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doi: 10.1007/s11906-010-0103-9pmid: 20424954
Production of considerable amounts of reactive oxygen species (ROS) eventually leads to oxidative stress. A key role of oxidative stress is evident in the pathologic mechanisms of endothelial dysfunction and associated cardiovascular diseases. Vascular enzymes such as NADPH oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase are involved in the production of ROS. The question remains whether pharmacologic approaches can effectively combat the excessive ROS production in the vasculature. Interestingly, existing registered cardiovascular drugs can directly or indirectly act as antioxidants, thereby preventing the damaging effects of ROS. Moreover, new compounds targeting NADPH oxidases have been developed. Finally, food-derived compounds appear to be effective inhibitors of oxidative stress and preserve vascular function.
Tjugen, Trygve; Flaa, Arnljot; Kjeldsen, Sverre
doi: 10.1007/s11906-010-0104-8pmid: 20431967
Five decades ago, hypertension was a debated risk factor for the development of cardiovascular disease. After further studies and the introduction of antihypertensive medications, few, if any, have doubted the important role hypertension plays as a cardiovascular risk factor. Today, a growing body of evidence emphasizes the relationship between heart rate and hypertension, and heart rate and cardiovascular disease, which makes the measurement of heart rate an important component of the cardiovascular risk assessment. Current European guidelines for managing arterial hypertension recommend the measurement of heart rate for risk stratification, but there still are no recommendations for treatment. This review discusses the evidence for a relationship between heart rate and cardiovascular mortality and morbidity and hypertension.
Xia, Huijing; Lazartigues, Eric
doi: 10.1007/s11906-010-0105-7pmid: 20424953
Angiotensin-converting enzyme 2 (ACE2) is a new component of the renin-angiotensin system (RAS). Accumulating evidence shows that ACE2 provides protective effects in peripheral tissues and has great potential for the treatment of RAS-related diseases. The role of ACE2 in the central nervous system is not well established. However, in recent years, much more progress has been made on the studies of this carboxypeptidase in the central regulation of blood pressure and cardiovascular function in general. It has been shown that brain ACE2 interacts with the other components of the RAS (ACE, angiotensin II, and angiotensin II type 1 receptor), protects baroreflex and autonomic function, stimulates nitric oxide release, reduces oxidative stress, and prevents the development of or attenuates hypertension. These data support the critical role of ACE2 in the central regulation of cardiovascular function. This review summarizes recently published data on the central effects of ACE2 in the regulation of cardiovascular function.
Taylor, Jeremy; Bisognano, John
doi: 10.1007/s11906-010-0106-6pmid: 20424952
Hypertension is a leading cause of morbidity and mortality worldwide. Despite the development of new medications, an alarmingly high proportion of patients are not reaching their target blood pressure goals, so nonpharmacologic therapies have been attracting more interest. Chronic baroreceptor stimulation of the carotid sinus has been shown to reduce blood pressure by inhibiting the sympathetic nervous system, particularly the renal sympathetic tone. This finding has led to the development of implantable carotid sinus stimulators, which have now been studied in both animals and humans, as a means for treating chronic hypertension. The enthusiasm for this modality has led to ongoing studies, which will provide more information on its safety and efficacy in patients with resistant hypertension. The early study results using baroreflex stimulation therapy are promising and suggest that it may play a significant role in controlling blood pressure in the future.
doi: 10.1007/s11906-010-0107-5pmid: 20424951
Cardiovascular disease is still the leading cause of death in North America. To improve outcomes, it will likely be necessary to identify new potentially treatable conditions. Sleep apnea affects approximately 50% of patients with cardiovascular disease and is associated with increased cardiovascular risk. Continuous positive airway pressure is currently the treatment of choice and has many short-term favorable effects. The long-term benefits, however, remain elusive. Further, it may not be the ideal treatment for central sleep apnea, and the benefits of alternatives such adaptive servo-ventilation are currently being tested. Randomized controlled trials are now needed to determine whether treating sleep apnea will improve survival and reduce cardiovascular disease risk. Until better evidence becomes available, testing for sleep apnea cannot be recommended as part of the routine cardiovascular disease risk assessment, nor can its treatment be recommended for the prevention or management of cardiovascular disease in asymptomatic patients.
doi: 10.1007/s11906-010-0112-8pmid: 20424946
Obstructive sleep apnea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure. However, these studies do indicate a wide variation in the blood pressure effects of CPAP, with some patients, on an individual basis, manifesting a large antihypertensive benefit. OSA is particularly common in patients with resistant hypertension. The reason for this high prevalence of OSA is not fully explained, but data from our laboratory suggest that it may be related to the high occurrence of hyperaldosteronism in patients with resistant hypertension. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid in the neck, which then contributes to increased upper airway resistance.
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