2020
DOI: 10.1007/s10741-020-10029-x
|View full text |Cite
|
Sign up to set email alerts
|

Hemodynamic effects of ivabradine use in combination with intravenous inotropic therapy in advanced heart failure

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
9
0

Year Published

2021
2021
2024
2024

Publication Types

Select...
7

Relationship

0
7

Authors

Journals

citations
Cited by 10 publications
(10 citation statements)
references
References 57 publications
1
9
0
Order By: Relevance
“…Chiu MH et al presented a case series of five patients with cardiogenic shock started on ivabradine who were unable to tolerate beta-blockers and using inotropic support. At 24h after initiation, they observed a reduction in HR (106±6.8 to 91.6±6.4 b.p.m., P = 0.04), and observed an increase in SvO2 (51±9 to 65±5%, P < 0.04), SV (37±8 to 49±13 mL, P < 0.04) [13], which supports the hypothesis that adding ivabradine, a rate control agent without negative inotropic effect, may blunt inotrope-induced tachycardia and its associated deleterious effects, while optimizing cardiac output by increasing SV [7]. However, the effects have not been reported in more severe patients, and the present case had lower cardiac output and lower SV compared with past studies.…”
Section: Discussionsupporting
confidence: 73%
See 1 more Smart Citation
“…Chiu MH et al presented a case series of five patients with cardiogenic shock started on ivabradine who were unable to tolerate beta-blockers and using inotropic support. At 24h after initiation, they observed a reduction in HR (106±6.8 to 91.6±6.4 b.p.m., P = 0.04), and observed an increase in SvO2 (51±9 to 65±5%, P < 0.04), SV (37±8 to 49±13 mL, P < 0.04) [13], which supports the hypothesis that adding ivabradine, a rate control agent without negative inotropic effect, may blunt inotrope-induced tachycardia and its associated deleterious effects, while optimizing cardiac output by increasing SV [7]. However, the effects have not been reported in more severe patients, and the present case had lower cardiac output and lower SV compared with past studies.…”
Section: Discussionsupporting
confidence: 73%
“…Many severe heart failure patients have sinus tachycardia as a compensatory mechanism to maintain cardiac output. However, excessive sinus tachycardia, especially caused by intravenous inotropes, can increase myocardial oxygen consumption, decrease coronary perfusion, decrease ventricular filling and SV [7]. Increased heart rate is a risk of worsening heart failure in patients with sinus rhythm [8][9][10].…”
Section: Discussionmentioning
confidence: 99%
“…28,56 Third, excessive chronotropy in the setting of RV systolic dysfunction will promote an impaired force-frequency relationship, 57 increased myocardial oxygen demand, 58 and compromised coronary artery perfusion further exacerbating the impairment in heart function. 59,60 Finally, augmentation of LV afterload in the setting of decreased left heart preload due to poor pulmonary venous return and ventricular interaction will further compromise systemic blood flow. 14,61 The adoption of certain pharmacologic treatments as a standard of care in neonatology, despite almost universal lack of benefit, is not unique to dopamine use.…”
Section: Physiology-based Therapeutic Framework For Aphmentioning
confidence: 99%
“…Based on these data and international society guidelines, we recommend the use of β-blockers in all patients with AdvHF, with a preference for those with more mi-nor hypotensive effects (bisoprolol and sustained-release metoprolol), starting with low doses (bisoprolol 1.25 mg or metoprolol succinate 12.5 mg) and cautious and slow up-titration (50% increase every 2-4 weeks). In patients with AdvHF in whom β-blockers are not tolerated or for whom heart rate (in sinus rhythm) remains over 70 beats per minute on maximum-tolerated β-blockers, ivabradine should be considered [33].…”
Section: β-Blockersmentioning
confidence: 99%