Device-based Therapies Research Articles

Occipital neurostimulation in primary headaches: update

A subset of headache patients are chronic and results refractory to standard medical treatments, they are unsatisfied or unable to tolerate the side effects of medications. In the lack of more effective prophylactic treatment, there is need of alternative approach. Migraine is conceptualized as a chronic and potentially progressive disorder. It is conceivable that more aggressive therapeutic efforts could be warranted in drug-refractory chronic migraine. In this prospective, the new, device-based therapies that allow to affect brain function in less invasive ways may represent a therapeutic opportunity. Peripheral occipital neurostimulation resulted in several trials and case reports to be beneficial in a large variety of headache and craniofacial pain disorders, with chronic primary headache the most studied. We comment on our experience in the application of ONS in drug-refractory chronic cluster headache and chronic migraine patients.

Cardiac contractility modulation in patients with advanced heart failure

Cardiac contractility modulation (CCM) is a novel device-based therapy for heart failure that involves applying electrical signals during the absolute refractory period of the myocardial action potential. This therapy has been shown to augment the strength of left ventricular contraction independent of myocardial oxygen consumption in animal models as well as human studies of patients with heart failure and reduced ejection fractions. The mechanism underlying CCM is an alteration of myocardial calcium handling in a fashion that extends beyond the traditional pharmacological effects of inotropic agents. Analysis of myocardial tissue from both animal models and human hearts treated by CCM demonstrates a shift of abnormally expressed genes towards normal function, positively affecting pathways involving proteins that regulate calcium cycling and myocardial contraction. CCM effects are proven to be independent of QRS duration; however, clinical studies to date have primarily focused on patients with normal QRS since cardiac resynchronization therapy is a well-established option for patients with heart failure and a prolonged QRS duration. Clinical trials show that CCM improves exercise tolerance, as measured by VO2,peak and quality of life, assessed by the Minnesota Living with Heart Failure Questionnaire. The device is currently available for the treatment of heart failure in Europe. Approval in the USA is pending additional testing currently underway using a protocol approved by the US FDA.

The human frontal lobes and frontal network systems: an evolutionary, clinical, and treatment perspective.

Frontal lobe syndromes, better termed as frontal network systems, are relatively unique in that they may manifest from almost any brain region, due to their widespread connectivity. The understandings of the manifold expressions seen clinically are helped by considering evolutionary origins, the contribution of the state-dependent ascending monoaminergic neurotransmitter systems, and cerebral connectivity. Hence, the so-called networktopathies may be a better term for the syndromes encountered clinically. An increasing array of metric tests are becoming available that complement that long standing history of qualitative bedside assessments pioneered by Alexander Luria, for example. An understanding of the vast panoply of frontal systems' syndromes has been pivotal in understanding and diagnosing the most common dementia syndrome under the age of 60, for example, frontotemporal lobe degeneration. New treatment options are also progressively becoming available, with recent evidence of dopaminergic augmentation, for example, being helpful in traumatic brain injury. The latter include not only psychopharmacological options but also device-based therapies including mirror visual feedback therapy.

The role of vitamin D in chronic heart failure

Despite advanced medical and device-based therapies, congestive heart failure (CHF) remains a major medical problem, associated with significant morbidity and mortality. Vitamin D deficiency is prevalent in CHF and is associated with poor outcomes. In this manuscript we review the evidence linking vitamin D deficiency and CHF and discuss potential mechanisms involved, as well the clinical data on vitamin D supplementation in CHF patients. A clear relationship has been established between Vitamin D deficiency and increased mortality and morbidity in CHF. However, the mechanism involved is not clearly understood. Recent clinical and experimental evidence have identified the renin-angiotensin-aldosterone system and inflammatory cytokines as likely mediators that can lead to poor clinical outcomes via the cardiorenal syndrome. Clinical data on vitamin D supplementation also remain unestablished, with potential clinical benefits recently reported in patients with vitamin D deficiency. Nonetheless, large-scale randomized clinical trials are lacking. Vitamin D is an emerging agent with tremendous potential and may represent a novel target for therapy in CHF. Further studies are needed to identify the mechanism(s) involved in the pathophysiology as well as to adequately examine the role of Vitamin D measurement and supplementation in patients with CHF.

Device-based Therapies for Resistant Hypertension

Hypertension is universally considered the most detrimental among cardiovascular risk factors. Despite the overwhelming evidence of benefits deriving from lowering blood pressure, its control among the hypertensive population is still unsatisfactory. Resistant hypertension has a non negligible prevalence among hypertensive patients, and it is associated with a worse cardiovascular prognosis. There is need of new therapeutic approaches for reducing cardiovascular risk in this population. Sympathetic nervous system is known to play a major role in development and maintenance of essential hypertension, thus in the past decades several efforts have been made to counteract its overactivation. Novel non-pharmacological, promising approaches targeting sympathetic nervous system are now available, such as renal denervation and baroceptor-activating therapy. This review is aimed at describing essential clinical aspects of resistant hypertension, physiopatological basis of autonomic modulation as a target for hypertension treatment, and the available clinical evidence about efficacy and safety of device-based therapies for resistant hypertension. Present limitations and future perspectives were also considered.

Device-based therapies for onychomycosis

Device-based therapies for onychomycosis

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Diabetes mellitus is associated with adverse prognosis in chronic heart failure of ischaemic and non-ischaemic aetiology.

It is unclear whether diabetes mellitus (DM) is an adverse prognostic factor in chronic heart failure (CHF) of ischaemic and non-ischaemic aetiology managed with contemporary evidence-based care. In total, 1091 outpatients with CHF with reduced ejection fraction were prospectively observed for a mean of 960 days. Total and cardiovascular mortality was quantified after accounting for potential confounders. In total, 25.7% of patients had DM; this group was more likely to have CHF of ischaemic aetiology and was more symptomatic. Patients with DM received comparable medical- and device-based therapies, except for greater doses of loop diuretic. DM was associated with approximately doubled crude and adjusted risk of total and cardiovascular mortality. The association of diabetes with these outcomes in patients with ischaemic and non-ischaemic cardiomyopathies was of similar magnitude. In spite of advances in the management of CHF, DM remains a major adverse prognostic feature, irrespective of ischaemic/non-ischaemic aetiology.

Correction

HomeCirculationVol. 127, No. 3Correction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection Originally published22 Jan 2013https://doi.org/10.1161/CIR.0b013e318283168fCirculation. 2013;127:e357–e359This article corrects the following2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm AbnormalitiesIn the article by Tracy et al, “2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society,” which published ahead of print on September 10, 2012, and appeared in the October 2, 2012, issue of the journal (Circulation. 2012;126:1784-1800), several corrections were needed.On page 1784, the Heart Rhythm Society was a full partner on the guideline and should be added to the subtitle. The complete title of the document read, “2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.” It has been changed to read, “2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society.”On page 1784, in the footnotes, fourth paragraph, the complete title of the document read, “2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.” It has been changed to read, “2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society.”On page 1787, section 1.1, first paragraph, the fourth line read, “ . . .data reported through January 2012,. . . .” It has been changed to read, “ . . .data reported through February 2012,. . . .”On page 1789, in Table 2, for Class IIa, recommendation 4, in the “Comments” column, the comment read, “ . . .need for pacing rather than NYHA class); class changed. . . .” It has been changed to read “ . . .need for pacing rather than NYHA class; class changed. . . .”On page 1790, in the second column, the second complete paragraph, the third sentence read, “ . . .5,356 patients.43” It has been changed to read, “ . . .5,356 patients.43a”On page 1790, in the second column, the second complete paragraph, the 10th sentence read, “ . . .statistically significant (P=0.0001).43” It has been changed to read, “ . . . statistically significant (P=0.0001).43a”On page 1795, a new reference (reference 43a) has been added. It reads, “43a. Sipahi I, Chou JC, Hyden M, et al. Effect of QRS morphology on clinical event reduction with cardiac resynchronization therapy: meta-analysis of randomized controlled trials. Am Heart J. 2012;163:260–7.”On page 1800, “Appendix 3. Indications for CRT Therapy—Algorithm” required clarification and improved consistency with the approved recommendations. It has been replaced in its entirety. The original algorithm appeared as:The revised algorithm, as shown below, appears in the current online version of the article.These corrections have been made to the current online version of the article, which is available at http://circ.ahajournals.org/content/126/14/1784.full.pdf.Download figureDownload PowerPointDownload figureDownload PowerPoint Previous Back to top Next FiguresReferencesRelatedDetailsCited By Itoh M, Yoshida A, Fukuzawa K, Kiuchi K, Imamura K, Fujiwara R, Suzuki A, Nakanishi T, Yamashita S, Matsumoto A and Hirata K (2013) Time-dependent effect of cardiac resynchronization therapy on ventricular repolarization and ventricular arrhythmias, Europace, 10.1093/europace/eut145, 15:12, (1798-1804), Online publication date: 1-Dec-2013. Related articles2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm AbnormalitiesCynthia M. Tracy, et al. Circulation. 2012;126:1784-1800 January 22, 2013Vol 127, Issue 3 Advertisement Article InformationMetrics © 2013 American Heart Association, Inc.https://doi.org/10.1161/CIR.0b013e318283168f Originally publishedJanuary 22, 2013 PDF download Advertisement SubjectsEthics and Policy

2012 ACCF/AHA/HRS Focused Update Incorporated Into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities

Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons Andrew E. Epstein, MD, FACC, FAHA, FHRS, Chair ; John P. DiMarco, MD, PhD, FACC, FHRS; Kenneth A. Ellenbogen. MD, FACC, FAHA, FHRS; N.A. Mark Estes III, MD, FACC, FAHA, FHRS; Roger A.

Resistant Hypertension: A Comprehensive Overview

Hypertension is a common, undertreated disease and a major risk factor for cardiovascular, cerebrovascular and renal disease. As many as 20-30% of hypertensive patients have resistant hypertension, defined as uncontrolled blood pressure despite 3 or more antihypertensive drugs including a diuretic, typically combined with a calcium-channel blocker and an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. Patients with resistant hypertension can often be controlled by adding a mineralocorticoid receptor antagonist and/or vasodilating beta-blocker. A significant number of patients will have a treatable secondary cause of resistant hypertension such as obesity, sleep apnea, renal insufficiency, primary aldosteronism or renal artery stenosis. For patients whose hypertension is refractory to preferred antihypertensives, use of third-line antihypertensives such as sympatholytics or vasodilators may be effective but consideration should be given to investigational device-based antihypertensive therapies. Renal artery angioplasty/ stenting can be useful in selected cases of renal artery stenosis, while renal sympathetic denervation holds promise for resistant essential hypertension.

2012 ACCF/AHA/HRS Focused Update Incorporated Into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities

Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons Andrew E. Epstein, MD, FACC, FAHA, FHRS, Chair ; John P. DiMarco, MD, PhD, FACC, FHRS; Kenneth A. Ellenbogen. MD, FACC, FAHA, FHRS; N.A. Mark Estes III, MD, FACC, FAHA, FHRS; Roger A.

Medical devices for the treatment of onychomycosis

Device-based therapies are the most rapidly expanding area of onychomycosis treatment. Traditional pharmacotherapy of onychomycosis has a low to moderate efficacy and is associated with adverse reactions and drug interactions that limit its use in many patients. These new therapies include laser systems, photodynamic therapy, iontophoresis, and ultrasound. Device-based therapies are procedures conducted in the clinic by a trained professional, which mitigates the requirement for long-term patient compliance. In addition, the drug component of these therapies is topical, preventing the adverse events associated with systemic antifungal administration, and potentially allowing for the treatment of individuals who were previously excluded due to drug interactions. Device-based therapy is a nascent field, so clinical data is still in an emergent stage; however, preliminary clinical trials of laser, photodynamic therapy, and iontophoresis suggest that some devices may have a degree of efficacy. More studies are required to better determine their ability to treat onychomycosis.

CKD and Sudden Cardiac Death

Multiple studies demonstrate a strong independent association between CKD and cardiovascular events including death, heart failure, and myocardial infarction. This review focuses on recent clinical studies that expand this spectrum of adverse cardiovascular events to include ventricular arrhythmias and sudden cardiac death. In addition, experimental models suggest structural remodeling of the heart and electrophysiologic changes in this population. These processes may explain the increased arrhythmic risk in kidney disease and aid in identifying patients who are at higher risk for sudden cardiac death. Finally, we review here the data to support the use of pharmacologic and device-based therapies for both the primary and secondary prevention of sudden cardiac death.

2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities

Andrew E. Epstein, MD, FACC, FAHA, FHRS, Chair; John P. DiMarco, MD, PhD, FACC, FHRS; Kenneth A. Ellenbogen, MD, FACC, FAHA, FHRS; N.A. Mark Estes III, MD, FACC, FAHA, FHRS; Roger A. Freedman, MD, FACC, FHRS; Leonard S. Gettes, MD, FACC, FAHA; A. Marc Gillinov, MD, FACC, FAHA; Gabriel Gregoratos, MD

2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities

Developed in Collaboration With the American Association for Thoracic Surgery, Heart Failure Society of America, and Society of Thoracic Surgeons

HRS/ACCF Expert Consensus Statement on Pacemaker Device and Mode Selection

The most recent American College of Cardiology Foundation/American Heart Association/Heart Rhythm Society (ACCF/AHA/HRS) guidelines related to pacemaker implantation were published as part of a larger document related to device-based therapy.1 While this document provides some comments on pacemaker mode selection and algorithms to guide selection, it does not provide specific recommendations regarding choices for single- or dual-chamber devices. Over the past 15 years multiple randomized trials have compared a number of cardiovascular outcomes among patients randomized to atrial or dual-chamber pacing vs those randomized to ventricular pacing.

Device Therapy to Modulate the Autonomic Nervous System to Treat Heart Failure

Heart failure is the final common pathway in many forms of heart disease, and is associated with excessive morbidity and mortality. Pathophysiologic alterations in the interaction between the heart and the autonomic nervous system in advanced heart failure have been noted for decades. Over the last decade, great advances have been made in the medical and surgical treatment of heart failure - and some of these modalities target the neuro-cardiac axis. Despite these advances, many patients progress to end-stage heart failure and death. Recently, device-based therapy targeting the neuro-cardiac axis with various forms of neuromodulatory stimuli has been shown to improve heart function in experimental heart failure models. These include spinal cord stimulation, vagal nerve stimulation, and baroreflex modulation. Human trials are now underway to evaluate the safety and efficacy of these device-based neuromodulatory modalities in the heart failure population.

Lowering of blood pressure by chronic suppression of central sympathetic outflow: insight from prolonged baroreflex activation

Device-based therapy for resistant hypertension by electrical activation of the carotid baroreflex is currently undergoing active clinical investigation, and initial findings from clinical trials have been published. The purpose of this mini-review is to summarize the experimental studies that have provided a conceptual understanding of the mechanisms that account for the long-term lowering of arterial pressure with baroreflex activation. The well established mechanisms mediating the role of the baroreflex in short-term regulation of arterial pressure by rapid changes in peripheral resistance and cardiac function are often extended to long-term pressure control, and the more sluggish actions of the baroreflex on renal excretory function are often not taken into consideration. However, because clinical, experimental, and theoretical evidence indicates that the kidneys play a dominant role in long-term control of arterial pressure, this review focuses on the mechanisms that link baroreflex-mediated reductions in central sympathetic outflow with increases in renal excretory function that lead to sustained reductions in arterial pressure.

Electromagnetic depression treatment nears approval

Deep transcranial magnetic stimulation adds to psychiatry's arsenal of electronic remedies — A new type of brain stimulation device for combating difficult-to-treat cases of major depressive disorder is likely to break into the large American market soon. Its maker, Jerusalem-based Brainsway, plans to apply to the U.S. Food and Drug Administration for permission to market the device this month. The move follows initial results from a large-scale trial of the system, in which 30.4 percent of treated patients went into remission and 36.7 percent showed significant improvement. Research into devicebased treatments for psychiatric problems has grown rapidly, and if the FDA gives its go-ahead, Brainsway's system will become the fourth device-based therapy to go on the market since 2005.