Left Ventricular Torsion Shear Angle Volume Approach for Noninvasive Evaluation of Diastolic Dysfunction in Preserved Ejection Fraction

Objective: The aim of this study was to quantify left ventricular torsion by newly applied cardiovascular magnetic resonance feature tracking (CMR-FT), and to evaluate the clinical value of the ventricular torsion as a sensitive indicator of cardiac function by comparison of preoperative and postoperative torsion.Methods: A total of 54 volunteers and 36 patients with previous myocardial infarction (MI) and LV ejection fraction (EF) between 30%-50% were screened preoperatively or postoperatively by MRI. The patients’ short axis views of the whole heart were acquired, and all patients had a scar area >75% in at least one of the anterior or inferior segments. Their apical and basal rotation values were analyzed by feature tracking, and the correlation analysis was performed for the improvement of LV torsion and ejection fraction after CABG. The intra- and inter-observer reliabilities of torsion measured by CMR-FT were assessed.Results: In normal hearts, the apex rotated counterclockwise in the systolic period with the peak rotation as 10.2 ± 4.8°, and the base rotated clockwise as the peak value was 7.0 ± 3.3°. There was a timing hiatus between the apex and base untwisting, during which period the heart recoils and its suction sets the stage for the following rapid filling period. The postoperative torsion and rotation significantly improved compared with preoperative ones. However, the traditional indicator of cardiac function, ejection fraction, didn’t show significant improvement.Conclusion: Left ventricular torsion derived from CMR-FT, which does not require specialized CMR sequences, was sensitive to patients with low ejection fraction whose cardiac function significantly improved after CABG. The rapid acquisition of this measurement has potential for the assessment of cardiac function in clinical practice.

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Opportunistic screening models for high-risk men and women to detect diastolic dysfunction and heart failure with preserved ejection fraction in the community

European Journal of Preventive Cardiology ◽

10.1177/2047487318816774 ◽

2018 ◽

Vol 26 (6) ◽

pp. 613-623 ◽

Cited By ~ 8

Author(s):

Aisha Gohar ◽

Rogier F Kievit ◽

Gideon B Valstar ◽

Arno W Hoes ◽

Evelien E Van Riet ◽

...

Keyword(s):

Heart Failure ◽

High Risk ◽

Ejection Fraction ◽

Diastolic Dysfunction ◽

Left Ventricular Diastolic Dysfunction ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Preserved Ejection Fraction ◽

Men And Women ◽

Ventricular Diastolic Dysfunction

Background The prevalence of undetected left ventricular diastolic dysfunction is high, especially in the elderly with comorbidities. Left ventricular diastolic dysfunction is a prognostic indicator of heart failure, in particularly of heart failure with preserved ejection fraction and of future cardiovascular and all-cause mortality. Therefore we aimed to develop sex-specific diagnostic models to enable the early identification of men and women at high-risk of left ventricular diastolic dysfunction with or without symptoms of heart failure who require more aggressive preventative strategies. Design Individual patient data from four primary care heart failure-screening studies were analysed (1371 participants, excluding patients classified as heart failure and left ventricular ejection fraction <50%). Methods Eleven candidate predictors were entered into logistic regression models to be associated with the presence of left ventricular diastolic dysfunction/heart failure with preserved ejection fraction in men and women separately. Internal-external cross-validation was performed to develop and validate the models. Results Increased age and β-blocker therapy remained as predictors in both the models for men and women. The model for men additionally consisted of increased body mass index, moderate to severe shortness of breath, increased pulse pressure and history of ischaemic heart disease. The models performed moderately and similarly well in men (c-statistics range 0.60–0.75) and women (c-statistics range 0.51–0.76) and the performance improved significantly following the addition of N-terminal pro b-type natriuretic peptide (c-statistics range 0.61–0.80 in women and 0.68–0.80 in men). Conclusions We provide an easy-to-use screening tool for use in the community, which can improve the early detection of left ventricular diastolic dysfunction/heart failure with preserved ejection fraction in high-risk men and women and optimise tailoring of preventive interventions.

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Preload-corrected dynamic Starling mechanism in patients with heart failure with preserved ejection fraction

Journal of Applied Physiology ◽

10.1152/japplphysiol.00718.2017 ◽

2018 ◽

Vol 124 (1) ◽

pp. 76-82 ◽

Cited By ~ 3

Author(s):

Michinari Hieda ◽

Erin Howden ◽

Shigeki Shibata ◽

Takashi Tarumi ◽

Justin Lawley ◽

...

Keyword(s):

Heart Failure ◽

Ejection Fraction ◽

Diastolic Dysfunction ◽

Diastolic Pressure ◽

Left Ventricular Diastolic Dysfunction ◽

Left Ventricular ◽

Preserved Ejection Fraction ◽

Dynamic Modulation ◽

Power Spectral ◽

Ventricular Diastolic Dysfunction

The beat-to-beat dynamic Starling mechanism (DSM), the dynamic modulation of stroke volume (SV) because of breath-by-breath changes in left-ventricular end-diastolic pressure (LVEDP), reflects ventricular-arterial coupling. The purpose of this study was to test whether the LVEDP-SV relationship remained impaired in heart failure with preserved ejection fraction (HFpEF) patients after normalization of LVEDP. Right heart catheterization and model-flow analysis of the arterial pressure waveform were performed while preload was manipulated using lower-body negative pressure to alter LVEDP. The DSM was compared at similar levels of LVEDP between HFpEF patients ( n = 10) and age-matched healthy controls ( n = 12) (HFpEF vs. controls: 10.9 ± 3.8 vs. 11.2 ± 1.3 mmHg, P = 1.00). Transfer function analysis between diastolic pulmonary artery pressure (PAD) representing dynamic changes in LVEDP vs. SV index was applied to obtain gain and coherence of the DSM. The DSM gain was significantly lower in HFpEF patients than in the controls, even at a similar level of LVEDP (0.46 ± 0.19 vs. 0.99 ± 0.39 ml·m−2·mmHg−1, P = 0.0018). Moreover, the power spectral density of PAD, the input variability, was greater in the HFpEF group than the controls (0.75 ± 0.38 vs. 0.28 ± 0.26 mmHg2, P = 0.01). Conversely, the power spectral density of SV index, the output variability, was not different between the groups ( P = 0.97). There was no difference in the coherence, which confirms the reliability of the linear transfer function between the two groups (0.71 ± 0.13 vs. 0.77 ± 0.19, P = 0.87). The DSM gain in HFpEF patients is impaired compared with age-matched controls even at a similar level of LVEDP, which may reflect intrinsic LV diastolic dysfunction and incompetence of ventricular-arterial coupling. NEW & NOTEWORTHY The beat-to-beat dynamic Starling mechanism (DSM), the dynamic modulation of stroke volume because of breath-by-breath changes in left-ventricular end-diastolic pressure (LVEDP), reflects ventricular-arterial coupling. Although the DSM gain is impaired in heart failure with preserved ejection fraction (HFpEF) patients, it is not clear whether this is because of higher LVEDP or left-ventricular diastolic dysfunction. The DSM gain in HFpEF patients is severely impaired, even at a similar level of LVEDP, which may reflect intrinsic left-ventricular diastolic dysfunction.

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ASSOCIATION OF LEFT VENTRICULAR DIASTOLIC DYSFUNCTION WITH ELEVATED NT-pro-BNP IN GENERAL INTENSIVE CARE UNIT PATIENTS WITH PRESERVED EJECTION FRACTION

Shock ◽

10.1097/shk.0b013e3181ad31f8 ◽

2010 ◽

Vol 33 (2) ◽

pp. 141-148 ◽

Cited By ~ 29

Author(s):

Ignatios Ikonomidis ◽

Maria Nikolaou ◽

Ioanna Dimopoulou ◽

Ioannis Paraskevaidis ◽

John Lekakis ◽

...

Keyword(s):

Intensive Care Unit ◽

Intensive Care ◽

Ejection Fraction ◽

Diastolic Dysfunction ◽

Left Ventricular Diastolic Dysfunction ◽

Left Ventricular ◽

General Intensive Care Unit ◽

Preserved Ejection Fraction ◽

Ventricular Diastolic Dysfunction

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Myocardial hypertrophy and its role in heart failure with preserved ejection fraction

Journal of Applied Physiology ◽

10.1152/japplphysiol.00374.2015 ◽

2015 ◽

Vol 119 (10) ◽

pp. 1233-1242 ◽

Cited By ~ 51

Author(s):

Frank R. Heinzel ◽

Felix Hohendanner ◽

Ge Jin ◽

Simon Sedej ◽

Frank Edelmann

Keyword(s):

Heart Failure ◽

Ejection Fraction ◽

Diastolic Dysfunction ◽

Clinical Evidence ◽

Mechanical Load ◽

Contractile Function ◽

Surrogate Marker ◽

Left Ventricular ◽

Structural Abnormality ◽

Preserved Ejection Fraction

Left ventricular hypertrophy (LVH) is the most common myocardial structural abnormality associated with heart failure with preserved ejection fraction (HFpEF). LVH is driven by neurohumoral activation, increased mechanical load, and cytokines associated with arterial hypertension, chronic kidney disease, diabetes, and other comorbidities. Here we discuss the experimental and clinical evidence that links LVH to diastolic dysfunction and qualifies LVH as one diagnostic marker for HFpEF. Mechanisms leading to diastolic dysfunction in LVH are incompletely understood, but may include extracellular matrix changes, vascular dysfunction, as well as altered cardiomyocyte mechano-elastical properties. Beating cardiomyocytes from HFpEF patients have not yet been studied, but we and others have shown increased Ca2+ turnover and impaired relaxation in cardiomyocytes from hypertrophied hearts. Structural myocardial remodeling can lead to heterogeneity in regional myocardial contractile function, which contributes to diastolic dysfunction in HFpEF. In the clinical setting of patients with compound comorbidities, diastolic dysfunction may occur independently of LVH. This may be one explanation why current approaches to reduce LVH have not been effective to improve symptoms and prognosis in HFpEF. Exercise training, on the other hand, in clinical trials improved exercise tolerance and diastolic function, but did not reduce LVH. Thus current clinical evidence does not support regression of LVH as a surrogate marker for (short-term) improvement of HFpEF.

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MO062CHRONIC KIDNEY DISEASE, INFLAMMATION, AND HEART FAILURE WITH PRESERVED EJECTION FRACTION: A RENAL-CARDIO AXIS?

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa140.mo062 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Alejandro Chade ◽

Maxx Williams ◽

Jason Engel ◽

Gene Bidwell

Keyword(s):

Heart Failure ◽

Cardiovascular Risk ◽

Kidney Disease ◽

Ejection Fraction ◽

Diastolic Dysfunction ◽

Left Ventricular ◽

Swine Model ◽

Preserved Ejection Fraction ◽

Renal Inflammation ◽

Tnf Α

Abstract Background and Aims Inflammation contributes to progressive renal dysfunction and increases cardiovascular mortality of patients with chronic kidney disease (CKD). The association of CKD and heart failure with preserved ejection fraction (HFpEF) is observed in up to 50%, suggesting the possibility of a shared pathophysiology. CKD and HFpEF are commonly associated with inflammation. Using a novel swine model of CKD and HFpEF, we propose that a renal-cardio inflammatory axis drives diastolic dysfunction and HFpEF in CKD and that targeting renal inflammation will improve cardiac health and reduce cardiovascular risk. Methods We developed a biopolymer-fused peptide of nuclear-factor kappa (NFk)B (ELP-p50i) that we show it blocks its activity in vitro and in vivo. NFkB is a key pro-inflammatory transcription factor that is upregulated in CKD. To test our hypothesis, we induced CKD in 10 pigs via bilateral renovascular disease and dyslipidemia. Pigs were observed for 6 weeks, renal hemodynamics quantified (multi-detector CT), then randomized to single intra-renal ELP-p50i or placebo (n=5 each), and studies repeated 8 weeks later accompanied by echocardiographic assessment. Blood pressure was continuously measured (telemetry). Blood was collected to measure circulating TNF-α and biomarkers of HF (ANP, BNP). Furthermore, kidneys and hearts were used to quantify expression of factors involved in NFkB signaling. Results CKD led to a significant loss of renal function, accompanied by left ventricular hypertrophy and diastolic dysfunction with pEF, increased renal mRNA expression of TNF-α and canonical and non-canonical mediators of NFkB signaling, and elevated systemic TNF-α, ANP, and BNP, indicating renal and cardiac dysfunction. Most of these changes were improved after intra-renal ELP-p50i, although cardiac inflammatory signaling was unchanged (Figure) suggesting the kidney as a source of inflammation that can target the heart in CKD. Conclusion We show that a renal anti-inflammatory strategy via targeted inhibition of renal NFkB improves renal and cardiac function in CKD, suggesting an inflammatory renal-cardio axis. The translational pathological features of CKD and HFpEF combined with the predictive power of the model may contribute to advance the field towards new treatments targeting renal inflammation to reduce cardiovascular risk in CKD.

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