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Published on: June 14, 2016
Pacing-induced cardiomyopathy: pathophysiological insights through matrix metalloproteinases
Fozia Z Ahmed1, Rajdeep S Khattar, Amir M Zaidi
1Manchester Heart Centre, Manchester Royal Infirmary, Oxford Road, Manchester, M13 9WL, UK, foziaahmed@doctors.org.uk.
Chronic right ventricular pacing can cause heart dysfunction. Matrix metalloproteinases (MMPs) are implicated in pacing-induced cardiomyopathy (PiCMP) development, suggesting new prevention strategies.
Area of Science:
- Cardiology
- Biochemistry
Background:
- Pacing-induced ventricular dysfunction and cardiomyopathy (PiCMP) are known complications of chronic right ventricular pacing.
- Myocardial perfusion and sympathetic innervation changes contribute to pacing-induced heart disease, but other mechanisms are likely involved.
Purpose of the Study:
- To review the clinical epidemiology of pacing-induced ventricular dysfunction.
- To explore the role of matrix metalloproteinases (MMPs) in the development of PiCMP using insights from animal models.
- To discuss potential pacing strategies for preventing pacing-induced ventricular dysfunction.
Main Methods:
- Literature review of clinical epidemiology of pacing-induced ventricular dysfunction.
- Analysis of data from animal models to understand MMP expression and function in PiCMP.
- Exploration of preventative pacing strategies.
Main Results:
- Matrix metalloproteinases (MMPs) are key in extracellular matrix degradation and left ventricular remodeling in heart failure.
- While MMP roles in other cardiomyopathies are defined, their specific involvement in PiCMP is not well-reported.
- Animal models offer insights into how altered MMP expression and function contribute to PiCMP.
Conclusions:
- Matrix metalloproteinases (MMPs) are likely involved in the pathophysiology of pacing-induced cardiomyopathy (PiCMP).
- Further research into MMPs in PiCMP could lead to novel therapeutic and preventative strategies.
- Optimizing pacing strategies may mitigate the risk of developing pacing-induced ventricular dysfunction.
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