Prognostic Significance of Left Ventricular Mass Change During Treatment of Hypertension

Devereux, Richard B.; Wachtell, Kristian; Gerdts, Eva; Boman, Krister K.; Nieminen, Markku S.; Papademetriou, Vasilios; Rokkedal, Jens; Harris, Katherine E.; Aurup, Peter; Dahlöf, Björn

doi:10.1001/jama.292.19.2350

Cited by 782 publications

(465 citation statements)

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“…Consistent with the latter observations, measures of subclinical cardiac and vascular disease also improved in parallel to the reduction in BP on antihypertensive medication. In the LIFE study, the prevalence of LV hypertrophy decreased from 70% at baseline to 23% over 5 years of antihypertensive treatment, and such regression in LV mass was associated with reduced relative risks of CVD events 28. In other clinical trials, antihypertensive treatment was associated with benign structural remodeling of the common carotid artery 29, 30.…”

Section: Discussionmentioning

confidence: 96%

Residual Cardiovascular Risk in Individuals on Blood Pressure–Lowering Treatment

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Enserro

Sullivan

et al. 2015

JAHA

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BackgroundHypertensive individuals on blood pressure (BP)–lowering treatment with BP in the normal or high‐normal range have higher cardiovascular risk than untreated persons with usual BP in the same range. This residual risk (relative and absolute) is not well quantified and may be attributable in part to the higher burden of subclinical disease in treated individuals.Methods and ResultsWe assigned 3024 Framingham Offspring Cohort participants to 5 categories based on systolic BP (SBP) and diastolic BP (DBP) and use of BP‐lowering treatment: (1) untreated SBP/DBP <120/80 mm Hg; (2) untreated SBP/DB ≥120/80 to <140/90 mm Hg; (3) treated SBP/DBP <140/90 mm Hg; (4) untreated SBP/DBP ≥140/90 mm Hg; and (5) treated SBP/DBP ≥140/90 mm Hg. A composite subclinical disease score was constructed, including information on left ventricular hypertrophy, systolic dysfunction, carotid ultrasound abnormality, peripheral artery disease, and microalbuminuria. The prevalence of subclinical disease rose across BP groups, as did the event rates for incident cardiovascular disease (449 events, median follow‐up of 11 years; group 1, 0.65 event per 100 person‐years; group 5, 3.20 events per 100 person‐years; P<0.0001 for trend). On multivariable adjustment, treated hypertensives in groups 3 and 5 had 50% (95% CI 13% to 99%) and 28% (95% CI −6% to 73%) higher hazards, respectively, of developing cardiovascular disease compared with their untreated counterparts with similar levels of BP (groups 1 and 2 and group 4, respectively). The increased risk of cardiovascular disease in treated hypertensives was attributable in part to greater subclinical disease burden.ConclusionsTreated hypertensives have higher subclinical cardiovascular disease burden, which partly explains their higher cardiovascular disease risk compared with untreated persons with similar BP levels.

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Section: Discussionmentioning

confidence: 96%

Residual Cardiovascular Risk in Individuals on Blood Pressure–Lowering Treatment

Lieb

Enserro

Sullivan

et al. 2015

JAHA

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“…[6][7][8] In the Losartan Intervention For End Point Reduction in Hypertension (LIFE) study, 9,10 losartan-based antihypertensive treatment, compared with an atenolol-based regimen, led to a lower rate of cardiovascular events, especially stroke, 11 and greater regression of LVH, 12,13 which was in turn associated with reduced rates of cardiovascular events. 14,15 In view of the greater effect of losartan-based therapy on LVH and the known association between LVH and MI, an unexpected result of the LIFE study was the lack of a lower rate of MI in losartan-treated patients. 11 Animal experiments have identified an important role of increased myocardial oxygen demand in sensitizing the hypertrophied LV in hypertension to greater size of infarction, as well as arrhythmia, when coronary arterial blood flow is reduced.…”

Section: Eft Ventricular (Lv) Hypertrophy (Lvh) Is a Cardinal Manifmentioning

confidence: 99%

Left Ventricular Wall Stress–Mass–Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients

et al. 2015

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Abstract-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 mass×wall stress×heart 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 P≤0.001). 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 P≤0.001), 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. (Hypertension. 2015;66:945-953.

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“…[3][4][5] In selected subsets of nondiabetic patients, LVH also precedes new onset of diabetes mellitus, 6 suggesting that hypertensive target organ damage might be also a marker of complex metabolic changes associated with the evolution of arterial hypertension.Prevention of the development of target organ damage should be, therefore, the main goal of management of arterial hypertension. 7,8 The most modifiable parameter to achieve this goal is the effective control of blood pressure (BP) using appropriate antihypertensive medications.…”

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confidence: 99%

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confidence: 99%

“…1,2 The effect of LVH on incident cardiovascular events is independent of conventional risk factors and of coronary artery disease. [3][4][5] In selected subsets of nondiabetic patients, LVH also precedes new onset of diabetes mellitus, 6 suggesting that hypertensive target organ damage might be also a marker of complex metabolic changes associated with the evolution of arterial hypertension.…”

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confidence: 99%

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Development of Left Ventricular Hypertrophy in Treated Hypertensive Outpatients

et al. 2017

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L eft ventricular (LV) hypertrophy (LVH) is a marker of target organ damage in hypertension and helps stratifying cardiovascular risk.1,2 The effect of LVH on incident cardiovascular events is independent of conventional risk factors and of coronary artery disease. [3][4][5] In selected subsets of nondiabetic patients, LVH also precedes new onset of diabetes mellitus, 6 suggesting that hypertensive target organ damage might be also a marker of complex metabolic changes associated with the evolution of arterial hypertension.Prevention of the development of target organ damage should be, therefore, the main goal of management of arterial hypertension. 7,8 The most modifiable parameter to achieve this goal is the effective control of blood pressure (BP) using appropriate antihypertensive medications. There is no information on whether LVH could develop during antihypertensive regimen. However, we recently demonstrated that carotid plaque can develop in a specific patient phenotype, independently of optimal BP control. 10 In that study, we found that risk of incident carotid plaque was higher in older diabetic or smoker patients with chronic renal failure and higher initial intima-media thickness complex, suggesting that earlier antihypertensive management might be more beneficial to reduce and prevent target organ damage.In the present analysis, we evaluate whether LVH occurs during antihypertensive therapy and whether a specific phenotype can be identified at risk of incident LVH, in a large treated hypertensive population from a regional Italian registry. Methods Study PopulationHypertensive patients were selected from the Campania Salute Network (CSN) Registry. The CSN is an open registry collecting information from general practitioners and community hospitals networked with the Hypertension Research Center of the Federico Abstract-There is little information on left ventricular (LV) hypertrophy (LVH) development during antihypertensive treatment. We evaluate incident LVH in a treated hypertensive cohort, the Campania Salute Network registry. We analyzed prospectively 4290 hypertensives (aged 50.3±11.1 years, 40% women) with at least 1-year follow-up, without LVH at baseline. Incident LVH was defined as the first detection of echocardiographic LV mass index ≥47 in women or ≥50 g/m 2.7 in men. During a median 48-month follow-up, 915 patients (21.3%) developed LVH. They were older, more frequently women, and obese (P<0.0001), with initial higher fasting glucose, diastolic and systolic blood pressure, LV mass index, lower heart rate and glomerular filtration rate, longer hypertension history and follow-up, and higher average systolic blood pressure during follow-up (all P<0.05), despite a more frequent treatment with Ca ++ -channel blockers and diuretics (both P<0.02). At multivariable Cox regression, incident LVH was independently associated with older age, female sex, obesity, higher average systolic blood pressure during follow-up, and initial greater LV mass index (all P<0.02). By categorizing patients a...

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Prognostic Significance of Left Ventricular Mass Change During Treatment of Hypertension

Cited by 782 publications

References 36 publications

Residual Cardiovascular Risk in Individuals on Blood Pressure–Lowering Treatment

Residual Cardiovascular Risk in Individuals on Blood Pressure–Lowering Treatment

Left Ventricular Wall Stress–Mass–Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients

Development of Left Ventricular Hypertrophy in Treated Hypertensive Outpatients

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