Right Ventricular Dysfunction Is the Strongest Determinant of Abnormal Left Ventricular Ejection Fraction in Pulmonary Arterial Hypertension

2017 ◽  
Vol 36 (4) ◽  
pp. S361
Author(s):  
T. Meeran ◽  
J.R. PO ◽  
A. Elapavaluru ◽  
R.L. Benza ◽  
A. Raina
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Arterial Hypertension ◽  
Ventricular Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Pulmonary Arterial

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.

scholarly journals Forward Left Ventricular Ejection Fraction as a Predictor of Postoperative Left Ventricular Dysfunction in Patients with Degenerative Mitral Regurgitation

2021 ◽  
Vol 10 (14) ◽  
pp. 3013
Author(s):  
Juyoun Kim ◽  
Jae-Sik Nam ◽  
Youngdo Kim ◽  
Ji-Hyun Chin ◽  
In-Cheol Choi
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Mitral Regurgitation ◽  
Ejection Fraction ◽  
Left Ventricular Dysfunction ◽  
Predictive Value ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Normal Lvef

Background: Left ventricular dysfunction (LVD) can occur immediately after mitral valve repair (MVr) for degenerative mitral regurgitation (DMR) in some patients with normal preoperative left ventricular ejection fraction (LVEF). This study investigated whether forward LVEF, calculated as left ventricular outflow tract stroke volume divided by left ventricular end-diastolic volume, could predict LVD immediately after MVr in patients with DMR and normal LVEF. Methods: Echocardiographic and clinical data were retrospectively evaluated in 234 patients with DMR ≥ moderate and preoperative LVEF ≥ 60%. LVD and non-LVD were defined as LVEF < 50% and ≥50%, respectively, as measured by echocardiography after MVr and before discharge. Results: Of the 234 patients, 52 (22.2%) developed LVD at median three days (interquartile range: 3–4 days). Preoperative forward LVEF in the LVD and non-LVD groups were 24.0% (18.9–29.5%) and 33.2% (26.4–39.4%), respectively (p < 0.001). Receiver operating characteristic (ROC) analyses showed that forward LVEF was predictive of LVD, with an area under the ROC curve of 0.79 (95% confidence interval: 0.73–0.86), and an optimal cut-off was 31.8% (sensitivity: 88.5%, specificity: 58.2%, positive predictive value: 37.7%, and negative predictive value: 94.6%). Preoperative forward LVEF significantly correlated with preoperative mitral regurgitant volume (correlation coefficient [CC] = −0.86, p < 0.001) and regurgitant fraction (CC = −0.98, p < 0.001), but not with preoperative LVEF (CC = 0.112, p = 0.088). Conclusion: Preoperative forward LVEF could be useful in predicting postoperative LVD immediately after MVr in patients with DMR and normal LVEF, with an optimal cut-off of 31.8%.

scholarly journals Parasympathetic effects on cardiac electrophysiology during exercise and recovery in patients with left ventricular dysfunction

2009 ◽  
Vol 297 (2) ◽  
pp. H743-H749 ◽  
Author(s):  
Alexandru B. Chicos ◽  
Prince J. Kannankeril ◽  
Alan H. Kadish ◽  
Jeffrey J. Goldberger
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Sudden Death ◽  
Ejection Fraction ◽  
Left Ventricular Dysfunction ◽  
Cardiac Electrophysiology ◽  
Cycle Length ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Depressed parasympathetic activity has been proposed to be associated with an increased risk of sudden death. Parasympathetic effects (PE) on cardiac electrophysiology during exercise and recovery have not been studied in patients with left ventricular dysfunction. We performed noninvasive electrophysiological studies (NI-EPS) and characterized the electrophysiological properties of the sinus node, atrioventricular (AV) node, and ventricle in subjects with depressed left ventricular ejection fraction and dual-chamber defibrillators. NI-EPS were performed during rest, exercise, and recovery at baseline and after parasympathetic blockade with atropine to assess PE (the difference between parameter values in the 2 conditions). Ten subjects (9 men: age, 60 ± 9 yr; and left ventricular ejection fraction, 29 ± 8%) completed the study. All NI-EPS parameters decreased during exercise and trended toward rest values during recovery. PE at rest, during exercise, and during recovery, respectively, were on sinus cycle length, 320 ± 71 ( P = 0.0001), 105 ± 60 ( P = 0.0003), and 155 ± 82 ms ( P = 0.0002); on AV block cycle length, 137 ± 136 ( P = 0.09), 37 ± 19 ( P = 0.002), and 61 ± 39 ms ( P = 0.006); on AV interval, 58 ± 32 ( P = 0.035), 22 ± 13 ( P = 0.002), and 36 ± 20 ms ( P = 0.001); on ventricular effective refractory period, 15.8 ± 11.3 ( P = 0.02), 4.7 ± 15.2 ( P = 0.38), and 6.8 ± 15.5 ms ( P = 0.20); and on QT interval, 13 ± 12 ( P = 0.13), 3 ± 17 ( P = 0.6), and 20 ± 23 ( P = 0.04). In conclusion, we describe for the first time the changes in cardiac electrophysiology and PE during rest, exercise, and recovery in subjects with left ventricular dysfunction. PEs are preserved in these patients. Thus the role of autonomic changes in the pathophysiology of sudden death requires further exploration.

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