Malignant and Benign Phenotypes of Multimorbidity in Heart Failure: Implications for Clinical Practice.

BACKGROUND: The impact of different patterns of multimorbidity in heart failure (HF) on health outcomes is unknown. OBJECTIVES: The aim of this study was to test the hypothesis that, independent of the extent of comorbidity, there are distinctive phenotypes of multimorbidity that convey an increased risk for premature mortality in patients hospitalized with HF. METHODS: We analyzed the clinical profile and health outcomes of 787 patients hospitalized with HF participating in a multidisciplinary HF management program with a minimum 12-month follow-up. A Classification and Regression Tree model was applied to explore the distinctive combinations of 10 most prevalent concurrent conditions (other than coronary artery disease and hypertension) associated with 12-month all-cause mortality. RESULTS: Mean (SD) age was 74 (12) years (59% men), and 65% had left ventricular systolic dysfunction. Most patients (88%) had 3 or more comorbid conditions, with a mean of 4.3 concurrent conditions in addition to HF. A total of 248 patients (32%) died (median, 663 [IQR, 492-910] days), including 142 deaths (18%) within 12 months. Patients with concurrent dysrhythmia, anemia, and respiratory disease experienced significantly higher 12-month all-cause mortality than those without these conditions (36.1% vs 3.6%, respectively; hazard ratio, 6.1 [95% confidence interval, 2.0-19.1]). Overall, this "malignant" phenotype of multimorbidity was associated with not only a markedly increased risk of all-cause mortality but also more unplanned readmissions, longer inpatient stays, and highest costs in the short (30-day) and longer terms when compared with more "benign" phenotypes of multimorbidity. CONCLUSIONS: We found a differential pattern of health outcomes according to pattern of comorbidity present in older patients hospitalized with HF and exposed to postdischarge, multidisciplinary management.

Exploring the potential to remain "Young @ Heart": initial findings of a multi-centre, randomised study of nurse-led, home-based intervention in a hybrid health care system.

BACKGROUND: Disease management programs have been shown to improve health outcomes in high risk individuals in many but not all health care systems. METHODS: Young @ Heart is a multi-centre, randomised controlled study of a nurse-led, home-based intervention (HBI) program vs. usual care (UC) in privately insured patients in Australia aged ≥ 45 years following an acute cardiac admission. Intensity of HBI is tailored to an individual's clinical stability, management and risk profile. The primary endpoint is the rate of all-cause stay during a mean of 2.5 years follow-up. RESULTS: A target of 602 adults (72% men) were randomised to HBI (n=306) or UC (n=296); their initial profiles being well matched. At baseline, 71% were overweight (body mass index 29.7 ± 3.9 kg/m(2)) and 66% had an elevated blood pressure (153 ± 18/89 ± 7 mm Hg). Over half had a history of smoking and 39% had a sub-optimal total cholesterol level >4 mmol/L. Overall, 62% (376 cases) were treated for coronary artery disease (27% with multi-vessel disease and 39% underwent cardiac revascularisation). A further 20% (120 cases) were treated for a cardiac arrhythmia (predominantly atrial fibrillation) and 19% type 2 diabetes mellitus. At 7-14 days post-discharge, 293 (96%) HBI patients received a home visit triggering urgent clinical review and/or enhanced clinical management in many patients. CONCLUSIONS: The Young @ Heart intervention is a well accepted and potentially effective intervention to reduce recurrent hospital stay in privately insured cardiac patients in Australia.

Postprandial response of adiponectin, interleukin-6, tumor necrosis factor-alpha, and C-reactive protein to a high-fat dietary load.

OBJECTIVE: Circulating levels of adiponectin are low in obesity and metabolic disorders associated with increasing fat mass including insulin resistance and dyslipidemia. Body fat stores may be positively related to intake of dietary fat, but little is known of mechanisms by which serum adiponectin may be regulated through diet. We investigated acute effects of a high-fat load and changes in fatty acid saturation on circulating adiponectin and associated mediators of inflammation including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP). METHODS: A high-fat test meal (59 +/- 4 g fat; 71% of energy as fat) containing a high ( approximately 71:29) or low ( approximately 55:45) ratio of saturated:unsaturated fatty acids was given at breakfast on two occasions. Blood samples were collected at 0 (baseline), 1, 3, and 6 h for measurement of adiponectin, IL-6, TNF-alpha, and high-sensitivity CRP. A fat-exclusion lunch, snack, and dinner were also given and blood samples collected at 10 and 24 h. RESULTS: Eighteen healthy, lean men completed the trial. There was no evidence of acute change in circulating adiponectin in response to the lipid bolus or a differential effect of fatty acid saturation on adiponectin, high-sensitivity CRP, or IL-6 (P > 0.05). IL-6 increased over 6 h on both treatments (time, P < 0.05). TNF-alpha decreased on the high saturated:unsaturated fatty acid treatment (treatment by time, P < 0.05). There were no significant correlations between circulating adiponectin and insulin on either dietary treatment in these normoglycemic subjects. CONCLUSION: Acute changes in the content of saturated and unsaturated fatty acids had no adverse effect on postprandial circulation of the adipose-related factors adiponectin, IL-6, TNF-alpha, or high-sensitivity CRP.

No evidence of an effect of alterations in dietary fatty acids on fasting adiponectin over 3 weeks.

OBJECTIVE: Little is known about the effects of alterations in fatty acid classes on adiponectin, a hormone secreted by the adipocyte known to be important in the development of diabetes and cardiovascular disease (CVD). Any factor, including diet, that may positively influence adiponectin gene expression or increase circulating levels might be useful for improving such metabolic abnormalities. We investigated the effects of alterations in dietary fatty acid saturation on fasting serum adiponectin and associated peptides. METHODS AND PROCEDURES: Double-blind, randomized, crossover, 2 x 3-week residential intervention trial where 18 mildly hyperlipidemic adult men were provided with a high saturated:unsaturated fat (SFA:USFA) and lower SFA:USFA treatment separated by an uncontrolled 4-week washout. Only fatty acid profile was altered between treatments. Fasting blood samples were collected on days 0, 1, 7, 14, 21, 22 of each intervention period for the measurement of adiponectin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsC-RP), leptin, and ghrelin. RESULTS: Body weight was kept constant (+/-1 kg) throughout each treatment. There was no detectable difference in fasting adiponectin at baseline (mean day 0 + day 1) between the treatment groups (mean +/- s.d.; high(SFA:USFA) = 7.0 +/- 1.7 vs. low(SFA:USFA) = 6.7 +/- 1.4 microg/ml, P > 0.05). There were neither significant between-treatment effects of fatty acid saturation (diet x time, P > 0.05) on serum adiponectin nor any significant between-treatment effects on serum TNF-alpha, IL-6, hsC-RP, leptin, or ghrelin (P > 0.05). DISCUSSION: Fasting serum adiponectin was not detectably affected by alterations in dietary fatty acid profile in mildly hyperlipidemic men. There was no evidence that an increase in SFA content of the diet significantly worsened fasting serum adiponectin over a 3-week intervention period.