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The Advanced HEART FAILURE Patient
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Eran Kalmanovich, Philippe Gaudard, François Roubille
Patients with advanced HF are often unable to tolerate β-blockers at large doses or at all. In the REMATCH trial, 129 patients who were ineligible for heart transplant were randomized to receive a left ventricular assist device (LVAD) (n=68) or optimal medical management (n=61), of which only 22% tolerated β-blockers. In COPERNICUS, although low blood pressure was a risk marker and a frequent reason to withhold β-blockers, the benefit of carvedilol was similar in patients with low and preserved systolic blood pressure prior to treatment.14 The negative chronotropic effect appears to be a key to the positive effects of β-blockers. In the placebo group of the Systolic Heart Failure Treatment with the If Inhibitor Ivabradine Trial (SHIFT), which enrolled patients with HFrEF in NYHA classes II–IV, a heart rate of >86 beats per minute was associated with a two-fold higher incidence of the primary endpoint of cardiovascular death and hospitalization for HF compared to <72 beats per minute; the risk was calculated to be 3% higher for every beat per minute higher baseline heart rate.15 Another analysis suggests that the benefit of β-blockers is directly related not to the dosage, but rather to the degree of heart rate reduction.16 Therefore, it is imperative to initiate β-blockers usage to treat advanced HF as the benefits outweigh the risks.
Trauma Physiology and Metabolism
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Increases in heart rate, termed positively chronotropic effects, are mediated, both directly and indirectly, by the sympathetic division of the autonomic nervous system. Conversely, stimulation of the parasympathetic division via the vagus nerve exerts a negatively chronotropic effect, decreasing the heart rate. Pharmacological inhibition of the sympathetic response, for example, with beta-blockers, will also result in a decreased heart rate.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Inotropic substances are those that alter myocardial contractility. A positive inotrope increases contractility, thereby increasing stroke volume and cardiac output, and a negative inotrope decreases contractility. Many inotropic agents also have chronotropic properties (affecting heart rate) and vasoactive properties and therefore can be somewhat complex to manage. For a summary of inotropic agents and their action, please see Table 6.11.
The current and future status of inotropes in heart failure management
Published in Expert Review of Cardiovascular Therapy, 2023
Angelos Arfaras-Melainis, Ioannis Ventoulis, Effie Polyzogopoulou, Antonios Boultadakis, John Parissis
Epinephrine, an endogenous catecholamine, elicits dose-dependent effects. At lower doses of up to 0.01 μg/kg/min, epinephrine preferentially activates beta-2 peripheral adrenergic receptors, resulting in vasodilation. However, at higher infusion rates of >0.2 μg/kg/min, it preferentially acts on beta-1 and alpha-1 receptors, with a subsequent net positive inotropic and vasoconstrictive effect. It is noteworthy that its vasoconstrictive effect is not only limited to the arterial periphery, but interestingly it is also exerted on the pulmonary arterial and venous vasculature as well [8,39]. As mentioned, epinephrine has significant inotropic, chronotropic and vasoconstrictive properties. However, its clinical use has been limited primarily to cases of cardiac arrest. Levy et al. in 2011 compared the use of epinephrine with a regimen which included the combination of norepinephrine and dobutamine in patients with cardiogenic shock. The study revealed that, while the two treatment strategies produced comparable hemodynamic results, the epinephrine group had significantly higher rates of lacticaemia with acidosis, tachyarrhythmias and gastric mucosal hypoperfusion [45]. To further corroborate these findings, the CardShock study, investigating trends and outcomes in the use of pressors and inotropes, found that the use of epinephrine was independently associated with worse mortality at 90 days and also with renal and cardiac impairment [46].
Epicardial adipose tissue, obesity, and the occurrence of atrial fibrillation: an overview of pathophysiology and treatment methods
Published in Expert Review of Cardiovascular Therapy, 2022
Juan Pablo Scarano Pereira, Eloise Owen, Alessandro Martinino, Kiran Akmal, Mohamed Abouelazayem, Yitka Graham, Sylvia Weiner, Nasser Sakran, Lukas R. Dekker, Chetan Parmar, Sjaak Pouwels
Rate-control therapies for managing AF aim to prevent tachyarrhythmia-related cardiac injury, worsening ventricular function, and the improvement of patient symptoms [83,86]. Adequate rate-control in AF is defined as maintaining a ventricular rate of 60–80 beats per minute at rest and 90–115 beats per min during exercise [87]. Pharmacological therapies aim to achieve a negative chronotropic effect by depressing atrioventricular node conduction lowering the ventricular rate [88]. Rate-control therapies include beta-blockers, non-dihydropyridine calcium channel antagonists, and cardiac glycosides medications, which have been found to be highly effective and non-inferior to other AF therapies [83,89]. The AFFIRM study reported that 85% of patients had maintained sinus rhythm after 5 years of rate-control therapy [90]. The RACE (Race Control Efficacy in Permanent Atrial Fibrillation) study was a prominent randomized controlled trial, which showed that rate-control was as effective as rhythm-control therapies and was associated with fewer hospitalizations [91].
Heart rate response and chronotropic incompetence during cardiopulmonary exercise testing in childhood acute lymphoblastic leukemia survivors
Published in Pediatric Hematology and Oncology, 2021
Émilie Bertrand, Maxime Caru, Valérie Lemay, Gregor Andelfinger, Caroline Laverdiere, Maja Krajinovic, Daniel Sinnett, Daniel Curnier
Chronotropic incompetence (CI) is defined as the HR’s inability to increase during and at the peak of a cardiopulmonary exercise test (CPET).19 The manifestation of CI is a predictor of mortality in cardiac20 and healthy populations.21 Recently, CI was associated with exercise intolerance in adult survivors of childhood cancer,22 while one third had a cardiac autonomic dysfunction associated with a lower exercise capacity.23 Further investigations of CI are necessary to better understand long-term treatment-related cardiac complications in childhood ALL survivors. In this sense, cardiopulmonary exercise testing focusing on analyses of CI could provide early information about treatment’s negative cardiac effects. Toward this goal, the first aim of this study was to examine survivors’ HR response during a maximal CPET, while the second aim was to identify survivors with CI.