Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study

Abstract Abnormal QRS duration and amplitudes on the electrocardiogram are indicative of cardiac pathology and are associated with adverse outcomes. The causal nature of these associations remains uncertain and could be due to QRS abnormalities being a symptom of cardiac damage rather than a factor...

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Autores principales:	M. Yldau Van Der Ende, Tom Hendriks, Dirk J. Van Veldhuisen, Harold Snieder, Niek Verweij, Pim Van Der Harst
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f1bc57e891134ba69b260cd894fdc478
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spelling	oai:doaj.org-article:f1bc57e891134ba69b260cd894fdc4782021-12-02T15:08:23ZCausal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study10.1038/s41598-018-24002-02045-2322https://doaj.org/article/f1bc57e891134ba69b260cd894fdc4782018-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-24002-0https://doaj.org/toc/2045-2322Abstract Abnormal QRS duration and amplitudes on the electrocardiogram are indicative of cardiac pathology and are associated with adverse outcomes. The causal nature of these associations remains uncertain and could be due to QRS abnormalities being a symptom of cardiac damage rather than a factor on the causal pathway. By performing Mendelian randomization (MR) analyses using summary statistics of genome wide association study consortia with sample sizes between 20,687 and 339,224 individuals, we aimed to determine which cardiovascular risk factors causally lead to changes in QRS duration and amplitude (Sokolow-Lyon, Cornell and 12-leadsum products). Additionally, we aimed to determine whether QRS traits have a causal relationship with mortality and longevity. We performed inverse-variance weighted MR as main analyses and MR-Egger regression and weighted median estimation as sensitivity analyses. We found evidence for a causal relationship between higher blood pressure and larger QRS amplitudes (systolic blood pressure on Cornell: 55SNPs, causal effect estimate per 1 mmHg = 9.77 millimeters·milliseconds (SE = 1.38,P = 1.20 × 10−12) and diastolic blood pressure on Cornell: 57SNPs, causal effect estimate per 1 mmHg = 14.89 millimeters·milliseconds (SE = 1.82,P = 3.08 × 10−16), but not QRS duration. Genetically predicted QRS traits were not associated with longevity, suggesting a more prominent role of acquired factors in explaining the well-known link between QRS abnormalities and outcome.M. Yldau Van Der EndeTom HendriksDirk J. Van VeldhuisenHarold SniederNiek VerweijPim Van Der HarstNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-7 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q M. Yldau Van Der Ende Tom Hendriks Dirk J. Van Veldhuisen Harold Snieder Niek Verweij Pim Van Der Harst Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study
description	Abstract Abnormal QRS duration and amplitudes on the electrocardiogram are indicative of cardiac pathology and are associated with adverse outcomes. The causal nature of these associations remains uncertain and could be due to QRS abnormalities being a symptom of cardiac damage rather than a factor on the causal pathway. By performing Mendelian randomization (MR) analyses using summary statistics of genome wide association study consortia with sample sizes between 20,687 and 339,224 individuals, we aimed to determine which cardiovascular risk factors causally lead to changes in QRS duration and amplitude (Sokolow-Lyon, Cornell and 12-leadsum products). Additionally, we aimed to determine whether QRS traits have a causal relationship with mortality and longevity. We performed inverse-variance weighted MR as main analyses and MR-Egger regression and weighted median estimation as sensitivity analyses. We found evidence for a causal relationship between higher blood pressure and larger QRS amplitudes (systolic blood pressure on Cornell: 55SNPs, causal effect estimate per 1 mmHg = 9.77 millimeters·milliseconds (SE = 1.38,P = 1.20 × 10−12) and diastolic blood pressure on Cornell: 57SNPs, causal effect estimate per 1 mmHg = 14.89 millimeters·milliseconds (SE = 1.82,P = 3.08 × 10−16), but not QRS duration. Genetically predicted QRS traits were not associated with longevity, suggesting a more prominent role of acquired factors in explaining the well-known link between QRS abnormalities and outcome.
format	article
author	M. Yldau Van Der Ende Tom Hendriks Dirk J. Van Veldhuisen Harold Snieder Niek Verweij Pim Van Der Harst
author_facet	M. Yldau Van Der Ende Tom Hendriks Dirk J. Van Veldhuisen Harold Snieder Niek Verweij Pim Van Der Harst
author_sort	M. Yldau Van Der Ende
title	Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study
title_short	Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study
title_full	Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study
title_fullStr	Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study
title_full_unstemmed	Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study
title_sort	causal pathways from blood pressure to larger qrs amplitudes: a mendelian randomization study
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/f1bc57e891134ba69b260cd894fdc478
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Causal Pathways from Blood Pressure to Larger QRS Amplitudes: a Mendelian Randomization Study

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