Review Article

Role of Mitogen-Activated Protein Kinase Pathways in Multifactorial Adverse Cardiac Remodeling Associated with Metabolic Syndrome

Table 1

Different disorders in metabolic syndrome are associated with cardiac structural and functional changes.

Metabolic syndrome characteristicAdverse cardiac remodellingReferenceMethod of assessment

Obese women have higher end-diastolic septal and posterior wall thickness, left ventricle mass, and relative wall thickness than nonobese[13]Echocardiography and tissue Doppler imaging
ObesityUncomplicated severe obesity is associated with adapted and appropriate changes in cardiac structure and function[14]Echocardiography
Reduced left ventricle systolic and diastolic function and increased myocardial reflectivity characterize obese patients as compared to referents[15]Transthoracic echocardiography, myocardial Doppler-derived systolic and early diastolic velocity, strain and strain rate imaging, and tissue characterization with cyclic variation and calibrated integrated backscatter

Diabetes, fasting glucose, and fasting insulin levels are associated with left ventricular hypertrophy[16]Echocardiography and laboratory testing
DiabetesIncreased heart size in obese men[17]Autopsy
Postmortem analysis of obese patients that died from gastric bypass complication revealed cardiac hypertrophy[18] Autopsy

HypertensionLeft ventricle mass is positively associated with the number of metabolic risk factors in normotensive and hypertensive participants[19]Echocardiography

Increased left ventricular mass and reduce left ventricular relaxation[20]Echocardiography was used to assess pulse-wave Doppler and tissue Doppler imaging
Metabolic syndrome
(defined as a cluster of all previously cited disorders [2])
Ventricular diastolic dysfunction, mean left ventricular mass, and left ventricular diameter significantly increase with the number of features of the metabolic syndrome[21] Structured clinical interview with a physician, ECG and a transthoracic M-mode, and 2D echocardiogram
High levels of IL-6 that could be observed in metabolic syndrome induce cardiac fibrosis[22]Blood-perfused isolated heart
Cardiotrophin-1 treatment, mimicking the upregulated level found in metabolic syndrome, induces cardiac fibrosis[23]Echocardiography, Doppler, and echo tracking device and ex vivo approach