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Cardiomyopathy II: Dilated Cardiomyopathy

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...

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Preconditioning the diabetic human myocardium.

Vivek Sivaraman¹, Derek J Hausenloy, Abigail M Wynne

¹The Hatter Cardiovascular Institute, University College London, UK.

Journal of Cellular and Molecular Medicine

|June 11, 2009

Summary

This summary is machine-generated.

Diabetic hearts require a prolonged hypoxic preconditioning protocol to achieve cardioprotection, unlike non-diabetic hearts. This is linked to lower Akt phosphorylation in diabetic myocardium, suggesting a potential therapeutic target.

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Area of Science:

Cardiology
Diabetology
Molecular Biology

Background:

Ischaemic preconditioning (IPC) is a phenomenon where brief episodes of ischemia protect the heart from subsequent longer ischemic insults.
Diabetes mellitus is associated with increased cardiovascular risk and altered myocardial responses to stress.

Purpose of the Study:

To investigate the efficacy of IPC in human diabetic myocardium.
To explore the role of the PI3K-Akt signaling pathway in diabetic hearts' response to IPC.

Main Methods:

Human right atrial appendages from diabetic and non-diabetic patients were used.
Trabeculae were subjected to hypoxia and reoxygenation with varying IPC protocols.
Contractile function recovery was measured.
Western blot analysis assessed Akt phosphorylation levels.

Main Results:

Standard IPC improved function in non-diabetic, but not diabetic, atrial trabeculae.
A prolonged IPC protocol significantly improved function in diabetic atrial trabeculae.
Diabetic myocardium showed significantly lower basal levels of phosphorylated Akt compared to non-diabetic myocardium.

Conclusions:

The threshold for effective IPC is elevated in human diabetic myocardium.
Down-regulation of the PI3K-Akt pathway may contribute to the blunted IPC response in diabetic hearts.
Prolonged IPC may be a viable strategy to confer cardioprotection in diabetic patients.