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Journal Article
Research Support, Non-U.S. Gov't
Association between electrocardiographic and echocardiographic markers of stage B heart failure and cardiovascular outcome.
ESC Heart Failure 2017 November
AIMS: The detection of non-ischaemic (mainly hypertension, diabetes, and obesity) stage B heart failure (SBHF) may facilitate the recognition of those at risk of progression to overt HF and HF prevention. We sought the relationship of specific electrocardiographic (ECG) markers of SBHF to echocardiographic features of SBHF and their prognostic value for development of HF. The ECG markers were Cornell product (Cornell-P), P-wave terminal force in lead V1 (PTFV1), ST depression in lead V5 V6 (minSTmV5V6), and increased heart rate. Echocardiographic assessment of SBHF included left ventricular hypertrophy (LVH), impaired global longitudinal strain (GLS), and diastolic dysfunction (DD).
METHOD AND RESULTS: Asymptomatic subjects ≥65 years without prior cardiac history, but with HF risks, were recruited from the local community. At baseline, they underwent clinical assessment, 12-lead ECG, and comprehensive echocardiography. New HF was assessed clinically at mean follow-up of 14 ± 4 months, and echocardiography was repeated in subjects with HF. Of the 447 study subjects (age 71 ± 5, 47% men) with SBHF, 13% had LVH, 32% impaired GLS, and 65% ≥grade I DD (10% ≥grade II DD). Forty were lost to follow-up. Clinical HF developed in 47 of 407, of whom 20% had echocardiographic LVH, 51% abnormal GLS, and 76% DD at baseline. Baseline LVH and abnormal GLS (not grade I DD) were independently associated with outcomes (clinical HF and cardiovascular death). Cornell-P and heart rate (not minSTmV5V6 nor PTFV1) were independently associated with LVH, impaired GLS, and DD. Cornell-P and minSTV5V6 (not heart rate nor PTFV1) were independently associated with outcomes. More ECG abnormalities improved sensitivity, but ECG-markers were not independent of or incremental to echocardiographic markers to predict HF in SBHF.
CONCLUSIONS: In this elderly study population, ECG markers showed low diagnostic sensitivity for non-ischaemic SBHF and low prognostic value for outcomes. Cornell-P and minSTmV5V6 had predictive value for outcomes in non-ischaemic SBHF independent of age, gender, and common comorbidities but were not incremental to echocardiography.
METHOD AND RESULTS: Asymptomatic subjects ≥65 years without prior cardiac history, but with HF risks, were recruited from the local community. At baseline, they underwent clinical assessment, 12-lead ECG, and comprehensive echocardiography. New HF was assessed clinically at mean follow-up of 14 ± 4 months, and echocardiography was repeated in subjects with HF. Of the 447 study subjects (age 71 ± 5, 47% men) with SBHF, 13% had LVH, 32% impaired GLS, and 65% ≥grade I DD (10% ≥grade II DD). Forty were lost to follow-up. Clinical HF developed in 47 of 407, of whom 20% had echocardiographic LVH, 51% abnormal GLS, and 76% DD at baseline. Baseline LVH and abnormal GLS (not grade I DD) were independently associated with outcomes (clinical HF and cardiovascular death). Cornell-P and heart rate (not minSTmV5V6 nor PTFV1) were independently associated with LVH, impaired GLS, and DD. Cornell-P and minSTV5V6 (not heart rate nor PTFV1) were independently associated with outcomes. More ECG abnormalities improved sensitivity, but ECG-markers were not independent of or incremental to echocardiographic markers to predict HF in SBHF.
CONCLUSIONS: In this elderly study population, ECG markers showed low diagnostic sensitivity for non-ischaemic SBHF and low prognostic value for outcomes. Cornell-P and minSTmV5V6 had predictive value for outcomes in non-ischaemic SBHF independent of age, gender, and common comorbidities but were not incremental to echocardiography.
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