- Email: [email protected]
Global systolic load, left ventricular hypertrophy, and atrial fibrillation
Global systolic load, left ventricular hypertrophy, and atrial fibrillation
Treatment of global systolic load, left ventricular hypertrophy, and atrial fibrillation We wish to thank Dr Jolobe for his comments and interest in our work. We agree that vascular disease should be considered an important contributor to the global load that is applied on the left ventricle (LV). Indeed, newer estimates of aortic stenosis severity (Zva = systolic blood pressure + [mean aortic gradient/stroke volume]) try to account for the composite impact of both vascular and valvular degeneration. 1 Thus, a pharmacological targeting of vascular resistance may be a plausible way by which the sum of these essentially serially coupled resistances could be reduced. However, to the best of our knowledge, there is no randomized trial that tests whether lowering of global LV afterload, or its individual components, reduces newonset atrial fibrillation (AF) in aortic stenosis. Notwithstanding, the hypothesis is credible and indeed there is evidence from hypertensive patients with electrocardiographic left ventricular hypertrophy to support that lowering of LV afterload, in particular central blood pressure, reduces AF. 2 Mechanism may be that lowering of LV afterload reduces LV hypertrophy, resulting in a lower likelihood of new-onset AF. 3 Moreover, reninangiotensin-based antihypertensive treatment as compared to atenolol has been shown to induce a greater reduction in left atrial volume and translate into less AF independent of LV mass. 4 Lowering of central blood pressure, either by renin-angiotensin system inhibitors or aldosterone-blocking agents as epelerone, as suggested by Dr. Jolobe, might be a novel therapeutic target to lower the likelihood of new-onset AF in aortic stenosis and, perhaps, some of the excess morbidity associated with additional AF in these patients.
Am Heart J 2012;164:e13. 0002-8703/$ - see front matter http://dx.doi.org/10.1016/j.ahj.2012.07.017
Casper N. Bang, MD Anders M. Greve, MD Department of Cardiology
The Heart Center Rigshospitalet, Copenhagen, Denmark E-mail: [email protected] Kristian Wachtell, MD, PhD, DMSc Department of Cardiology
The Heart Center Rigshospitalet, Copenhagen, Denmark Department of Cardiology Gentofte University Hospital, Hellerup, Denmark Lars Kober, MD, DMSc Department of Cardiology
The Heart Center Rigshospitalet, Copenhagen, Denmark
References 1. Briand M, Dumesnil JG, Kadem L, et al. Reduced systemic arterial compliance impacts significantly on left ventricular afterload and function in aortic stenosis: implications for diagnosis and treatment. J Am Coll Cardiol 2005;46:291-8. 2. Wachtell K, Lehto M, Gerdts E, et al. Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol: the Losartan Intervention For End Point Reduction in Hypertension (LIFE) study. J Am Coll Cardiol 2005;45:712-9. 3. Okin PM, Wachtell K, Devereux RB, et al. Regression of electrocardiographic left ventricular hypertrophy and decreased incidence of new-onset atrial fibrillation in patients with hypertension. JAMA 2006; 296:1242-8. 4. Wachtell K, Gerdts E, Aurigemma GP, et al. In-treatment reduced left atrial diameter during antihypertensive treatment is associated with reduced new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy: the LIFE Study. Blood Press 2010;19:169-75.
Treatment of global systolic load, left ventricular hypertrophy, and atrial fibrillation We wish to thank Dr Jolobe for his comments and interest in our work. We agree that vascular disease should be considered an important contributor to the global load that is applied on the left ventricle (LV). Indeed, newer estimates of aortic stenosis severity (Zva = systolic blood pressure + [mean aortic gradient/stroke volume]) try to account for the composite impact of both vascular and valvular degeneration. 1 Thus, a pharmacological targeting of vascular resistance may be a plausible way by which the sum of these essentially serially coupled resistances could be reduced. However, to the best of our knowledge, there is no randomized trial that tests whether lowering of global LV afterload, or its individual components, reduces newonset atrial fibrillation (AF) in aortic stenosis. Notwithstanding, the hypothesis is credible and indeed there is evidence from hypertensive patients with electrocardiographic left ventricular hypertrophy to support that lowering of LV afterload, in particular central blood pressure, reduces AF. 2 Mechanism may be that lowering of LV afterload reduces LV hypertrophy, resulting in a lower likelihood of new-onset AF. 3 Moreover, reninangiotensin-based antihypertensive treatment as compared to atenolol has been shown to induce a greater reduction in left atrial volume and translate into less AF independent of LV mass. 4 Lowering of central blood pressure, either by renin-angiotensin system inhibitors or aldosterone-blocking agents as epelerone, as suggested by Dr. Jolobe, might be a novel therapeutic target to lower the likelihood of new-onset AF in aortic stenosis and, perhaps, some of the excess morbidity associated with additional AF in these patients.
Am Heart J 2012;164:e13. 0002-8703/$ - see front matter http://dx.doi.org/10.1016/j.ahj.2012.07.017
Casper N. Bang, MD Anders M. Greve, MD Department of Cardiology
The Heart Center Rigshospitalet, Copenhagen, Denmark E-mail: [email protected] Kristian Wachtell, MD, PhD, DMSc Department of Cardiology
The Heart Center Rigshospitalet, Copenhagen, Denmark Department of Cardiology Gentofte University Hospital, Hellerup, Denmark Lars Kober, MD, DMSc Department of Cardiology
The Heart Center Rigshospitalet, Copenhagen, Denmark
References 1. Briand M, Dumesnil JG, Kadem L, et al. Reduced systemic arterial compliance impacts significantly on left ventricular afterload and function in aortic stenosis: implications for diagnosis and treatment. J Am Coll Cardiol 2005;46:291-8. 2. Wachtell K, Lehto M, Gerdts E, et al. Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol: the Losartan Intervention For End Point Reduction in Hypertension (LIFE) study. J Am Coll Cardiol 2005;45:712-9. 3. Okin PM, Wachtell K, Devereux RB, et al. Regression of electrocardiographic left ventricular hypertrophy and decreased incidence of new-onset atrial fibrillation in patients with hypertension. JAMA 2006; 296:1242-8. 4. Wachtell K, Gerdts E, Aurigemma GP, et al. In-treatment reduced left atrial diameter during antihypertensive treatment is associated with reduced new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy: the LIFE Study. Blood Press 2010;19:169-75.