odds ratio per SD 1.37 and 1.45, respectively; P<0.01). On follow-up, 297 of 5803 participants experienced a first CVD event. Presence of TOD was associated with a 33% greater hazard of incident CVD (95% CI , 0-77%; P<0.05), which was attenuated upon adjustment for baseline arterial stiffness measures by 5-21%. Conclusions Elevated arterial stiffness is associated with presence of TOD and may partially mediate the relations of TOD with incident CVD . Our observations in a large community-based sample suggest that mitigating arterial stiffness may lower the burden of TOD and, in turn, clinical CVD .
AbstractList Background Excess transmission of pressure pulsatility caused by increased arterial stiffness may incur microcirculatory damage in end organs (target organ damage [TOD]) and, in turn, elevate risk for cardiovascular disease (CVD) events. Methods and Results We related arterial stiffness measures (carotid‐femoral pulse wave velocity, mean arterial pressure, central pulse pressure) to the prevalence and incidence of TOD (defined as albuminuria and/or echocardiographic left ventricular hypertrophy) in up to 6203 Framingham Study participants (mean age 50±15 years, 54% women). We then related presence of TOD to incident CVD in multivariable Cox regression models without and with adjustment for arterial stiffness measures. Cross‐sectionally, greater arterial stiffness was associated with a higher prevalence of TOD (adjusted odds ratios ranging from 1.23 to 1.54 per SD increment in arterial stiffness measure, P<0.01). Prospectively, increased carotid‐femoral pulse wave velocity was associated with incident albuminuria (odds ratio per SD 1.28, 95% CI, 1.02–1.61; P<0.05), whereas higher mean arterial pressure and central pulse pressure were associated with incident left ventricular hypertrophy (odds ratio per SD 1.37 and 1.45, respectively; P<0.01). On follow‐up, 297 of 5803 participants experienced a first CVD event. Presence of TOD was associated with a 33% greater hazard of incident CVD (95% CI, 0–77%; P<0.05), which was attenuated upon adjustment for baseline arterial stiffness measures by 5–21%. Conclusions Elevated arterial stiffness is associated with presence of TOD and may partially mediate the relations of TOD with incident CVD. Our observations in a large community‐based sample suggest that mitigating arterial stiffness may lower the burden of TOD and, in turn, clinical CVD.
Background Excess transmission of pressure pulsatility caused by increased arterial stiffness may incur microcirculatory damage in end organs (target organ damage [TOD] ) and, in turn, elevate risk for cardiovascular disease ( CVD ) events. Methods and Results We related arterial stiffness measures (carotid-femoral pulse wave velocity, mean arterial pressure, central pulse pressure) to the prevalence and incidence of TOD (defined as albuminuria and/or echocardiographic left ventricular hypertrophy) in up to 6203 Framingham Study participants (mean age 50±15 years, 54% women). We then related presence of TOD to incident CVD in multivariable Cox regression models without and with adjustment for arterial stiffness measures. Cross-sectionally, greater arterial stiffness was associated with a higher prevalence of TOD (adjusted odds ratios ranging from 1.23 to 1.54 per SD increment in arterial stiffness measure, P<0.01). Prospectively, increased carotid-femoral pulse wave velocity was associated with incident albuminuria (odds ratio per SD 1.28, 95% CI, 1.02-1.61; P<0.05), whereas higher mean arterial pressure and central pulse pressure were associated with incident left ventricular hypertrophy (odds ratio per SD 1.37 and 1.45, respectively; P<0.01). On follow-up, 297 of 5803 participants experienced a first CVD event. Presence of TOD was associated with a 33% greater hazard of incident CVD (95% CI , 0-77%; P<0.05), which was attenuated upon adjustment for baseline arterial stiffness measures by 5-21%. Conclusions Elevated arterial stiffness is associated with presence of TOD and may partially mediate the relations of TOD with incident CVD . Our observations in a large community-based sample suggest that mitigating arterial stiffness may lower the burden of TOD and, in turn, clinical CVD .Background Excess transmission of pressure pulsatility caused by increased arterial stiffness may incur microcirculatory damage in end organs (target organ damage [TOD] ) and, in turn, elevate risk for cardiovascular disease ( CVD ) events. Methods and Results We related arterial stiffness measures (carotid-femoral pulse wave velocity, mean arterial pressure, central pulse pressure) to the prevalence and incidence of TOD (defined as albuminuria and/or echocardiographic left ventricular hypertrophy) in up to 6203 Framingham Study participants (mean age 50±15 years, 54% women). We then related presence of TOD to incident CVD in multivariable Cox regression models without and with adjustment for arterial stiffness measures. Cross-sectionally, greater arterial stiffness was associated with a higher prevalence of TOD (adjusted odds ratios ranging from 1.23 to 1.54 per SD increment in arterial stiffness measure, P<0.01). Prospectively, increased carotid-femoral pulse wave velocity was associated with incident albuminuria (odds ratio per SD 1.28, 95% CI, 1.02-1.61; P<0.05), whereas higher mean arterial pressure and central pulse pressure were associated with incident left ventricular hypertrophy (odds ratio per SD 1.37 and 1.45, respectively; P<0.01). On follow-up, 297 of 5803 participants experienced a first CVD event. Presence of TOD was associated with a 33% greater hazard of incident CVD (95% CI , 0-77%; P<0.05), which was attenuated upon adjustment for baseline arterial stiffness measures by 5-21%. Conclusions Elevated arterial stiffness is associated with presence of TOD and may partially mediate the relations of TOD with incident CVD . Our observations in a large community-based sample suggest that mitigating arterial stiffness may lower the burden of TOD and, in turn, clinical CVD .
Author Vasan, Ramachandran S.
Short, Meghan I.
Xanthakis, Vanessa
DeCarli, Charles
Cheng, Susan
Mitchell, Gary F.
Niiranen, Teemu J.
Seshadri, Sudha
AuthorAffiliation 3 Section of Cardiology Department of Medicine Boston University School of Medicine Boston MA
4 Department of Epidemiology Boston University School of Public Health Boston MA
2 Section of Preventive Medicine Department of Medicine Boston University School of Medicine Boston MA
10 Biggs Institute for Alzheimer's Disease University of Texas Health Sciences Center at San Antonio TX
11 Cardiovascular Engineering, Inc. Norwood MA
9 Smidt Heart Institute Cedars‐Sinai Medical Center Los Angeles CA
7 Department of Public Health Solutions National Institute for Health and Welfare Turku Finland
8 University of California Davis CA
5 Department of Biostatistics Boston University School of Public Health Boston MA
6 Department of Medicine Turku University Hospital and University of Turku Finland
1 National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham MA
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– name: 4 Department of Epidemiology Boston University School of Public Health Boston MA
– name: 8 University of California Davis CA
– name: 9 Smidt Heart Institute Cedars‐Sinai Medical Center Los Angeles CA
– name: 7 Department of Public Health Solutions National Institute for Health and Welfare Turku Finland
– name: 5 Department of Biostatistics Boston University School of Public Health Boston MA
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  givenname: Ramachandran S.
  surname: Vasan
  fullname: Vasan, Ramachandran S.
  organization: National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham MA, Section of Preventive Medicine Department of Medicine Boston University School of Medicine Boston MA, Section of Cardiology Department of Medicine Boston University School of Medicine Boston MA, Department of Epidemiology Boston University School of Public Health Boston MA
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  givenname: Meghan I.
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  fullname: Short, Meghan I.
  organization: Department of Biostatistics Boston University School of Public Health Boston MA
– sequence: 3
  givenname: Teemu J.
  surname: Niiranen
  fullname: Niiranen, Teemu J.
  organization: National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham MA, Department of Medicine Turku University Hospital and University of Turku Finland, Department of Public Health Solutions National Institute for Health and Welfare Turku Finland
– sequence: 4
  givenname: Vanessa
  surname: Xanthakis
  fullname: Xanthakis, Vanessa
  organization: National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham MA, Section of Preventive Medicine Department of Medicine Boston University School of Medicine Boston MA, Department of Biostatistics Boston University School of Public Health Boston MA
– sequence: 5
  givenname: Charles
  surname: DeCarli
  fullname: DeCarli, Charles
  organization: University of California Davis CA
– sequence: 6
  givenname: Susan
  surname: Cheng
  fullname: Cheng, Susan
  organization: National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham MA, Smidt Heart Institute Cedars‐Sinai Medical Center Los Angeles CA
– sequence: 7
  givenname: Sudha
  surname: Seshadri
  fullname: Seshadri, Sudha
  organization: National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham MA, Biggs Institute for Alzheimer's Disease University of Texas Health Sciences Center at San Antonio TX
– sequence: 8
  givenname: Gary F.
  surname: Mitchell
  fullname: Mitchell, Gary F.
  organization: Cardiovascular Engineering, Inc. Norwood MA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31303106$$D View this record in MEDLINE/PubMed
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Issue 14
Keywords arterial stiffness
cardiovascular disease
epidemiology
pulse wave velocity
target organ damage
Language English
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Snippet Background Excess transmission of pressure pulsatility caused by increased arterial stiffness may incur microcirculatory damage in end organs (target organ...
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SubjectTerms Adult
Aged
Albuminuria - epidemiology
Angina Pectoris - epidemiology
Angina, Unstable - epidemiology
Arterial Pressure - physiology
arterial stiffness
cardiovascular disease
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - mortality
Carotid-Femoral Pulse Wave Velocity
Cohort Studies
Echocardiography
epidemiology
Female
Heart Failure - epidemiology
Humans
Hypertrophy, Left Ventricular - diagnostic imaging
Hypertrophy, Left Ventricular - epidemiology
Incidence
Intermittent Claudication - epidemiology
Ischemic Attack, Transient - epidemiology
Longitudinal Studies
Male
Manometry
Middle Aged
Myocardial Infarction - epidemiology
Myocardial Infarction - mortality
Original Research
Prospective Studies
pulse wave velocity
Stroke - epidemiology
target organ damage
Vascular Stiffness - physiology
Title Interrelations Between Arterial Stiffness, Target Organ Damage, and Cardiovascular Disease Outcomes
URI https://www.ncbi.nlm.nih.gov/pubmed/31303106
https://www.proquest.com/docview/2258159504
https://pubmed.ncbi.nlm.nih.gov/PMC6662123
https://doaj.org/article/bd13f8560482475388b2d4707ac670df
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