Bhatia RS, Tu JV, Lee DS, Austin PC, Fang J, Haouzi A, Gong Y, Liu PP. Outcome of heart failure with preserved ejection fraction in a population-based study

Heart & Stroke/Richard Lewar Centre of Excellence, University of Toronto, and the Division of Cardiology, Toronto General Hospital, University Health Network, Toronto, ON, Canada.
New England Journal of Medicine (Impact Factor: 55.87). 08/2006; 355(3):260-9. DOI: 10.1056/NEJMoa051530
Source: PubMed


The importance of heart failure with preserved ejection fraction is increasingly recognized. We conducted a study to evaluate the epidemiologic features and outcomes of patients with heart failure with preserved ejection fraction and to compare the findings with those from patients who had heart failure with reduced ejection fraction.
From April 1, 1999, through March 31, 2001, we studied 2802 patients admitted to 103 hospitals in the province of Ontario, Canada, with a discharge diagnosis of heart failure whose ejection fraction had also been assessed. The patients were categorized in three groups: those with an ejection fraction of less than 40 percent (heart failure with reduced ejection fraction), those with an ejection fraction of 40 to 50 percent (heart failure with borderline ejection fraction), and those with an ejection fraction of more than 50 percent (heart failure with preserved ejection fraction). Two groups were studied in detail: those with an ejection fraction of less than 40 percent and those with an ejection fraction of more than 50 percent. The main outcome measures were death within one year and readmission to the hospital for heart failure.
Thirty-one percent of the patients had an ejection fraction of more than 50 percent. Patients with heart failure with preserved ejection fraction were more likely to be older and female and to have a history of hypertension and atrial fibrillation. The presenting history and clinical examination findings were similar for the two groups. The unadjusted mortality rates for patients with an ejection fraction of more than 50 percent were not significantly different from those for patients with an ejection fraction of less than 40 percent at 30 days (5 percent vs. 7 percent, P=0.08) and at 1 year (22 percent vs. 26 percent, P=0.07); the adjusted one-year mortality rates were also not significantly different in the two groups (hazard ratio, 1.13; 95 percent confidence interval, 0.94 to 1.36; P=0.18). The rates of readmission for heart failure and of in-hospital complications did not differ between the two groups.
Among patients presenting with new-onset heart failure, a substantial proportion had an ejection fraction of more than 50 percent. The survival of patients with heart failure with preserved ejection fraction was similar to that of patients with reduced ejection fraction.

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Available from: Peter P Liu, May 10, 2014
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    • "These findings indicate that myocardial wall thickness and ejection fraction are independent risk factors for mortality.[29] This observation may explain why heart failure with a reduced ejection fraction has the same mortality as HFNEF when presenting symptoms are similar.[30] [31] These data would also explain why measures of myocardial mechanics such as global longitudinal and circumferential strain are better markers of mortality and morbidity than ejection fraction.[32] "
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    ABSTRACT: The purpose of this study was to determine the mathematical relationship between left ventricular ejection fraction and global myocardial strain. A reduction in myocardial strain would be expected to cause a fall in ejection fraction. However, there is abundant evidence that abnormalities of myocardial strain can occur with a normal ejection fraction. Explanations such as a compensatory increase in radial or circumferential strain are not supported by clinical studies. We set out to determine the biomechanical relationship between ejection fraction, wall thickness and global myocardial strain.
    04/2015; 55. DOI:10.1016/j.ijcha.2015.03.007
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    • "The high prevalence of patients with heart failure with a preserved ejection fraction (HFpEF) has highlighted the important role of left ventricular (LV) diastolic dysfunction in the development of heart failure (HF) [7] [8]. In addition, diastolic dysfunction is associated with poor prognosis, particularly in patients with advanced HF and a reduced ejection fraction [9]. "
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    ABSTRACT: Albuminuria is an established risk factor for mortality and cardiovascular events in high-risk populations. However, few studies have evaluated the relationship between normoalbuminuria and left ventricular (LV) diastolic function. The present study evaluated the impact of the low-grade albuminuria on LV diastolic function in patients with coronary artery disease (CAD).
    IJC Metabolic and Endocrine 01/2015; 106. DOI:10.1016/j.ijcme.2015.01.006
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    • "Cardiac fibrosis decreases cardiac compliance and contributes to heart failure with preserved ejection fraction (HFpEF). [9] Although HFpEF is similar to heart failure with reduced ejection fraction in terms of incidence and mortality, [10] in contrast, no therapies have been found to be effective for treating HFpEF. [11] If subclinical LPS contributes to HFpEF, this may provide novel targets to ameliorate this burgeoning problem. "
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    ABSTRACT: Background Exposure to subclinical levels of lipopolysaccharide (LPS) occurs commonly and is seemingly well tolerated. However, recurrent LPS exposure induces cardiac fibrosis over 2 to 3 months in a murine model, not mediated by the renin-angiotensin system. Subclinical LPS induces cardiac fibrosis by unique mechanisms. Methods In C57/Bl6 mice, LPS (10 mg/kg) or saline (control) were injected intraperitoneally once a week for 1–4 weeks. Mice showed no signs of distress, change in activity, appetite, or weight loss. Mice were euthanized after 3 days, 1, 2, or 4 weeks to measure cardiac expression of fibrosis-related genes and potential mediators (measured by QRT-PCR), including micro-RNA (miR) and NADPH oxidase (NOX). Collagen fraction area of the left ventricle was measured with picrosirius red staining. Cardiac fibroblasts isolated from adult mouse hearts were incubated with 0, 0.1, 1.0 or 10 ng/ml LPS for 48 hours. Results Cardiac miR expression profiling demonstrated decreased miR-29c after 3 and 7 days following LPS, which were confirmed by QRT-PCR. The earliest changes in fibrosis-related genes and mediators that occurred 3 days after LPS were increased cardiac expression of TIMP-1 and NOX-2 (but not of NOX-4). This persisted at 1 and 2 weeks, with additional increases in collagen Iα1, collagen IIIα1, MMP2, MMP9, TIMP1, TIMP2, and periostin. There was no change in TGF-β or connective tissue growth factor. Collagen fraction area of the left ventricle increased after 2 and 4 weeks of LPS. LPS decreased miR-29c and increased NOX-2 in isolated cardiac fibroblasts. Conclusions Recurrent exposure to subclinical LPS induces cardiac fibrosis after 2–4 weeks. Early changes 3 days after LPS were decreased miR-29c and increased NOX2 and TIMP1, which persisted at 1 and 2 weeks, along with widespread activation of fibrosis-related genes. Decreased miR-29c and increased NOX2, which induce cardiac fibrosis in other conditions, may uniquely mediate LPS-induced cardiac fibrosis.
    PLoS ONE 09/2014; 9(9):e107556. DOI:10.1371/journal.pone.0107556 · 3.23 Impact Factor
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