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Oxygen uptake efficiency plateau best predicts early death in heart failure.

ABSTRACT: The responses of oxygen uptake efficiency (ie, oxygen uptake/ventilation = VO(2)/VE) and its highest plateau (OUEP) during incremental cardiopulmonary exercise testing (CPET) in patients with chronic left heart failure (HF) have not been previously reported. We planned to test the hypothesis that OUEP during CPET is the best single predictor of early death in HF.We evaluated OUEP, slope of VO(2) to log(VE) (oxygen uptake efficiency slope), oscillatory breathing, and all usual resting and CPET measurements in 508 patients with low-ejection-fraction (< 35%) HF. Each had further evaluations at other sites, including cardiac catheterization. Outcomes were 6-month all-reason mortality and morbidity (death or > 24 h cardiac hospitalization). Statistical analyses included area under curve of receiver operating characteristics, ORs, univariate and multivariate Cox regression, and Kaplan-Meier plots.OUEP, which requires only moderate exercise, was often reduced in patients with HF. A low % predicted OUEP was the single best predictor of mortality (P < .0001), with an OR of 13.0 (P < .001). When combined with oscillatory breathing, the OR increased to 56.3, superior to all other resting or exercise parameters or combinations of parameters. Other statistical analyses and morbidity analysis confirmed those findings.OUEP is often reduced in patients with HF. Low % predicted OUEP (< 65% predicted) is the single best predictor of early death, better than any other CPET or other cardiovascular measurement. Paired with oscillatory breathing, it is even more powerful.

SUBMITTER: Sun XG

PROVIDER: S-EPMC4694089 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature

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Oxygen uptake efficiency plateau best predicts early death in heart failure.

Sun Xing-Guo XG Hansen James E JE Stringer William W WW

Chest 20111026 5

<h4>Background</h4>The responses of oxygen uptake efficiency (ie, oxygen uptake/ventilation = VO(2)/VE) and its highest plateau (OUEP) during incremental cardiopulmonary exercise testing (CPET) in patients with chronic left heart failure (HF) have not been previously reported. We planned to test the hypothesis that OUEP during CPET is the best single predictor of early death in HF.<h4>Methods</h4>We evaluated OUEP, slope of VO(2) to log(VE) (oxygen uptake efficiency slope), oscillatory breathing ...[more]

PMID: 22030802

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Project description:BackgroundMyocardial oxygen consumption (MVO2) and its coupling to contractile work are fundamentals of cardiac function and may be involved causally in the transition from compensated left ventricular hypertrophy to failure. Nevertheless, these processes have not been studied previously in patients with aortic valve stenosis (AS).Methods and resultsParticipants underwent 11C-acetate positron emission tomography, cardiovascular magnetic resonance, and echocardiography to measure MVO2 and myocardial external efficiency (MEE) defined as the ratio of left ventricular stroke work and the energy equivalent of MVO2. We studied 10 healthy controls (group A), 37 asymptomatic AS patients with left ventricular ejection fraction ?50% (group B), 12 symptomatic AS patients with left ventricular ejection fraction ?50% (group C), and 9 symptomatic AS patients with left ventricular ejection fraction <50% (group D). MVO2 did not differ among groups A, B, C, and D (0.105±0.02, 0.117±0.024, 0.129±0.032, and 0.104±0.026 mL/min per gram, respectively; P=0.07), whereas MEE was reduced in group D (21.0±1.6%, 22.3±3.3%, 22.1±4.2%, and 17.3±4.7%, respectively; P<0.05). Similarly, patients with global longitudinal strain greater than -12% and paradoxical low-flow, low-gradient AS had impaired MEE (P<0.05 versus controls). The ability to discriminate between symptomatic and asymptomatic patients was superior for global longitudinal strain compared with MVO2 and MEE (area under the curve 0.98, 0.48, and 0.61, respectively; P<0.05).ConclusionsAS patients display a persistent ability to maintain normal MVO2 and MEE (ie, the ability to convert energy into stroke work); however, patients with left ventricular ejection fraction <50%; global longitudinal strain greater than -12%; or paradoxical low-flow, low-gradient AS demonstrate reduced MEE. These findings suggest that mitochondrial uncoupling contributes to the dismal prognosis in patients with reduced contractile function or paradoxical low-flow, low-gradient AS.

Project description:AimsThe outpatient diuretic dose is a marker of diuretic resistance and prognosis in chronic heart failure (HF). Still, the impact of the preadmission dose on diuretic efficiency (DE) and prognosis in acute HF is not fully known.Methods and resultsWe conducted an observational and prospective study. All patients admitted for acute HF treated with intravenous diuretic and at least one criterion of congestion on admission were evaluated. Decongestion [physical examination, hemoconcentration, N-terminal pro-brain natriuretic peptide (NT-proBNP) change, and lung ultrasound], DE (weight loss and urine output per unit of 40 mg furosemide), and urinary sodium were monitored on the fifth day of admission. DE was dichotomized into high-low based on the median value. A multivariate Cox regression analysis was conducted to find predictors of HF readmission or mortality. A total of 105 patients were included between July 2017 and July 2019. Mean age was 74.5 ± 12.0 years, 64.8% were male, 33.3% had de novo HF, and mean left ventricular ejection fraction was 46 ± 17%. Median follow-up was 26 [15-35] months. Low DE based on weight loss was associated with a higher previous dose of furosemide (odds ratio [OR] 1.01 [1.00-1.02]), thiazide treatment before admission (OR 9.37 [2.19-40.14]), and lower diastolic blood pressure (OR 0.95 [0.91-0.98]) in the multivariate regression model. Only previous dose of furosemide (OR 1.01 [1.00-1.02]) and haemoglobin at admission (OR 0.76 [0.58-0.99]) were associated with low DE based on urine output in the multivariate analysis. The correlation between the previous dose of furosemide and DE based on weight loss was poor (r = -0.12; P = 0.209) and with DE based on urine output was weak to moderate (r = -0.33; P < 0.001). Low DE based on weight loss and urine output was associated with lesser decongestion measured by NT-proBNP (P = 0.011; P = 0.007), hemoconcentration (P = 0.006; P = 0.044), and lung ultrasound (P = 0.034; P = 0.029), but not by physical examination (P = 0.506; P = 0.560). Survival and event-free survival in acute decompensated HF (ADHF) were lower than in de novo HF; a preadmission dose of furosemide > 80 mg in ADHF identified patients with particularly poor prognosis (log-rank < 0.001). In ADHF, the preadmission dose of furosemide (hazard ratio [HR] 1.34 [1.08-1.67] per 40 mg) and NT-proBNP at admission (HR 1.03 [1.01-1.06] per 1000 pg/mL) were independently associated with mortality or HF readmission in the multivariate Cox regression analysis.ConclusionsThe outpatient dose of furosemide before acute HF admission predicts DE and must be taken into account when deciding on the initial diuretic dose. In ADHF, the outpatient dose of furosemide can predict long-term prognosis better than DE during hospitalization.

Project description:BACKGROUNDSudden cardiac death (SCD) remains a worldwide public health problem in need of better noninvasive predictive tools. Current guidelines for primary preventive SCD therapies, such as implantable cardioverter defibrillators (ICDs), are based on left ventricular ejection fraction (LVEF), but these guidelines are imprecise: fewer than 5% of ICDs deliver lifesaving therapy per year. Impaired cardiac metabolism and ATP depletion cause arrhythmias in experimental models, but to our knowledge a link between arrhythmias and cardiac energetic abnormalities in people has not been explored, nor has the potential for metabolically predicting clinical SCD risk.METHODSWe prospectively measured myocardial energy metabolism noninvasively with phosphorus magnetic resonance spectroscopy in patients with no history of significant arrhythmias prior to scheduled ICD implantation for primary prevention in the setting of reduced LVEF (≤35%).RESULTSBy 2 different analyses, low myocardial ATP significantly predicted the composite of subsequent appropriate ICD firings for life-threatening arrhythmias and cardiac death over approximately 10 years. Life-threatening arrhythmia risk was approximately 3-fold higher in patients with low ATP and independent of established risk factors, including LVEF. In patients with normal ATP, rates of appropriate ICD firings were several-fold lower than reported rates of ICD complications and inappropriate firings.CONCLUSIONTo the best of our knowledge, these are the first data linking in vivo myocardial ATP depletion and subsequent significant arrhythmic events in people, suggesting an energetic component to clinical life-threatening ventricular arrhythmogenesis. The findings support investigation of metabolic strategies that limit ATP loss to treat or prevent life-threatening cardiac arrhythmias and herald noninvasive metabolic imaging as a complementary SCD risk stratification tool.TRIAL REGISTRATIONClinicalTrials.gov NCT00181233.FUNDINGThis work was supported by the DW Reynolds Foundation, the NIH (grants HL61912, HL056882, HL103812, HL132181, HL140034), and Russell H. Morgan and Clarence Doodeman endowments at Johns Hopkins.

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Oxygen uptake efficiency plateau best predicts early death in heart failure.

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Oxygen uptake efficiency plateau best predicts early death in heart failure.

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