The sympathetic nervous system is an effective homeostatic mechanism for modulating hemodynamics in times of stress and illness. Unfortunately, in some patients, this mechanism escapes physiologic control and through various mechanisms leads to resistant hypertension. Antihypertensive drug therapy is successful only to a point, leaving a significant percentage of patients nationwide with blood pressure measurements above guidelines despite being treated with at least three agents at maximally tolerated doses, consistent with a diagnosis of resistant hypertension. Novel methods of modifying the activity of the sympathetic nervous system have been studied in animals, and this review discusses the data in support of one of the techniques at the forefront of non-pharmacologic blood pressure therapy.

Hypertension is a complex syndrome that increases the risk of developing other medical comorbidities and interacts with other medical conditions to increase the risk of target end-organ damage such as cardiovascular disease, stroke, and renal disease. Hypertension remains under-recognized and poorly controlled in the USA and worldwide. In some patients, hypertension is resistant to optimal medical therapy. Over the last few decades, there has been an increasing understanding of the role of the sympathetic nervous system in the development and maintenance of hypertension. This update reviews the physiology and role of the sympathetic nervous system in hypertension and pharmacological and interventional treatments directed at nervous system involvement in secondary hypertension.

Hypertension (HTN) is a worldwide epidemic. When untreated, HTN places patients at an elevated risk for several health conditions, including cardiovascular disease and end-organ damage. This effect is particularly pronounced in a subset of patients who experience treatment-resistant HTN despite the utilization of conventional medication and lifestyle interventions. For these challenging patients, ongoing research efforts continue to explore and develop novel nonpharmacologic therapies for resistant HTN. One such avenue is the regulation of the sympathetic nervous system, a large component of circulatory physiology. Innovative therapies have evolved to harness the ability to deliver electrical stimulation to baroreceptors in an effort to modulate the sympathetic system involvement in HTN. This review discusses baroreflex activation therapy and its role in the management of resistant HTN.

Summary: Therapy for acute myocardial infarction has advanced dramatically since the early 1980s with the use of early intravenous fibrinolytic therapy. Combining low-dose fibrinolysis and platelet lysis appears to provide an additional increase in infarct-related artery (IRA) patency, but the largescale mortality reduction trials evaluating this strategy are just getting under way. Recently, considerable attention has shifted away from the epicardial arteries to the microvasculature. Contemporary evidence suggests that epicardial patency does not necessarily translate to actual perfusion at the myocardial level. Techniques to evaluate beyond thrombolysis in myocardial infarction (TIMI) epicardial flow are now available and validated. In addition, there are promising treatments for the prevention or alleviation of certain forms of microvascular obstruction. This review attempts to clarify the confusion surrounding epicardial flow and "myocardial malperfusion" and to provide some insight into the next direction in acute myocardial infarction therapeutics.