In medically treated patients with heart failure, treatment of coexisting obstructive sleep apnea by continuous positive airway pressure reduces systolic blood pressure and improves left ventricular systolic function. Obstructive sleep apnea may thus have an adverse effect in heart failure that can be addressed by targeted therapy.

Treatment of coexisting OSA by CPAP in HF patients lowers daytime MSNA, systolic BP, and HR. Inhibition of increased central sympathetic vasoconstrictor outflow is one mechanism by which nocturnal CPAP reduces awake BP in HF patients with moderate to severe OSA.

Abstract-Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking. Whether coexisting sleep apnea augments daytime MSNA in HF is unknown. We tested the hypothesis that its presence exerts additive effects on MSNA during wakefulness. Overnight sleep studies and morning MSNA recordings were performed on 60 subjects with ejection fraction Ͻ45%. Of these, 43 had an apnea-hypopnea index Ն15 per hour. Subjects with and subjects without sleep apnea were similar for age, ejection fraction, HF etiology, body mass index, blood pressure, and heart rate.

Background-Activation of the sympathetic nervous system has important prognostic implications in chronic heart failure.Nonselective versus selective ␤-adrenergic receptor antagonists may have differential effects on norepinephrine release from nerve terminals mediated by prejunctional ␤ 2 -adrenergic receptors. Methods and Results-Thirty-six patients with chronic heart failure were randomized to the nonselective ␤-blocker carvedilol or the selective ␤-blocker metoprolol (double-blind). Measurements of hemodynamics and cardiac and systemic norepinephrine spillover as well as microneurographic recordings of muscle sympathetic nerve traffic were made before and after 4 months of therapy. In the carvedilol group (nϭ17), there were significant reductions in both total body (Ϫ1.7Ϯ0.5 nmol/min, PϽ0.01) and cardiac norepinephrine spillover (Ϫ87Ϯ29 pmol/min, PϽ0.01). By contrast, in the metoprolol group (nϭ14), there were no significant changes in total body or cardiac norepinephrine spillover. Responses in the carvedilol group were significantly different from those observed in the metoprolol group (PϽ0.05). Both agents caused a reduction in heart rate and increases in pulse pressure, although mean arterial pressure did not change. Importantly, microneurographic measures of sympathetic nerve traffic to skeletal muscle did not change in either group. Conclusions-Therapy with carvedilol caused significant decreases in systemic and cardiac norepinephrine spillover, an indirect measure of norepinephrine release. Such changes were not observed in patients treated with metoprolol. There was no effect of either agent on sympathetic efferent neuronal discharge to skeletal muscle. These findings suggest that carvedilol, a nonselective ␤-blocker, caused its sympathoinhibitory effect by blocking peripheral, prejunctional ␤-adrenergic receptors. (Circulation. 2001;104:2194-2199.)

In postmenopausal women, acute dynamic exercise elicits sustained increases in FMD that could facilitate post-exercise hypotension in this population. These observations reinforce the concept of exercise as an important non-pharmacological intervention to modify cardiovascular risk in postmenopausal women.

Carvedilol did not increase CVC, blunt the calf vasoconstrictor response to handgrip or attenuate the gain of the neuroeffector transfer function, indicating the absence of functionally important peripheral alpha(1)-adrenoceptor antagonism during long-term treatment of CHF.

How Occupational Health can Contribute in a Disaster and What We should Prepare for the Future—Lessons Learned through Support Activities of a Medical School at the Fukushima Daiichi Nuclear Power Plant in Summer 2011: Koji MORI, et al. Department of Occupational Health Practice and Management, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan— Background A nuclear accident occurred at the Fukushima Daiichi Nuclear Power Plant of Tokyo Electric Power Company (TEPCO) as a result of a mega‐earthquake and tsunami in March, 2011. A large number of workers were engaged in response and recovery operations under a complex structure of involved companies. They were exposed not only to radiation but also to other health hazards. TEPCO implemented programs to prevent radiation exposure, but had no effective systems for managing the other health risks and few occupational health (OH) professionals contributed to the health risk management. Activities: The University of Occupational and Environmental Health (UOEH), Japan, dispatched physicians to a quake‐proof building at the plant to provide first‐aid services from mid‐May, 2011, and took a strategic approach to protecting workers from existing health risks. UOEH presented recommendations on OH systems and preventive measures against heat stress to the Government and TEPCO. The Ministry of Health, Labour, and Welfare issued guidelines to TEPCO and contractors. TEPCO implemented a comprehensive program against heat stress according to the guidelines and in cooperation with UOEH. As a result, we successfully prevented severe heat illness during summer 2011. Discussion From our experiences, we believe that the following recommendations should be considered: 1) the role of OH and the participation of experts should be defined in emergency response plans; 2) regulations should allow the national government and main companies involved to lead safety and health initiatives for all workers at disaster sites; and 3) OH professionals, response manuals and drills should be organized at a national level.

We have documented a pre-junctional h-2 adrenoceptor mediated reduction in cardiac norepinephrine spillover (CNES) in heart failure patients receiving chronic h-blockade. Our present objective was to ascertain the consequence of this decrease for vagal heart rate (HR) regulation by determining CNES, arterial baroreflex sensitivity for HR (BRS) and arterial baroreflex modulation of muscle sympathetic nerve activity (MSNA) before and upon 4 months of h-blockade with either carvedilol or metoprolol. In 19 heart failure patients in sinus rhythm (age: 55F2 [meanFS.E.]; ejection fraction: 20F2%), h-blockade increased BRS from 4.8F0.9 to 7.9F1.3 ms/mm Hg ( Pb0.005) but had no effect on arterial baroreflex modulation of MSNA. Changes in CNES and BRS were inversely related (r=À0.52; n=16, Pb0.05). Chronic hblockade in heart failure augments reflex vagal control of HR at an efferent site of interaction involving blockade of cardiac sympathetic prejunctional h-2 adrenoceptors that facilitate NE release.