ANP but not BNP Reflects Early Left Diastolic Dysfunction in Type 1 Diabetics with Myocardial Dysinnervation

doi:10.1055/s-2003-41306

Cited by 15 publications

(2 citation statements)

References 32 publications

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“… 30 Moreover, elevated plasma atrial natriuretic peptide levels have been associated with early LVDD in patients with diabetes. 31 This transcriptional remodeling has been associated with increased myocardial oxidative stress, and although causality is not clearly established it is noteworthy that deletion of nuclear factor erythroid 2‐related factor 2, a master regulator of the endogenous antioxidant defense system, is sufficient to exacerbate return to the fetal gene program in hearts of mice subjected to pressure overload by constriction of the transverse aorta. 32 , 33 Therefore, accelerated return to the fetal gene program in hypertensive ucp3 +/‐ rats may also be rooted in the excessive ROS generation caused by partial loss of the mitochondrial anion carrier.…”

Section: Discussionmentioning

confidence: 99%

UCP3 (Uncoupling Protein 3) Insufficiency Exacerbates Left Ventricular Diastolic Dysfunction During Angiotensin II‐Induced Hypertension

Chen

Ashraf

et al. 2021

JAHA

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Background Left ventricular diastolic dysfunction, an early stage in the pathogenesis of heart failure with preserved ejection fraction, is exacerbated by joint exposure to hypertension and obesity; however, the molecular mechanisms involved remain uncertain. The mitochondrial UCP3 (uncoupling protein 3) is downregulated in the heart with obesity. Here, we used a rat model of UCP3 haploinsufficiency (ucp3 +/‐ ) to test the hypothesis that decreased UCP3 promotes left ventricular diastolic dysfunction during hypertension. Methods and Results Ucp3 +/‐ rats and ucp3 +/+ littermates fed a high‐salt diet (HS; 2% NaCl) and treated with angiotensin II (190 ng/kg per min for 28 days) experienced a similar rise in blood pressure (158±4 versus 155±7 mm Hg). However, UCP3 insufficiency worsened diastolic dysfunction according to echocardiographic assessment of left ventricular filling pressures (E/e’; 18.8±1.0 versus 14.9±0.6; P <0.05) and the isovolumic relaxation time (24.7±0.6 versus 21.3±0.5 ms; P <0.05), as well as invasive monitoring of the diastolic time constant (Tau; 15.5±0.8 versus 12.7±0.2 ms; P <0.05). Exercise tolerance on a treadmill also decreased for HS/angiotensin II‐treated ucp3 +/‐ rats. Histological and molecular analyses further revealed that UCP3 insufficiency accelerated left ventricular concentric remodeling, detrimental interstitial matrix remodeling, and fetal gene reprogramming during hypertension. Moreover, UCP3 insufficiency increased oxidative stress and led to greater impairment of protein kinase G signaling. Conclusions Our findings identified UCP3 insufficiency as a cause for increased incidence of left ventricular diastolic dysfunction during hypertension. The results add further support to the use of antioxidants targeting mitochondrial reactive oxygen species as an adjuvant therapy for preventing heart failure with preserved ejection fraction in individuals with obesity.

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Section: Discussionmentioning

confidence: 99%

UCP3 (Uncoupling Protein 3) Insufficiency Exacerbates Left Ventricular Diastolic Dysfunction During Angiotensin II‐Induced Hypertension

Chen

Ashraf

et al. 2021

JAHA

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“…In T1DM patients, high circulating NT-proBNP levels identify left ventricular systolic dysfunction in 96% cases [ 103 ], whereas ANP was elevated after early diastolic dysfunction and cardiac sympathetic dysinnervation [ 104 ]. However, both peptides were useful sensors for diastolic dysfunction in diabetic patients who were symptomatic, had a restrictive filling pattern or pseudo-normalized mitral flow pattern, but not in those subjects asymptomatic or with relaxation abnormalities [ 100 ].…”

Section: Diagnosis Of Diabetic Cardiomyopathymentioning

confidence: 99%

Diagnostic approaches for diabetic cardiomyopathy

Lorenzo-Almorós

Tuñón

Orejas

et al. 2017

Cardiovasc Diabetol

194

165

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Diabetic cardiomyopathy (DCM) is a cardiac dysfunction which affects approximately 12% of diabetic patients, leading to overt heart failure and death. However, there is not an efficient and specific methodology for DCM diagnosis, possibly because molecular mechanisms are not fully elucidated, and it remains asymptomatic for many years. Also, DCM frequently coexists with other comorbidities such as hypertension, obesity, dyslipidemia, and vasculopathies. Thus, human DCM is not specifically identified after heart failure is established. In this sense, echocardiography has been traditionally considered the gold standard imaging test to evaluate the presence of cardiac dysfunction, although other techniques may cover earlier DCM detection by quantification of altered myocardial metabolism and strain. In this sense, Phase-Magnetic Resonance Imaging and 2D/3D-Speckle Tracking Echocardiography may potentially diagnose and stratify diabetic patients. Additionally, this information could be completed with a quantification of specific plasma biomarkers related to related to initial stages of the disease. Cardiotrophin-1, activin A, insulin-like growth factor binding protein-7 (IGFBP-7) and Heart fatty-acid binding protein have demonstrated a stable positive correlation with cardiac hypertrophy, contractibility and steatosis responses. Thus, we suggest a combination of minimally-invasive diagnosis tools for human DCM recognition based on imaging techniques and measurements of related plasma biomarkers.

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Clinical Applications in Extra-Cardiac Diseases

Clerico

Passino

Emdin

Natriuretic Peptides

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ANP but not BNP Reflects Early Left Diastolic Dysfunction in Type 1 Diabetics with Myocardial Dysinnervation

Abstract: In Type 1 diabetes, impaired diastolic function is associated with elevated ANP and catecholamine plasma levels that are normalized after ACE inhibition. Thus, ANP but not BNP appears to be a sensitive biochemical marker for early diastolic dysfunction in Type 1 diabetes.

Cited by 15 publications

References 32 publications

UCP3 (Uncoupling Protein 3) Insufficiency Exacerbates Left Ventricular Diastolic Dysfunction During Angiotensin II‐Induced Hypertension

UCP3 (Uncoupling Protein 3) Insufficiency Exacerbates Left Ventricular Diastolic Dysfunction During Angiotensin II‐Induced Hypertension

Diagnostic approaches for diabetic cardiomyopathy

Clinical Applications in Extra-Cardiac Diseases

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