Key result
Severe insulin resistance is linked to ~5-point worse global longitudinal strain at 24 months.
Why the study?
The exact pathophysiological sequence translating metabolic dysregulation and systemic insulin resistance into structural cardiac decline and left ventricular diastolic dysfunction remains poorly quantified in normoglycemic populations.
Does severe systemic hyperinsulinemia impair subclinical myocardial mechanics and promote left ventricular diastolic dysfunction in non-diabetic adult patients with varying degrees of metabolic syndrome?
Cohort (n=215)
Does severe systemic hyperinsulinemia impair subclinical myocardial mechanics and promote left ventricular diastolic dysfunction in non-diabetic adult patients with varying degrees of metabolic syndrome?
Severe insulin resistance in non-diabetic patients independently drives progressive left ventricular hypertrophy, elevated filling pressures, and impaired global longitudinal strain over 24 months, highlighting a potential pre-diabetic therapeutic window to prevent HFpEF.
Answers are grounded in this paper and cite their sources.
May link insulin resistance to diastolic dysfunction independent of glucose or CAD; leaves open causal validation before any practice change.
Systemic insulin resistance functions as a primary pathological catalyst for adverse myocardial remodeling, directly precipitating left ventricular diastolic dysfunction independent of overt hyperglycemia or obstructive coronary artery disease. The exact pathophysiological sequence translating metabolic dysregulation into structural cardiac decline remains poorly quantified in normoglycemic populations. This prospective longitudinal investigation aimed to evaluate the isolated impact of severe systemic hyperinsulinemia on subclinical myocardial mechanics, utilizing advanced tissue Doppler imaging and two-dimensional speckle-tracking echocardiography over a 24-month follow-up trajectory. A strictly selected cohort of 215 non-diabetic adult patients exhibiting varying degrees of metabolic syndrome was stratified based on baseline Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) quartiles. Serial echocardiographic analyses demonstrated a profound, dose-dependent deterioration in myocardial relaxation and compliance among highly insulin-resistant subjects. Patients in the highest HOMA-IR quartile (> 4.5) experienced an accelerated expansion of the Left Ventricular Mass Index from 92.4 ± 8.1 g/m2 at baseline to 118.6 ± 10.4 g/m2 at the final follow-up, alongside a critical elevation in the E/e' ratio reaching 14.2 ± 1.5, indicating severely elevated left ventricular filling pressures. Global longitudinal strain, a highly sensitive marker of early contractile failure, degraded significantly in the severe hyperinsulinemic group (-16.4 ± 1.2%) compared to the insulin-sensitive control cohort (-21.5 ± 0.9%). Multivariate regression confirmed fasting insulin levels as the strongest independent predictor of myocardial collagen deposition and diastolic stiffness, overriding the mechanical stress of concurrent prehypertension. Targeting the insulin-signaling cascade proactively at the pre-diabetic stage presents a vital therapeutic opportunity to arrest fibrotic myocardial remodeling and prevent the inevitable progression toward heart failure with preserved ejection fraction.
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Abdulhamidova Saydinsa (2026) conducted a cohort in Severe insulin resistance and metabolic syndrome in non-diabetic patients (n=215). Severe systemic hyperinsulinemia / insulin resistance (highest HOMA-IR quartile > 4.5) vs. Insulin-sensitive control cohort (lower HOMA-IR quartiles) was evaluated on Subclinical myocardial mechanics and remodeling (Left Ventricular Mass Index, E/e' ratio, and global longitudinal strain). Severe insulin resistance (HOMA-IR >4.5) significantly degraded global longitudinal strain (-16.4% vs -21.5% in controls) and increased LV mass index (to 118.6 g/m2) and E/e' (to 14.2) at 24 months.
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