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dc.contributor.authorKhanji, Men_US
dc.contributor.authorBalawon, Aen_US
dc.contributor.authorBoubertakh, Ren_US
dc.contributor.authorZemrak, Fen_US
dc.contributor.authorCollier, Den_US
dc.contributor.authorCaulfield, MJen_US
dc.contributor.authorPetersen, SEen_US
dc.description.abstractOBJECTIVE: Hypertension remains a major cause of cardiovascular morbidity and mortality worldwide. Persistent blood pressure (BP) elevation may lead to left ventricular (LV) hypertrophy and heart failure. We wanted to assess the impact of high BP on LV function in an asymptomatic cohort, with no evidence of LV hypertrophy. DESIGN AND METHOD: We included all 96 asymptomatic volunteers scanned with cardiovascular magnetic resonance (CMR) as part of the HAPPY London primary prevention study. BP was taken sitting, from the left arm with at least 2 consistent measures. We compared those with elevated clinic BP (systolic >140mmHg and/or diastolic >90mmHg) to those with a 'normal' BP, regardless of whether on BP treatment. CMR at 1.5 Tesla was performed within 2 weeks of the clinic. RESULTS: Average age was 64.5 years and 74% were males, similar in both groups. Half were taking antihypertensive medication in both groups. 31 participants had elevated clinic BP and the remaining 65 had normal BP. Mean BPs were: 150mmHg ± 8 / 86mmHg ± 11 in high BP group and 127mmHg ± 8 / 77mmHg ± 7 in the normal (Table 1).(Figure is included in full-text article.)LV ejection fraction (EF) was significantly elevated in the high BP group (68% vs. 64%, p < 0.05; Figure 1), despite similar indexed LV myocardial mass.Systolic BP was correlated with LVEF (Cor coeffeicient = 0.26, p = 0.01, t = 2.62, CI 0.06 - 0.44). In a multiple regression model both systolic BP and BP treatment, but not diastolic BP, were predictors for LV EF (r2 = 0.17, p < 0.001), independent of diastolic BP, LV myocardial mass, BP treatment, age and heart rate. CONCLUSIONS: We believe this is the first description of this relationship. Thus in the absence of LV hypertrophy, asymptomatic individuals who have elevated clinic BP have a higher EF compared to those with normal BP. Sustained hyperdynamic circulation may be a contributory mechanism for future hypertrophy, heart failure and other long-term complications.Preliminary data suggests this increased EF may settle with improved BP control. It is possible that we may need to consider an EF correction factor based on BP.en_US
dc.format.extente46 - ?en_US
dc.typeConference Proceeding
dc.rights.holderWolters Kluwer Health, Inc.
pubs.notesNot knownen_US
pubs.volume33 Suppl 1en_US

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