Abstract 20086: Influence of Central Apneas and Chemoreflex Activation on Heart Failure Related Pulmonary Arterial Hypertension

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Valentina Raglianti ◽  
Alberto Giannoni ◽  
Annamaria Del Franco ◽  
Gianluca Mirizzi ◽  
Alberto Aimo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Passive Component ◽  
Ventricular Ejection Fraction ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Central Apneas

Introduction: Pulmonary arterial hypertension (PAH) is an acknowledged independent prognostic factor in patients with heart failure (HF). Beyond a “passive” component due to the increased left ventricular pressure, an “active” component due to pulmonary vascular reactivity is frequently observed. However, the mechanism behind pulmonary vasoconstriction is not fully understood. Hypothesis: We hypothesized that central apneas (Cheyne-Stokes respiration [[Unable to Display Character: &#8211;]] CSR) through chemoreflex stimulation may contribute to PAH in HF. Methods: we studied 56 HF patients (left ventricular ejection fraction <50%), on stable optimal pharmacological treatment, without increased left ventriculare pressure (excluding patients with severe mitral disease and severe diastolic dysfunction). All patients underwent echocardiographic and neurohormonal assessment, 24-hour cardiorespiratory screening for CSR (patients with obstructive events were excluded) and chemoreflex test for hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses (by rebreathing technique) . Results: Thirteen patients (23%) showed CSR, as defined by a 24 hour AHI > of 15. HF patients with CSR compared with patients with normal breathing, presented higher systolic arterial pulmonary pressure (SPAP: 40.1±7.6 vs 33.1±5.9, p<0.01) at echocardiography, despite similar systolic and diastolic function (data not shown). Furthermore, patients with central apneas also presented with enhanced HVR (median 0.78, interquartile range -IR 0.48-1.22 vs 0.43, IR 0.19-0.69 L/min/%, p<0.05) and HCVR (1.18, IR 0.98-1.35 vs 0.75, IR 0.51-0.95 L/min/mmHg, p<0.01) as well as increased plasma norepinephrine levels (546, IR 371-732 vs 393, IR 229-538 pg/mL, p<0.05). SPAP was indeed correlated with AHI (Spearman’s Rho, R=0.44, p<0.01), HCVR (R=0.48, p<0.001), HVR (R=0.33, p<0.05) and norepinephrine levels (R=0.31, p<0.05). Conclusions: In patients with systolic HF, the presence of diurnal-nocturnal CSR, likely via recurrent hypoxia and hypercapnia cycles, may determine a chemoreflex mediated adrenergic discharge and a consequent pulmonary vasoconstriction, responsible of the undesirable increase in pulmonary arterial pressure.

scholarly journals Cardiac sympathetic dysfunction in pulmonary arterial hypertension: lesson from left-sided heart failure

2019 ◽  
Vol 9 (3) ◽  
pp. 204589401986862 ◽  
Author(s):  
Valentina Mercurio ◽  
Teresa Pellegrino ◽  
Giorgio Bosso ◽  
Giacomo Campi ◽  
Paolo Parrella ◽  
...  
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Pulmonary Arterial Hypertension ◽  
Left Ventricular Ejection Fraction ◽  
Arterial Hypertension ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Pulmonary Arterial ◽  
Sympathetic Nervous

Sympathetic nervous system hyperactivity has a well-recognized role in the pathophysiology of heart failure with reduced left ventricular ejection fraction. Alterations in sympathetic nervous system have been related to the pathophysiology of pulmonary arterial hypertension, but it is unclear whether cardiac sympathetic nervous system is impaired and how sympathetic dysfunction correlates with hemodynamics and clinical status in pulmonary arterial hypertension patients. The aim of this study was to evaluate the cardiac sympathetic nervous system activity by means of123Iodine-metaiodobenzylguanidine nuclear imaging in pulmonary arterial hypertension patients and to explore its possible correlation with markers of disease severity. Twelve consecutive pulmonary arterial hypertension patients (nine women, median age 56.5 (17.8), eight idiopathic and four connective tissue-associated pulmonary arterial hypertension) underwent cardiac123Iodine-metaiodobenzylguanidine scintigraphy. The results were compared with those of 12 subjects with a negative history of cardiovascular or pulmonary disease who underwent the same nuclear imaging test because of a suspected paraganglioma or pheochromocytoma, with a negative result (controls), and 12 patients with heart failure with reduced left ventricular ejection fraction. Hemodynamics, echocardiography, six-minute walking distance, cardiopulmonary exercise testing, and N-terminal pro brain natriuretic peptide were collected in pulmonary arterial hypertension patients within one week from123Iodine-metaiodobenzylguanidine scintigraphy. Cardiac123Iodine-metaiodobenzylguanidine uptake, assessed as early and late heart-to-mediastinum ratio, was significantly lower in pulmonary arterial hypertension compared to controls (p = 0.001), but similar to heart failure with reduced left ventricular ejection fraction. Myocardial123Iodine-metaiodobenzylguanidine turnover, expressed as washout rate, was similar in pulmonary arterial hypertension and heart failure with reduced left ventricular ejection fraction and significantly higher compared to controls (p = 0.016). In the pulmonary arterial hypertension group, both early and late heart-to-mediastinum ratios and washout rate correlated with parameters of pulmonary arterial hypertension severity including pulmonary vascular resistance, right atrial pressure, tricuspid annular plane systolic excursion, N-terminal pro brain natriuretic peptide, and peak VO2. Although we evaluated a small number of subjects, our study showed a significant impairment in cardiac sympathetic nervous system in pulmonary arterial hypertension, similarly to that observed in heart failure with reduced left ventricular ejection fraction. This impairment correlated with indices of pulmonary arterial hypertension severity. Cardiac sympathetic dysfunction may be a contributing factor to the development of right-sided heart failure in pulmonary arterial hypertension.

Prevalence and Predictors of Pulmonary Arterial Hypertension in Hemoglobin E/ β-Thalassemia Patients.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2015-2015 ◽  
Author(s):  
Suporn Chuncharunee ◽  
Vichai Atichartakarn ◽  
Napaporn Archararit ◽  
Umaporn Udomsubpayakul ◽  
Atiporn Ingsathit ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Univariate Analysis ◽  
Cellular Adhesion ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Low Grade ◽  
Ventricular Ejection Fraction ◽  
Hemoglobin E ◽  
Pulmonary Arterial

Abstract Abstract 2015 Poster Board I-1037 Introduction: Pulmonary arterial hypertension (PAH) associated with thalassemia (Thal) hemoglobinopathy is now an accepted clinical entity. Most of the reports are in sickle cell disease and splenectomized β-Thal patients. Once manifested, it connotes poor prognosis. We herein present its prevalence and predictors in hemoglobin E/β-Thal (E/β-Thal) patients. Patients and Methods: One hundred and ten clinically stable E/β-Thal outpatients, on no medication aside from folic acid and who received no blood transfusion in the preceding 4 weeks were studied. All gave written informed consent, and study protocol was approved by the institution ethics committee on studies in humans (#0774/2548). Echocardiogram was used to estimate systolic PA pressure (SPAP). PAH was defined as an estimated SPAP ≥36 mmHg. Clinical features and laboratory data were stratified according to the presence or absence of PAH, and statistical analysis was done by STATA version 10 (Stata Corp, Texas), considering a P value <0.05 as statistically significant. Predictors of PAH were considered in univariate analysis. Results: There were 110 patients, 56 of whom were female and 61 were asplenic. PAH was present in 41 patients (37.3%), all of whom had normal left ventricular ejection fraction. There was no gender difference between the 2 groups (p=0.055). Selected statistically significant results are shown in the table. Conclusions: Prevalence of PAH in E/β-Thal patients is 37.3% without gender preponderance. Predictors are asplenia, more severe hemolysis, higher number of circulating (activated) platelets and nucleated RBCs, increased chronic low grade inflammation and increased cellular adhesion between blood and endothelial cells. These changes could facilitate development of thrombotic pulmonary arteriopathy, the underlying basis of PAH. Serum NT pro BNP assay can be utilized as a predictor or a screener of PAH in these patients. Disclosures: No relevant conflicts of interest to declare.

scholarly journals A Hospital Based Study of Pulmonary Arterial Hypertension in Various Stages of Chronic Kidney Disease and Associated Risk Factors among Patients Attending a Tertiary Care Hospital in Ujjain, Madhya Pradesh

2021 ◽  
Vol 8 (20) ◽  
pp. 1500-1504
Author(s):  
Rajesh Deshpande ◽  
Amit Kumar Yadav ◽  
Vipin Porwal
Keyword(s):  
Chronic Kidney Disease ◽  
Pulmonary Arterial Hypertension ◽  
Kidney Disease ◽  
Arterial Hypertension ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Corticomedullary Differentiation ◽  
Pulmonary Arterial

BACKGROUND Multiple mechanisms have been identified contributing to pulmonary arterial hypertension (PAH) in chronic kidney disease (CKD) patients and it is one of the important sequelae of CKD and needs early detection. We wanted to study PAH in various stages of CKD and its association with renal and cardiovascular parameters. METHODS This was an observational study. PAH was diagnosed if mean pulmonary artery pressure (MPAP) was ≥ 25 mmHg using 2D - Doppler echocardiography in 96 CKD patients. Staging of CKD was done as per Kidney Disease Improving Global Outcomes (KDIGO) stages 1 - 5. Age, gender, diabetes, hypertension, stages of CKD, corticomedullary differentiation (CMD), estimated glomerular filtration rate (EGFR), urinary albumin creatinine ratio (UACR), left ventricular ejection fraction (LVEF) and left ventricular hypertrophy (LVH) were included as risk factors. Data was analysed by calculating percentage, mean, standard deviation, chi square and t test. P value < 0.05 was taken as statistically significant. RESULTS PAH was detected in 37 (38.5 %) of CKD patients. Prevalence of PAH increased with stages of CKD being highest (59 %) in stage 5 and this was found to be statistically significant (P = 0.04). PAH was detected earliest in stage 2 (23.5 %). Lower mean eGFR ml / min / 1.733m2 (24.43 ± 17.8 vs 40.98 ± 25.7, P = 0.001) altered corticomedullary differentiation (50.9 % vs 20.5 % p = 0.003), reduced LVEF (81 % vs 26.7 % P = 0.000) and LVH (65 % vs 19.6 %, P = 0.000) were significantly associated with PAH in CKD patients. CONCLUSIONS PAH in CKD patients increases with CKD stages. Onset of PAH in CKD patients may be earlier and significantly associated with left ventricular dysfunction. KEYWORDS Pulmonary Arterial Hypertension, Chronic Kidney Disease, Left Ventricular Ejection Fraction, Left Ventricular Hypertrophy

scholarly journals Plasma aldosterone levels are elevated in patients with pulmonary arterial hypertension in the absence of left ventricular heart failure: a pilot study

2013 ◽  
Vol 15 (3) ◽  
pp. 277-283 ◽  
Author(s):  
Bradley A. Maron ◽  
Alexander R. Opotowsky ◽  
Michael J. Landzberg ◽  
Joseph Loscalzo ◽  
Aaron B. Waxman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pilot Study ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Left Ventricular ◽  
Plasma Aldosterone ◽  
Pulmonary Arterial

scholarly journals In Chronic Cardiac Decompensation with Reduced Left Ventricular Ejection Fraction, Phosphodiesterase-5 Inhibition Exerts Significant Effects on some Clinical, Functional and Hemodynamic Outcomes: a Meta-Analysis

2017 ◽  
Author(s):  
Renato De Vecchis ◽  
Carmelina Ariano
Keyword(s):  
Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Meta Analysis ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Pulmonary Arterial ◽  
Phosphodiesterase 5

Background:&nbsp;In&nbsp; patients with pulmonary arterial&nbsp; hypertension, substantial&nbsp; clinical benefits have been reported with the use of phosphodiesterase-5 inhibitors(PDE5i) . Moreover, some studies would have proven&nbsp; useful effects&nbsp; of PDE5i&nbsp; also&nbsp; on&nbsp;&nbsp; the clinical picture of the&nbsp; pulmonary hypertension(PH) secondary to left-sided chronic heart failure(CHF). Methods:&nbsp;We performed a meta-analysis comprising randomized controlled trials ( RCTs) which had compared&nbsp; PDE5i ( mostly sildenafil) with&nbsp; placebo in CHF patients.&nbsp;Results:&nbsp;14 studies, including 928&nbsp; patients overall , were admitted to the&nbsp; meta-analysis. In&nbsp;&nbsp; heart failure with reduced left ventricular ejection fraction(HFREF), PDE5i,&nbsp; compared to placebo, significantly improved the composite of death and hospitalization (OR= 0.28; 95% CI: 0.10 to 0.74). They also improved peak VO2&nbsp; (difference in means[MD]: 3.76; 95% CI: 3.27 to 4.25), six-minutes walk distance ( (6MWD)(&nbsp; MD, 22.7 meters ; 95% CI, 8.19 to 37.21) and pulmonary arterial systolic pressure (MD: -11.52 mmHg; 95% CI: -15.56 to -7.49). Conversely, in&nbsp;&nbsp; CHF with preserved left ventricular ejection fraction ( HFpEF), PDE5i&nbsp; were shown&nbsp; not to yield&nbsp; any&nbsp; beneficial effect&nbsp; concerning&nbsp; the investigated endpoints.&nbsp;Conclusions:&nbsp;In HFREF, PDE5i&nbsp; were shown&nbsp; to improve&nbsp; the composite of death and hospitalization, as well as&nbsp;&nbsp;&nbsp; exercise capacity and pulmonary hemodynamics. Conversely,&nbsp; in HFpEF, no significant clinical, ergospirometric or hemodynamic &nbsp;betterment&nbsp; was achieved&nbsp; using PDE5i treatment.

P3525Buspirone effect on chemoreflex and central apneas in heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Borrelli ◽  
A Giannoni ◽  
G Mirizzi ◽  
M Emdin ◽  
C Passino
Keyword(s):  
Heart Failure ◽  
Randomized Study ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Apnea Hypopnea Index ◽  
Double Blind ◽  
Ventricular Ejection Fraction ◽  
Central Apneas ◽  
Carbon Dioxide Co2 ◽  
Co2 Chemosensitivity

Abstract Background Increased chemosensitivity to carbon dioxide (CO2) is an important trigger of central apneas in heart failure (HF), contributing to HF progression and mortality. We hypothesized that buspirone, a 5HT1A receptor agonist that inhibits serotonergic chemoreceptor neuron firing in animals, can decrease CO2 chemosensitivity, thus preventing CA in patients with HF. Methods Sixteen patients with systolic HF (age 71.3±5.8 years, left ventricular ejection fraction 29.8±7.8%) and moderate-severe central apneas (nighttime apnea/hypopnea index AHI≥15 events/hour) underwent a double-blind, placebo-controlled, cross over, randomized study of oral buspirone administration (45 mg/day for 1 week). Results Buspirone reduced CO2 chemosensitivity compared to placebo (1.2 IR [1.1–1.5] vs. 2.0 [1.6–2.2] L/min/mmHg, p=0.008). Furthermore, buspirone improved: the AHI at nighttime (16.5 [8.5–24.7] vs. 27.5 [23.0–37.3] events/hour, p=0.002), and daytime (8.0 [2.3–11.5] vs. 11.5 [6.3–18.8] events/hour, p=0.006); the central apnea index at nighttime (4.0 [1.0–19.0] vs. 12.5 [8.3–27.3] events/hour, p=0.01) and daytime (1.0 [0.0–3.0] vs. 4.0 [1.3–6.0] events/hour, p=0.009); and the oxygen desaturation index at nighttime (4.7 [1.0–11.0] vs. 20.0 [8.7–26.5] events/hour, p=0.004) and daytime (0.2 [0.1–0.7] vs. 1.2 [0.3–4.8] events/hour, p=0.005). Buspirone showed a good safety profile and had no effect on neurohormones, arrhythmias, exercise capacity and mood/daytime sleepiness. Conclusion Buspirone reduces CO2 chemosensitivity and inhibits central apneas both during the day and the night in patients with systolic HF.

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