Preclinical Alterations in Myocardial Microstructure in People with Metabolic Syndrome

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Abstract

Objective

Metabolic syndrome (MetS) can lead to myocardial fibrosis, diastolic dysfunction and eventual heart failure. We evaluated alterations in myocardial microstructure in people with MetS using a novel algorithm to characterize ultrasonic signal intensity variation.

Methods

Among 254 participants without existing cardiovascular disease (mean age 42 ± 11 years, 75% women), there were 162 with MetS, 47 with obesity without MetS, and 45 non-obese controls. Standard echocardiography was performed, and a novel validated computational algorithm was used to investigate myocardial microstructure based on sonographic signal intensity and distribution. We examined the signal intensity coefficient (SIC, left ventricular microstructure).

Results

The SIC was significantly higher in people with MetS compared with people with (P<0.001) and without obesity (P=0.04), even after adjustment for age, sex, body mass index, hypertension, diabetes mellitus and triglyceride to HDL cholesterol (TG/HDL) ratio (P<0.05 for all). Clinical correlates of SIC included TG concentrations (r=0.21, P=0.0007) and the TG/HDL ratio (r=0.2, P=0.001).

Conclusions

Our findings suggest that preclinical MetS and dyslipidemia in particular, are associated with altered myocardial signal intensity variation. Future studies are needed to determine whether the SIC may help detect subclinical disease in people with metabolic disease, with the ultimate goal of targeting preventive efforts.

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Most cited references 32

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Use of metabolic markers to identify overweight individuals who are insulin resistant.

Tracey McLaughlin, Fahim Abbasi, Karen Cheal … (2003)

Insulin resistance is more common in overweight individuals and is associated with increased risk for type 2 diabetes mellitus and cardiovascular disease. Given the current epidemic of obesity and the fact that lifestyle interventions, such as weight loss and exercise, decrease insulin resistance, a relatively simple means to identify overweight individuals who are insulin resistant would be clinically useful. To evaluate the ability of metabolic markers associated with insulin resistance and increased risk for cardiovascular disease to identify the subset of overweight individuals who are insulin resistant. Cross-sectional study. General clinical research center. 258 nondiabetic, overweight volunteers. Body mass index; fasting glucose, insulin, lipid and lipoprotein concentrations; and insulin-mediated glucose disposal as quantified by the steady-state plasma glucose concentration during the insulin suppression test. Overweight was defined as body mass index of 25 kg/m2 or greater, and insulin resistance was defined as being in the top tertile of steady-state plasma glucose concentrations. Receiver-operating characteristic curve analysis was used to identify the best markers of insulin resistance; optimal cut-points were identified and analyzed for predictive power. Plasma triglyceride concentration, ratio of triglyceride to high-density lipoprotein cholesterol concentrations, and insulin concentration were the most useful metabolic markers in identifying insulin-resistant individuals. The optimal cut-points were 1.47 mmol/L (130 mg/dL) for triglyceride, 1.8 in SI units (3.0 in traditional units) for the triglyceride-high-density lipoprotein cholesterol ratio, and 109 pmol/L for insulin. Respective sensitivity and specificity for these cut-points were 67%, 64%, and 57% and 71%, 68%, and 85%. Their ability to identify insulin-resistant individuals was similar to the ability of the criteria proposed by the Adult Treatment Panel III to diagnose the metabolic syndrome (sensitivity, 52%, and specificity, 85%). Three relatively simple metabolic markers can help identify overweight individuals who are sufficiently insulin resistant to be at increased risk for various adverse outcomes. In the absence of a standardized insulin assay, we suggest that the most practical approach to identify overweight individuals who are insulin resistant is to use the cut-points for either triglyceride concentration or the triglyceride-high-density lipoprotein cholesterol concentration ratio.

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Relationship Between Left Ventricular Structural and Metabolic Remodeling in Type 2 Diabetes.

Eylem Levelt, Masliza Mahmod, Stefan K Piechnik … (2016)

Concentric left ventricular (LV) remodeling is associated with adverse cardiovascular events and is frequently observed in patients with type 2 diabetes mellitus (T2DM). Despite this, the cause of concentric remodeling in diabetes per se is unclear, but it may be related to cardiac steatosis and impaired myocardial energetics. Thus, we investigated the relationship between myocardial metabolic changes and LV remodeling in T2DM. Forty-six nonhypertensive patients with T2DM and 20 matched control subjects underwent cardiovascular magnetic resonance to assess LV remodeling (LV mass-to-LV end diastolic volume ratio), function, tissue characterization before and after contrast using T1 mapping, and (1)H and (31)P magnetic resonance spectroscopy for myocardial triglyceride content (MTG) and phosphocreatine-to-ATP ratio, respectively. When compared with BMI- and blood pressure-matched control subjects, subjects with diabetes were associated with concentric LV remodeling, higher MTG, impaired myocardial energetics, and impaired systolic strain indicating a subtle contractile dysfunction. Importantly, cardiac steatosis independently predicted concentric remodeling and systolic strain. Extracellular volume fraction was unchanged, indicating the absence of fibrosis. In conclusion, cardiac steatosis may contribute to concentric remodeling and contractile dysfunction of the LV in diabetes. Because cardiac steatosis is modifiable, strategies aimed at reducing MTG may be beneficial in reversing concentric remodeling and improving contractile function in the hearts of patients with diabetes.

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Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities.

Michele Cavalera, Nikolaos G Frangogiannis, Junhong Wang (2014)

Cardiac fibrosis is strongly associated with obesity and metabolic dysfunction and may contribute to the increased incidence of heart failure, atrial arrhythmias, and sudden cardiac death in obese subjects. This review discusses the evidence linking obesity and myocardial fibrosis in animal models and human patients, focusing on the fundamental pathophysiological alterations that may trigger fibrogenic signaling, the cellular effectors of fibrosis, and the molecular signals that may regulate the fibrotic response. Obesity is associated with a wide range of pathophysiological alterations (such as pressure and volume overload, metabolic dysregulation, neurohumoral activation, and systemic inflammation); their relative role in mediating cardiac fibrosis is poorly defined. Activation of fibroblasts likely plays a major role in obesity-associated fibrosis; however, inflammatory cells, cardiomyocytes, and vascular cells may also contribute to fibrogenic signaling. Several molecular processes have been implicated in regulation of the fibrotic response in obesity. Activation of the renin-angiotensin-aldosterone system, induction of transforming growth factor β, oxidative stress, advanced glycation end-products, endothelin 1, Rho-kinase signaling, leptin-mediated actions, and upregulation of matricellular proteins (such as thrombospondin 1) may play a role in the development of fibrosis in models of obesity and metabolic dysfunction. Moreover, experimental evidence suggests that obesity and insulin resistance profoundly affect the fibrotic and remodeling response after cardiac injury. Understanding the pathways implicated in obesity-associated fibrosis may lead to the development of novel therapies to prevent heart failure and attenuate postinfarction cardiac remodeling in patients with obesity. Copyright © 2014 Elsevier Inc. All rights reserved.

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Author and article information

Journal

Journal ID (nlm-journal-id): 101264860

Journal ID (pubmed-jr-id): 32902

Journal ID (nlm-ta): Obesity (Silver Spring)

Journal ID (iso-abbrev): Obesity (Silver Spring)

Title: Obesity (Silver Spring, Md.)

ISSN (Print): 1930-7381

ISSN (Electronic): 1930-739X

Publication date Nihms-submitted: 23 June 2017

Publication date (Electronic): 24 July 2017

Publication date (Print): September 2017

Publication date PMC-release: 24 January 2018

Volume: 25

Issue: 9

Pages: 1516-1522

Affiliations

[1 ]Cardiovascular Research Center and Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, MA

[2 ]Cardiovascular Center, Tufts Medical Center, Boston, MA

[3 ]Temple Heart and Vascular Institute, Temple University, Philadelphia, PA

[4 ]Harvard Medical School, Boston, MA

[5 ]Cardiovascular Medicine Section, Department of Medicine, Boston University, Boston, MA

[6 ]Whitaker Cardiovascular Institute, Boston University, Boston, MA

[7 ]Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA

Author notes

Correspondence to: Jennifer E. Ho, MD Massachusetts General Hospital, 185 Cambridge Street, CPZN #3192, Boston, MA 02114, Phone: 617-724-6411, Fax: 617-643-3451, jho1@ 123456partners.org

[*]

Denotes equal contribution

Article

Manuscript ID: NIHMS887522

DOI: 10.1002/oby.21936

PMC ID: 5578717

PubMed ID: 28737258

SO-VID: b766d652-95b8-40cb-8a43-71ee48134c65

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Preclinical Alterations in Myocardial Microstructure in People with Metabolic Syndrome

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Abstract

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Most cited references 32

Use of metabolic markers to identify overweight individuals who are insulin resistant.

Relationship Between Left Ventricular Structural and Metabolic Remodeling in Type 2 Diabetes.

Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities.

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