Table 2 Limitations and drawbacks for the use of conventional metabolic therapies against DCM

Metformin

Dependence on plasma glucose reduction

[15,19]

Inconsistent recovery of cardiac function

Potential induction of myocardial fibrosis

Sulfonylureas

Higher risk of total cardiovascular events (except gliclazide)

[13,23]

Hypoglycemia

Weight gain

DPP-4 inhibitors

Higher risk of subclinical cardiac dysfunction and HF hospitalization

[28,30,39,40]

Inconsistent recovery of cardiac function and remodelling

Higher risk of myocardial hypertrophy with effective dose

GLP-1R agonists

Lack of data from large clinical trials on cardiovascular outcome

Statins

Dependence on plasma lipid reduction and vascular remodelling

[41,42]

Adverse impact on insulin production and sensitivity

Higher risk of total cardiovascular events (torcetrapib)

PPARα agonists

Dependence on plasma lipid reduction

[31,38,43]

Inconsistent recovery of cardiac function (fenofibrate)

DCM-like phenotype by experimental PPARα agonism

PPARγ agonists

Dependence on plasma lipid reduction

[29,44,45]

Higher risk of HF (pioglitazone)

Higher risk of total cardiovascular events (rosiglitazone)

Inconsistent recovery of cardiac function (rosiglitazone)

Potential induction of myocardial hypertrophy (rosiglitazone)

DCM-like phenotype by experimental PPARγ agonism