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- Reil, J. C., et al.
(författare)
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Heart rate reduction in cardiovascular disease and therapy
- 2011
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Ingår i: Clinical research in cardiology. - : Springer Science and Business Media LLC. - 1861-0692 .- 1861-0684. ; 100:1, s. 11-19
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Tidskriftsartikel (refereegranskat)abstract
- Heart rate influences myocardial oxygen demand, coronary blood flow, and myocardial function. Clinical and experimental studies support an association between elevated resting heart rate and a broad range of maladaptive effects on the function and structure of the cardiovascular system. Heart rate has been shown to be an important predictor of mortality in cardiovascular disorders such as coronary artery disease, myocardial infarction, and chronic heart failure. This review summarizes the specific influence of heart rate on vascular morphology and function as well as on myocardial lesions leading from early impact on vascular homeostasis to myocardial hemodynamics in chronic heart failure. Heart rate can be easily determined during physical examination of the patient and therefore allows a simple hint on prognosis and efficiency of therapy.
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| 2. |
- Tardif, J. C., et al.
(författare)
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Effects of selective heart rate reduction with ivabradine on left ventricular remodelling and function: results from the SHIFT echocardiography substudy
- 2011
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Ingår i: European heart journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 32:20, s. 2507-15
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: The SHIFT echocardiographic substudy evaluated the effects of ivabradine on left ventricular (LV) remodelling in heart failure (HF). METHODS AND RESULTS: Eligible patients had chronic HF and systolic dysfunction [LV ejection fraction (LVEF) /=70 bpm. Patients were randomly allocated to ivabradine or placebo, superimposed on background therapy for HF. Complete echocardiographic data at baseline and 8 months were available for 411 patients (ivabradine 208, placebo 203). Treatment with ivabradine reduced LVESVI (primary substudy endpoint) vs. placebo [-7.0 +/- 16.3 vs. -0.9 +/- 17.1 mL/m(2); difference (SE), -5.8 (1.6), 95% CI -8.8 to -2.7, P< 0.001]. The reduction in LVESVI was independent of beta-blocker use, HF aetiology, and baseline LVEF. Ivabradine also improved LV end-diastolic volume index (-7.9 +/- 18.9 vs. -1.8 +/- 19.0 mL/m(2), P= 0.002) and LVEF (+2.4 +/- 7.7 vs. -0.1 +/- 8.0%, P< 0.001). The incidence of the SHIFT primary composite outcome (cardiovascular mortality or hospitalization for worsening HF) was higher in patients with LVESVI above the median (59 mL/m2) at baseline (HR 1.62, 95% CI 1.03-2.56, P= 0.04). Patients with the largest relative reductions in LVESVI had the lowest event rates. CONCLUSION: Ivabradine reverses cardiac remodelling in patients with HF and LV systolic dysfunction.
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