Indication

Heart failure associated with type 2 diabetes mellitus

Heart failure associated with type 2 diabetes mellitus is a high-risk cardiovascular complication characterized by the inability of the heart to maintain adequate systemic perfusion or to do so only under elevated filling pressures in individuals with type 2 diabetes mellitus. Read more about Heart failure associated with type 2 diabetes mellitus

25 drugs 23 manufacturers

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Drugs that treat it

Common Heart failure associated with type 2 diabetes mellitus therapies.

Showing 1–9 of 25 drugs

INVOKANA (canagliflozin)

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+3
JANSSEN PHARM.

FARXIGA (dapagliflozin)

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+4
AstraZeneca Pharmaceuticals

INPEFA (sotagliflozin)

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·CHRONIC HEART FAILURE·+2
LEXICON PHARMAC

DAPAGLIFLOZIN

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+4
A-S MEDICATION

FARXIGA (dapagliflozin)

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+4
A-S MEDICATION

INVOKANA (canagliflozin)

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+3
A-S MEDICATION

DAPAGLIFLOZIN

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+4
PRASCO LABS

DAPAGLIFLOZIN

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+4
BRYANT RANCH PR

DAPAGLIFLOZIN

ANTIHYPERGLYCEMIC-SOD/GLUC COTRANSPORT-2 (SGLT2) INHIBITORS·TYPE 2 DIABETES MELLITUS·+4
AJANTA PHARMA L
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About Heart failure associated with type 2 diabetes mellitus.

Heart failure associated with type 2 diabetes mellitus is a high-risk cardiovascular complication characterized by the inability of the heart to maintain adequate systemic perfusion or to do so only under elevated filling pressures in individuals with type 2 diabetes mellitus.

Affecting the cardiovascular and metabolic systems, this clinical state can manifest across preserved, mildly reduced, or reduced left ventricular ejection fraction phenotypes.

Pathophysiologically, persistent hyperglycemia, hyperinsulinemia, and insulin resistance induce myocardial lipotoxicity, advanced glycation end-product accumulation, systemic microvascular inflammation, and neurohormonal overactivation.

These interrelated mechanisms drive myocardial fibrosis, adverse ventricular remodeling, and impaired diastolic and systolic function, substantially increasing the risk of cardiovascular mortality and hospitalizations.

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