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 |
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| Hlavní autori: | , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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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 . |
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| 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 |
| AuthorAffiliation_xml | – name: 6 Department of Medicine Turku University Hospital and University of Turku Finland – name: 2 Section of Preventive Medicine Department of Medicine Boston University School of Medicine Boston MA – name: 3 Section of Cardiology Department of Medicine Boston University School of Medicine Boston MA – name: 11 Cardiovascular Engineering, Inc. Norwood MA – name: 1 National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study Framingham MA – 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 – name: 10 Biggs Institute for Alzheimer's Disease University of Texas Health Sciences Center at San Antonio TX |
| Author_xml | – sequence: 1 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 – sequence: 2 givenname: Meghan I. surname: Short 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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| Cites_doi | 10.1161/HYPERTENSIONAHA.111.177469 10.1212/WNL.0000000000002368 10.1001/2012.jama.10503 10.2174/1874609811205020157 10.1097/HJH.0000000000000686 10.1161/STROKEAHA.116.012949 10.1177/1753944709338942 10.1161/CIRCULATIONAHA.105.555235 10.1152/japplphysiol.90549.2008 10.2105/AJPH.41.3.279 10.1681/ASN.2009010074 10.1093/aje/kwm021 10.1159/000324215 10.1016/j.jacc.2015.08.888 10.1038/jhh.2013.103 10.5114/aoms.2017.69240 10.1161/CIRCULATIONAHA.109.914507 10.1161/CIRCULATIONAHA.110.989145 10.1016/j.neurobiolaging.2013.08.026 10.1053/j.ajkd.2011.08.015 10.1681/ASN.V1341034 10.1093/oxfordjournals.aje.a112813 10.1161/STROKEAHA.112.656744 10.1161/HYPERTENSIONAHA.116.08749 10.1016/j.jacc.2012.07.054 10.1001/jama.292.19.2343 10.1161/01.HYP.0000128420.01881.aa 10.2147/CIA.S133691 10.1161/JAHA.115.002189 10.1093/eurheartj/ehy339 10.1016/j.neurobiolaging.2004.05.004 10.1161/CIRCULATIONAHA.109.886655 10.2337/diacare.10.4.414 10.1161/JAHA.115.002693 10.1001/jama.292.19.2350 10.1093/brain/awr253 10.2337/dc11-2245 10.1161/01.HYP.0000154082.72286.2a 10.1161/JAHA.116.004168 10.1016/j.echo.2014.10.003 10.1161/CIRCRESAHA.118.312563 10.1161/HYPERTENSIONAHA.109.136655 10.1161/HYPERTENSIONAHA.111.00430 10.1053/j.ajkd.2018.04.018 |
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| Copyright | 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. |
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| Keywords | arterial stiffness cardiovascular disease epidemiology pulse wave velocity target organ damage |
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| References | e_1_3_1_21_2 e_1_3_1_43_2 e_1_3_1_22_2 e_1_3_1_44_2 e_1_3_1_23_2 e_1_3_1_45_2 e_1_3_1_46_2 e_1_3_1_8_2 e_1_3_1_7_2 e_1_3_1_40_2 e_1_3_1_41_2 e_1_3_1_9_2 e_1_3_1_20_2 e_1_3_1_42_2 e_1_3_1_4_2 e_1_3_1_29_2 e_1_3_1_3_2 e_1_3_1_6_2 e_1_3_1_5_2 e_1_3_1_25_2 e_1_3_1_48_2 e_1_3_1_26_2 e_1_3_1_47_2 e_1_3_1_2_2 e_1_3_1_27_2 e_1_3_1_28_2 e_1_3_1_49_2 Quan SF (e_1_3_1_24_2) 1997; 20 e_1_3_1_32_2 e_1_3_1_33_2 e_1_3_1_34_2 Kannel WB (e_1_3_1_36_2) 1987 e_1_3_1_35_2 e_1_3_1_13_2 e_1_3_1_12_2 e_1_3_1_11_2 e_1_3_1_30_2 e_1_3_1_10_2 e_1_3_1_31_2 e_1_3_1_17_2 e_1_3_1_16_2 e_1_3_1_15_2 e_1_3_1_14_2 e_1_3_1_37_2 e_1_3_1_19_2 e_1_3_1_38_2 e_1_3_1_18_2 e_1_3_1_39_2 |
| References_xml | – ident: e_1_3_1_11_2 doi: 10.1161/HYPERTENSIONAHA.111.177469 – volume-title: Section 34: some risk factors related to the annual incidence of cardiovascular disease and death in pooled repeated biennial measurements. Framingham Heart Study, 30 Year Follow‐Up year: 1987 ident: e_1_3_1_36_2 – ident: e_1_3_1_16_2 doi: 10.1212/WNL.0000000000002368 – ident: e_1_3_1_29_2 doi: 10.1001/2012.jama.10503 – ident: e_1_3_1_12_2 doi: 10.2174/1874609811205020157 – ident: e_1_3_1_19_2 doi: 10.1097/HJH.0000000000000686 – ident: e_1_3_1_13_2 doi: 10.1161/STROKEAHA.116.012949 – ident: e_1_3_1_10_2 doi: 10.1177/1753944709338942 – ident: e_1_3_1_43_2 doi: 10.1161/CIRCULATIONAHA.105.555235 – ident: e_1_3_1_7_2 doi: 10.1152/japplphysiol.90549.2008 – ident: e_1_3_1_21_2 doi: 10.2105/AJPH.41.3.279 – ident: e_1_3_1_15_2 doi: 10.1681/ASN.2009010074 – ident: e_1_3_1_23_2 doi: 10.1093/aje/kwm021 – ident: e_1_3_1_45_2 doi: 10.1159/000324215 – ident: e_1_3_1_40_2 doi: 10.1016/j.jacc.2015.08.888 – ident: e_1_3_1_41_2 doi: 10.1038/jhh.2013.103 – ident: e_1_3_1_44_2 doi: 10.5114/aoms.2017.69240 – ident: e_1_3_1_27_2 doi: 10.1161/CIRCULATIONAHA.109.914507 – ident: e_1_3_1_35_2 doi: 10.1161/CIRCULATIONAHA.110.989145 – ident: e_1_3_1_9_2 doi: 10.1016/j.neurobiolaging.2013.08.026 – ident: e_1_3_1_17_2 doi: 10.1053/j.ajkd.2011.08.015 – ident: e_1_3_1_26_2 – ident: e_1_3_1_32_2 doi: 10.1681/ASN.V1341034 – ident: e_1_3_1_25_2 – ident: e_1_3_1_22_2 doi: 10.1093/oxfordjournals.aje.a112813 – ident: e_1_3_1_33_2 doi: 10.1161/STROKEAHA.112.656744 – ident: e_1_3_1_38_2 doi: 10.1161/HYPERTENSIONAHA.116.08749 – ident: e_1_3_1_42_2 doi: 10.1016/j.jacc.2012.07.054 – ident: e_1_3_1_4_2 doi: 10.1001/jama.292.19.2343 – ident: e_1_3_1_28_2 doi: 10.1161/01.HYP.0000128420.01881.aa – ident: e_1_3_1_47_2 doi: 10.2147/CIA.S133691 – ident: e_1_3_1_39_2 doi: 10.1161/JAHA.115.002189 – ident: e_1_3_1_2_2 doi: 10.1093/eurheartj/ehy339 – ident: e_1_3_1_34_2 doi: 10.1016/j.neurobiolaging.2004.05.004 – ident: e_1_3_1_37_2 doi: 10.1161/CIRCULATIONAHA.109.886655 – ident: e_1_3_1_31_2 doi: 10.2337/diacare.10.4.414 – ident: e_1_3_1_14_2 doi: 10.1161/JAHA.115.002693 – ident: e_1_3_1_3_2 doi: 10.1001/jama.292.19.2350 – ident: e_1_3_1_8_2 doi: 10.1093/brain/awr253 – ident: e_1_3_1_18_2 doi: 10.2337/dc11-2245 – ident: e_1_3_1_6_2 doi: 10.1161/01.HYP.0000154082.72286.2a – ident: e_1_3_1_46_2 doi: 10.1161/JAHA.116.004168 – volume: 20 start-page: 1077 year: 1997 ident: e_1_3_1_24_2 article-title: The Sleep Heart Health Study: design, rationale, and methods publication-title: Sleep – ident: e_1_3_1_30_2 doi: 10.1016/j.echo.2014.10.003 – ident: e_1_3_1_49_2 doi: 10.1161/CIRCRESAHA.118.312563 – ident: e_1_3_1_5_2 doi: 10.1161/HYPERTENSIONAHA.109.136655 – ident: e_1_3_1_20_2 doi: 10.1161/HYPERTENSIONAHA.111.00430 – ident: e_1_3_1_48_2 doi: 10.1053/j.ajkd.2018.04.018 |
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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 |
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