Prognostic Value of Insulin Resistance Assessed by HOMA-IR in Non-Diabetic Patients with Decompensated Heart Failure

Author(s):  
Yanina Castillo Costa ◽  
Víctor Mauro ◽  
Enrique Fairman ◽  
Adrián Charask ◽  
Lisandro Olguín ◽  
...  
2020 ◽  
Vol 72 (1) ◽  
Author(s):  
Yasser Gaber Metwally ◽  
Heba Kamal Sedrak ◽  
Inass Fahiem Shaltout

Abstract Background Although B-blockers provide unequivocal benefits in heart failure (HF) management, some B-blockers worsen insulin resistance. It will be a promising strategy to recruit such a B blocker that did not worsen or can even improve insulin resistance (IR). So, this study aimed to assess the effect of two of the third-generation B-blockers (carvedilol versus nebivolol) on insulin sensitivity state in non-diabetic patients with non-ischemic cardiomyopathy with heart failure. Results Out of 43 patients enrolled, 58.1% represented the carvedilol group while 41.9% represented the nebivolol group. Nebivolol improves insulin resistance-related variables (fasting glucose, fasting insulin, and HOMA-IR; P < 0.001, 0.01, and 0.01 respectively). The percentage of change at homeostasis model of assessment (HOMA-IR), indicative of insulin sensitivity status, between baseline versus at 3-months follow-up level of intra-group comparison was increased by 4.58% in the carvedilol arm whereas it was decreased by 11.67% in the nebivolol arm, and the difference on the intragroup level of comparison was significant (P < 0.001 and 0.01 respectively). Conclusion Nebivolol improves insulin resistance-related variables .Nebivolol may be recommended as the B blocker of the first choice for those with non-ischemic cardiomyopathy heart failure with evident insulin resistance; however, larger scaled prospective multicenter randomized trials are needed for confirming our favorable results.


2020 ◽  
Vol 43 (4) ◽  
pp. 329-337
Author(s):  
Yuhui Huang ◽  
Yunhong Wang ◽  
Yan Huang ◽  
Mei Zhai ◽  
Qiong Zhou ◽  
...  

2016 ◽  
Vol 4 (1) ◽  
pp. 68-77 ◽  
Author(s):  
W.H. Wilson Tang ◽  
Yuping Wu ◽  
Justin L. Grodin ◽  
Amy P. Hsu ◽  
Adrian F. Hernandez ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S R R Siqueira ◽  
S M Ayub-Ferreira ◽  
P R Chizzola ◽  
V M C Salemi ◽  
S H G Lage ◽  
...  

Abstract Introduction The occurrence of right ventricular disfunction (RVD) is common in heart failure (HF) patients due to Chagas' disease (ChD). However, its clinical and prognostic value has not been studied during episodes of acute decompensated heart failure (ADHF). Purpose Evaluate the prognostic value of RVD in ADHF patients with ChD during hospitalization and after 180 days of discharge compared to other etiologies. Methods We analysed a prospective cohort of consecutive 768 patients admitted for ADHF between March 2013 and October 2018; 490 (63.7%) patients were male and the median age was 58 (48.3–66.8) years and left ventricular ejection fraction was 26% (median) (IQR 22–35%). We compared the clinical characteristics and the prognosis of ChD patients according to the presence of RVD in the echocardiogram to other etiologies. Results RVD was presented in 289 (37.6%) patients. Among patients with non-chagasic etiologies, those with RVD were younger [53 (41–62) vs 61 (52–70) years, p<0.0001], had high levels of BNP in the moment of hospitalization [1195 (606–2209) vs 886 (366– 555) pg/mL], p<0,0001], received more inotropes (79.2% vs 57.9%, p<0,0001), had longer hospitalization [35 (17–51) vs 21 (10–37) days, p<0.001] and more clinical signs of congestion as hepatomegaly (49% vs 28.6%, p<0.0001); jugular venous distension (68.3% vs 41.2%, p<0.0001) and leg edema (65.4% vs 49.2%, p=0.001). Among patients with ChD, those with RVD were older [61 (48- 66) vs 58 (48 - 67) years, p=0.017], and had more frequently signs of hypoperfusion (56.8% vs 36.5%, p=0.029), jugular venous distension (72.8% vs 52.8%, p=0.01) and hepatomegaly (56.8% vs 31.1%, p=0.011), higher BNP levels [1288 (567–2180) vs 1066 (472–2007) pg/mL, p=0.006] and more frequent use of intravenous inotropes (88.9% vs 67.1%, p=0.003); additionally ChD patients with RVD had a higher rate of death and transplant during hospitalization (51.2% vs 38.3%, p=0.001). When all groups were compared together, ChD patients with RVD had the highest rate of death, transplant and readmissions at 180-days of follow-up (Figure). Figure 1 Conclusion Patients with RVD demonstrated a distinct clinical presentation, biomarkers and worse prognosis in all etiologies. ChD patients with RVD in ADHF had the worst prognosis with the highest rate of death, heart transplant e rehospitalization in follow-up.


2009 ◽  
Vol 34 (3) ◽  
pp. 473-480 ◽  
Author(s):  
Joost J.F.P. Luiken

Cardiomyopathy and heart failure are frequent comorbid conditions in type-2 diabetic patients. However, it has become increasingly evident that insulin resistance, type-2 diabetes, and cardiomyopathy are not independent variables, and are linked through changes in metabolism. Specifically, elevated intracellular levels of long-chain fatty acid (LCFA) metabolites are a central feature in the development of cardiac insulin resistance, and their prolonged accumulation is an important cause of heart failure. In the insulin-resistant heart, the abundance of the LCFA transporters CD36 and FABPpm at the sarcolemma of cardiac myocytes appears to be markedly increased. Because circulating LCFA levels are increased in insulin resistance, the cardiac LCFA metabolizing machinery is confronted with drastic increases in substrate supply. Indeed, LCFA esterification into triacylglycerol and other lipid intermediates is increased, as is β-oxidation and reactive oxygen species production. Therapeutic strategies to normalize the cardiac LCFA flux would be most successful when the target is the rate-limiting step in cardiac LCFA utilization. Carnitine palmitoyltransferase (CPT)-I has long been considered to be this rate-limiting site and, accordingly, pharmacological inhibition of CPT-I, or β-oxidation enzymes, has been proposed as an insulin-resistance-antagonizing strategy. However, recent evidence indicates that, instead, sarcolemmal LCFA transport mediated by CD36 in concert with FABPpm provides a major site of flux control. In this review, it is proposed that a pharmacologically imposed net internalization of CD36 and FABPpm is the preferable strategy to limit LCFA entry and accumulation of LCFA metabolites, to regress cardiac insulin resistance and, eventually, prevent diabetic heart failure.


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