Left Ventricular Hypertrophy With Strain and Aortic Stenosis
ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes associated with ECG strain. One hundred and two patients (age, 70 years [range, 63-75 years]; male, 66%; aortic valve area, 0.9 cm(2) [range, 0.7-1.2 c...
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Published in | Circulation (New York, N.Y.) Vol. 130; no. 18; pp. 1607 - 1616 |
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Main Authors | , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hagerstown, MD
Lippincott Williams & Wilkins
28.10.2014
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Subjects | |
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Abstract | ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes associated with ECG strain.
One hundred and two patients (age, 70 years [range, 63-75 years]; male, 66%; aortic valve area, 0.9 cm(2) [range, 0.7-1.2 cm(2)]) underwent ECG, echocardiography, and cardiovascular magnetic resonance. They made up the mechanism cohort. Myocardial fibrosis was determined with late gadolinium enhancement (replacement fibrosis) and T1 mapping (diffuse fibrosis). The relationship between ECG strain and cardiovascular magnetic resonance was then assessed in an external validation cohort (n=64). The outcome cohort was made up of 140 patients from the Scottish Aortic Stenosis and Lipid Lowering Trial Impact on Regression (SALTIRE) study and was followed up for 10.6 years (1254 patient-years). Compared with those without left ventricular hypertrophy (n=51) and left ventricular hypertrophy without ECG strain (n=30), patients with ECG strain (n=21) had more severe aortic stenosis, increased left ventricular mass index, more myocardial injury (high-sensitivity plasma cardiac troponin I concentration, 4.3 ng/L [interquartile range, 2.5-7.3 ng/L] versus 7.3 ng/L [interquartile range, 3.2-20.8 ng/L] versus 18.6 ng/L [interquartile range, 9.0-45.2 ng/L], respectively; P<0.001) and increased diffuse fibrosis (extracellular volume fraction, 27.4±2.2% versus 27.2±2.9% versus 30.9±1.9%, respectively; P<0.001). All patients with ECG strain had midwall late gadolinium enhancement (positive and negative predictive values of 100% and 86%, respectively). Indeed, late gadolinium enhancement was independently associated with ECG strain (odds ratio, 1.73; 95% confidence interval, 1.08-2.77; P=0.02), a finding confirmed in the validation cohort. In the outcome cohort, ECG strain was an independent predictor of aortic valve replacement or cardiovascular death (hazard ratio, 2.67; 95% confidence interval, 1.35-5.27; P<0.01).
ECG strain is a specific marker of midwall myocardial fibrosis and predicts adverse clinical outcomes in aortic stenosis. |
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AbstractList | BACKGROUNDECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes associated with ECG strain. METHODS AND RESULTSOne hundred and two patients (age, 70 years [range, 63-75 years]; male, 66%; aortic valve area, 0.9 cm(2) [range, 0.7-1.2 cm(2)]) underwent ECG, echocardiography, and cardiovascular magnetic resonance. They made up the mechanism cohort. Myocardial fibrosis was determined with late gadolinium enhancement (replacement fibrosis) and T1 mapping (diffuse fibrosis). The relationship between ECG strain and cardiovascular magnetic resonance was then assessed in an external validation cohort (n=64). The outcome cohort was made up of 140 patients from the Scottish Aortic Stenosis and Lipid Lowering Trial Impact on Regression (SALTIRE) study and was followed up for 10.6 years (1254 patient-years). Compared with those without left ventricular hypertrophy (n=51) and left ventricular hypertrophy without ECG strain (n=30), patients with ECG strain (n=21) had more severe aortic stenosis, increased left ventricular mass index, more myocardial injury (high-sensitivity plasma cardiac troponin I concentration, 4.3 ng/L [interquartile range, 2.5-7.3 ng/L] versus 7.3 ng/L [interquartile range, 3.2-20.8 ng/L] versus 18.6 ng/L [interquartile range, 9.0-45.2 ng/L], respectively; P<0.001) and increased diffuse fibrosis (extracellular volume fraction, 27.4±2.2% versus 27.2±2.9% versus 30.9±1.9%, respectively; P<0.001). All patients with ECG strain had midwall late gadolinium enhancement (positive and negative predictive values of 100% and 86%, respectively). Indeed, late gadolinium enhancement was independently associated with ECG strain (odds ratio, 1.73; 95% confidence interval, 1.08-2.77; P=0.02), a finding confirmed in the validation cohort. In the outcome cohort, ECG strain was an independent predictor of aortic valve replacement or cardiovascular death (hazard ratio, 2.67; 95% confidence interval, 1.35-5.27; P<0.01). CONCLUSIONECG strain is a specific marker of midwall myocardial fibrosis and predicts adverse clinical outcomes in aortic stenosis. ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes associated with ECG strain. One hundred and two patients (age, 70 years [range, 63-75 years]; male, 66%; aortic valve area, 0.9 cm(2) [range, 0.7-1.2 cm(2)]) underwent ECG, echocardiography, and cardiovascular magnetic resonance. They made up the mechanism cohort. Myocardial fibrosis was determined with late gadolinium enhancement (replacement fibrosis) and T1 mapping (diffuse fibrosis). The relationship between ECG strain and cardiovascular magnetic resonance was then assessed in an external validation cohort (n=64). The outcome cohort was made up of 140 patients from the Scottish Aortic Stenosis and Lipid Lowering Trial Impact on Regression (SALTIRE) study and was followed up for 10.6 years (1254 patient-years). Compared with those without left ventricular hypertrophy (n=51) and left ventricular hypertrophy without ECG strain (n=30), patients with ECG strain (n=21) had more severe aortic stenosis, increased left ventricular mass index, more myocardial injury (high-sensitivity plasma cardiac troponin I concentration, 4.3 ng/L [interquartile range, 2.5-7.3 ng/L] versus 7.3 ng/L [interquartile range, 3.2-20.8 ng/L] versus 18.6 ng/L [interquartile range, 9.0-45.2 ng/L], respectively; P<0.001) and increased diffuse fibrosis (extracellular volume fraction, 27.4±2.2% versus 27.2±2.9% versus 30.9±1.9%, respectively; P<0.001). All patients with ECG strain had midwall late gadolinium enhancement (positive and negative predictive values of 100% and 86%, respectively). Indeed, late gadolinium enhancement was independently associated with ECG strain (odds ratio, 1.73; 95% confidence interval, 1.08-2.77; P=0.02), a finding confirmed in the validation cohort. In the outcome cohort, ECG strain was an independent predictor of aortic valve replacement or cardiovascular death (hazard ratio, 2.67; 95% confidence interval, 1.35-5.27; P<0.01). ECG strain is a specific marker of midwall myocardial fibrosis and predicts adverse clinical outcomes in aortic stenosis. Background— ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes associated with ECG strain. Methods and Results— One hundred and two patients (age, 70 years [range, 63–75 years]; male, 66%; aortic valve area, 0.9 cm 2 [range, 0.7–1.2 cm 2 ]) underwent ECG, echocardiography, and cardiovascular magnetic resonance. They made up the mechanism cohort. Myocardial fibrosis was determined with late gadolinium enhancement (replacement fibrosis) and T1 mapping (diffuse fibrosis). The relationship between ECG strain and cardiovascular magnetic resonance was then assessed in an external validation cohort (n=64). The outcome cohort was made up of 140 patients from the Scottish Aortic Stenosis and Lipid Lowering Trial Impact on Regression (SALTIRE) study and was followed up for 10.6 years (1254 patient-years). Compared with those without left ventricular hypertrophy (n=51) and left ventricular hypertrophy without ECG strain (n=30), patients with ECG strain (n=21) had more severe aortic stenosis, increased left ventricular mass index, more myocardial injury (high-sensitivity plasma cardiac troponin I concentration, 4.3 ng/L [interquartile range, 2.5–7.3 ng/L] versus 7.3 ng/L [interquartile range, 3.2–20.8 ng/L] versus 18.6 ng/L [interquartile range, 9.0–45.2 ng/L], respectively; P <0.001) and increased diffuse fibrosis (extracellular volume fraction, 27.4±2.2% versus 27.2±2.9% versus 30.9±1.9%, respectively; P <0.001). All patients with ECG strain had midwall late gadolinium enhancement (positive and negative predictive values of 100% and 86%, respectively). Indeed, late gadolinium enhancement was independently associated with ECG strain (odds ratio, 1.73; 95% confidence interval, 1.08–2.77; P =0.02), a finding confirmed in the validation cohort. In the outcome cohort, ECG strain was an independent predictor of aortic valve replacement or cardiovascular death (hazard ratio, 2.67; 95% confidence interval, 1.35–5.27; P <0.01). Conclusion— ECG strain is a specific marker of midwall myocardial fibrosis and predicts adverse clinical outcomes in aortic stenosis. |
Author | NEWBY, David E DWECK, Marc R SHAH, Anoop S. V T'NG CHOONG KWOK MCKILLOP, Graham ZAMVAR, Vipin COWELL, S. Joanna VASSILIOU, Vassilis SEMPLE, Scott BOON, Nicholas A DORIS, Mhairi CHIN, Calvin W. L MILLS, Nicholas L WHITE, Audrey C PRASAD, Sanjay K |
Author_xml | – sequence: 1 givenname: Anoop S. V surname: SHAH fullname: SHAH, Anoop S. V organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 2 givenname: Calvin W. L surname: CHIN fullname: CHIN, Calvin W. L organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 3 givenname: Nicholas A surname: BOON fullname: BOON, Nicholas A organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 4 givenname: Sanjay K surname: PRASAD fullname: PRASAD, Sanjay K organization: Royal Brompton Hospital, London, United Kingdom – sequence: 5 givenname: Nicholas L surname: MILLS fullname: MILLS, Nicholas L organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 6 givenname: David E surname: NEWBY fullname: NEWBY, David E organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 7 givenname: Marc R surname: DWECK fullname: DWECK, Marc R organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 8 givenname: Vassilis surname: VASSILIOU fullname: VASSILIOU, Vassilis organization: Royal Brompton Hospital, London, United Kingdom – sequence: 9 givenname: S. Joanna surname: COWELL fullname: COWELL, S. Joanna organization: NHS Lothian, Edinburgh, United Kingdom – sequence: 10 givenname: Mhairi surname: DORIS fullname: DORIS, Mhairi organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 11 surname: T'NG CHOONG KWOK fullname: T'NG CHOONG KWOK organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 12 givenname: Scott surname: SEMPLE fullname: SEMPLE, Scott organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 13 givenname: Vipin surname: ZAMVAR fullname: ZAMVAR, Vipin organization: Department of Cardiothoracic Surgery, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom – sequence: 14 givenname: Audrey C surname: WHITE fullname: WHITE, Audrey C organization: British Heart Foundation/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom – sequence: 15 givenname: Graham surname: MCKILLOP fullname: MCKILLOP, Graham organization: NHS Lothian, Edinburgh, United Kingdom |
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Keywords | Aortic stenosis Troponin I Fibrosis aortic valve stenosis hypertrophy, left ventricular Cardiovascular disease Circulatory system Cardiology Aortic valve Left ventricle Hypertrophy Strain fibrosis troponin I |
Language | English |
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References_xml | – ident: e_1_3_4_31_2 doi: 10.1055/s-2007-1012039 – ident: e_1_3_4_23_2 doi: 10.1093/eurheartj/ehm095 – ident: e_1_3_4_10_2 doi: 10.1016/0002-8703(68)90035-5 – ident: e_1_3_4_12_2 doi: 10.1016/j.echo.2008.11.029 – ident: e_1_3_4_9_2 doi: 10.1056/NEJMoa043876 – volume: 13 start-page: 182 year: 2004 ident: e_1_3_4_30_2 article-title: Influence of atypical symptoms and electrocardiographic signs of left ventricular hypertrophy or ST-segment/T-wave abnormalities on the natural history of otherwise asymptomatic adults with moderate to severe aortic stenosis: preliminary communication. publication-title: J Heart Valve Dis contributor: fullname: Hering D – ident: e_1_3_4_21_2 doi: 10.1093/eurheartj/ehu189 – ident: e_1_3_4_13_2 doi: 10.1016/j.echo.2005.10.005 – ident: e_1_3_4_20_2 doi: 10.1016/j.amjcard.2011.02.346 – ident: e_1_3_4_18_2 doi: 10.1093/ehjci/jet245 – ident: e_1_3_4_3_2 doi: 10.1161/01.CIR.101.4.423 – ident: e_1_3_4_4_2 doi: 10.1161/hc0102.101365 – ident: e_1_3_4_7_2 doi: 10.1161/circulationaha.111.049759 – ident: e_1_3_4_15_2 doi: 10.1161/CIRCULATIONAHA.109.930636 – ident: e_1_3_4_19_2 doi: 10.1002/jmri.21119 – ident: e_1_3_4_29_2 doi: 10.1016/S0735-1097(02)02171-X – ident: e_1_3_4_8_2 doi: 10.1080/10976640600572889 – ident: e_1_3_4_11_2 doi: 10.1016/j.jacc.2008.12.015 – ident: e_1_3_4_26_2 doi: 10.1016/0735-1097(89)90314-8 – ident: e_1_3_4_5_2 doi: 10.1161/01.CIR.0000051865.66123.B7 – ident: e_1_3_4_14_2 doi: 10.1016/j.jacc.2011.03.064 – volume: 28 start-page: 1 year: 2014 ident: e_1_3_4_6_2 article-title: Markers of left ventricular decompensation in aortic stenosis. publication-title: Expert Rev Cardiovasc Ther contributor: fullname: Chin CW – ident: e_1_3_4_24_2 doi: 10.1093/eurheartj/ehs109 – ident: e_1_3_4_2_2 doi: 10.1016/j.jacc.2012.02.093 – ident: e_1_3_4_27_2 doi: 10.1161/01.CIR.102.1.48 – volume-title: ARCHITECT STAT high sensitivity troponin I [package insert] year: 2012 ident: e_1_3_4_22_2 – ident: e_1_3_4_17_2 doi: 10.1136/heartjnl-2012-302346 – ident: e_1_3_4_16_2 doi: 10.1186/1532-429X-14-88 – ident: e_1_3_4_28_2 doi: 10.1016/0735-1097(92)90360-Y – ident: e_1_3_4_25_2 doi: 10.1016/j.amjcard.2011.03.084 |
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Snippet | ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes associated... Background— ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and... BACKGROUNDECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes... |
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SubjectTerms | Aged Aged, 80 and over Aortic Valve Stenosis - diagnosis Aortic Valve Stenosis - mortality Aortic Valve Stenosis - physiopathology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Echocardiography Electrocardiography Female Fibrosis - mortality Fibrosis - physiopathology Heart Function Tests Humans Hypertrophy, Left Ventricular - diagnosis Hypertrophy, Left Ventricular - mortality Hypertrophy, Left Ventricular - physiopathology Logistic Models Magnetic Resonance Imaging Male Medical sciences Middle Aged Multivariate Analysis Outcome Assessment, Health Care Predictive Value of Tests Prognosis Proportional Hazards Models Randomized Controlled Trials as Topic Stroke Volume Troponin I - blood |
Title | Left Ventricular Hypertrophy With Strain and Aortic Stenosis |
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