Renal Denervation and Atrial Fibrillation (page 172)
Obstructive sleep apnea (OSA) causes combined sympathovagal activation potentially leading to hypertension and increased susceptibility to atrial fibrillation. Modulation of sympathetic activity by renal denervation (RDN) reduces sympathetic activity, and high blood pressure, apnea-hypopnea index (OSA severity) and improves glucose metabolism in resistant hypertension. Whether RDN displays antiarrhythmic effects or attenuates postapneic hemodynamic changes in OSA is unknown. In a pig model for OSA, RDN but not atenolol reduced OSA-induced atrial fibrillation inducibility (20% versus 100% at baseline; P=0.0001) by attenuating OSA-induced shortening of atrial refractoriness. Administration of atropine after RDN or atenolol completely inhibited OSA-induced atrial electrophysiological changes. This antiarrhythmic effect of RDN was not mediated by changes in sensitivity of the intrinsic cardiac autonomic system. In addition, the postapneic blood pressure rise was inhibited by RDN and not modified by atenolol. Apart from the described antiarrhythmic electrophysiological effects of RDN, RDN might be able to attenuate the development of an atrial proarrhythmic structural substrate by inhibiting postapneic blood pressure surges, as shown in this study. Modulation of the autonomic nervous system by RDN might be useful to reduce atrial arrhythmogenesis and hypertension in OSA but needs to be tested in clinical studies before these experimental findings can be implemented into clinical practice.
Arterial Load and Myocardial Wall Stress (page 64)
Myocardial wall stress (MWS) is a primary determinant of myocardial oxygen consumption and a key stimulus for myocardial hypertrophy and fibrosis. We assessed the influence of sex and arterial properties on time-resolved systolic MWS among 1214 middle-aged adults. We found that, for any given end-diastolic left ventricular geometry and output, peak MWS (an early systolic phenomenon) is determined by systemic vascular resistance (which depends on the microvasculature) and proximal aortic characteristic impedance (which depends on ascending aortic diameter and wall stiffness). The area under the MWS curve during ejection was determined by systemic vascular resistance, total arterial compliance, and wave reflection timing, whereas end-systolic MWS was determined by systemic vascular resistance and wave reflection magnitude. Our study demonstrates the importance of the microvasculature and the aortic root as determinants of peak MWS and confirms the importance of wave reflections as determinants of late systolic load and, therefore, the loading sequence. It confirms the relatively low levels of late systolic MWS in the presence of a normal ejection fraction. These support the idea that wave reflections are important determinants of left ventricular hypertrophy and dysfunction and that the loading sequence may be more important than absolute MWS levels.
For any given end-diastolic geometry, cardiac output, and arterial hemodynamic function, women demonstrated a higher MWS, suggesting a less efficient myocardial-arterial coupling in women, which may be related to the differential susceptibility of women to heart failure.
Hypertension in Aortic Stenosis (page 90)
Hypertension in patients with aortic valve stenosis may influence assessment of stenosis severity, as well as left ventricular structure. The present prospective study evaluated in 1616 patients with initially asymptomatic aortic stenosis who were randomized to double-blind, placebo-controlled combination treatment with simvastatin and ezetimibe followed by annual echocardiography in the Simvastatin Ezetimibe in Aortic Stenosis Study the impact of hypertension on clinical outcome and change in left ventricular structure during progression of aortic valve stenosis. The primary study end point included combined cardiovascular death, aortic valve events, and ischemic cardiovascular events. Aortic stenosis progression rate did not differ between hypertensive and normotensive subjects. During an average of 4.3 years of follow-up, the prevalence of concentric left ventricular hypertrophy increased 3 times in both groups. However, the presence of hypertension was associated with a 51% higher incidence of abnormal left ventricular geometry. Furthermore, hypertension was associated with a higher rate of ischemic cardiovascular events and 2-fold increased mortality, independent of aortic stenosis severity, abnormal left ventricular geometry, in-treatment systolic blood pressure, and study treatment allocation.
- © 2012 American Heart Association, Inc.