The impact of diabetes on left ventricular filling pattern in normotensive and hypertensive adults: the strong heart study

Liu, Jennifer E.; Palmieri, Vittorio; Roman, Mary J.; Bella, J.N.; Fabsitz, Richard R.; Howard, Barbara V.; Welty, Thomas K.; Lee, Elisa T.; Devereux, Richard B.

doi:10.1016/s0735-1097(01)01230-x

Cited by 309 publications

(183 citation statements)

References 37 publications

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“…Previous work has established that diastolic abnormalities occur early in the course of diabetic cardiomyopathy and prevalence estimates of between 30 and 61% have been reported for asymptomatic left ventricular diastolic dysfunction [19,44,45]. Our results are supported by those of the Strong Heart Study, in which diastolic abnormalities in diabetic patients were found to be independent of left ventricular mass and left ventricular systolic function [46]. The mechanisms contributing to the pathogenesis of diastolic dysfunction in some diabetic patients, but not others, are not fully established, although some pointers do exist.…”

Section: Discussionsupporting

confidence: 88%

“…Secondly, altered diastolic function in type 2 diabetes is associated with reduced myocardial metabolism, assessed using magnetic resonance imaging [48]. It is possible that the degree of hyperglycaemia may also play a role, as a higher fasting glucose and glycated haemoglobin are associated with abnormal left ventricular relaxation in diabetic patients [46].…”

Section: Discussionmentioning

confidence: 99%

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The epidemiology of left ventricular hypertrophy in type 2 diabetes mellitus

2005

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Aims/hypothesis: Patients with type 2 diabetes mellitus are at greater cardiovascular risk than the general population. Although it is widely acknowledged that diabetes is a risk factor for coronary artery disease, the increased prevalence of potentially lethal left ventricular abnormalities in this population is less well appreciated. Methods: We carried out an echocardiographic study of 500 subjects with type 2 diabetes mellitus to assess the prevalence of left ventricular hypertrophy (LVH) and left ventricular systolic dysfunction (LVSD). We also assessed whether abnormalities in diastolic filling parameters were present. Results: Of the 371 patients in whom left ventricular mass could be successfully assessed, 264 had LVH (71%). Left ventricular systolic dysfunction was much less common, being present in 16/385 patients (4.2%). Long axis contraction was abnormal in 29/429 patients (6.8%). Diastolic filling abnormalities were present in 178/435 (41%) of patients who could be classified using the selected criteria. Conclusions: We conclude that left ventricular abnormalities are common in type 2 diabetic patients. As medical therapy is available for both LVH and LVSD and has been demonstrated to reduce cardiovascular death, these left ventricular abnormalities could be ideal targets for screening, followed by selective therapeutic intervention.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

The epidemiology of left ventricular hypertrophy in type 2 diabetes mellitus

2005

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“…The STZ mouse model employed here is characterized by an initial decline of diastolic function, which is commonly found in the diabetic population 1, 49, 50, 51, 52. LV filling patterns in STZ‐treated mice are altered in the first month after onset of hyperglycemia, whereas EF is still preserved.…”

Section: Discussionmentioning

confidence: 99%

Reduction in Kv Current Enhances the Temporal Dispersion of the Action Potential in Diabetic Myocytes: Insights From a Novel Repolarization Algorithm

Meo

Meste

Signore

et al. 2016

JAHA

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BackgroundDiabetes is associated with prolongation of the QT interval of the electrocardiogram and enhanced dispersion of ventricular repolarization, factors that, together with atherosclerosis and myocardial ischemia, may promote the occurrence of electrical disorders. Thus, we tested the possibility that alterations in transmembrane ionic currents reduce the repolarization reserve of myocytes, leading to action potential (AP) prolongation and enhanced beat‐to‐beat variability of repolarization.Methods and ResultsDiabetes was induced in mice with streptozotocin (STZ), and effects of hyperglycemia on electrical properties of whole heart and myocytes were studied with respect to an untreated control group (Ctrl) using electrocardiographic recordings in vivo, ex vivo perfused hearts, and single‐cell patch‐clamp analysis. Additionally, a newly developed algorithm was introduced to obtain detailed information of the impact of high glucose on AP profile. Compared to Ctrl, hyperglycemia in STZ‐treated animals was coupled with prolongation of the QT interval, enhanced temporal dispersion of electrical recovery, and susceptibility to ventricular arrhythmias, defects observed, in part, in the Akita mutant mouse model of type I diabetes. AP was prolonged and beat‐to‐beat variability of repolarization was enhanced in diabetic myocytes, with respect to Ctrl cells. Density of Kv K+ and L‐type Ca2+ currents were decreased in STZ myocytes, in comparison to cells from normoglycemic mice. Pharmacological reduction of Kv currents in Ctrl cells lengthened AP duration and increased temporal dispersion of repolarization, reiterating features identified in diabetic myocytes.ConclusionsReductions in the repolarizing K+ currents may contribute to electrical disturbances of the diabetic heart.

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“…DCM is defined as structural and functional myocardial impairments in diabetic patients without coronary artery disease or hypertension. It is mainly characterized by myocardial hypertrophy and fibrosis, metabolic dysregulation, and defects in myocardial contractile properties (Liu et al., 2001). Considerable progress has been made in DCM management.…”

Section: Introductionmentioning

confidence: 99%

Glucagon‐like peptide‐1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway

Wang

et al. 2018

Aging Cell

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SummaryLipotoxicity cardiomyopathy is the result of excessive accumulation and oxidation of toxic lipids in the heart. It is a major threat to patients with diabetes. Glucagon‐like peptide‐1 (GLP‐1) has aroused considerable interest as a novel therapeutic target for diabetes mellitus because it stimulates insulin secretion. Here, we investigated the effects and mechanisms of the GLP‐1 analog exendin‐4 and the dipeptidyl peptidase‐4 inhibitor saxagliptin on cardiac lipid metabolism in diabetic mice (DM). The increased myocardial lipid accumulation, oxidative stress, apoptosis, and cardiac remodeling and dysfunction induced in DM by low streptozotocin doses and high‐fat diets were significantly reversed by exendin‐4 and saxagliptin treatments for 8 weeks. We found that exendin‐4 inhibited abnormal activation of the (PPARα)‐CD36 pathway by stimulating protein kinase A (PKA) but suppressing the Rho‐associated protein kinase (ROCK) pathway in DM hearts, palmitic acid (PA)‐treated rat h9c2 cardiomyocytes (CMs), and isolated adult mouse CMs. Cardioprotection in DM mediated by exendin‐4 was abolished by combination therapy with the PPARα agonist wy‐14643 but mimicked by PPARα gene deficiency. Therefore, the PPARα pathway accounted for the effects of exendin‐4. This conclusion was confirmed in cardiac‐restricted overexpression of PPARα mediated by adeno‐associated virus serotype‐9 containing a cardiac troponin T promoter. Our results provide the first direct evidence that GLP‐1 protects cardiac function by inhibiting the ROCK/PPARα pathway, thereby ameliorating lipotoxicity in diabetic cardiomyopathy.

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The impact of diabetes on left ventricular filling pattern in normotensive and hypertensive adults: the strong heart study

Cited by 309 publications

References 37 publications

The epidemiology of left ventricular hypertrophy in type 2 diabetes mellitus

The epidemiology of left ventricular hypertrophy in type 2 diabetes mellitus

Reduction in Kv Current Enhances the Temporal Dispersion of the Action Potential in Diabetic Myocytes: Insights From a Novel Repolarization Algorithm

Glucagon‐like peptide‐1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway

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