Empagliflozin, an SGLT2 inhibitor, reduces cardiovascular mortality in Type 2 diabetes beyond glycaemic control. The haemodynamic mechanism MOST responsible for cardiac benefit is:

• A Osmotic diuresis and natriuresis reducing preload, afterload, and ventricular wall stress ✓
• B Direct negative chronotropy reducing myocardial oxygen demand
• C Upregulation of GLP-1 receptors on cardiomyocytes improving contractility
• D Inhibition of cardiac SGLT1 transporters reducing glucose uptake in ischemic myocardium

Explanation

The cardiovascular mortality benefit of SGLT2 inhibitors in HFrEF/HFpEF is largely attributed to their diuretic and natriuretic effects — osmotic diuresis from glucosuria reduces plasma volume, preload, afterload, and ventricular filling pressure. This 'pseudo-Fontan' unloading mechanism is similar to loop diuretics but without neurohormonal activation. There is also evidence of direct myocardial metabolic effects (ketone body utilization), but the haemodynamic benefit is primary. SGLT2 inhibitors do not act via GLP-1 receptors.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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