Patients with HFrEF who were treated with less than 50% of recommended dose of ACE-inhibitors/ARBs and beta-blockers seemed to have a greater risk of death and/or heart failure hospitalization compared with patients reaching ≥100%.
This study was performed because of observed differences between dye dilution cardiac output and the Fick cardiac output, calculated from estimated oxygen consumption according to LaFarge and Miettinen, and to find a better formula for assumed oxygen consumption. In 250 patients who underwent left and right heart catheterization, the oxygen consumption VO2 (ml.min-1) was calculated using Fick's principle. Either pulmonary or systemic flow, as measured by dye dilution, was used in combination with the concordant arteriovenous oxygen concentration difference. In 130 patients, who matched the age of the LaFarge and Miettinen population, the obtained values of oxygen consumption VO2(dd) were compared with the estimated oxygen consumption values VO2(lfm), found using the LaFarge and Miettinen formulae. The VO2(lfm) was significantly lower than VO2(dd); -21.8 +/- 29.3 ml.min-1 (mean +/- SD), P < 0.001, 95% confidence interval (95% CI) -26.9 to -16.7, limits of agreement (LA) -80.4 to 36.9. A new regression formula for the assumed oxygen consumption VO2(ass) was derived in 250 patients by stepwise multiple regression analysis. The VO2(dd) was used as a dependent variable, and body surface area BSA (m2). Sex (0 for female, 1 for male), Age (years), Heart rate (min-1) and the presence of a left to right shunt as independent variables. The best fitting formula is expressed as: VO2(ass) = (157.3 x BSA + 10.0 x Sex - 10.5 x In Age + 4.8) ml.min-1, where ln Age = the natural logarithm of the age. This formula was validated prospectively in 60 patients. A non-significant difference between VO2(ass) and VO2(dd) was found; mean 2.0 +/- 23.4 ml.min-1, P = 0.771, 95% Cl = -4.0 to +8.0, LA -44.7 to +48.7. In conclusion, assumed oxygen consumption values, using our new formula, are in better agreement with the actual values than those found according to LaFarge and Miettinen's formulae.
Cycle length-dependent contractile mechanisms, including postextrasystolic potentiation and mechanical restitution, determine the varying left ventricular systolic performance during atrial fibrillation over the entire range of intervals. Beat-to-beat changes in preload, consistent with the Frank-Starling mechanism, also play a role, but their influence is diminished after long preceding and short prepreceding intervals.
There is much symptomatic similarity between acute kidney disease and acute heart disease. Both may present with shortness of breath and chest discomfort, and thus it is not surprising that biomarkers of acute myocardial and renal disease often coexist in many physicians' diagnostic work-up schedules. In this review we explore the similarities and differences between current and future tests of myocardial and renal injury and function, with particular emphasis on the diagnostic utility of currently available biomarkers to assist with the diagnosis of cardiorenal syndromes. Imaging studies have not traditionally been viewed as clinical biomarkers, but as tests of structure and function; they contribute to the diagnostic process, and we believe that they should be considered alongside more traditional biomarkers such as blood and urine measurements of circulating proteins and metabolites. We discuss the place of natriuretic peptides, novel tests of kidney damage as well as kidney function and conclude with a discussion of their place in guiding future research studies whose goals must include better characterization of the degree of dysfunction imposed on one organ system by failure of the other.
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