Failing Heart of Patients With Type 2 Diabetes Mellitus Can Adapt to Extreme Short-term Increases in Circulating Lipids and Does Not Display Features of Acute Myocardial Lipotoxicity

Nielsen, Roni; Nørrelund, Helene; Kampmann, Ulla; Kim, Won Yong; Ringgaard, Steffen; Schär, Michael; Møller, Niels; Bøtker, Hans Erik; Wiggers, Henrik

doi:10.1161/circheartfailure.113.000187

Cited by 20 publications

(10 citation statements)

References 34 publications

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“…The results from short-term studies have shown disappointing effects of increases in substrate accessibility on left ventricular function in patients with T2D and HF. 25 26 This indicates that possible beneficial effects of metabolic intervention may require long-term intervention. In the present randomized trial, patients with T2D and HF underwent 4 months of glycemic optimization.…”

Section: Discussionmentioning

confidence: 99%

Effect of tighter glycemic control on cardiac function, exercise capacity, and muscle strength in heart failure patients with type 2 diabetes: a randomized study

Nielsen

Wiggers

Thomsen

et al. 2016

BMJ Open Diab Res Care

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ObjectivesIn patients with type 2 diabetes (T2D) and heart failure (HF), the optimal glycemic target is uncertain, and evidence-based data are lacking. Therefore, we performed a randomized study on the effect of optimized glycemic control on left ventricular function, exercise capacity, muscle strength, and body composition.Design and methods40 patients with T2D and HF (left ventricular ejection fraction (LVEF) 35±12% and hemoglobin A1c (HbA1c) 8.4±0.7% (68±0.8 mmol/mol)) were randomized to either 4-month optimization (OPT group) or non-optimization (non-OPT group) of glycemic control. Patients underwent dobutamine stress echocardiography, cardiopulmonary exercise test, 6 min hall-walk test (6-MWT), muscle strength examination, and dual X-ray absorptiometry scanning at baseline and at follow-up.Results39 patients completed the study. HbA1c decreased in the OPT versus the non-OPT group (8.4±0.8% (68±9 mmol/mol) to 7.6±0.7% (60±7 mmol/mol) vs 8.3±0.7% (67±10 mmol/mol) to 8.4±1.0% (68±11 mmol/mol); p<0.001). There was no difference between the groups with respect to changes in myocardial contractile reserve (LVEF (p=0.18)), oxygen consumption (p=0.55), exercise capacity (p=0.12), and 6-MWT (p=0.84). Muscle strength decreased in the non-OPT compared with the OPT group (37.2±8.1 to 34.8±8.3 kg vs 34.9±10.2 to 35.4±10.7 kg; p=0.01), in line with a non-significant decrease in lean (p=0.07) and fat (p=0.07) tissue mass in the non-OPT group. Hypoglycemia and fluid retention did not differ between groups.Conclusions4 months of optimization of glycemic control was associated with preserved muscle strength and lean body mass in patients with T2D and HF compared with lenient control, and had no deleterious effect on left ventricular contractile function and seemed to be safe.Trial registration numberNCT01213784; pre-results.

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Section: Discussionmentioning

confidence: 99%

Effect of tighter glycemic control on cardiac function, exercise capacity, and muscle strength in heart failure patients with type 2 diabetes: a randomized study

Nielsen

Wiggers

Thomsen

et al. 2016

BMJ Open Diab Res Care

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“…This may be due to the long standing type 2 diabetes [ 9 ], which increase the possibility of depressed sympathetic activity [ 23 ]. Nielsen et al [ 26 ] observed a tendency towards increased heart rate ( p = 0.08) due to high levels of lipid infusion versus low lipid infusion controls—this indicates that fast food may increase heart rate more than healthy foods.…”

Section: Discussionmentioning

confidence: 99%

Fast food increases postprandial cardiac workload in type 2 diabetes independent of pre-exercise: A pilot study

Hollekim-Strand

Malmo

Follestad

et al. 2015

Nutr J

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BackgroundType 2 diabetes aggravates the postprandial metabolic effects of food, which increase cardiovascular risk. We investigated the acute effects of fast food on postprandial left ventricular (LV) function and the potential effects of pre-exercise in type 2 diabetes individuals.MethodsWe used a cross-over study including 10 type 2 diabetes individuals (7 male and 3 females; 53.4 ± 8.1 years; 28.3 ± 3.8 kg/m2; type 2 diabetes duration 3.1 ± 1.8 years) and 10 controls (7 male and 3 females; 52.8 ± 10.1 years; 28.5 ± 4.2 kg/m2) performing high intensity interval exercise (HIIE; 40 min, 4 × 4min intervals, 90–95 % HRmax), moderate intensity exercise (MIE; 47 min, 70 % HRmax) and no exercise (NE) in a random order 16–18 hours prior to fast-food ingestion. Baseline echocardiography, blood pressure and biochemical measurements were recorded prior to and 16–18 hours after exercise, and 30 minutes, 2 hours and 4 hours after fast food ingestion.ResultsLV diastolic (peak early diastolic tissue velocity, peak early diastolic filling velocity), and systolic workload (global strain rate, peak systolic tissue velocity, rate pressure product) increased after consumption of fast food in both groups. In contrast to controls, the type 2 diabetes group had prolonged elevations in resting heart rate and indications of prolonged elevations in diastolic workload (peak early diastolic tissue velocity) as well as reduced systolic blood pressure after fast food consumption. No significant modifications due to exercise in the postprandial phase were seen in any group.ConclusionsOur findings indicate that fast-food induces greater and sustained overall cardiac workload in type 2 diabetes individuals versus body mass index and age matched controls; exercise 16–18 hours pre-meal has no acute effects to the postprandial phase.Trial registrationClinicalTrials.gov: NCT01991769.

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“…Echocardiography was performed using a GE VIVID 9E system (GE Medical System) with a 2.5‐MHz transducer and analyzed offline using EchoPAC version 113 (GE‐Vingmed Ultrasound), as described previously . Continuous‐wave Doppler imaging from multiple acoustic windows was used to explore the highest transaortic velocity and peak and mean gradients.…”

Section: Methodsmentioning

confidence: 99%

Myocardial Oxygen Consumption and Efficiency in Aortic Valve Stenosis Patients With and Without Heart Failure

Hansson

Sørensen

Harms

et al. 2017

JAHA

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BackgroundMyocardial oxygen consumption (MVO2) and its coupling to contractile work are fundamentals of cardiac function and may be involved causally in the transition from compensated left ventricular hypertrophy to failure. Nevertheless, these processes have not been studied previously in patients with aortic valve stenosis (AS).Methods and ResultsParticipants underwent 11C‐acetate positron emission tomography, cardiovascular magnetic resonance, and echocardiography to measure MVO2 and myocardial external efficiency (MEE) defined as the ratio of left ventricular stroke work and the energy equivalent of MVO2. We studied 10 healthy controls (group A), 37 asymptomatic AS patients with left ventricular ejection fraction ≥50% (group B), 12 symptomatic AS patients with left ventricular ejection fraction ≥50% (group C), and 9 symptomatic AS patients with left ventricular ejection fraction <50% (group D). MVO2 did not differ among groups A, B, C, and D (0.105±0.02, 0.117±0.024, 0.129±0.032, and 0.104±0.026 mL/min per gram, respectively; P=0.07), whereas MEE was reduced in group D (21.0±1.6%, 22.3±3.3%, 22.1±4.2%, and 17.3±4.7%, respectively; P<0.05). Similarly, patients with global longitudinal strain greater than −12% and paradoxical low‐flow, low‐gradient AS had impaired MEE (P<0.05 versus controls). The ability to discriminate between symptomatic and asymptomatic patients was superior for global longitudinal strain compared with MVO2 and MEE (area under the curve 0.98, 0.48, and 0.61, respectively; P<0.05).ConclusionsAS patients display a persistent ability to maintain normal MVO2 and MEE (ie, the ability to convert energy into stroke work); however, patients with left ventricular ejection fraction <50%; global longitudinal strain greater than −12%; or paradoxical low‐flow, low‐gradient AS demonstrate reduced MEE. These findings suggest that mitochondrial uncoupling contributes to the dismal prognosis in patients with reduced contractile function or paradoxical low‐flow, low‐gradient AS.

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Failing Heart of Patients With Type 2 Diabetes Mellitus Can Adapt to Extreme Short-term Increases in Circulating Lipids and Does Not Display Features of Acute Myocardial Lipotoxicity

Abstract: We hypothesized that (1) short-term extreme changes in FFA and triglyceride levels affect MyLC in patients with T2D and HF, and that (2) suppressed as opposed to increased circulating FFA and triglyceride increase myocardial contractility and cardiopulmonary exercise capacity.

Cited by 20 publications

References 34 publications

Effect of tighter glycemic control on cardiac function, exercise capacity, and muscle strength in heart failure patients with type 2 diabetes: a randomized study

Effect of tighter glycemic control on cardiac function, exercise capacity, and muscle strength in heart failure patients with type 2 diabetes: a randomized study

Fast food increases postprandial cardiac workload in type 2 diabetes independent of pre-exercise: A pilot study

Myocardial Oxygen Consumption and Efficiency in Aortic Valve Stenosis Patients With and Without Heart Failure

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