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Diane Barker

Publications and source records attributed to Diane Barker.

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Exercise duration and peak systolic blood pressure are predictive of mortality in ambulatory patients with mild-moderate chronic heart failure.

BACKGROUND AND AIMS: It is a prevailing concept in chronic heart failure (CHF) that ventricular remodelling (evaluated via imaging) and neurohormonal activation (via biomarkers) exert major influences, such that the need to subject patients to haemodynamic evaluations and exercise testing has been questioned. We sought to investigate whether exercise and haemodynamic parameters lack independent prognostic value in a cohort of unselected ambulatory patients with mild-moderate CHF. METHODS: Eighty-five consecutive patients with stable CHF in New York Heart Association functional classes I-IV, aged 55 +/- 12 years, 84% males, left ventricular ejection fraction (LVEF) 37 +/- 15%, participated in this study. Survivors were followed for a median of 5.08 years. All subjects underwent cardiopulmonary exercise testing to measure standard parameters including peak oxygen consumption, exercise duration and blood pressure. A sample of venous blood was taken to determine the N-terminal pro-brain natriuretic peptide (N-BNP) level. Echocardiography was performed at rest to measure LVEF. Predictors of mortality were sought using the Cox proportional hazards model. RESULTS: All-cause mortality was 19% (16 deaths, 95% CI 11-29%). Age and LVEF did not independently predict mortality. Although various parameters including New York Heart Association class, peak oxygen consumption and N-BNP level were all predictive of outcome on univariate analysis, multivariate analysis identified reduced exercise duration and peak systolic blood pressure (SBP) to be the only independent predictors of all-cause mortality. Hazard ratios of 0.78 (95% CI 0.65-0.93, p = 0.007) and 0.79 (95% CI 0.66-0.95, p = 0.01) were associated with an increase in exercise duration of 1 min and 10 mm Hg peak SBP, respectively. CONCLUSIONS: Two simple parameters (exercise duration and peak SBP) that are easily measured by standard exercise testing are the strongest independent predictors of mortality which outperform LVEF and N-BNP in ambulatory patients with mild-moderate CHF.

Adult↗

Comparison and relation of indirect and direct dynamic indexes of cardiac pumping capacity in chronic heart failure.

Cardiac power output (CPO), the product of cardiac output (CO) and mean arterial pressure (MAP), is a direct measure of cardiac pumping capability and is strongly indicative of prognosis and exercise ability in patients with chronic heart failure (CHF). However, it is not as easily measured as indirect indicators of cardiac function, such as peak oxygen consumption (VO(2)) or peak "circulatory power" (CircP), the product of VO(2) and MAP. The relation between direct and indirect indexes of cardiac pumping capacity was evaluated in 219 ambulatory patients with CHF. CircP was found to have a direct and consistent relation with CPO, overall (R = 0.93, p <0.0001) and at peak exercise (R = 0.84, p < 0.0001). The results suggest CircP to be an adequate measure of cardiac pumping capacity when the more directly measured CPO is not available.

Cardiac Output↗

How do different indicators of cardiac pump function impact upon the long-term prognosis of patients with chronic heart failure?

BACKGROUND: The prognosis of patients with mild-moderate chronic heart failure (CHF) over a long-term follow-up period is more difficult to predict than for patients with more severe CHF in the short term. This study assessed the prognostic value of various indicators of cardiac pump function to gain insight into how different aspects of organ function impact upon prognosis. METHODS: Unselected, consecutive patients with CHF (n = 219, 166 men, mean [+/-SD] age 56 +/- 13 years) who underwent symptom limited cardiopulmonary treadmill exercise testing with noninvasive estimation of cardiac output using carbon dioxide rebreathing techniques were followed up for a median period of 8.6 +/- 1.0 years in survivors. Cardiac power output (CPO) was calculated from the product of cardiac output and mean arterial pressure and cardiac reserve was estimated by subtracting resting from peak exercise CPO or cardiac output (CO). RESULTS: All-cause mortality was 36% (78 deaths). Survivors had a significantly greater cardiac pumping reserve with the greatest difference seen in CPO reserve (+57%) and CO reserve (+49%) (both P < .001). Although various direct and indirect indicators of cardiac function were predictive of outcome on univariate analyses, multivariate analysis using the Cox proportional hazards model identified CO reserve to be the independent variable predictive of all-cause mortality, with a hazard ratio (95% CI) of 0.682 (0.612-0.757, P < .001) for each L/min increase in cardiac output reserve. Survival at 10 years in patients with tertiles of good, moderate, or poor cardiac output reserve was 89%, 63%, and 36.1%, respectively (P < .001). CONCLUSION: In this long-term follow-up study involving a cohort of unselected ambulatory patients with mild-moderate CHF, cardiac pumping reserve measured noninvasively by cardiopulmonary exercise testing was found to be the strongest independent predictor of prognosis.

Chronic Disease↗

Fiftieth anniversary of aldosterone: from discovery to cardiovascular therapy.

Half a century after the elucidation of its molecular structure, aldosterone is generating the greatest interest, not in the fields of endocrinology or renal medicine but in cardiology-where aldosterone over-activation is now perceived as detrimental in heart failure (HF) and ischaemic heart disease. Clinically, excess aldosterone is associated with higher morbidity and mortality after myocardial infarction (MI) and HF. The Randomised Aldactone Evaluation Study (RALES) study in severe chronic heart failure and the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival (EPHESUS) study in post-MI heart failure have shown that use of non-selective and selective aldosterone receptor antagonists, respectively, improves prognosis. The pathophysiological mechanisms underpinning these damaging aldosterone-mediated cardiovascular effects are still being elucidated, but prime candidates include cardiomyocyte necrosis and apoptosis, and myocardial fibrosis resulting in adverse cardiac remodelling, coronary vasculopathy, tachyarrhythmia and positive feedback activation of the renin-angiotensin-aldosterone system. Practical points for consideration when instigating therapy include preferential use of aldosterone receptor antagonists to maintain electrolyte balance whenever loop or thiazide diuretics are used (vulnerable HF patients require higher ranges of potassium and magnesium to minimise propensity for tachyarrthythmia), for renoprotection and for counteracting aldosterone breakthrough despite adequate ACE inhibition; use of the minimum doses of loop diuretics required to lessen activation of the renin-angiotensin-aldosterone system in HF; use of selective aldosterone receptor antagonists to avoid gynaecomastia/mastalgia and impotence; and prophylactic use of aldosterone receptor antagonists to improve prognosis.

Aldosterone↗