Change search
ReferencesLink to record
Permanent link

Direct link
Left Ventricular Wall Stress-Mass-Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients LIFE Study
Show others and affiliations
2015 (English)In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 66, no 5, 945-953 p.Article in journal (Refereed) Published
Abstract [en]

In the Losartan Intervention for End Point Reduction in Hypertension (LIFE) study, 4.8 years' losartan- versus atenolol-based antihypertensive treatment reduced left ventricular hypertrophy and cardiovascular end points, including cardiovascular death and stroke. However, there was no difference in myocardial infarction (MI), possibly related to greater reduction in myocardial oxygen demand by atenolol-based treatment. Myocardial oxygen demand was assessed indirectly by the left ventricular massxwall stressxheart rate (triple product) in 905 LIFE participants. The triple product was included as time-varying covariate in Cox models assessing predictors of the LIFE primary composite end point (cardiovascular death, MI, or stroke), its individual components, and all-cause mortality. At baseline, the triple product in both treatment groups was, compared with normal adults, elevated in 70% of patients. During randomized treatment, the triple product was reduced more by atenolol, with prevalences of elevated triple product of 39% versus 51% on losartan (both P0.001). In Cox regression analyses adjusting for age, smoking, diabetes mellitus, and prior stroke, MI, and heart failure, 1 SD lower triple product was associated with 23% (95% confidence interval 13%-32%) fewer composite end points, 31% (18%-41%) less cardiovascular mortality, 30% (15%-41%) lower MI, and 22% (11%-33%) lower all-cause mortality (all P0.001), without association with stroke (P=0.34). Although losartan-based therapy reduced ventricular mass more, greater heart rate reduction with atenolol resulted in larger reduction of the triple product. Lower triple product during antihypertensive treatment was strongly, independently associated with lower rates of the LIFE primary composite end point, cardiovascular death, and MI, but not stroke.

Place, publisher, year, edition, pages
2015. Vol. 66, no 5, 945-953 p.
Keyword [en]
hypertension, hypertrophy, myocardial infarction, oxygen, prognosis, VEREUX RB, 1986, AMERICAN JOURNAL OF CARDIOLOGY, V57, P450 vereux RB, 2004, JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, V292, P2350, LLSPERGER KC, 1988, CIRCULATION RESEARCH, V63, P87, VEREUX RB, 1993, CIRCULATION, V88, P1444 hlof B, 1997, AMERICAN JOURNAL OF HYPERTENSION, V10, P705 nonymous], 1981, N Engl J Med, V304, P801 hlof B, 2002, LANCET, V359, P995 hiller N B, 1989, Journal of the American Society of Echocardiography : official publication of the erican Society of Echocardiography, V2, P358 vereux RB, 2000, JOURNAL OF HYPERTENSION, V18, P1129 in PM, 2003, CIRCULATION, V108, P684
National Category
Cardiac and Cardiovascular Systems
URN: urn:nbn:se:umu:diva-110989DOI: 10.1161/HYPERTENSIONAHA.114.05582ISI: 000362354500006PubMedID: 26418019OAI: diva2:872246
Available from: 2015-11-18 Created: 2015-11-02 Last updated: 2015-11-18Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Boman, Kurt
By organisation
In the same journal
Cardiac and Cardiovascular Systems

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 33 hits
ReferencesLink to record
Permanent link

Direct link