Dataset Information

Myocardial strain for heart failure with preserved ejection fraction but without diastolic dysfunction.

ABSTRACT:

Aims

Some patients with apparent heart failure (HF) have an ejection fraction (EF) ≥ 50% and elevated levels of natriuretic peptides (NPs), but no significant diastolic dysfunction. Among these, some may have HF, others may not. Myocardial strain is an excellent prognostic factor.

Methods and results

Among 4312 consecutive patients with acute HF from three tertiary hospitals, we included 355 patients with EF of ≥50% and elevated levels of NPs, without significant diastolic dysfunction. Patients were classified as having impaired global longitudinal strain (GLS < 16%) or normal GLS (GLS ≥ 16%). The primary endpoint was 5 year all-cause mortality. The mean age was 70.3 years and 49% were female. Overall, 107 patients (30.1%) died at 5 years. As per the definition, 176 (49.6%) patients had impaired GLS and 179 (50.4%) had normal GLS. Patients with normal GLS had lower 5 year all-cause mortality than those with impaired GLS (P < 0.001). When comparing with the 11 365 age-matched and sex-matched controls, patients with normal GLS had the same long-term survival as the controls (P = 0.834), whereas those with impaired GLS had 48% increased risk of all-cause mortality (hazard ratio, 1.48; 95% confidence interval, 1.17-1.89).

Conclusions

Among patients with apparent HF and preserved EF but without diastolic dysfunction, those with impaired GLS may be considered to have HF.

SUBMITTER: Park JJ

PROVIDER: S-EPMC9715819 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Publications

Myocardial strain for heart failure with preserved ejection fraction but without diastolic dysfunction.

Park Jin Joo JJ Hwang In-Chang IC Kang Si-Hyuck SH Park Jun-Bean JB Park Jae-Hyeong JH Cho Goo-Yeong GY

ESC heart failure 20220712 5

<h4>Aims</h4>Some patients with apparent heart failure (HF) have an ejection fraction (EF) ≥ 50% and elevated levels of natriuretic peptides (NPs), but no significant diastolic dysfunction. Among these, some may have HF, others may not. Myocardial strain is an excellent prognostic factor.<h4>Methods and results</h4>Among 4312 consecutive patients with acute HF from three tertiary hospitals, we included 355 patients with EF of ≥50% and elevated levels of NPs, without significant diastolic dysfunc ...[more]

PMID: 35821568

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Project description:AimsThe diagnostic and treatment of patients with heart failure with preserved ejection fraction (HFpEF) are both hampered by an incomplete understanding of the pathophysiology of the disease. Novel imaging tools to adequately identify these patients from individuals with a normal cardiac function and respectively patients with HF with reduced EF are warranted. Computing multilayer myocardial strain with feature tracking is a fast and accurate method to assess cardiac deformation. Our purpose was to assess the HFpEF diagnostic ability of multilayer strain parameters and compare their sensitivity and specificity with other established parameters.Methods and resultsWe included 20 patients with a diagnosis of HFpEF and, respectively, 20 matched controls. We assessed using feature-tracking cardiac magnetic resonance longitudinal and circumferential myocardial strain at three distinct layers of the myocardium: subendocardial (Endo-), mid-myocardial (Myo-), and subepicardial (Epi-). Comparatively, we additionally assessed various others clinical, imaging, and biochemical parameters with a putative role in HFpEF diagnostic: left ventricular end-diastolic volume (LVEDV), left ventricular mass (LVM), interventricular septum (IVS) wall thickness and free wall thickness, left atrial volume and strain, septal and lateral mitral annular early diastolic velocity (e`), E/e´ ratio, and plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP). Global longitudinal strain (GLS) is significantly impaired at Endo (-20.8 ± 4.0 vs. -23.2 ± 3.4, P = 0.046), Myo- (-18.0 ± 3.0 vs. -21.0 ± 2.5, P = 0.002), and Epi- (-12.2 ± 2.0 vs. -16.2 ± 2.5, P < 0.001) levels. Compared with any other imaging parameter, an Epi-GLS lower than 13% shows the highest ability to detect patients with HFpEF [area under the curve (AUC) = 0.90 (0.81-1), P < 0.001] and in tandem with NT-proBNP can diagnose with maximal sensibility (93%) and specificity (100%), patients with HFpEF from normal, composed variable [AUC = 0.98 (0.95-1), P < 0.001]. In a logistic regression model, a composite predictive variable taking into account both GLS Epi and NT-proBNP values in each individual subject reached a sensitivity of 89% and a specificity of 100% with an AUC of 0.98 (0.95-1), P < 0.001, to detect HFpEF.ConclusionsEpi-GLS is a promising new imaging parameter to be considered in the clinical assessment of HFpEF patients. Given its excellent specificity, in tandem with a highly sensitive parameter such as NT-proBNP, Epi-GLS holds the potential to greatly improve the current diagnostic algorithms.

Project description:BACKGROUND:The role of coronary microvascular disease and its impact on functional and energetic reserve in heart failure with preserved ejection fraction (HFpEF) remains unclear. We hypothesized that in response to submaximal pharmacologic stress (dobutamine), patients with HFpEF have impairment in left ventricular (LV) myocardial mechanical (external work [EW]), energetic (myocardial O2 consumption [MVO2]), and myocardial blood flow (MBF) reserve. We further assessed whether coupling of MBF to EW is impaired in HFpEF and associated with compensatory increases or pathological decreases in myocardial O2 extraction. Lastly, we assessed whether coupling of MVO2 to EW (mechanical efficiency) was impaired in HFpEF. METHODS AND RESULTS:In prospectively enrolled patients with HFpEF (n=19) and age/sex-matched healthy controls (n=19), we performed 11C-acetate positron emission tomography assessing MVO2 and MBF at rest and during dobutamine infusion. EW was calculated as stroke volume (echo)×end-systolic pressure×heart rate. At rest, compared with controls, patients with HFpEF had higher LV EW, MVO2, and MBF. With dobutamine, LV EW, MVO2, and MBF increased in both HFpEF and controls; however, the magnitude of increases was significantly smaller in HFpEF. In both groups, MBF increased in relation to EW, but in HFpEF, the slope of the relationship was significantly smaller than in controls. Myocardial O2 extraction was increased in HFpEF. Mechanical efficiency was similar in HFpEF and controls. In a post hoc analysis, HFpEF patients with LV hypertrophy (n=10) had significant reductions in LV mechanical efficiency relative to controls. CONCLUSIONS:In HFpEF during submaximal dobutamine stress, there is myocardial mechanical-, energetic- and flow-reserve dysfunction with impaired coupling of blood flow to demand and slight increases in myocardial O2 extraction. These findings provide evidence that coronary microvascular dysfunction is present in HFpEF, limits O2 supply relative to demand, and is associated with reserve dysfunction.

Project description:Heart failure with preserved ejection fraction (HFpEF) is an increasingly studied entity accounting for 50% of all diagnosed heart failure and that has claimed its own dignity being markedly different from heart failure with reduced EF in terms of etiology and natural history (Graziani et al., 2018). Recently, a growing body of evidence points the finger toward microvascular dysfunction as the major determinant of the pathological cascade that justifies clinical manifestations (Crea et al., 2017). The high burden of comorbidities such as metabolic syndrome, hypertension, atrial fibrillation, chronic kidney disease, obstructive sleep apnea, and similar, could lead to a systemic inflammatory state that impacts the physiology of the endothelium and the perivascular environment, engaging complex molecular pathways that ultimately converge to myocardial fibrosis, stiffening, and dysfunction (Paulus and Tschope, 2013). These changes could even self-perpetrate with a positive feedback where hypoxia and locally released inflammatory cytokines trigger interstitial fibrosis and hypertrophy (Ohanyan et al., 2018). Identifying microvascular dysfunction both as the cause and the maintenance mechanism of this condition has opened the field to explore specific pharmacological targets like nitric oxide (NO) pathway, sarcomeric titin, transforming growth factor beta (TGF-β) pathway, immunomodulators or adenosine receptors, trying to tackle the endothelial impairment that lies in the background of this syndrome (Graziani et al., 2018;Lam et al., 2018). Yet, many questions remain, and the new data collected still lack a translation to improved treatment strategies. To further elaborate on this tangled and exponentially growing topic, we will review the evidence favoring a microvasculature-driven etiology of this condition, its clinical correlations, the proposed diagnostic workup, and the available/hypothesized therapeutic options to address microvascular dysfunction in the failing heart.

Dataset Information

Myocardial strain for heart failure with preserved ejection fraction but without diastolic dysfunction.

Aims

Methods and results

Conclusions

Publications

Myocardial strain for heart failure with preserved ejection fraction but without diastolic dysfunction.

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