The role of endothelial nitric oxide synthase −786 T/C polymorphism in cardiac instability following aneurysmal subarachnoid hemorrhage

Philipp Hendrix, Paul M. Foreman, Mark R. Harrigan, Winfield S. Fisher, Nilesh A. Vyas, Robert H. Lipsky, Minkuan Lin, Beverly C. Walters, R. Shane Tubbs, Mohammadali Mohajel Shoja, Jean Francois Pittet, Mali Mathru, Christoph J. Griessenauer

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Introduction Cardiac abnormalities are observed frequently after aneurysmal subarachnoid hemorrhage (aSAH). A subset of aSAH patients develops neurogenic cardiomyopathy, likely induced by catecholamine excess. Genetic polymorphisms of the endothelial nitric oxide synthase (eNOS) gene have been linked to decreased nitric oxide (NO) levels, coronary artery spasm, and myocardial infarction. The role of the eNOS single nucleotide polymorphism (SNP) −786 T/C in cardiac instability following aSAH has not been previously investigated. Methods From 2012 to 2015, aSAH patients were prospectively enrolled in the Cerebral Aneurysm Renin Angiotensin System (CARAS) study at two academic institutions. Blood samples were used to assess the eNOS SNP -786 T/C rs2070744 through 5'exonuclease (Taqman) genotyping assays. Associations between this polymorphism and cardiac instability following aSAH were analyzed. Results Multivariable analysis demonstrated a dominant effect of the C allele of eNOS SNP -786 T/C on cardiac instability in patients with aSAH. A lower Glasgow Coma Scale score and a history of ischemic vascular disease were also associated with cardiac instability. Furthermore, cardiac instability independently predicted poor functional outcome upon discharge from the hospital. Conclusions The C allele of the eNOS SNP -786 T/C was independently associated with an increased risk for cardiac instability following aSAH. Cardiac instability itself was a risk factor for an unfavorable functional outcome upon discharge from the hospital.

Original languageEnglish (US)
Pages (from-to)52-56
Number of pages5
JournalNitric Oxide - Biology and Chemistry
Volume71
DOIs
StatePublished - Dec 1 2017
Externally publishedYes

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Nitric Oxide Synthase Type III
Subarachnoid Hemorrhage
Polymorphism
Single Nucleotide Polymorphism
Nucleotides
Alleles
Phosphodiesterase I
Glasgow Coma Scale
Angiotensins
Spasm
Intracranial Aneurysm
Genetic Polymorphisms
Renin-Angiotensin System
Cardiomyopathies
Vascular Diseases
Renin
Catecholamines
Assays
Coronary Vessels
Nitric Oxide

Keywords

  • Cardiac instability
  • Cardiomyopathy
  • Endothelial nitric oxide synthase
  • eNOS
  • eNOS SNP -786 T/C
  • Subarachnoid hemorrhage

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Clinical Biochemistry
  • Cancer Research

Cite this

The role of endothelial nitric oxide synthase −786 T/C polymorphism in cardiac instability following aneurysmal subarachnoid hemorrhage. / Hendrix, Philipp; Foreman, Paul M.; Harrigan, Mark R.; Fisher, Winfield S.; Vyas, Nilesh A.; Lipsky, Robert H.; Lin, Minkuan; Walters, Beverly C.; Tubbs, R. Shane; Mohajel Shoja, Mohammadali; Pittet, Jean Francois; Mathru, Mali; Griessenauer, Christoph J.

In: Nitric Oxide - Biology and Chemistry, Vol. 71, 01.12.2017, p. 52-56.

Research output: Contribution to journalArticle

Hendrix, P, Foreman, PM, Harrigan, MR, Fisher, WS, Vyas, NA, Lipsky, RH, Lin, M, Walters, BC, Tubbs, RS, Mohajel Shoja, M, Pittet, JF, Mathru, M & Griessenauer, CJ 2017, 'The role of endothelial nitric oxide synthase −786 T/C polymorphism in cardiac instability following aneurysmal subarachnoid hemorrhage', Nitric Oxide - Biology and Chemistry, vol. 71, pp. 52-56. https://doi.org/10.1016/j.niox.2017.10.008
Hendrix, Philipp ; Foreman, Paul M. ; Harrigan, Mark R. ; Fisher, Winfield S. ; Vyas, Nilesh A. ; Lipsky, Robert H. ; Lin, Minkuan ; Walters, Beverly C. ; Tubbs, R. Shane ; Mohajel Shoja, Mohammadali ; Pittet, Jean Francois ; Mathru, Mali ; Griessenauer, Christoph J. / The role of endothelial nitric oxide synthase −786 T/C polymorphism in cardiac instability following aneurysmal subarachnoid hemorrhage. In: Nitric Oxide - Biology and Chemistry. 2017 ; Vol. 71. pp. 52-56.
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abstract = "Introduction Cardiac abnormalities are observed frequently after aneurysmal subarachnoid hemorrhage (aSAH). A subset of aSAH patients develops neurogenic cardiomyopathy, likely induced by catecholamine excess. Genetic polymorphisms of the endothelial nitric oxide synthase (eNOS) gene have been linked to decreased nitric oxide (NO) levels, coronary artery spasm, and myocardial infarction. The role of the eNOS single nucleotide polymorphism (SNP) −786 T/C in cardiac instability following aSAH has not been previously investigated. Methods From 2012 to 2015, aSAH patients were prospectively enrolled in the Cerebral Aneurysm Renin Angiotensin System (CARAS) study at two academic institutions. Blood samples were used to assess the eNOS SNP -786 T/C rs2070744 through 5'exonuclease (Taqman) genotyping assays. Associations between this polymorphism and cardiac instability following aSAH were analyzed. Results Multivariable analysis demonstrated a dominant effect of the C allele of eNOS SNP -786 T/C on cardiac instability in patients with aSAH. A lower Glasgow Coma Scale score and a history of ischemic vascular disease were also associated with cardiac instability. Furthermore, cardiac instability independently predicted poor functional outcome upon discharge from the hospital. Conclusions The C allele of the eNOS SNP -786 T/C was independently associated with an increased risk for cardiac instability following aSAH. Cardiac instability itself was a risk factor for an unfavorable functional outcome upon discharge from the hospital.",
keywords = "Cardiac instability, Cardiomyopathy, Endothelial nitric oxide synthase, eNOS, eNOS SNP -786 T/C, Subarachnoid hemorrhage",
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T1 - The role of endothelial nitric oxide synthase −786 T/C polymorphism in cardiac instability following aneurysmal subarachnoid hemorrhage

AU - Hendrix, Philipp

AU - Foreman, Paul M.

AU - Harrigan, Mark R.

AU - Fisher, Winfield S.

AU - Vyas, Nilesh A.

AU - Lipsky, Robert H.

AU - Lin, Minkuan

AU - Walters, Beverly C.

AU - Tubbs, R. Shane

AU - Mohajel Shoja, Mohammadali

AU - Pittet, Jean Francois

AU - Mathru, Mali

AU - Griessenauer, Christoph J.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - Introduction Cardiac abnormalities are observed frequently after aneurysmal subarachnoid hemorrhage (aSAH). A subset of aSAH patients develops neurogenic cardiomyopathy, likely induced by catecholamine excess. Genetic polymorphisms of the endothelial nitric oxide synthase (eNOS) gene have been linked to decreased nitric oxide (NO) levels, coronary artery spasm, and myocardial infarction. The role of the eNOS single nucleotide polymorphism (SNP) −786 T/C in cardiac instability following aSAH has not been previously investigated. Methods From 2012 to 2015, aSAH patients were prospectively enrolled in the Cerebral Aneurysm Renin Angiotensin System (CARAS) study at two academic institutions. Blood samples were used to assess the eNOS SNP -786 T/C rs2070744 through 5'exonuclease (Taqman) genotyping assays. Associations between this polymorphism and cardiac instability following aSAH were analyzed. Results Multivariable analysis demonstrated a dominant effect of the C allele of eNOS SNP -786 T/C on cardiac instability in patients with aSAH. A lower Glasgow Coma Scale score and a history of ischemic vascular disease were also associated with cardiac instability. Furthermore, cardiac instability independently predicted poor functional outcome upon discharge from the hospital. Conclusions The C allele of the eNOS SNP -786 T/C was independently associated with an increased risk for cardiac instability following aSAH. Cardiac instability itself was a risk factor for an unfavorable functional outcome upon discharge from the hospital.

AB - Introduction Cardiac abnormalities are observed frequently after aneurysmal subarachnoid hemorrhage (aSAH). A subset of aSAH patients develops neurogenic cardiomyopathy, likely induced by catecholamine excess. Genetic polymorphisms of the endothelial nitric oxide synthase (eNOS) gene have been linked to decreased nitric oxide (NO) levels, coronary artery spasm, and myocardial infarction. The role of the eNOS single nucleotide polymorphism (SNP) −786 T/C in cardiac instability following aSAH has not been previously investigated. Methods From 2012 to 2015, aSAH patients were prospectively enrolled in the Cerebral Aneurysm Renin Angiotensin System (CARAS) study at two academic institutions. Blood samples were used to assess the eNOS SNP -786 T/C rs2070744 through 5'exonuclease (Taqman) genotyping assays. Associations between this polymorphism and cardiac instability following aSAH were analyzed. Results Multivariable analysis demonstrated a dominant effect of the C allele of eNOS SNP -786 T/C on cardiac instability in patients with aSAH. A lower Glasgow Coma Scale score and a history of ischemic vascular disease were also associated with cardiac instability. Furthermore, cardiac instability independently predicted poor functional outcome upon discharge from the hospital. Conclusions The C allele of the eNOS SNP -786 T/C was independently associated with an increased risk for cardiac instability following aSAH. Cardiac instability itself was a risk factor for an unfavorable functional outcome upon discharge from the hospital.

KW - Cardiac instability

KW - Cardiomyopathy

KW - Endothelial nitric oxide synthase

KW - eNOS

KW - eNOS SNP -786 T/C

KW - Subarachnoid hemorrhage

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SN - 1089-8603

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