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Augmentation of central arterial pressure in mild primary hyperparathyroidism
Primary hyperparathyroidism (PHPT) is associated with increased cardiovascular risk, although the mechanisms involved remain unclear. Recent evidence has shown increased pulse pressure to be a powerful predictor of cardiovascular events. As increases in pulse pressure are due largely to arterial sti...
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Published in: | The journal of clinical endocrinology and metabolism 2000-10, Vol.85 (10), p.3515-3519 |
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description | Primary hyperparathyroidism (PHPT) is associated with increased cardiovascular risk, although the mechanisms involved remain unclear. Recent evidence has shown increased pulse pressure to be a powerful predictor of cardiovascular events. As increases in pulse pressure are due largely to arterial stiffening, we measured arterial stiffness in 21 subjects with PHPT (18 women and 3 men; 46-71 yr old) and 21 age- and sex-matched healthy controls using pulse wave analysis, a technique that measures peripheral arterial pressure waveforms and generates corresponding central aortic waveforms. This allows determination of the augmentation of central pressure resulting from wave reflection and augmentation index, a measure of vessel stiffness. Metabolic parameters were also measured. The serum calcium level among PHPT subjects was (mean +/- SD) 2.74+/-0.14 mmol/L. pulse wave analysis showed that both augmentation and the augmentation index were significantly higher in the PHPT group vs. controls [16+/-5 vs. 10+/-4 mm Hg (P < 0.001) and 36+/-9% vs. 25+/-6% (P < 0.001)] despite comparable brachial systolic pressures between groups (136+/-13 vs. 134+/-18 mm Hg). Patients with PHPT had higher fasting serum insulin levels [median (range), 15.8 (7.4-39.4) vs. 11.6 (5.1-23) mU/L; P < 0.05] and triglyceride (1.6+/-0.6 vs. 1.2+/-0.4 mmol/L; P < 0.05), but lower high density lipoprotein cholesterol (1.4+/-0.4 vs. 1.6+/-0.3 mmol/L; P < 0.05). These data indicate that subjects with mild PHPT (calcium, |
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C ; PAGE, M. D ; JOHN, R ; WHEELER, M. H ; COCKCROFT, J. R ; SCANLON, M. F ; DAVIES, J. S</creator><creatorcontrib>SMITH, J. C ; PAGE, M. D ; JOHN, R ; WHEELER, M. H ; COCKCROFT, J. R ; SCANLON, M. F ; DAVIES, J. S</creatorcontrib><description><![CDATA[Primary hyperparathyroidism (PHPT) is associated with increased cardiovascular risk, although the mechanisms involved remain unclear. Recent evidence has shown increased pulse pressure to be a powerful predictor of cardiovascular events. As increases in pulse pressure are due largely to arterial stiffening, we measured arterial stiffness in 21 subjects with PHPT (18 women and 3 men; 46-71 yr old) and 21 age- and sex-matched healthy controls using pulse wave analysis, a technique that measures peripheral arterial pressure waveforms and generates corresponding central aortic waveforms. This allows determination of the augmentation of central pressure resulting from wave reflection and augmentation index, a measure of vessel stiffness. Metabolic parameters were also measured. The serum calcium level among PHPT subjects was (mean +/- SD) 2.74+/-0.14 mmol/L. pulse wave analysis showed that both augmentation and the augmentation index were significantly higher in the PHPT group vs. controls [16+/-5 vs. 10+/-4 mm Hg (P < 0.001) and 36+/-9% vs. 25+/-6% (P < 0.001)] despite comparable brachial systolic pressures between groups (136+/-13 vs. 134+/-18 mm Hg). Patients with PHPT had higher fasting serum insulin levels [median (range), 15.8 (7.4-39.4) vs. 11.6 (5.1-23) mU/L; P < 0.05] and triglyceride (1.6+/-0.6 vs. 1.2+/-0.4 mmol/L; P < 0.05), but lower high density lipoprotein cholesterol (1.4+/-0.4 vs. 1.6+/-0.3 mmol/L; P < 0.05). These data indicate that subjects with mild PHPT (calcium, <3.0 mmol/L) have increased arterial stiffness, as evidenced by higher augmentation of central aortic pressures. Enhanced vessel stiffness may arise from a combination of structural and functional vascular changes due to hypercalcemia and/or metabolic abnormalities. Increased vascular stiffness in subjects with PHPT may account in part for the increased cardiovascular risk in this group.]]></description><identifier>ISSN: 0021-972X</identifier><identifier>EISSN: 1945-7197</identifier><identifier>DOI: 10.1210/jc.85.10.3515</identifier><identifier>PMID: 11061493</identifier><identifier>CODEN: JCEMAZ</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Aged ; Aging - physiology ; Arteries - pathology ; Biological and medical sciences ; Blood Glucose - metabolism ; Blood Pressure - physiology ; Calcium - blood ; Endocrinopathies ; Female ; Humans ; Hyperparathyroidism - pathology ; Hyperparathyroidism - physiopathology ; Lipids - blood ; Male ; Medical sciences ; Middle Aged ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Parathyroid Hormone - blood ; Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases) ; Risk Factors</subject><ispartof>The journal of clinical endocrinology and metabolism, 2000-10, Vol.85 (10), p.3515-3519</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c251t-9dc75e0316f986a687f408d3d75831091827df937fbe0cb05b1ba26a14ec0fe33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1526891$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11061493$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SMITH, J. C</creatorcontrib><creatorcontrib>PAGE, M. D</creatorcontrib><creatorcontrib>JOHN, R</creatorcontrib><creatorcontrib>WHEELER, M. H</creatorcontrib><creatorcontrib>COCKCROFT, J. R</creatorcontrib><creatorcontrib>SCANLON, M. F</creatorcontrib><creatorcontrib>DAVIES, J. S</creatorcontrib><title>Augmentation of central arterial pressure in mild primary hyperparathyroidism</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description><![CDATA[Primary hyperparathyroidism (PHPT) is associated with increased cardiovascular risk, although the mechanisms involved remain unclear. Recent evidence has shown increased pulse pressure to be a powerful predictor of cardiovascular events. As increases in pulse pressure are due largely to arterial stiffening, we measured arterial stiffness in 21 subjects with PHPT (18 women and 3 men; 46-71 yr old) and 21 age- and sex-matched healthy controls using pulse wave analysis, a technique that measures peripheral arterial pressure waveforms and generates corresponding central aortic waveforms. This allows determination of the augmentation of central pressure resulting from wave reflection and augmentation index, a measure of vessel stiffness. Metabolic parameters were also measured. The serum calcium level among PHPT subjects was (mean +/- SD) 2.74+/-0.14 mmol/L. pulse wave analysis showed that both augmentation and the augmentation index were significantly higher in the PHPT group vs. controls [16+/-5 vs. 10+/-4 mm Hg (P < 0.001) and 36+/-9% vs. 25+/-6% (P < 0.001)] despite comparable brachial systolic pressures between groups (136+/-13 vs. 134+/-18 mm Hg). Patients with PHPT had higher fasting serum insulin levels [median (range), 15.8 (7.4-39.4) vs. 11.6 (5.1-23) mU/L; P < 0.05] and triglyceride (1.6+/-0.6 vs. 1.2+/-0.4 mmol/L; P < 0.05), but lower high density lipoprotein cholesterol (1.4+/-0.4 vs. 1.6+/-0.3 mmol/L; P < 0.05). These data indicate that subjects with mild PHPT (calcium, <3.0 mmol/L) have increased arterial stiffness, as evidenced by higher augmentation of central aortic pressures. Enhanced vessel stiffness may arise from a combination of structural and functional vascular changes due to hypercalcemia and/or metabolic abnormalities. Increased vascular stiffness in subjects with PHPT may account in part for the increased cardiovascular risk in this group.]]></description><subject>Aged</subject><subject>Aging - physiology</subject><subject>Arteries - pathology</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Blood Pressure - physiology</subject><subject>Calcium - blood</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>Humans</subject><subject>Hyperparathyroidism - pathology</subject><subject>Hyperparathyroidism - physiopathology</subject><subject>Lipids - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Parathyroid Hormone - blood</subject><subject>Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)</subject><subject>Risk Factors</subject><issn>0021-972X</issn><issn>1945-7197</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNpF0EtLxDAQB_AgiruuHr1KD-KtayaPJjkuiy9Y8aLgraR5uFn6MmkP--0tWPE08x9-DMMgdA14DQTw_cGsJV9PiXLgJ2gJivFcgBKnaIkxgVwJ8rlAFykdMAbGOD1HCwBcAFN0iV4341fj2kEPoWuzzmdmClHXmY6Di2Fq-uhSGqPLQps1obbTIDQ6HrP9sXex11EP-2Psgg2puURnXtfJXc11hT4eH963z_nu7ellu9nlhnAYcmWN4A5TKLyShS6k8AxLS63gkgJWIImwXlHhK4dNhXkFlSaFBuYM9o7SFbr73dvH7nt0aSibkIyra926bkylIFQSVsAEb2Y4Vo2z5Xx7-feACdzOQCejax91a0L6d5wUUgH9AZpdalo</recordid><startdate>20001001</startdate><enddate>20001001</enddate><creator>SMITH, J. C</creator><creator>PAGE, M. D</creator><creator>JOHN, R</creator><creator>WHEELER, M. H</creator><creator>COCKCROFT, J. R</creator><creator>SCANLON, M. F</creator><creator>DAVIES, J. S</creator><general>Endocrine Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20001001</creationdate><title>Augmentation of central arterial pressure in mild primary hyperparathyroidism</title><author>SMITH, J. C ; PAGE, M. D ; JOHN, R ; WHEELER, M. H ; COCKCROFT, J. R ; SCANLON, M. F ; DAVIES, J. S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c251t-9dc75e0316f986a687f408d3d75831091827df937fbe0cb05b1ba26a14ec0fe33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Aged</topic><topic>Aging - physiology</topic><topic>Arteries - pathology</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Blood Pressure - physiology</topic><topic>Calcium - blood</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>Humans</topic><topic>Hyperparathyroidism - pathology</topic><topic>Hyperparathyroidism - physiopathology</topic><topic>Lipids - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Parathyroid Hormone - blood</topic><topic>Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SMITH, J. C</creatorcontrib><creatorcontrib>PAGE, M. D</creatorcontrib><creatorcontrib>JOHN, R</creatorcontrib><creatorcontrib>WHEELER, M. H</creatorcontrib><creatorcontrib>COCKCROFT, J. R</creatorcontrib><creatorcontrib>SCANLON, M. F</creatorcontrib><creatorcontrib>DAVIES, J. S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of clinical endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SMITH, J. C</au><au>PAGE, M. D</au><au>JOHN, R</au><au>WHEELER, M. H</au><au>COCKCROFT, J. R</au><au>SCANLON, M. F</au><au>DAVIES, J. S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Augmentation of central arterial pressure in mild primary hyperparathyroidism</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>2000-10-01</date><risdate>2000</risdate><volume>85</volume><issue>10</issue><spage>3515</spage><epage>3519</epage><pages>3515-3519</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><coden>JCEMAZ</coden><abstract><![CDATA[Primary hyperparathyroidism (PHPT) is associated with increased cardiovascular risk, although the mechanisms involved remain unclear. Recent evidence has shown increased pulse pressure to be a powerful predictor of cardiovascular events. As increases in pulse pressure are due largely to arterial stiffening, we measured arterial stiffness in 21 subjects with PHPT (18 women and 3 men; 46-71 yr old) and 21 age- and sex-matched healthy controls using pulse wave analysis, a technique that measures peripheral arterial pressure waveforms and generates corresponding central aortic waveforms. This allows determination of the augmentation of central pressure resulting from wave reflection and augmentation index, a measure of vessel stiffness. Metabolic parameters were also measured. The serum calcium level among PHPT subjects was (mean +/- SD) 2.74+/-0.14 mmol/L. pulse wave analysis showed that both augmentation and the augmentation index were significantly higher in the PHPT group vs. controls [16+/-5 vs. 10+/-4 mm Hg (P < 0.001) and 36+/-9% vs. 25+/-6% (P < 0.001)] despite comparable brachial systolic pressures between groups (136+/-13 vs. 134+/-18 mm Hg). Patients with PHPT had higher fasting serum insulin levels [median (range), 15.8 (7.4-39.4) vs. 11.6 (5.1-23) mU/L; P < 0.05] and triglyceride (1.6+/-0.6 vs. 1.2+/-0.4 mmol/L; P < 0.05), but lower high density lipoprotein cholesterol (1.4+/-0.4 vs. 1.6+/-0.3 mmol/L; P < 0.05). These data indicate that subjects with mild PHPT (calcium, <3.0 mmol/L) have increased arterial stiffness, as evidenced by higher augmentation of central aortic pressures. Enhanced vessel stiffness may arise from a combination of structural and functional vascular changes due to hypercalcemia and/or metabolic abnormalities. Increased vascular stiffness in subjects with PHPT may account in part for the increased cardiovascular risk in this group.]]></abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>11061493</pmid><doi>10.1210/jc.85.10.3515</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Aging - physiology Arteries - pathology Biological and medical sciences Blood Glucose - metabolism Blood Pressure - physiology Calcium - blood Endocrinopathies Female Humans Hyperparathyroidism - pathology Hyperparathyroidism - physiopathology Lipids - blood Male Medical sciences Middle Aged Non tumoral diseases. Target tissue resistance. Benign neoplasms Parathyroid Hormone - blood Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases) Risk Factors |
title | Augmentation of central arterial pressure in mild primary hyperparathyroidism |
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