Heart failure with preserved ejection fraction; the other half of the heart failure, how it stands in 2013
Kunal Bikram ShahaRikesh TamrakarMan Bahadur KCDeewakar SharmaYadav Deo BhattSujeeb RajbhandariRajit SharmaRabindra Simkhada
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Abstract:
Last two decade, heart failure with preserved ejection fraction was deprived from being considered as a part of spectrum of heart failure. May be heart failure with preserved ejection fraction was common but not recognized by cardiology fraternity. Heart failure with reduced ejection fraction and heart failure with preserved ejection fraction each make up about half of the overall heart failure burden. But the paradox is: morbidity and mortality in heart failure with preserved ejection fraction despite being similar to patients with heart failure with reduced ejection fraction, today’s cardiology community has not much to offer in terms of mortality reducing treatment. The term diastolic heart failure has been well replaced by heart failure with preserved ejection fraction because multiple non-diastolic abnormalities in cardiovascular function also contribute to heart failure with preserved ejection fraction and diastolic dysfunction always accompanied heart failure with reduced ejection fraction. Diagnosis of heart failure with preserved ejection fraction is an uphill task since it relies upon careful clinical evaluation, doppler (pulse wave and tissue) echocardiography, and invasive hemodynamic assessment after exclusion of potential noncardiac causes of symptoms suggestive of heart failure. Patients with heart failure with preserved ejection fraction are usually older women with a history of hypertension. Obesity, coronary artery disease, diabetes mellitus, and atrial fibrillation are also highly prevalent in heart failure with preserved ejection fraction. Cornerstone of treatment of this entity revolves around treatment of underlying cause and symptom guided therapy. Nepalese Heart Journal | Volume 10 | No.1 | November 2013| Pages 46-56 DOI: http://dx.doi.org/10.3126/njh.v10i1.9747Keywords:
Diastolic heart failure
Owing to the overwhelming obesity epidemic, preserved ejection fraction heart failure commonly ensues in patients with severe obesity and the obese phenotype of preserved ejection fraction heart failure is now commonplace in clinical practice. Severe obesity and preserved ejection fraction heart failure share congruent cardiovascular, immune, and renal derangements that make it difficult to ascertain whether the obese phenotype of preserved ejection fraction heart failure is the convergence of two highly prevalent conditions or severe obesity enables the development and progression of the syndrome of preserved ejection fraction heart failure. Nevertheless, the obese phenotype of preserved ejection fraction heart failure provides a unique opportunity to assess whether sustained and sizeable loss of excess body weight via metabolic bariatric surgery reverses the concentric left ventricular remodeling that patients with preserved ejection fraction heart failure commonly display.
Ventricular remodeling
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PREVIEWCongestive heart failure caused by abnormal diastolic function may be far more common than previously recognized. The diastolic disorder must be distinguished from systolic abnormalities because treatment is significantly different. Although prognosis is better with diastolic dysfunction than with systolic dysfunction, mortality and morbidity continue to be high in elderly patients. Drs Spencer and Lang describe the mechanisms, symptoms, diagnosis, and management of diastolic heart failure.
Diastolic heart failure
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Diastolic heart failure
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Diastolic heart failure
Concomitant
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Background: Recent trial data suggest that stratification of patients with heart failure with preserved ejection fraction (HFpEF) according to left ventricular ejection fraction (LVEF) provides a means for dissecting different treatment responses. However, the differential pathophysiologic considerations have rarely been described. Methods: This prospective, single-center study analyzed consecutive symptomatic patients with HFpEF diagnosed according to the 2016 European Society of Cardiology heart failure guidelines. Patients were grouped into LVEF 50% to 60% and LVEF >60% cohorts. All patients underwent cardiac magnetic resonance imaging. Transfemoral cardiac catheterization was performed to derive load-dependent and load-independent left ventricular (LV) properties on pressure–volume loop analyses. Results: Fifty-six patients with HFpEF were enrolled and divided into LVEF 50% to 60% (n=21) and LVEF >60% (n=35) cohorts. On cardiac magnetic resonance imaging, the LVEF >60% cohort showed lower LV end-diastolic volumes ( P =0.019) and end-systolic volumes ( P =0.001) than the LVEF 50% to 60% cohort; stroke volume ( P =0.821) did not differ between the cohorts. Extracellular volume fraction was higher in the LVEF 50% to 60% cohort than in the LVEF >60% cohort (0.332 versus 0.309; P =0.018). Pressure-volume loop analyses demonstrated higher baseline LV contractility (end-systolic elastance, 1.85 vs 1.33 mm Hg/mL; P <0.001) and passive diastolic stiffness (β constant, 0.032 versus 0.018; P =0.004) in the LVEF >60% cohort. Ventriculo-arterial coupling (end-systolic elastance/arterial elastance) at rest was in the range of optimized stroke work in the LVEF >60% cohort but was impaired in the LVEF 50% to 60% cohort (1.01 versus 0.80; P =0.005). During handgrip exercise, patients with LVEF >60% had higher increases in end-systolic elastance (1.85 versus 0.82 mm Hg/mL; P =0.023), attenuated increases in indexed end-systolic volume (−1 versus 7 mL/m²; P <0.004), and more exaggerated increases in LV filling pressures (8 vs 5 mm Hg; P =0.023). LV stroke volume decreased in the LVEF >60% cohort ( P =0.007) under exertion. Conclusions: Patients with HFpEF in whom LVEF ranged from 50% to 60% demonstrated reduced contractility, impaired ventriculo-arterial coupling, and higher extracellular volume fraction. In contrast, patients with HFpEF and a LVEF >60% demonstrated a hypercontractile state with excessive LV afterload and diminished preload reserve. A LVEF-based stratification of patients with HFpEF identified distinct morphologic and pathophysiologic subphenotypes.
Fraction (chemistry)
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OBJECTIVE: To determine the variation in indexed stroke volume (LVSVi) in children with varying left ventricle ejection fraction (LVEF) using cardiac magnetic imaging (CMR) and its correlation with various cardiac factors. METHODS: This observational comparative study was conducted at The Children’s Hospital, Lahore, Pakistan from December 2018 to November 2021. All children below 18 years’ age presenting to hospital for CMR for tissue characterization, having normal vital organs function and no clinical signs of heart failure were included in the study. Relevant clinical data was recorded. CMR was performed using 1.5T Philips Ingenia MRI scanner. The data were analyzed with varying LVEF and correlation of LVSVi with various cardiac factors including indexed left ventricular end diastolic volume (LVEDVi), cardiac output (CO) and heart rate (HR). RESULTS: Out of 175 patients, 170 children up to 18 years old completed the test with mean age 14.3±3.3 years. Mean LVSVi was 42+12 ml/m2 which followed Frank Starling curve except in children with LVEF <36%. Mean LVEDVi was 86±34 ml/m2. LVSVi did not correlate with heart rate or indexed ventricular systolic volumes acting as an independent variable. Minimum LVSVi remained similar all groups as demonstrated through centile distribution. CONCLUSION: Indexed stroke volume is an independent variable in children having normal vital organs function with varying LVEF. It can serve as an independent monitoring parameter for clinical management of children with impaired ejection fraction.
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Diastolic heart failure
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Objective To develop a new method for measuring stroke volume and ejection fraction in the infarct and non infarct area with three dimensional color kinesis(CK) technique.Methods A set of left ventricular two dimensional CK images at end systole were acquired in 20 patients with old myocardial infarction using multiplane transesophageal echocardiographic technique and inputted into a self made three dimensional reconstruction system to reconstruct three dimensional CK images of the entire left ventricle,infarct area and non infarct area.The following parameters were calculated from the three groups of three dimensional CK images: stroke volume,wall segment averaged stroke volume,ejection fraction and wall segment averaged ejection fraction.Results Stroke volume and ejection fraction in the infarct and non infarct area were significantly lower than the corresponding values in the entire left ventricle(P 0.01 ).The wall segment averaged stroke volume and ejection fraction decreased progressively in the order of non infarct area,entire left ventricle and infarct area(P 0.01 ～ 0.05 ).The regional and wall segment averaged stroke volume and ejection fraction were the lowest in the infarct area(P 0.01 ).Conclusions The systolic function in the entire left ventricle,infarct area and non infarct area can be accurately measured with three dimensional CK technique.This new method is of value in assessing left ventricular regional function and myocardial viability as well as in therapeutic decision making and prognostic estimation,and therefore,deserves further investigation.
Stroke
End-systolic volume
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Patients with heart failure and a normal left ventricular ejection fraction have significantly reduced left ventricular long-axis function. This paper proposes an explanation for this apparent paradox and suggests a new mechanism of "diastolic" heart failure.The effect of changes in left ventricular hypertrophy on stroke volume and ejection fraction in non-dilated left ventricles was calculated using the area-length method. Further, the effect of a reduction in long-axis shortening on these parameters was determined.Increasing left ventricular hypertrophy resulted in augmentation of systolic wall thickening and ejection fraction but not stroke volume when long-axis shortening was normal. In the presence of abnormal long-axis function, stroke volume was reduced but ejection fraction was preserved.The model predicts that the normal ejection fraction in patients with heart failure may be explained by the presence of left ventricular hypertrophy. The resulting amplified radial thickening in the setting of reduced long-axis shortening explains the preservation of ejection fraction. The reduced stroke volume in the precompensated state rather than diastolic dysfunction may be the cause of heart failure.
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Left Ventricles
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Left atrial (LA) storage fraction is defined as the ratio of storage volume of the left atrium (LA) during ventricular systole to left ventricular (LV) stroke volume. To test their hypothesis that left atrial (LA) storage fraction is increased to compensate for impaired LV filling in the heart of aged subjects or with impaired LV ejection fraction, the authors studied 33 "normal" subjects and 25 patients with coronary artery disease. LA volume was measured by LA cineangiocardiography, and LV stroke volume and LV ejection fraction were measured by LV cineangiocardiography. To further evaluate the determi nants of changes in LA storage fraction, they measured the ratio of LA active release volume to LV stroke volume, and the ratio of LA passive release volume to LV stroke volume. In "normal" subjects, LA storage fraction was increased with age ( r = 0.584, P < 0.01). In patients with coronary artery disease, LA storage fraction was increased as LV ejection fraction was decreased ( r = -0.525, P < 0.01). In both cases, LA active release fraction was significantly associated with changes in LA storage fraction rather than in LA passive release fraction. They conclude that LA storage fraction may be an important determinant of LV filling mainly through the LA active release fraction.
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