ABSTRACT
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.
Subject(s)
Baroreflex/physiology , Hypertension/therapy , Animals , Clinical Trials as Topic , Drug Resistance, Neoplasm , Follow-Up Studies , Humans , Hypertension/physiopathology , Sympathetic Nervous System/physiologySubject(s)
Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antihypertensive Agents/therapeutic use , Isoquinolines/therapeutic use , Prodrugs , Ramipril/therapeutic use , Tetrahydroisoquinolines , Captopril/therapeutic use , Cardiovascular Diseases/complications , Cardiovascular Diseases/drug therapy , Clinical Trials as Topic , Enalapril/therapeutic use , Heart Failure/drug therapy , Humans , Indoles/therapeutic use , Myocardial Infarction/prevention & control , Perindopril/therapeutic use , Quinapril , Stroke/prevention & control , Stroke Volume , Treatment Outcome , Ventricular Dysfunction, Left/drug therapyABSTRACT
Despite advances in medical and surgical therapy, heart failure (HF) remains a common and serious problem. An association between HF and sleep-related breathing disorders has been recognized since Cheyne's observations in 1818, but only recently have treatment options targeting sleep-related breathing disorders become available. This overview will consider the clinical features, pathophysiology, and treatment options of sleep-related breathing disorders in patients with HF.
Subject(s)
Heart Failure/complications , Sleep Apnea Syndromes/complications , Cheyne-Stokes Respiration , Heart Failure/physiopathology , Humans , Polysomnography , Sleep Apnea Syndromes/physiopathology , Sleep Apnea Syndromes/therapy , Sleep Apnea, Central/complications , Sleep Apnea, Central/physiopathology , Sleep Apnea, Obstructive/complications , Sleep Apnea, Obstructive/physiopathologyABSTRACT
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 large-scale 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.
