Neuromodulation to Treat Patients With Heart Failure With Preserved Ejection Fraction
| Status: | Recruiting |
|---|---|
| Conditions: | Cardiology |
| Therapuetic Areas: | Cardiology / Vascular Diseases |
| Healthy: | No |
| Age Range: | 21 - 90 |
| Updated: | 12/20/2017 |
| Start Date: | December 12, 2017 |
| End Date: | December 31, 2019 |
| Contact: | Kathy Bright, RN, MBA |
| Email: | kathy-wileman-bright@ouhsc.edu |
| Phone: | 405-271-2229 |
Neuromodulation of Inflammation to Treat Heart Failure With Preserved Ejection Fraction
Heart failure with preserved ejection fraction (HFpEF) is a leading cause of mortality in the
elderly. Outcomes of patients with HFpEF are poor and so far, no treatment has been shown to
decrease morbidity or mortality. Recent animal and human studies suggest that a systemic
proinflammatory state, produced by comorbidities, including aging, plays a central role in
the development of HFpEF, supporting the notion that attenuating the proinflammatory state is
an attractive therapeutic target for HFpEF. We have previously shown that low-level
transcutaneous electrical stimulation of the vagus nerve (tVNS) suppresses inflammation in
patients with atrial fibrillation. The overall objective of this proposal is to examine the
effects of tVNS on diastolic dysfunction, exercise capacity and inflammation in patients with
HFpEF. Our specific aims include: 1. To examine the effect of intermittent (1 hour daily for
3 months) tVNS on diastolic dysfunction and exercise capacity, relative to sham stimulation,
in patients with HFpEF and 2. To examine the effect of intermittent (1 hour daily for 3
months) LLTS on inflammatory cytokines relative to sham stimulation, in patients with HFpEF.
The proposed proof-of-concept studies will provide the basis for the design of further human
studies using LLTS among populations with HFpEF. In light of the increasing number of elderly
patients with HFpEF and the poor success of the currently available treatment options, an
alternative and novel approach such as tVNS has the potential to impact clinical practice and
improve health outcomes among a large number of patients. It is anticipated that these
investigations will contribute to the broader understanding of the role of inflammation in
the pathogenesis of HFpEF and how its inhibition can be used to provide therapeutic effects.
Moreover, it is anticipated that a better understanding of how modulation of inflammation
affects one of the hallmarks of HFpEF, diastolic dysfunction, will lead to the development of
novel pharmacological and non-pharmacological approaches to treat this disease.
elderly. Outcomes of patients with HFpEF are poor and so far, no treatment has been shown to
decrease morbidity or mortality. Recent animal and human studies suggest that a systemic
proinflammatory state, produced by comorbidities, including aging, plays a central role in
the development of HFpEF, supporting the notion that attenuating the proinflammatory state is
an attractive therapeutic target for HFpEF. We have previously shown that low-level
transcutaneous electrical stimulation of the vagus nerve (tVNS) suppresses inflammation in
patients with atrial fibrillation. The overall objective of this proposal is to examine the
effects of tVNS on diastolic dysfunction, exercise capacity and inflammation in patients with
HFpEF. Our specific aims include: 1. To examine the effect of intermittent (1 hour daily for
3 months) tVNS on diastolic dysfunction and exercise capacity, relative to sham stimulation,
in patients with HFpEF and 2. To examine the effect of intermittent (1 hour daily for 3
months) LLTS on inflammatory cytokines relative to sham stimulation, in patients with HFpEF.
The proposed proof-of-concept studies will provide the basis for the design of further human
studies using LLTS among populations with HFpEF. In light of the increasing number of elderly
patients with HFpEF and the poor success of the currently available treatment options, an
alternative and novel approach such as tVNS has the potential to impact clinical practice and
improve health outcomes among a large number of patients. It is anticipated that these
investigations will contribute to the broader understanding of the role of inflammation in
the pathogenesis of HFpEF and how its inhibition can be used to provide therapeutic effects.
Moreover, it is anticipated that a better understanding of how modulation of inflammation
affects one of the hallmarks of HFpEF, diastolic dysfunction, will lead to the development of
novel pharmacological and non-pharmacological approaches to treat this disease.
Inclusion Criteria:
- HFpEF, defined as signs and symptoms of heart failure, LV ejection fraction ≥50%,
brain natriuretic peptide ≥35pg/mL and echocardiographic evidence of diastolic
dysfunction (left atrial volume index ≥34mL/m2, mitral E-wave velocity/mitral annular
velocity ratio [E/e']≥13 and e'<9cm/s) plus 2 of the following 4 comorbidities:
- age ≥ 65,
- diabetes,
- hypertension and
- obesity, defined as body mass index ≥30kg/m2
Exclusion Criteria:
- LV ejection fraction <40%
- significant valvular disorder (i.e., prosthetic valve or hemodynamically significant
valvular diseases)
- recent (<6 months) stroke, myocardial infarction or hospitalization for heart failure
- severe heart failure (class III or IV)
- end stage kidney disease
- recurrent vasovagal syncope
- history of vagotomy
- pregnancy
- sick sinus syndrome and 2nd or 3rd degree AV block (without a pacemaker).
We found this trial at
1
site
940 NE 13th St
Oklahoma City, Oklahoma 73190
Oklahoma City, Oklahoma 73190
(405) 271-6458
Principal Investigator: Stavros Stavrakis, MD, PhD
Phone: 405-271-2229
University of Oklahoma Health Sciences Center The OU Health Sciences Center is composed of seven...
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