Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol

Dahlöf, Björn; Devereux, Richard B.; Kjeldsen, Sverre E.; Julius, Stevo; Beevers, Gareth; Fairé, Ulf dé; Fyhrquist, Frej; Ibsen, Hans; Kristiansson, Krister; Lederballe‐Pedersen, Ole; Lindholm, Lars; Nieminen, Markku S.; Omvik, Per; Oparil, Suzanne; Wedel, Hans

doi:10.1016/s0140-6736(02)08089-3

Cited by 4,764 publications

(3,210 citation statements)

References 26 publications

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“…What are the clinical implications of the results presented from the SILVHIA 13,16 and LIFE studies, 14,44 comparing an ARB (irbesartan and losartan, respectively), with a b 1 -adrenoceptor blocker (atenolol)? So far, the effects of irbesartan and losartan are consistent and supportive.…”

Section: Future Perspectivementioning

confidence: 99%

“…13,14 Reduction in LV mass in turn reduces the repolarization time and its dispersion, [15][16][17] the incidence and severity of ventricular arrhythmias 2 and the risk for cardiovascular events. 18,19 We have recently shown that regression of LV mass induced by the angiotensin II type 1 receptor blocker (ARB) irbesartan rather than by the b 1 -selective adrenoceptor blocker atenolol is accompanied by improved repolarization.…”

Section: Introductionmentioning

confidence: 99%

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Cardiac repolarization and its relation to ventricular geometry and rate in reverse remodelling during antihypertensive therapy with irbesartan or atenolol: results from the SILVHIA study

et al. 2007

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Hypertensive left ventricular (LV) hypertrophy is associated with a substantial risk for malignant arrhythmias and sudden death. According to recent results, antihypertensive therapy with the angiotensin II type 1 receptor blocker irbesartan reverses both structural and electrical remodelling. However, the relation between the LV geometric pattern (concentric vs eccentric) and electrical reverse remodelling has not been characterized, neither has the relation between repolarization and rate (QT/RR and JT/RR relation), which presumably reflects the propensity for bradycardia-dependent ventricular arrhythmia. In this study, repeat echocardiographic and electrocardiographic measurements were performed in hypertensive patients with LV hypertrophy, randomized to double-blind therapy with irbesartan (n ¼ 44) or the b 1 -adrenoceptor blocker atenolol (n ¼ 48) for 48 weeks; 53 patients had concentric and 39 eccentric LV hypertrophy. In addition, 37 matched hypertensive subjects without LV hypertrophy and no current therapy served as controls. Irbesartan induced structural and electrophysiological reverse remodelling, independent of LV geometry. In contrast, atenolol had similar beneficial effect only in patients with concentric LV hypertrophy, while the response in those with eccentric hypertrophy was unfavourable with both prolonged repolarization time and an increased QT/RR slope (suggesting reverse-use dependence). In conclusion, there is a significant geometry-related difference in the reverse remodelling processes induced by irbesartan and atenolol. Echocardiographic characterization of the geometry in hypertension-induced LV hypertrophy might become an important step in the selection of optimal antihypertensive therapy.

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Section: Future Perspectivementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cardiac repolarization and its relation to ventricular geometry and rate in reverse remodelling during antihypertensive therapy with irbesartan or atenolol: results from the SILVHIA study

et al. 2007

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“…Whereas patients with LVH represent a risk group for adverse outcomes, progression to reduced LV systolic function, let alone major adverse cardiac events, occurs in a minority 3. Recent studies by our group have demonstrated that presence of LVH in conjunction with elevated soluble biomarkers for myocardial injury (high‐sensitivity cardiac troponin T; hs‐cTnT) and hemodynamic stress (amino‐terminal pro‐B‐type natriuretic peptide; NT‐proBNP) can identify a “malignant” phenotype of LVH more likely to progress to HF or death in both middle‐aged and older individuals 2, 4…”

Section: Introductionmentioning

confidence: 99%

“Malignant” Left Ventricular Hypertrophy Identifies Subjects at High Risk for Progression to Asymptomatic Left Ventricular Dysfunction, Heart Failure, and Death: MESA (Multi‐Ethnic Study of Atherosclerosis)

Peters

Seliger

Christenson

et al. 2018

JAHA

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BackgroundAs heart failure (HF)‐associated morbidity and mortality continue to escalate, enhanced focus on prevention is increasingly important. “Malignant” left ventricular (LV) hypertrophy (LVH): LVH combined with an elevated cardiac biomarker reflecting either injury (high‐sensitivity cardiac troponin T), or strain (amino‐terminal pro‐B‐type natriuretic peptide) has predicted accelerated progression to HF. We sought to determine whether malignant LVH identified community‐dwelling adults initially free of cardiovascular disease at high risk of asymptomatic decline in LV ejection fraction or a clinical cardiovascular event.Methods and ResultsA total of 4985 of 6814 individuals without prevalent cardiovascular disease underwent baseline cardiac magnetic resonance for LVH in combination with measurement of plasma high‐sensitivity cardiac troponin T and amino‐terminal pro‐B‐type natriuretic peptide as part of MESA (Multi‐Ethnic Study of Atherosclerosis) and were subsequently divided into 4 groups: (1) No LVH, no elevated biomarkers (n=2206; 44.3%); (2) No LVH, ≥1 elevated biomarkers (n=2275; 45.7%); (3) LVH, no elevated biomarkers (n=153; 3.0%); and (4) LVH, ≥1 elevated biomarkers (malignant LVH; n=351; 7.0%). Cardiac magnetic resonance was repeated 10 years later (n=2831) for assessment of LV ejection fraction <50%. Median follow‐up was 12.2 years. Malignant LVH was associated with 7.0‐, 3.5‐, and 2.6‐fold adjusted increases in incidence of HF, cardiovascular death, and asymptomatic LV dysfunction, respectively, versus group 1. New‐onset HF was predominately HF with reduced ejection fraction (9.5‐fold increase).ConclusionsMalignant LVH is predictive of progression to asymptomatic LV dysfunction, HF (particularly HF with reduced ejection fraction), and cardiovascular death. Consequently, malignant LVH represents a high‐risk phenotype among individuals without known cardiovascular disease, which should be targeted for increased surveillance and more‐aggressive therapies.

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“…Currently, the choice of the drug for the initial treatment of hypertension is very strongly debuted. Although ARBs have been shown superior to b-blockers in the LIFE study 24 and ACEI better than diuretics in the Captopril Prevention Project (CAPPP) trial, 25 these findings have not been confirmed. On the contrary, the Antihypertensive and Lipid-Lowering Treatment to prevent Heart Attack Trial (ALLHAT) results suggest that chlorothalidone was better than lisinopril, both in lowering BP and diminishing cardiovascular events, but no differential effects of drug class on PP were found when all participants were considered.…”

Section: Discussionmentioning

confidence: 99%

Differential pulse pressure response to various antihypertensive drug families

et al. 2006

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Pulse pressure (PP) is emerging as a major pressure predictor of cardiac disease. The study comprised 10 185 untreated patients with essential hypertension. A total of 5395 men and 4790 women 56713 years old, with uncomplicated essential hypertension, after a 15-day washout period and after 6 months of antihypertensive monotherapy were included. All patients included in the final cohort were responders and had normalized their blood pressure. PP was decreased least with diuretics (À5 mm Hg) and most with angiotensin II receptor blockers (ARBs) and calcium antagonists (À15 mm Hg), followed by angiotensin-converting enzyme inhibitors (ACEI) (À12 mm Hg) a-and b-blockers (À10 and À9 mm Hg), differentiating among antihypertensive classes (Po0.001). The magnitude of PP fall was related to the degree of left ventricular (LV) mass reduction (Po0.001), seen best with ARBs (r ¼ 0.42) and least with ACEIs (r ¼ 0.18). Of the antihypertensive medications used in everyday practice, PP decrease may be achieved best with ARBs and calcium antagonists, whereas diuretics confer poor response. PP was decreased least with diuretics (À5 mm Hg) and most with ARBs and calcium channel blockers (À15 mm Hg), followed by ACEI (À12 mm Hg) a-and b-blockers (À10 and À9 mm Hg), differentiating among antihypertensive classes (Po0.001). Of the antihypertensive medications used in everyday practice, PP decrease may be achieved best with ARBs and calcium antagonists.

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Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol

Cited by 4,764 publications

References 26 publications

Cardiac repolarization and its relation to ventricular geometry and rate in reverse remodelling during antihypertensive therapy with irbesartan or atenolol: results from the SILVHIA study

Cardiac repolarization and its relation to ventricular geometry and rate in reverse remodelling during antihypertensive therapy with irbesartan or atenolol: results from the SILVHIA study

“Malignant” Left Ventricular Hypertrophy Identifies Subjects at High Risk for Progression to Asymptomatic Left Ventricular Dysfunction, Heart Failure, and Death: MESA (Multi‐Ethnic Study of Atherosclerosis)

Differential pulse pressure response to various antihypertensive drug families

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