Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

Atrial natriuretic peptide and sodium homeostasis in compensated heart failure

1996 ◽  
Vol 271 (5) ◽  
pp. R1353-R1363 ◽  
Author(s):  
T. E. Lohmeier ◽  
H. L. Mizelle ◽  
G. A. Reinhart ◽  
J. P. Montani ◽  
C. E. Hord ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Left Ventricular ◽  
Sodium Balance ◽  
Plasma Norepinephrine ◽  
Norepinephrine Concentration ◽  
Atrial Natriuretic

The purpose of this study was to determine whether high plasma levels of atrial natriuretic peptide (ANP) in compensated heart failure are important in the maintenance of sodium balance. This was achieved by subjecting eight dogs to bilateral atrial appendectomy (APX) to blunt the ANP response to pacing-induced heart failure. Five intact dogs served as controls. In controls, 14 days of left ventricular pacing at 240 beats/min produced a sustained fall in cardiac output and mean arterial pressure of approximately 40 and 20%, respectively; compared with cardiac output, reductions in renal blood flow (up to approximately 25%) were less pronounced and even smaller decrements in GFR occurred (up to 9%). Despite these changes and a threefold elevation in plasma norepinephrine concentration, plasma renin activity (PRA) did not increase and sodium balance was achieved during the second week of pacing in association with a six- to eightfold rise in plasma levels of ANP. Similar responses occurred in four dogs in which APX was relatively ineffective in blunting the ANP response to pacing. In marked contrast, there were substantial increments in PRA and in plasma norepinephrine concentration, and marked sodium and water retention during the last week of pacing in four dogs with APX and severely deficient ANP. These results indicate that ANP plays a critical role in promoting sodium excretion in the early stages of cardiac dysfunction.

P3531Continual measurement of arterial dP/dtmax enables mini-invasive monitoring of left ventricular contractility in acute heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Vondrakova ◽  
D V Vondrakova ◽  
A K Kruger ◽  
M J Janotka ◽  
P N Neuzil ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Intensive Care ◽  
Acute Heart Failure ◽  
Hemodynamic Monitoring ◽  
Continuous Wave ◽  
Left Ventricular ◽  
Waveform Analysis ◽  
Arterial Line ◽  
Arterial Blood

Abstract Introduction Continuous reliable evaluating of left ventricular (LV) contractile function in patients with advanced heart failure requiring intensive care remains challenging. Recently, continual monitoring of dP/dtmax from arterial line became available for hemodynamic monitoring. However, the relation between arterial dP/dtmax and LV dP/dtmax measurement is not fully understood. Purpose The aim of our study was to determine the relation of arterial dP/dtmax and LV dP/dtmax assessed by echocardiography in patients with acute heart failure. Methods Forty-eight patients with acute heart failure requiring intensive care and hemodynamic monitoring were recruited into the study (mean age 70.4 years, 65% were males). Hemodynamic variables including arterial dP/dtmax were continually monitored using arterial line pressure waveform analysis. LV dP/dtmax was assessed using continuous-wave Doppler analysis of mitral regurgitation flow. Results The values from continual arterial dP/dtmax monitoring significantly correlated with the LV dP/dtmax assessed by echocardiography (r=0.72, 95% confidence interval [CI] 0.54–0.83, P<0.0001). Linear regression revealed that (LV dP/dtmax) = 0.87×(arterial dP/dtmax) + 291, P<0.0001. Arterial dP/dtmax significantly correlated also with the stroke volume (r=0.55, P<0.0001), cardiac output (r=0.32, P=0.0289), mean arterial blood pressure (r=0.43, P=0.0155) and systolic blood pressure (r=0.79, P<0001). On the other hand arterial dP/dtmax did not correlate with the systemic vascular resistance (SVR), heart rate, dynamic arterial elastance, diastolic blood pressure or central venous pressure. Conclusion Our results revealed that arterial dP/dtmax values tightly and highly significantly correlate with LV dP/dtmax. Arterial dP/dtmax could be, therefore, used for continual monitoring of LV contractility. Acknowledgement/Funding Institutional grant MH CZ - DRO (Na Homolce Hospital- NNH, 00023884), IG150501

scholarly journals Comparison between Spironolactone and Eplerenone on LV Systolic Function in Patients with Chronic Heart Failure

2020 ◽  
Vol 16 (2) ◽  
pp. 65-70
Author(s):  
Md Noornabi Khondokar ◽  
Khurshed Ahmed ◽  
Mohammad Ashraf Hossain ◽  
Rakibulh Rashed ◽  
Mohamed Mausool Siraj ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Side Effects ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Systolic Function ◽  
Nyha Class ◽  
Left Ventricular ◽  
Group I ◽  
Lv Systolic Function

Background:Chronic heart failure (CHF) is the most common and prognostically unfavorable outcome of many diseases of the cardiovascular system. Clinical trials have demonstrated mortality and morbidity benefits of mineralocorticoid receptor antagonists (MRAs) in patients with heart failure. These studies have used either eplerenone or spironolactone as the MRA. Eplerenone is a selective aldosterone antagonist expected to have a lower incidence of hormonal side effects than spironolactone. The present study is designed to compare these two drugs in chronic heart failure patients as no head to head trial between these two drugs is found regarding improvement of systolic function, tolerability and safety. The aim of this study is to compare the effects of eplerenone and spironolactone on LV systolic function in patients with chronic heart failure in a single center. Methods:It was a randomized clinical trial single blind study. A total of 224 cases of chronic heart failure with reduced ejection fraction and NYHA class III or IV were selected by random sampling, from July 2017 to June 2018. Each patient was randomly allocated into either of the two arms, and was continued receiving treatment with either spironolactone (Arm-I) or eplerenone(Arm-II). Each patient was evaluated clinically, biochemically and echocardiographically at the beginning of treatment (baseline) at 1 month and at the end of 6th month. Echocardiography was performed to find out change in left ventricular systolic function. Result: After 6 months of treatment, ejection fraction was found higher in the eplerenonearm (40.3 ± 6.5 versus 38.3 ± 4.6%; P < 0.05). Ejection fraction (EF) changes were 6.2% in eplerenone group and 4.1% in spironolactonearm. A significant reduction in left ventricular end-systolic volume (21.9±2.5 in group I versus 14.9±5.7 in group II; P < 0.05) and left ventricular systolic diameter (48.7±4.0 in arm I versus 45.2±4.9 in arm II; P<0.05) occurred after 6 months of treatment. But no significant differences were observed in left ventricular end-diastolic volume (187.8±37.4 versus 184.5±33.9; P=0.101) and left ventricular diastolic diameter (60.1±4.5 versus 61.0±4.9; P=0.0818) between arms. Assessment of blood pressure six months after treatment shows, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were improved in both arms but difference between two arms were statistically non-significant (p>0.05). Conclusion: In this study, the improvement in systolic function was more in eplerenone arm, which also had fewer adverse side effects when compared to spironolactone arm. So, it can be concluded that eplerenone can be advised in patient with chronic heart failure in addition to other drugs that are used to treat heart failure. University Heart Journal Vol. 16, No. 2, Jul 2020; 65-70

Heart Rate and Systolic Arterial Blood Pressure Variabilities in the Progression of Chronic Heart Failure

1996 ◽  
Vol 91 (s1) ◽  
pp. 37-39 ◽  
Author(s):  
Stefano Guzzetti ◽  
Chiara Cogliati ◽  
Silvia Mezzetti ◽  
Maurizio Turiel ◽  
Federico Lombardi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Chronic Heart Failure ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Systolic Arterial Blood Pressure

scholarly journals Arterial Hypertension and Heart Failure in General Practice

2020 ◽  
Vol 0 (1-2) ◽  
pp. 85-88
Author(s):  
В. М. Ждан ◽  
О. Є. Кітура ◽  
Є. М. Кітура ◽  
М. Ю. Бабаніна ◽  
М. В. Ткаченко
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Arterial Hypertension ◽  
Beta Blockers ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Lv Remodeling ◽  
Hemodynamic Overload ◽  
European Society Of Cardiology

The Framingham study demonstrated that myocardial infarction (25% of cases) and arterial hypertension (AH) (75% of cases) caused the development of chronic heart failure (CHF). The most significant predictor of CHF development was an increase in systolic blood pressure (SBP) and pulse pressure and each increase in SBP by 20 mm Hg and pulse blood pressure by 16 mm Hg led to an increase in the incidence of CHF by 52% and 55%, respectively. The presented clinical case of a patient with CHF, developed due to long-term hypertension, considered the mechanisms of CHF development, as well as the issue of pharmacotherapy of AH in combination with chronic heart failure with systolic dysfunction. The key mechanisms that directly lead to the development of CHF in AH are hemodynamic overload, reduction of myocardial contractility, left ventricular hypertrophy (LVH). The likelihood of CHF development in patients with AH is by 4 times higher, whilst in patients with LVH it is by 15 times higher. Along with LVH, one of the early manifestations of LV remodeling in AH is the development of diastolic dysfunction, which precedes the development of systolic abnormalities in AH and LVH. Antihypertensive therapy resulted in reduction of the incidence of CHF by approximately 52% compared to patients who did not receive adequate therapy. The decrease in the incidence of CHF was linearly dependent on the decrease in SBP: each decrease of SBP by 10 mm Hg led to a 26% reduction in the relative risk in CHF development. It has been established that AH is not only one of the leading etiological factors in CHF development, but also have similar key links in pathogenesis. The strategy for the selection of pathogenetic pharmacotherapy should be determined taking into account the above circumstance. Currently, the European Society of Cardiology recommends prescribing beta-blockers to all patients with stable CHF Class II–IV as a standard treatment in combination with ACE inhibitors and diuretics in the absence of contraindications. In addition to RAAS blockers, medications for patients with AH in combination with systolic CHF can be supplemented with thiazide or loop diuretics, as well as mineralocorticoid receptor ant agonists (MRA).

scholarly journals Effect of empagliflozin on ketone bodies in patients with stable chronic heart failure

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
R. Pietschner ◽  
J. Kolwelter ◽  
A. Bosch ◽  
K. Striepe ◽  
S. Jung ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Pulse Pressure ◽  
Ketone Bodies ◽  
Left Ventricular ◽  
Vascular Stiffness ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Central Pulse Pressure

Abstract Background Recent studies indicated that sodium glucose cotransporter (SGLT)2 inhibition increases levels of ketone bodies in the blood in patients with type 1 and 2 diabetes. Other studies suggested that in patients with chronic heart failure (CHF), increased myocardial oxygen demand can be provided by ketone bodies as a fuel substrate. Experimental studies reported that ketone bodies, specifically beta-hydroxybutyrate (β-OHB) may increase blood pressure (BP) by impairing endothelium-dependant relaxation, thereby leading to increased vascular stiffness. In our study we assessed whether the SGLT 2 inhibition with empagliflozin increases ketone bodies in patients with stable CHF and whether such an increase impairs BP and vascular function. Methods In a prospective, double blind, placebo controlled, parallel-group single centre study 75 patients with CHF (left ventricular ejection fraction 39.0 ± 8.2%) were randomised (2:1) to the SGLT-2 inhibitor empagliflozin 10 mg orally once daily or to placebo, 72 patients completed the study. After a run-in phase we evaluated at baseline BP by 24 h ambulatory blood pressure (ABP) monitoring, vascular stiffness parameters by the SphygmoCor system (AtCor Medical, Sydney, NSW, Australia) and fasting metabolic parameters, including β-OHB by an enzymatic assay (Beckman Coulter DxC 700 AU). The same measurements were repeated 12 weeks after treatment. In 19 of the 72 patients serum levels of β-OHB were beneath the lower border of our assay (< 0.05 mmol/l) therefore being excluded from the subsequent analysis. Results In patients with stable CHF, treatment with empagliflozin (n = 36) was followed by an increase of β-OHB by 33.39% (p = 0.017), reduction in 24 h systolic (p = 0.038) and diastolic (p = 0.085) ABP, weight loss (p = 0.003) and decrease of central systolic BP (p = 0.008) and central pulse pressure (p = 0.008). The increase in β-OHB was related to an attenuated decrease of empagliflozin-induced 24 h systolic (r = 0.321, p = 0.069) and diastolic (r = 0.516, p = 0.002) ABP and less reduction of central systolic BP (r = 0.470, p = 0.009) and central pulse pressure (r = 0.391, p = 0.033). No significant changes were seen in any of these parameters after 12 weeks of treatment in the placebo group (n = 17). Conclusion In patients with stable CHF ketone bodies as assessed by β-OHB increased after treatment with empagliflozin. This increase led to an attenuation of the beneficial effects of empagliflozin on BP and vascular parameters. Trial registration The study was registered at http://www.clinicaltrials.gov (NCT03128528).

Mechanisms involved in central cardiovascular effects of prostaglandin F2 alpha

1982 ◽  
Vol 242 (5) ◽  
pp. R545-R551 ◽  
Author(s):  
G. Feuerstein ◽  
C. J. Helke ◽  
R. L. Zerbe ◽  
D. M. Jacobowitz ◽  
I. J. Kopin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rectal Temperature ◽  
Cardiovascular Effects ◽  
Plasma Norepinephrine ◽  
Central Administration ◽  
Prostaglandin F2 Alpha ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Bilateral Vagotomy

Prostaglandin F2 alpha (PGF2 alpha) injected into the cerebroventricular system (icv) of halothane-anesthetized rats increased the arterial blood pressure, heart rate, and rectal temperature. These effects were accompanied by a preferential increase in plasma norepinephrine concentration. Plasma levels of epinephrine, renin, and vasopressin were not changed in the PGF2 alpha-icv-treated rats. Bilateral vagotomy did not affect the PGF2 alpha-induced hypertension and tachycardia nor was there any change in the selective increase in plasma norepinephrine concentration. Hexamethonium pretreatment suppressed, in a dose-response manner, the increases in blood pressure, heart rate, and rectal temperature in response to PGF2 alpha-icv. Plasma norepinephrine and epinephrine levels were not altered by PGF2 alpha-icv in hexamethonium-treated rats, but plasma vasopressin concentration was markedly elevated in all hexamethonium-infused rats. These results suggest that selective central activation of the sympathetic nervous system underlies the profound cardiovascular and temperature responses elicited by central administration of PGF2 alpha.

Left ventricular shape changes during the course of evolving heart failure

1992 ◽  
Vol 263 (1) ◽  
pp. H266-H270 ◽  
Author(s):  
H. N. Sabbah ◽  
T. Kono ◽  
P. D. Stein ◽  
G. B. Mancini ◽  
S. Goldstein
Keyword(s):  
Heart Failure ◽  
Left Ventricular ◽  
Minor Axis ◽  
Plasma Norepinephrine ◽  
End Diastolic Volume ◽  
Lv Dysfunction ◽  
Norepinephrine Concentration ◽  
Lv Ejection Fraction ◽  
Left Ventricular Shape ◽  
Shape Changes

The temporal relationship between left ventricular (LV) shape changes and the development of LV dysfunction, dilation, and sympathoadrenergic hyperactivity was examined in 10 dogs with chronic heart failure produced by multiple sequential intracoronary microembolizations. LV shape was quantitated from serial ventriculograms based on the ratio of the major to minor axis at end systole and end diastole. Measurements were made at baseline (before embolizations) and were repeated at 2, 8, and 16 wk after the last embolization. A significant increase of LV sphericity was present at 2 wk, with only minimal changes occurring thereafter. Despite the tendency for LV shape changes to plateau between 2 and 16 wk, LV ejection fraction continued to decline (31 +/- 1 vs. 20 +/- 2%; P less than 0.001), and LV end-diastolic volume continued to increase (86 +/- 6 vs. 103 +/- 9 ml; P less than 0.01) as did plasma norepinephrine concentration (456 +/- 30 vs. 868 +/- 172 pg/ml; P less than 0.02). These data indicate that in the course of evolving heart failure, LV shape abnormalities precede the development of profound LV dysfunction, dilation, and overt activation of the sympathetic nervous system.

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