Link of Nonhemodynamic Factors to Hemodynamic Determinants of Left Ventricular Hypertrophy
Despite current evidence suggesting that hemodynamic load is the fundamental stimulus to begin the sequence of biological events leading to the development of left ventricular hypertrophy, genotype, gender, body size, and less easily recognizable environmental factors may contribute to generate the...
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Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2001-07, Vol.38 (1), p.13-18 |
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creator | de Simone, Giovanni Pasanisi, Fabrizio Contaldo, Franco |
description | Despite current evidence suggesting that hemodynamic load is the fundamental stimulus to begin the sequence of biological events leading to the development of left ventricular hypertrophy, genotype, gender, body size, and less easily recognizable environmental factors may contribute to generate the cascade of molecular changes that eventually yield the increase in protein synthesis needed to increase left ventricular mass. However, even nonhemodynamic factors such as gender and body size eventually regulate the growth of left ventricular mass by at least in part influencing loading conditions. Consideration of measurable factors, such as gender, body size, and hemodynamic load, allows evaluation of individual echocardiographic left ventricular mass as the deviation from the level that would be required to face a gender-specific hemodynamic load at a given body size. Values of left ventricular mass that are inappropriately high for individual gender, body size, and hemodynamic load are associated with a high cardiovascular risk phenotype, even independent of the presence of arterial hypertension. Thus, the condition of inappropriately high left ventricular mass may be recognized as a more advanced stage of pathological structural changes initially induced by overload, going beyond the compensatory needs. The biological process that yields inappropriate left ventricular mass is probably linked to the protracted activity over time of biological mediators of left ventricular hypertrophy, such as proto-oncogenes and other growth factors, neurohormones, and cytokines, inducing structural modifications that initially compensate imposed overload but eventually change the structure of myocardial tissue and the composition of motor units. |
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However, even nonhemodynamic factors such as gender and body size eventually regulate the growth of left ventricular mass by at least in part influencing loading conditions. Consideration of measurable factors, such as gender, body size, and hemodynamic load, allows evaluation of individual echocardiographic left ventricular mass as the deviation from the level that would be required to face a gender-specific hemodynamic load at a given body size. Values of left ventricular mass that are inappropriately high for individual gender, body size, and hemodynamic load are associated with a high cardiovascular risk phenotype, even independent of the presence of arterial hypertension. Thus, the condition of inappropriately high left ventricular mass may be recognized as a more advanced stage of pathological structural changes initially induced by overload, going beyond the compensatory needs. The biological process that yields inappropriate left ventricular mass is probably linked to the protracted activity over time of biological mediators of left ventricular hypertrophy, such as proto-oncogenes and other growth factors, neurohormones, and cytokines, inducing structural modifications that initially compensate imposed overload but eventually change the structure of myocardial tissue and the composition of motor units.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.38.1.13</identifier><identifier>PMID: 11463753</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Biological and medical sciences ; Blood Pressure ; Body Constitution ; Cardiology. 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However, even nonhemodynamic factors such as gender and body size eventually regulate the growth of left ventricular mass by at least in part influencing loading conditions. Consideration of measurable factors, such as gender, body size, and hemodynamic load, allows evaluation of individual echocardiographic left ventricular mass as the deviation from the level that would be required to face a gender-specific hemodynamic load at a given body size. Values of left ventricular mass that are inappropriately high for individual gender, body size, and hemodynamic load are associated with a high cardiovascular risk phenotype, even independent of the presence of arterial hypertension. Thus, the condition of inappropriately high left ventricular mass may be recognized as a more advanced stage of pathological structural changes initially induced by overload, going beyond the compensatory needs. The biological process that yields inappropriate left ventricular mass is probably linked to the protracted activity over time of biological mediators of left ventricular hypertrophy, such as proto-oncogenes and other growth factors, neurohormones, and cytokines, inducing structural modifications that initially compensate imposed overload but eventually change the structure of myocardial tissue and the composition of motor units.</description><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Body Constitution</subject><subject>Cardiology. Vascular system</subject><subject>Genotype</subject><subject>Growth Substances - metabolism</subject><subject>Heart</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Humans</subject><subject>Hypertrophy, Left Ventricular - genetics</subject><subject>Hypertrophy, Left Ventricular - metabolism</subject><subject>Hypertrophy, Left Ventricular - physiopathology</subject><subject>Medical sciences</subject><subject>Nutritional Physiological Phenomena</subject><subject>Sex Factors</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkdGL1DAQxoMo3nr66qMUEd9aM5k0yT7K6bnCoj6oqC8hzaa0d21Tk5Sj_71Zd8HDeRlm-M3HzDeEPAdaAQh4Q6Hq1rlCVUEF-IBsoGa85LXAh2RDYcvLLcCPC_IkxhtKgXMuH5MLAC5Q1rghv_b9dFv4tvjkp86N_rBOZuxtcW1s8iEWyRe7e-13Lrkw9pOZUjxO7V2biu9uSqG3y2BCsVtnF1Lwc7c-JY9aM0T37Jwvybfr91-vduX-84ePV2_3pa1R8VIxKRVtWYMogEkqpdlKg60CVNZxh3nZhrItIm2UcMidEIANp1S1B5EPvSSvT7pz8L8XF5Me-2jdMJjJ-SVqCdkHwWQGX_4H3vglTHk3zWjNFGPIMlSdIBt8jMG1eg79aMKqgeqj5ZqC3v38olFp0IB54MVZdWlGd_iHnz3OwKszYKI1QxvMZPt4T1bVKI8YP2F3fsgmx9thuXNBd84MqdM0B2dClSx_kcpclX9b-AfpOpby</recordid><startdate>200107</startdate><enddate>200107</enddate><creator>de Simone, Giovanni</creator><creator>Pasanisi, Fabrizio</creator><creator>Contaldo, Franco</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200107</creationdate><title>Link of Nonhemodynamic Factors to Hemodynamic Determinants of Left Ventricular Hypertrophy</title><author>de Simone, Giovanni ; Pasanisi, Fabrizio ; Contaldo, Franco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5384-827780f2b336127077a97a3f8138ce4e3114b029330b86e34e6613b4008fd6563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Body Constitution</topic><topic>Cardiology. Vascular system</topic><topic>Genotype</topic><topic>Growth Substances - metabolism</topic><topic>Heart</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Humans</topic><topic>Hypertrophy, Left Ventricular - genetics</topic><topic>Hypertrophy, Left Ventricular - metabolism</topic><topic>Hypertrophy, Left Ventricular - physiopathology</topic><topic>Medical sciences</topic><topic>Nutritional Physiological Phenomena</topic><topic>Sex Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Simone, Giovanni</creatorcontrib><creatorcontrib>Pasanisi, Fabrizio</creatorcontrib><creatorcontrib>Contaldo, Franco</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>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Simone, Giovanni</au><au>Pasanisi, Fabrizio</au><au>Contaldo, Franco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Link of Nonhemodynamic Factors to Hemodynamic Determinants of Left Ventricular Hypertrophy</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2001-07</date><risdate>2001</risdate><volume>38</volume><issue>1</issue><spage>13</spage><epage>18</epage><pages>13-18</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Despite current evidence suggesting that hemodynamic load is the fundamental stimulus to begin the sequence of biological events leading to the development of left ventricular hypertrophy, genotype, gender, body size, and less easily recognizable environmental factors may contribute to generate the cascade of molecular changes that eventually yield the increase in protein synthesis needed to increase left ventricular mass. However, even nonhemodynamic factors such as gender and body size eventually regulate the growth of left ventricular mass by at least in part influencing loading conditions. Consideration of measurable factors, such as gender, body size, and hemodynamic load, allows evaluation of individual echocardiographic left ventricular mass as the deviation from the level that would be required to face a gender-specific hemodynamic load at a given body size. Values of left ventricular mass that are inappropriately high for individual gender, body size, and hemodynamic load are associated with a high cardiovascular risk phenotype, even independent of the presence of arterial hypertension. Thus, the condition of inappropriately high left ventricular mass may be recognized as a more advanced stage of pathological structural changes initially induced by overload, going beyond the compensatory needs. 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subjects | Biological and medical sciences Blood Pressure Body Constitution Cardiology. Vascular system Genotype Growth Substances - metabolism Heart Heart failure, cardiogenic pulmonary edema, cardiac enlargement Humans Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - metabolism Hypertrophy, Left Ventricular - physiopathology Medical sciences Nutritional Physiological Phenomena Sex Factors |
title | Link of Nonhemodynamic Factors to Hemodynamic Determinants of Left Ventricular Hypertrophy |
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