Endothelial Dysfunction: A Link Among Preeclampsia, Recurrent Pregnancy Loss, and Future Cardiovascular Events?
We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholester...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2007-01, Vol.49 (1), p.90-95 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Germain, Alfredo M Romanik, Mary Carmen Guerra, Irene Solari, Sandra Reyes, María Soledad Johnson, Richard J Price, Karen Karumanchi, S Ananth Valdés, Gloria |
| description | We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated. |
| doi_str_mv | 10.1161/01.HYP.0000251522.18094.d4 |
| format | Article |
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Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000251522.18094.d4</identifier><identifier>PMID: 17116761</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Abortion, Habitual - blood ; Abortion, Habitual - physiopathology ; Adult ; Blood Pressure ; Cardiovascular Diseases - etiology ; Cholesterol - blood ; Diastole ; Endothelium, Vascular - physiopathology ; Female ; Humans ; Medical Records ; Placenta Diseases - etiology ; Pre-Eclampsia - blood ; Pre-Eclampsia - physiopathology ; Pregnancy ; Risk Factors ; Severity of Illness Index ; Time Factors ; Vasodilation</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2007-01, Vol.49 (1), p.90-95</ispartof><rights>2007 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3451-37b604bac86e58efd35268699a393a66990c6f161c5102b0bc8a1e7e2163a9063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17116761$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Germain, Alfredo M</creatorcontrib><creatorcontrib>Romanik, Mary Carmen</creatorcontrib><creatorcontrib>Guerra, Irene</creatorcontrib><creatorcontrib>Solari, Sandra</creatorcontrib><creatorcontrib>Reyes, María Soledad</creatorcontrib><creatorcontrib>Johnson, Richard J</creatorcontrib><creatorcontrib>Price, Karen</creatorcontrib><creatorcontrib>Karumanchi, S Ananth</creatorcontrib><creatorcontrib>Valdés, Gloria</creatorcontrib><title>Endothelial Dysfunction: A Link Among Preeclampsia, Recurrent Pregnancy Loss, and Future Cardiovascular Events?</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated.</description><subject>Abortion, Habitual - blood</subject><subject>Abortion, Habitual - physiopathology</subject><subject>Adult</subject><subject>Blood Pressure</subject><subject>Cardiovascular Diseases - etiology</subject><subject>Cholesterol - blood</subject><subject>Diastole</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Female</subject><subject>Humans</subject><subject>Medical Records</subject><subject>Placenta Diseases - etiology</subject><subject>Pre-Eclampsia - blood</subject><subject>Pre-Eclampsia - physiopathology</subject><subject>Pregnancy</subject><subject>Risk Factors</subject><subject>Severity of Illness Index</subject><subject>Time Factors</subject><subject>Vasodilation</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE9v1DAQxS0EokvhKyCLA6cmeGLHSXpBq2X7R1qJCoEEJ8txJt1Qx17spNV-e7zdlerLeEbvvdH8CPkELAeQ8IVBfvPnLmfpFSWURZFDzRqRd-IVWaReZKKU_DVZMGhE1gD8PiPvYvzLGAghqrfkDKoUVElYEL92nZ-2aAdt6bd97GdnpsG7S7qkm8E90OXo3T29C4jG6nEXB31Bf6CZQ0A3Heb3Tjuzpxsf4wXVrqNX8zQHpCsdusE_6mhmqwNdPyZ9_PqevOm1jfjhVM_Jr6v1z9VNtvl-fbtabjLDRQkZr1rJRKtNLbGsse94WchaNo3mDdcyfZiRfYJhSmBFy1pTa8AKC5BcN0zyc_L5mLsL_t-McVLjEA1aqx36OSpZ86pO_iS8PApNSBcE7NUuDKMOewVMHXArBirhVi-41TNu1Ylk_njaMrcjdi_WE98kEEfBk7cThvhg5ycMaovaTtvnSJHuygrGKgapyw5LgP8HwD2Llw</recordid><startdate>200701</startdate><enddate>200701</enddate><creator>Germain, Alfredo M</creator><creator>Romanik, Mary Carmen</creator><creator>Guerra, Irene</creator><creator>Solari, Sandra</creator><creator>Reyes, María Soledad</creator><creator>Johnson, Richard J</creator><creator>Price, Karen</creator><creator>Karumanchi, S Ananth</creator><creator>Valdés, Gloria</creator><general>American Heart Association, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200701</creationdate><title>Endothelial Dysfunction: A Link Among Preeclampsia, Recurrent Pregnancy Loss, and Future Cardiovascular Events?</title><author>Germain, Alfredo M ; Romanik, Mary Carmen ; Guerra, Irene ; Solari, Sandra ; Reyes, María Soledad ; Johnson, Richard J ; Price, Karen ; Karumanchi, S Ananth ; Valdés, Gloria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3451-37b604bac86e58efd35268699a393a66990c6f161c5102b0bc8a1e7e2163a9063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Abortion, Habitual - blood</topic><topic>Abortion, Habitual - physiopathology</topic><topic>Adult</topic><topic>Blood Pressure</topic><topic>Cardiovascular Diseases - etiology</topic><topic>Cholesterol - blood</topic><topic>Diastole</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Female</topic><topic>Humans</topic><topic>Medical Records</topic><topic>Placenta Diseases - etiology</topic><topic>Pre-Eclampsia - blood</topic><topic>Pre-Eclampsia - physiopathology</topic><topic>Pregnancy</topic><topic>Risk Factors</topic><topic>Severity of Illness Index</topic><topic>Time Factors</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Germain, Alfredo M</creatorcontrib><creatorcontrib>Romanik, Mary Carmen</creatorcontrib><creatorcontrib>Guerra, Irene</creatorcontrib><creatorcontrib>Solari, Sandra</creatorcontrib><creatorcontrib>Reyes, María Soledad</creatorcontrib><creatorcontrib>Johnson, Richard J</creatorcontrib><creatorcontrib>Price, Karen</creatorcontrib><creatorcontrib>Karumanchi, S Ananth</creatorcontrib><creatorcontrib>Valdés, Gloria</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Germain, Alfredo M</au><au>Romanik, Mary Carmen</au><au>Guerra, Irene</au><au>Solari, Sandra</au><au>Reyes, María Soledad</au><au>Johnson, Richard J</au><au>Price, Karen</au><au>Karumanchi, S Ananth</au><au>Valdés, Gloria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial Dysfunction: A Link Among Preeclampsia, Recurrent Pregnancy Loss, and Future Cardiovascular Events?</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2007-01</date><risdate>2007</risdate><volume>49</volume><issue>1</issue><spage>90</spage><epage>95</epage><pages>90-95</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><abstract>We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. 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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Abortion, Habitual - blood Abortion, Habitual - physiopathology Adult Blood Pressure Cardiovascular Diseases - etiology Cholesterol - blood Diastole Endothelium, Vascular - physiopathology Female Humans Medical Records Placenta Diseases - etiology Pre-Eclampsia - blood Pre-Eclampsia - physiopathology Pregnancy Risk Factors Severity of Illness Index Time Factors Vasodilation |
| title | Endothelial Dysfunction: A Link Among Preeclampsia, Recurrent Pregnancy Loss, and Future Cardiovascular Events? |
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