Introduction <p>The evaluation of diastolic function in patients with diabesity (i.e., combined obesity and type-2 diabetes mellitus) undergoing incretin-based therapy could facilitate its early detection and help prevent its progression to heart failure.</p> Methodology <p>In this small descriptive study, performed for exploratory and proof-of-concept purposes, a group of 15 diabesity cases with chest x-ray examinations (&lt; 1 month) before and after ≥ 12 months of incretin-based therapy (absent ventricular/valvular dysfunction) were identified. Standard diabesity characteristics (Body Weight (kg), Body Mass Index (kg/m<sup>2</sup>), and Hemoglobin A1c) and AI-model diagnostic predictions of pulmonary venous hypertension (aka “pulmonary congestion”) [None; Stage 1: vascular distention/redistribution but minimal interstitial edema; or Stage ≥ 2: vascular congestion with ≥ mild interstitial or alveolar edema] by validated AI-enabled chest x-ray staging, representing mean left atrial pressure in diastolic dysfunction, were evaluated pre- and post-therapy.</p> Results <p>According to weight-loss response to incretin therapy, cases clustered into equal-sized therapeutic categories as follows: (1) Significant Responders (9–30% decreases); (2) Insignificant Responders (0–2% decreases); and (3) Non-Responders (2–12% increases). Regarding hemoglobin A1c changes: (1) Significant Responders collectively decreased; (2) Insignificant Responders varied; and (3) Non-Responders were largely stable. Pre-therapy, all 15 cases demonstrated AI-enabled chest x-ray pulmonary venous hypertension staging evidence of diastolic dysfunction; post-therapy, 4 improved (especially the cases of greatest weight loss or hemoglobin A1c reduction), 5 were stable, and 6 worsened. Per therapeutic category, AI-enabled chest x-ray signs of functional response were: (1) Significant Responders (all demonstrating unequivocally decreased obesity and improved diabetes) collectively showed stable-decreased dysfunction; (2) Insignificant Responders (all demonstrating at most minimally decreased obesity, but stable-worsening diabetes in most) reflected stable-increased dysfunction in 60%; and (3) Non-Responders (all demonstrating increased obesity, but stable-improved diabetes) showed increased dysfunction in 80%.</p> Conclusion <p>AI-enabled chest x-ray pulmonary venous hypertension staging potentially detects background subclinical diastolic dysfunction in diabesity and monitors its functional response to incretin-based therapy. The confirmation (or disproof), and assessments of durability and generalizability, of these preliminary results await a larger more definitive and controlled prospective study on the subject.</p>

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AI-enabled chest x-ray potentially detects subclinical diastolic dysfunction in diabesity and monitors its functional responses to GLP-1 or GLP-1/GIP receptor agonists: initial exploration and proof-of-concept

  • Richard D. White,
  • Mutlu Demirer,
  • Barbaros Selnur Erdal,
  • Grace Lin

摘要

Introduction

The evaluation of diastolic function in patients with diabesity (i.e., combined obesity and type-2 diabetes mellitus) undergoing incretin-based therapy could facilitate its early detection and help prevent its progression to heart failure.

Methodology

In this small descriptive study, performed for exploratory and proof-of-concept purposes, a group of 15 diabesity cases with chest x-ray examinations (< 1 month) before and after ≥ 12 months of incretin-based therapy (absent ventricular/valvular dysfunction) were identified. Standard diabesity characteristics (Body Weight (kg), Body Mass Index (kg/m2), and Hemoglobin A1c) and AI-model diagnostic predictions of pulmonary venous hypertension (aka “pulmonary congestion”) [None; Stage 1: vascular distention/redistribution but minimal interstitial edema; or Stage ≥ 2: vascular congestion with ≥ mild interstitial or alveolar edema] by validated AI-enabled chest x-ray staging, representing mean left atrial pressure in diastolic dysfunction, were evaluated pre- and post-therapy.

Results

According to weight-loss response to incretin therapy, cases clustered into equal-sized therapeutic categories as follows: (1) Significant Responders (9–30% decreases); (2) Insignificant Responders (0–2% decreases); and (3) Non-Responders (2–12% increases). Regarding hemoglobin A1c changes: (1) Significant Responders collectively decreased; (2) Insignificant Responders varied; and (3) Non-Responders were largely stable. Pre-therapy, all 15 cases demonstrated AI-enabled chest x-ray pulmonary venous hypertension staging evidence of diastolic dysfunction; post-therapy, 4 improved (especially the cases of greatest weight loss or hemoglobin A1c reduction), 5 were stable, and 6 worsened. Per therapeutic category, AI-enabled chest x-ray signs of functional response were: (1) Significant Responders (all demonstrating unequivocally decreased obesity and improved diabetes) collectively showed stable-decreased dysfunction; (2) Insignificant Responders (all demonstrating at most minimally decreased obesity, but stable-worsening diabetes in most) reflected stable-increased dysfunction in 60%; and (3) Non-Responders (all demonstrating increased obesity, but stable-improved diabetes) showed increased dysfunction in 80%.

Conclusion

AI-enabled chest x-ray pulmonary venous hypertension staging potentially detects background subclinical diastolic dysfunction in diabesity and monitors its functional response to incretin-based therapy. The confirmation (or disproof), and assessments of durability and generalizability, of these preliminary results await a larger more definitive and controlled prospective study on the subject.