Search

Background The prognostic role of diabetes mellitus (DM) in heart failure (HF) patients is undefined, since DM is outweighed by several DM-related variables when confounders are considered. We determined the prognostic role of DM, treatment, and glycemic control in a real-life HF population. Methods 3927 HF patients included in the Metabolic Exercise Cardiac Kidney Index (MECKI) score database were evaluated with a median follow-up of 3.66 years (IQR 1.70–6.67). Data analysis considered survival between DM (n = 897) vs. non-DM (n = 3030) patients, and, in diabetics, between insulin (n = 304), oral antidiabetics (n = 479), and dietary only (n = 88) treatments. The role of glycemic control was evaluated grouping DM patients according to glycated hemoglobin (HbA1c): 8% (n = 149). All analyses were performed also adjusting for ejection fraction, renal function, hemoglobin, sodium, exercise peak oxygen uptake, and ventilation/carbon dioxide relationship slope. Study primary endpoint was the composite of cardiovascular death, urgent heart transplantation, or left ventricular assist device implantation. Secondary endpoints were cardiovascular and all causes death. Results For all endpoints, upon adjustment for confounders, DM status and insulin treatment or dietary regimen were not significantly associated with adverse long-term prognosis compared to non-DM and oral antidiabetic treated patients, respectively. A worse prognosis was observed in HbA1c >8% patients (Log-Rank p Conclusion In HF patients, DM, insulin treatment and dietary regimen are not adverse outcome predictors. The only condition related to long-term prognosis, considering potential confounders, is poor glycemic control.

The usefulness of β-blockers in heart failure (HF) patients with permanent atrial fibrillation (AF) has been questioned. Background: The usefulness of β-blockers in heart failure (HF) patients with permanent atrial fibrillation (AF) has been questioned. Methods and results: We analyzed data from HF patients (958 patients (801 males, 84%, age 67 ± 11 years)) with AF enrolled in the MECKI score database. We evaluated prognosis (composite of cardiovascular death, urgent heart transplant, or left ventricular assist device) of patients receiving β-blockers (n = 777, 81%) vs. those not treated with β-blockers (n = 181, 19%). We also analyzed the role β1-selectivity and the role of daily β-blocker dose. To account for different HF severity, Kaplan-Meier survival curves were normalized for relevant confounding factors and for treatment strategies. Dose was available in 629 patients. Median follow-up was 1312 (577–2304) days in the entire population, 1203 (614–2420) and 1325 (569–2300) days in patients not receiving and receiving β-blockers. 224 (23%, 54/1000 events/year), 163 (21%, 79/1000 events/year), and 61 (34%, 49/1000 events/year) events were recorded, respectively. At 10-year patients treated with β-blockers had a better outcome (HR 0.447, p < 0.01) with no effects as regards β1selective drugs (53%) vs. β1-β2 blockers (47%). Survival improved in parallel with β-blocker dose increase (HR 0.296, 0.496, 0.490 for the high, medium, and low dose vs. no β-blockers, p < 0.0001). Conclusion: HF patients with AF taking a β-blocker have a better outcome (with a survival improvement in parallel with daily dose but no differences as regards β1 selectivity) but this does not mean that β-blockers improve outcomes in these patients as we cannot control for all the potential confounders associated with β-blocker use.

Background Accurate identification of renal dysfunction (RD) is crucial to risk stratification in chronic heart failure (CHF). Patients with CHF are at special risk of having RD despite normal serum creatinine (SCr), owing to a decreased Cr generation. At low levels of SCr, the equations estimating renal function are less accurate. This study was aimed to assess and compare the prognostic value of formulas estimating renal function in CHF patients with normal SCr. Methods We studied 462 patients with systolic CHF and normal SCr. Creatinine clearance was estimated by the Cockcroft–Gault (eCrCl) and glomerular filtration rate by the 4-variable MDRD equation (eGFR); eCrCl normalized for body-surface area (eCrCl BSA ) was calculated. The primary outcome was all-cause mortality at 2years. Results Seventy five patients died. At multivariate Cox regression analysis, only eCrCl BSA was significantly associated with mortality ( p =0.006); eGFR ( p =0.24), eCrCl ( p =0.09) and BUN ( p =0.14) were not statistically significant predictors. The patients in the lowest eCrCl BSA quartile had an adjusted 2.1-fold (CI: 1.06–4.1) increased risk of mortality, compared with those in the referent quartile. Two-year survival was 70.4% in the lowest eCrCl BSA quartile and 89.7% in the referent quartile. Other independent predictors of mortality were ischemic etiology (RR: 2.16 [CI: 1.3–3.5], p =0.0017), NYHA III/IV class (RR: 2.45 [CI: 1.51–3.97], p =0.0003), LVEF p =0.014), and anemia (RR: 1.86 [CI: 1.16–2.99], p =0.009). Conclusions A sizeable proportion of CHF patients have prognostically significant RD despite normal SCr. Such patients represent a high-risk subgroup and can more accurately be identified by the CG formula corrected for BSA than the MDRD.

To investigate whether percent achieved of predicted peak exercise oxygen uptake (%VO2max) and recovery of oxygen consumption after exercise may provide prognostic information in chronic heart failure (CHF), we prospectively studied 196 patients with mild to moderate CHF. The following variables were examined: age, etiology of CHF, functional class, ejection fraction (EF), peak exercise oxygen uptake normalized for body weight (VO2max), %VO2max, time to reach 50% of the peak oxygen uptake after exercise (T1/2VO2max), presence of nonsustained ventricular tachycardia (NSVT) and inability to take ACE-inhibitors. VO2max was the most powerful predictor of cardiac death (P

This study was undertaken to assess the relation of ambulatory myocardial ischemia to heart rate changes and variability in exercise threshold in patients with chronic angina. The study involved 118 patients with chronic angina and proven coronary artery disease who had a ‘positive' exercise test result. All patients underwent a first exercise test followed by a 48-h period of ambulatory electrocardiographic monitoring. A second exercise test was performed 4 days later. A total of 101 ischemic episodes were recorded in 35 patients. The heart rate at the appearance of 1-mm ST segment depression during ambulatory electrocardiographic monitoring was ≥ 20 beats/min lower than that during exercise testing in 58 ischemic episodes (57%, Group A), 10–19 beats/min lower in 26 (26%, Group B), and ≤9 beats/min lower or higher in 17 (17%, Group C). Thirty-five percent of the Group A ischemic episodes, 69% of Group B, and 71% of Group C were preceded by an increase in heart rate of ≥10 beats/min. Thirty patients showed a variable exercise threshold. The prevalence of Group A and B ischemic episodes was not significantly different in patients with fixed or variable exercise threshold, whereas that of Group C episodes was 22% in the former and 0% in the latter ( P = 0.036). These results suggest that increased coronary tone may be one of the mechanisms contributing to modulate the occurrence of transient myocardial ischemia in most patients with chronic angina and transient myocardial ischemia at ambulatory electrocardiographic monitoring. This occurs regardless of whether the patients have a variable or fixed exercise threshold.

Background NT-proBNP has been associated with prognosis in acute decompensated heart failure (ADHF). Whether NT-proBNP provides additional prognostic information beyond that obtained from standard clinical variables is uncertain. We sought to assess whether N-terminal pro-B-type natriuretic peptide (NT-proBNP) determination improves risk reclassification of patients with ADHF and to develop and validate a point-based NT-proBNP risk score. Methods This study included 824 patients with ADHF (453 in the derivation cohort, 371 in the validation cohort). We compared two multivariable models predicting 1-year all-cause mortality, including clinical variables and clinical variables plus NT-proBNP. We calculated the net reclassification improvement (NRI) and the integrated discrimination improvement (IDI). Then, we developed and externally validated the NT-proBNP risk score. Results One-year mortalities for the derivation and validation cohorts were 28.3% and 23.4%, respectively. Multivariable predictors of mortality included chronic obstructive pulmonary disease, estimated glomerular filtration rate, sodium, hemoglobin, left ventricular ejection fraction, and moderate to severe tricuspid regurgitation. Adding NT-proBNP to the clinical variables only model significantly improved the NRI (0.129; p=0.0027) and the IDI (0.037; p=0.0005). In the derivation cohort, the NT-proBNP risk score had a C index of 0.839 (95% CI: 0.798–0.880) and the Hosmer–Lemeshow statistic was 1.23 (p=0.542), indicating good calibration. In the validation cohort, the risk score had a C index of 0.768 (95% CI: 0.711–0.817); the Hosmer–Lemeshow statistic was 2.76 (p=0.251), after recalibration. Conclusions The NT-proBNP risk score provides clinicians with a contemporary, accurate, easy-to-use, and validated predictive tool. Further validation in other datasets is advisable.

Atrial pacing can safely be utilized shortly after myocardial infarction. To evaluate the prognostic value of wall motion abnormalities induced by such pacing 83 consecutive patients with recent uncomplicated myocardial infarction underwent transthoracic cross-sectional echocardiography during transesophageal atrial pacing and upright bicycle exercise stress test. Patients were followed-up for 14 +/- 5 months. During the atrial pacing and the echocardiography, patients were defined at high risk if abnormalities of wall motion were detected in left ventricular regions remote from the infarcted area. Then, during the exercise stress test, high risk patients were those with ST segment depression greater than or equal to 1 mm. On the other hand, patients were considered to be at low risk if they had no abnormalities of wall motion during atrial pacing in remote regions or, in the case of the stress test, if they did not develop ST depression greater than or equal to 1 mm. Of the 83 patients, 21 had major cardiac events during the period of follow-up. Cardiac events occurred in 15/23 (65%) and 5/60 (8%, P less than 0.001) patients assigned to the groups adjudged to be at high and low risk, respectively, on the basis of echocardiographic results. Exercise testing was less reliable in identifying patients at risk of future cardiac events. Major events occurred in only 6 of the 19 patients with a positive stress test (32%, P less than 0.05 vs positive stress echocardiography) and in 14 of the 64 patients with a negative exercise stress test (22%, P = NS vs positive exercise stress test, P less than 0.05 vs negative atrial pacing echocardiography).

The effects of propionyl-L-carnitine on exercise tolerance of 12 patients with stable exertional angina were assessed in a double-blind, placebo-controlled, cross-over protocol using serial exercise tests. Compared to placebo, propionyl-L-carnitine significantly increased total work from 514 +/- 199 to 600 +/- 209 W (P less than 0.05) (17%) and prolonged exercise time and time to ischemic threshold from 515 +/- 115 to 565 +/- 109 sec (P less than 0.05) (10%) and from 375 +/- 102 to 427 +/- 93 sec (P less than 0.01) (14%), respectively. ST segment depression at the highest common work level was significantly reduced from 0.19 +/- 0.08 to 0.15 +/- 0.08 mV (P less than 0.05) (21%). No significant changes in heart rate, systolic blood pressure, and rate-pressure product at rest, at the highest common work level, on appearance of the ischemic threshold, or at peak exercise were observed after propionyl-L-carnitine treatment. No side effects were observed under propionyl-L-carnitine treatment. This study shows that propionyl-L-carnitine can significantly improve exercise tolerance in patients with stable angina. Our data seem to confirm that propionyl-L-carnitine most likely exerts its protective action via the metabolic pathway.