scholarly journals The Impact of Deep Y Descent on Hemodynamics in Patients With Heart Failure and Preserved Left Ventricular Systolic Function

2021 ◽  
Vol 8 ◽  
Author(s):  
Daisuke Harada ◽  
Hidetsugu Asanoi ◽  
Takahisa Noto ◽  
Junya Takagawa

Background: Influence of right ventricular diastolic function on the hemodynamics of heart failure (HF). We aimed to clarify the hemodynamic features of deep Y descent in the right atrial pressure waveform in patients with HF and preserved left ventricular systolic function.Methods: In total, 114 consecutive inpatients with HF who had preserved left ventricular systolic function (left ventricular ejection fraction ≥ 50%) and right heart catheterization were retrospectively enrolled in this study. The patients were divided into two groups according to right atrial pressure waveform, and those with Y descent deeper than X descent in the right atrial pressure waveform were assigned to the deep Y descent group. We enrolled another seven patients (two men, five women; mean age, 87 ± 6) with HF and preserved ejection fraction, and implanted a pacemaker to validate the results of this study.Results: The patients with deep Y descent had a higher rate of atrial fibrillation, higher right atrial pressure and mean pulmonary arterial pressure, and lower stroke volume and cardiac index than those with normal Y descent (76 vs. 7% p < 0.001, median 8 vs. 5 mmHg p = 0.001, median 24 vs. 21 mmHg p = 0.036, median 33 vs. 43 ml/m2p < 0.001, median 2.2 vs. 2.7 L/m2, p < 0.001). Multiple linear regression revealed a negative correlation between stroke volume index and pulmonary vascular resistance index (wood unit*m2) only in the patients with deep Y descent (estimated regression coefficient: −1.281, p = 0.022). A positive correlation was also observed between cardiac index and heart rate in this group (r = 0.321, p = 0.038). In the other seven patients, increasing the heart rate (from median 60 to 80/min, p = 0.001) significantly reduced the level of BNP (from median 419 to 335 pg/ml, p = 0.005).Conclusions: The hemodynamics of patients with HF with deep Y descent and preserved left ventricular systolic function resembled right ventricular restrictive physiology. Optimizing the heart rate may improve hemodynamics in these patients.

2013 ◽  
Vol 3 (2) ◽  
pp. 29 ◽  
Author(s):  
Giuseppe Cocco ◽  
Paul Jerie

Multicenter trials have demonstrated that in patients with sinus rhythm ivabradine is effective in the therapy of ischemic heart disease and of impaired left ventricular systolic function. Ivabradine is ineffective in atrial fibrillation. Many patients with symptomatic heart failure have diastolic dysfunction with preserved left ventricular systolic function, and many have asymptomatic paroxysmal atrial fibrillation. Ivabradine is not indicated in these conditions, but it happens that it is <em>erroneously</em> used. Digoxin is now considered an outdated and potentially dangerous drug and while effective in the mentioned conditions, is rarely used. The aim of the study was to compare the therapeutic effects of ivabradine in diastolic heart failure with preserved left ventricular systolic function. Patients were assigned to ivabradine or digoxin according to a randomization cross-over design. Data were single-blind analyzed. The analysis was performed using an intention-to-treat method. Forty-two coronary patients were selected. In spite of maximally tolerated therapy with renin-antagonists, diuretics and ?-blockers, they had congestive diastolic heart failure with preserved systolic function. Both ivabradine and digoxin had positive effects on dyspnea, Nterminal natriuretic peptide, heart rate, duration of 6-min. walk-test and signs of diastolic dysfunction, but digoxin was high-statistically more effective. Side-effects were irrelevant. Data were obtained in a single-center and from 42 patients with ischemic etiology of heart failure. The number of patients is small and does not allow assessing mortality. In coronary patients with symptomatic diastolic heart failure with preserved systolic function low-dose digoxin was significantly more effective than ivabradine and is much cheaper. One should be more critical about ivabradine and low-dose digoxin in diastolic heart failure. To avoid possible negative effects on the cardiac function and a severe reduction of the cardiac output the resting heart rate should not be decreased to &lt;65 beats/min.


2020 ◽  
Vol 132 (2) ◽  
pp. 321-329
Author(s):  
Alexandre Bedet ◽  
Guillaume Voiriot ◽  
Julien Ternacle ◽  
Elisabeth Marcos ◽  
Serge Adnot ◽  
...  

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Tachycardia is a hallmark of sepsis. An elevated heart rate could impair ventricular filling and increase myocardial oxygen demand. β-Blockers and ivabradine (a selective inhibitor of If channels in the sinoatrial node) are both able to control sinus tachycardia, with the latter drug being devoid of negative inotropic effect. This work aimed at assessing the hemodynamic effects of ivabradine as compared with a β-blocker (atenolol) during murine peritonitis. Methods Ivabradine (3 μg/g), atenolol (3 μg/g), or placebo was administered intraperitoneally 2 h after induction of peritonitis (cecal ligation and puncture) in male C57BL6 mice. The authors used invasive (left ventricular catheterization) and noninvasive (transthoracic echocardiography) monitoring to assess hemodynamics 20 h after surgery, including heart rate, blood pressure, left ventricular systolic, and diastolic function (n = 10 mice/group). The authors also assessed overall mortality 30 and 60 h after surgery in a distinct subset of animals (n = 20 mice/group). Descriptive data are presented as median (25th to 75th percentile). Results As compared with placebo (601 beats/min [547 to 612]), ivabradine (447 beats/min [430 to 496]) and atenolol (482 beats/min [412 to 505]) blunted sepsis-induced tachycardia assessed by transthoracic echocardiography in awake animals (P &lt; 0.001 and P = 0.004, respectively). Unlike ivabradine, atenolol reduced cardiac output, systolic blood pressure, and left ventricular systolic function (as assessed by ejection fraction, maximal left ventricular pressure rise, and anterior wall strain rate) as compared with septic mice receiving placebo. There was no difference in survival 60 h after sepsis induction with ivabradine (6 of 20, 30%) or atenolol (7 of 20, 35%), as compared with placebo (5 of 20, 25%; P = 0.224). Conclusions Heart rate control could be similarly achieved by ivabradine or atenolol, with preservation of blood pressure, cardiac output, and left ventricular systolic function with the former drug.


2001 ◽  
Vol 280 (1) ◽  
pp. H392-H400 ◽  
Author(s):  
Maartje De Vroomen ◽  
Paul Steendijk ◽  
Robbert H. Lopes Cardozo ◽  
Hens H. A. Brouwers ◽  
Frank Van Bel ◽  
...  

Respiratory distress syndrome (RDS) causes pulmonary hypertension. It is often suggested that this increased afterload for the right ventricle (RV) might lead to cardiac dysfunction. To examine this, we studied biventricular function in an experimental model. RDS was induced by lung lavages in seven newborn lambs. Five additional lambs served as controls. Cardiac function was quantified by indexes derived from end-systolic pressure-volume relations obtained by pressure-conductance catheters. After lung lavages, a twofold increase of mean pulmonary arterial pressure (from 15 to 34 mmHg) was obtained and lasted for the full 4-h study period. Stroke volume was maintained (5.2 ± 0.6 ml at baseline and 6.1 ± 1.4 ml at 4 h of RDS), while RV end-diastolic volume showed only a slight increase (from 6.5 ± 2.3 ml at baseline to 7.7 ± 1.3 ml at 4 h RDS). RV systolic function improved significantly, as indicated by a leftward shift and increased slope of the end-systolic pressure-volume relation. Left ventricular systolic function showed no changes. In control animals, pulmonary arterial pressure did not increase and right and left ventricular systolic function remained unaffected. In the face of increased RV afterload, the newborn heart is able to maintain cardiac output, primarily by improving systolic RV function through homeometric autoregulation.


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