Prevention of new-onset atrial fibrillation and its predictors with angiotensin II-receptor blockers in the treatment of hypertension and heart failure

Aksnes, Tonje A.; Flaa, Arnljot; Strand, A; Kjeldsen, Sverre E.

doi:10.1097/01.hjh.0000254378.26607.1f

Cited by 41 publications

(26 citation statements)

References 67 publications

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“…34,35 The benefit of renin-angiotensin inhibition in heart failure has been demonstrated in several randomized clinical trials. We have previously shown that the hypertrophy in the TG mice can be reversed by pharmacological suppression of the RAS, and future studies are required to determine whether reversal of ECC remodeling can be achieved by these means.…”

Section: Significance and Limitations Of The Modelmentioning

confidence: 99%

Angiotensin II–Mediated Adaptive and Maladaptive Remodeling of Cardiomyocyte Excitation–Contraction Coupling

Gusev

Domenighetti

Delbridge

et al. 2009

Circulation Research

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Abstract-Cardiac hypertrophy is associated with alterations in cardiomyocyte excitation-contraction coupling (ECC) and Ca 2ϩ handling. Chronic elevation of plasma angiotensin II (Ang II) is a major determinant in the pathogenesis of cardiac hypertrophy and congestive heart failure. However, the molecular mechanisms by which the direct actions of Ang II on cardiomyocytes contribute to ECC remodeling are not precisely known. This question was addressed using cardiac myocytes isolated from transgenic (TG1306/1R [TG]) mice exhibiting cardiac specific overexpression of angiotensinogen, which develop Ang II-mediated cardiac hypertrophy in the absence of hemodynamic overload. Electrophysiological techniques, photolysis of caged Ca 2ϩ and confocal Ca 2ϩ imaging were used to examine ECC remodeling at early (Ϸ20 weeks of age) and late (Ϸ60 weeks of age) time points during the development of cardiac dysfunction. In young TG mice, increased cardiac Ang II levels induced a hypertrophic response in cardiomyocyte, which was accompanied by an adaptive change of Ca 2ϩ signaling, specifically an upregulation of the Na ϩ /Ca 2ϩ exchangermediated Ca 2ϩ transport. In contrast, maladaptation was evident in older TG mice, as suggested by reduced sarcoplasmic reticulum Ca 2ϩ content resulting from a shift in the ratio of plasmalemmal Ca 2ϩ removal and sarcoplasmic reticulum Ca 2ϩ uptake. This was associated with a conserved ECC gain, consistent with a state of hypersensitivity in Ca 2ϩ -induced Ca 2ϩ release. Together, our data suggest that chronic elevation of cardiac Ang II levels significantly alters cardiomyocyte ECC in the long term, and thereby contractility, independently of hemodynamic overload and arterial hypertension. Key Words: cardiac excitation-contraction coupling Ⅲ remodeling Ⅲ sodium-calcium exchange Ⅲ angiotensin II Ⅲ hypertrophy H ypertension is a major risk factor for the genesis and progression of a variety of cardiovascular diseases including heart failure, stroke, and kidney dysfunction. Common therapies for the treatment of hypertension lower blood pressure via inhibition of the renin-angiotensin system (RAS). Drugs include inhibitors of the angiotensinconverting enzyme, as well as angiotensin II (Ang II) receptor type 1 (AT 1 ) antagonists, thus preventing the formation of Ang II or its binding to AT 1 receptors. 1,2 In addition to its effects on the vasculature, the RAS plays an important role in the development of cardiac hypertrophy. 3 Sustained activation of the RAS results in arterial hypertension, which in turn produces hemodynamic overload. The adaptation of the heart to this loading is characterized by a change in cardiac protein expression and substantial cardiac remodeling. In addition, Ang II also exerts direct growth-promoting effects on cardiac tissues, resulting in cardiomyocyte hypertrophy and mechanical dysfunction independently of hypertension. 4,5 Ang II activates several intracellular signal transduction pathways including mitogen-activated protein kinases and protein kinase C. 6,7 Therefore,...

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Section: Significance and Limitations Of The Modelmentioning

confidence: 99%

Angiotensin II–Mediated Adaptive and Maladaptive Remodeling of Cardiomyocyte Excitation–Contraction Coupling

Gusev

Domenighetti

Delbridge

et al. 2009

Circulation Research

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“…Recientemente se ha centrado la atención en la medición ecocardiográfica del tamaño auricular izquierdo como frecuente indicio de hipertrofia ventricular izquierda 374 y como predictor de los episodios cardiovasculares 375 , en paralelo con la evidencia creciente de que los fármacos antihipertensivos pueden tener efectos diferentes en el desarrollo de la fibrilación auricular 376 . Dos ensayos amplios en la hipertensión 377,378 han indicado que los antagonistas de los receptores de la angiotensina losartán y valsartán se asocian a una menor incidencia de fibrilación auricular de nueva aparición, en comparación con el bloqueador beta atenolol y el antagonista del calcio amlodipino, respectivamente.…”

Section: Corazónunclassified

“…Parece que es necesario un estricto control de la presión arterial cuando se administra un tratamiento anticoagulante, debido a que los ictus y los episodios hemorrágicos son más frecuentes cuando la presión arterial sistólica es ≥ 140 mmHg 629 . A la vista de los resultados obtenidos en análisis post-hoc de 2 ensayos recientes [376][377][378] , que indican menos incidencia de fibrilación auricular de nueva aparición con los antagonistas de los receptores de la angiotensina (véase el apartado 4.5.1), estos fármacos pueden ser preferibles, aunque es deseable obtener una confirmación en los ensayos clínicos en curso.…”

Section: Fibrilación Auricularunclassified

Guías de práctica clínica para el tratamiento de la hipertensión arterial 2007

2007

Revista Española de Cardiología

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“…4,10,11 Increased pulse pressure (PP), defined as the difference between systolic blood pressure (SBP) and diastolic blood pressure (DBP), is a marker of arterial stiffness.…”

mentioning

confidence: 99%

“…9 Prevention of AF is thus of great importance, and hypertension is currently the most prevalent, potentially modifiable risk factor, accounting for Ϸ14% to 22% of AF cases. 4,10,11 Increased pulse pressure (PP), defined as the difference between systolic blood pressure (SBP) and diastolic blood pressure (DBP), is a marker of arterial stiffness. 12 Studies have found PP to be an independent predictor of new-onset AF in both general 13 and hypertensive 14 populations.…”

mentioning

confidence: 99%

Association of Pulse Pressure With New-Onset Atrial Fibrillation in Patients With Hypertension and Left Ventricular Hypertrophy

et al. 2012

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Abstract-Previous studies have found pulse pressure (PP), a marker of arterial stiffness, to be an independent predictor of atrial fibrillation (AF) in general and hypertensive populations. We examined whether PP predicted new-onset AF in comparison with other blood pressure components in the Losartan Intervention For Endpoint reduction in hypertension study, a double-blind, randomized (losartan versus atenolol), parallel-group study, including 9193 patients with hypertension and electrocardiographic left ventricular hypertrophy. In 8810 patients with neither a history of AF nor AF at baseline, Minnesota coding of electrocardiograms confirmed new-onset AF in 353 patients (4.0%) during mean 4.9 years of follow-up. In multivariate Cox regression analyses, baseline and in-treatment PP and baseline and in-treatment systolic blood pressure predicted new-onset AF, independent of baseline age, height, weight, and Framingham Risk Score; sex, race, and treatment allocation; and in-treatment heart rate and Cornell product. PP was the strongest single blood pressure predictor of new-onset AF determined by the decrease in the Ϫ2 Log likelihood statistic, in comparison with systolic blood pressure, diastolic blood pressure, and mean arterial pressure. When evaluated in the same model, the predictive effect of systolic and diastolic blood pressures together was similar to that of PP. In this population of patients with hypertension and left ventricular hypertrophy, PP was the strongest single blood pressure predictor of new-onset AF, independent of other risk factors. Key Words: arrhythmia Ⅲ atenolol Ⅲ blood pressure Ⅲ hypertension Ⅲ losartan Ⅲ structural heart disease A trial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia, and the prevalence is increasing. 1 In the Rotterdam study, the prevalence of AF varied from 0.7% in the age group 55 to 59 years to 17.8% in those aged Ն85 years.2 AF incidence increases with age, 3 and other risk factors include diabetes, obesity, hypertension, left ventricular hypertrophy (LVH), coronary heart disease, congestive heart failure, valvular heart disease, and increased left atrial size by echocardiography.4-6 AF is associated with a 4-to 5-fold increased risk of ischemic stroke 7,8 and with a nearly doubled cardiovascular mortality risk.9 Prevention of AF is thus of great importance, and hypertension is currently the most prevalent, potentially modifiable risk factor, accounting for Ϸ14% to 22% of AF cases. 4,10,11 Increased pulse pressure (PP), defined as the difference between systolic blood pressure (SBP) and diastolic blood pressure (DBP), is a marker of arterial stiffness.12 Studies have found PP to be an independent predictor of new-onset AF in both general 13

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Prevention of new-onset atrial fibrillation and its predictors with angiotensin II-receptor blockers in the treatment of hypertension and heart failure

Cited by 41 publications

References 67 publications

Angiotensin II–Mediated Adaptive and Maladaptive Remodeling of Cardiomyocyte Excitation–Contraction Coupling

Angiotensin II–Mediated Adaptive and Maladaptive Remodeling of Cardiomyocyte Excitation–Contraction Coupling

Guías de práctica clínica para el tratamiento de la hipertensión arterial 2007

Association of Pulse Pressure With New-Onset Atrial Fibrillation in Patients With Hypertension and Left Ventricular Hypertrophy

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