scholarly journals Vasoresponsiveness in patients with heart failure (VASOR): protocol for a prospective observational study

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Marieke E. van Vessem ◽  
Saskia L. M. A. Beeres ◽  
Rob B. P. de Wilde ◽  
René de Vries ◽  
Remco R. Berendsen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Observational Study ◽  
Vascular Reactivity ◽  
Prospective Observational Study ◽  
Ex Vivo ◽  
Phase 1 ◽  
Resistance Arteries ◽  
Patients With Heart Failure

Abstract Background Vasoplegia is a severe complication which may occur after cardiac surgery, particularly in patients with heart failure. It is a result of activation of vasodilator pathways, inactivation of vasoconstrictor pathways and the resistance to vasopressors. However, the precise etiology remains unclear. The aim of the Vasoresponsiveness in patients with heart failure (VASOR) study is to objectify and characterize the altered vasoresponsiveness in patients with heart failure, before, during and after heart failure surgery and to identify the etiological factors involved. Methods This is a prospective, observational study conducted at Leiden University Medical Center. Patients with and patients without heart failure undergoing cardiac surgery on cardiopulmonary bypass are enrolled. The study is divided in two inclusion phases. During phase 1, 18 patients with and 18 patients without heart failure are enrolled. The vascular reactivity in response to a vasoconstrictor (phenylephrine) and a vasodilator (nitroglycerin) is assessed in vivo on different timepoints. The response to phenylephrine is assessed on t1 (before induction), t2 (before induction, after start of cardiotropic drugs and/or vasopressors), t3 (after induction), t4 (15 min after cessation of cardiopulmonary bypass) and t5 (1 day post-operatively). The response to nitroglycerin is assessed on t1 and t5. Furthermore, a sample of pre-pericardial fat tissue, containing resistance arteries, is collected intraoperatively. The ex vivo vascular reactivity is assessed by constructing concentrations response curves to various vasoactive substances using isolated resistance arteries. Next, expression of signaling proteins and receptors is assessed using immunohistochemistry and mRNA analysis. Furthermore, the groups are compared with respect to levels of organic compounds that can influence the cardiovascular system (e.g. copeptin, (nor)epinephrine, ANP, BNP, NTproBNP, angiotensin II, cortisol, aldosterone, renin and VMA levels). During inclusion phase 2, only the ex vivo vascular reactivity test is performed in patients with (N = 12) and without heart failure (N = 12). Discussion Understanding the difference in vascular responsiveness between patients with and without heart failure in detail, might yield therapeutic options or development of preventive strategies for vasoplegia, leading to safer surgical interventions and improvement in outcome. Trial registration The Netherlands Trial Register (NTR), NTR5647. Registered 26 January 2016.

Effect of testosterone on ex vivo vascular reactivity in man

2006 ◽  
Vol 111 (4) ◽  
pp. 265-274 ◽  
Author(s):  
Christopher J. Malkin ◽  
Richard D. Jones ◽  
T. Hugh Jones ◽  
Kevin S. Channer
Keyword(s):  
Heart Failure ◽  
Vascular Reactivity ◽  
Ex Vivo ◽  
Testosterone Replacement ◽  
Androgen Deficiency ◽  
Resistance Arteries ◽  
Patients With Heart Failure ◽  
Dose Dependent ◽  
Concentration Curves

Testosterone is reported to have an acute vasodilating action in vitro, an effect that may impart a favourable haemodynamic response in patients with chronic heart failure. However, the effect of chronic testosterone exposure on general vascular reactivity is poorly described. In the present study, fresh subcutaneous resistance arteries were obtained from patients with heart failure (n=10), healthy controls (n=9) and men with androgen-deficiency (n=17). All arteries were studied using a wire myograph to examine the effect of cumulative additions of testosterone (1 nmol/l–100 μmol/l) compared with vehicle control following maximal pre-constriction with KCl (1–100 μmol/l). The vascular reactivity of arteries from androgen-deficient patients was examined further by recording tension concentration curves to cumulative additions of noradrenaline (1 nmol/l–100 μmol/l) and U46619 (1–300 nmol/l), followed by relaxation concentration curves to additions of ACh (acetylcholine; 10 nmol/l–30 μmol/l) and SNP (sodium nitroprusside; 10 nmol–30 μmol/l) respectively. In all cases, statistical analysis was performed by ANOVA. Patients with proven androgen-deficiency were treated according to clinical recommendations for a minimum of 3 months and further arteries (n=19) were taken for experimentation using the same protocol. In all groups, testosterone was confirmed to be an acute concentration-dependent vasodilator at concentrations ≥1 μmol/l (P=0.0001). The dilating effect of testosterone was augmented in patients with androgen-deficiency prior to treatment, and this effect was abrogated following appropriate testosterone replacement. Testosterone therapy significantly reduced the normal vascular dilating response to ACh and SNP (P<0.01) and significantly increased the contractile response to noradrenaline (P<0.01), but not U46619. Testosterone is an acute dose-dependent vasodilator of resistance arteries. Physiological testosterone replacement attenuates general vascular reactivity in androgen-deficient subjects. The numerous perceived benefits of testosterone replacement may be offset by a decline in vascular reactivity and, therefore, further studies and careful monitoring of patients is recommended.

Abstract 15823: Diminished Vasoresponsiveness in Patients With Heart Failure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Olga Papazisi ◽  
Marieke E van Vessem ◽  
Saskia L Beeres ◽  
Rob B de Wilde ◽  
Remco R Berendsen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Clinical Outcome ◽  
Prospective Observational Study ◽  
Independent Predictor ◽  
Medical Center ◽  
Vascular Response ◽  
Patients With Heart Failure ◽  
Vascular Responsiveness

Introduction: Vasoplegia is a severe complication after cardiac surgery and is associated with impaired clinical outcome. Pre-operative heart failure (HF) is considered an independent predictor of post-operative vasoplegia. We hypothesize that HF patients are more susceptible to vasoplegia due to altered vascular responsiveness. In this study, vasoresponsiveness in patients undergoing cardiac surgery for HF is investigated. Methods: A prospective, observational study was conducted at Leiden University Medical Center. We included patients with HF (N=18) and without HF (N=18) who underwent cardiac surgery on cardiopulmonary bypass. Vasoresponsiveness was assessed at 4 different timepoints: 1) before induction, 2) after induction, 3) after cessation of cardiopulmonary bypass and 4) on the first postoperative day. The vascular response was recorded as change in systemic vascular resistance (SVR) after the administration of phenylephrine (bolus 2 μg/kg). Results: Thirty-six patients were included [67 (61-71) years, 78% male]. Vascular responsiveness was significantly attenuated in patients with HF compared to controls. The response to phenylephrine was already diminished at baseline in HF patients and was almost abolished after cessation of cardiopulmonary bypass (Figure). Roughly the same pattern of vasoresponsiveness was found when excluding patients that received norepinephrine. Moreover, HF patients required a significantly higher amount of noradrenaline [169.80 (IQR 14.77-318.97) ug/kg] compared to controls [3.61 (IQR 0-41.60) ug/kg] to maintain similar SVR during the first 24h postoperatively. Conclusions: The vascular responsiveness is altered in patients with HF and this might explain the higher prevalence of vasoplegia in this patient population.

Prognostic value of galectin-3 on admission in Chinese patients with heart failure: a prospective observational study

2017 ◽  
Vol 72 (2) ◽  
pp. 188-195 ◽  
Author(s):  
Hua Wang ◽  
Qingyong Chen ◽  
Yingying Li ◽  
Xianchao Jing ◽  
Tianya Liang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Observational Study ◽  
Prognostic Value ◽  
Prospective Observational Study ◽  
Chinese Patients ◽  
Patients With Heart Failure ◽  
Galectin 3

A prospective observational study of emboli exposure in open versus closed chamber cardiac surgery

Perfusion ◽  
2021 ◽  
pp. 026765912110238
Author(s):  
Ghazwan NS Jabur ◽  
Joseph Donnelly ◽  
Alan F Merry ◽  
Simon J Mitchell
Keyword(s):  
Cardiac Surgery ◽  
Observational Study ◽  
Prospective Observational Study ◽  
Phase 1 ◽  
Cerebral Arteries ◽  
Aortic Cross Clamp ◽  
Closed Chamber ◽  
Cerebral Laterality ◽  
Open Versus ◽  
The Right

Objective: Exposure to cerebral emboli is ubiquitous and may be harmful in cardiac surgery utilizing cardiopulmonary bypass. This was a prospective observational study aiming to compare emboli exposure in closed-chamber with open-chamber cardiac surgery, distinguish particulate from gaseous emboli and examine cerebral laterality in distribution. Methods: Forty patients underwent either closed-chamber procedures ( n = 20) or open-chamber procedures ( n = 20). Emboli (gaseous and solid) were detected using transcranial Doppler in both middle cerebral arteries in two monitoring phases: 1, initiation of bypass to the removal of the aortic cross-clamp; and 2, removal of aortic cross-clamp to 20 minutes after venous decannulation. Results: Total (median (interquartile range)) emboli counts (both phases) were 898 (499–1366) and 2617 (1007–5847) in closed-chamber and open-chamber surgeries, respectively. The vast majority were gaseous; median 794 (closed-chamber surgery) and 2240 (open-chamber surgery). When normalized for duration, there was no difference between emboli exposures in closed-chamber and open-chamber surgery in phase 1: 6.8 (3.6–15.2) versus 6.4 (2.0–18.1) emboli per minute, respectively. In phase 2, closed-chamber surgery cases were exposed to markedly fewer emboli than open-chamber surgery cases: 9.6 (5.1–14.9) versus 43.3 (19.7–60.3) emboli per minute, respectively. More emboli (total) passed into the right cerebral circulation: 985 (397–2422) right versus 376 (198–769) left. Conclusions: Patients undergoing open-chamber surgery are exposed to considerably higher numbers of cerebral arterial emboli after removal of the aortic cross-clamp than those undergoing closed-chamber surgery, and more emboli enter the right middle cerebral artery than the left. These results may help inform the evaluation of the pathophysiological impact of emboli exposure.

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