Key result
Complex fibrotic, inflammatory, and metabolic mechanisms drive LV diastolic dysfunction primarily diagnosed by echocardiography.
Left ventricular diastolic dysfunction is driven by complex cellular mechanisms including calcium dysregulation, altered titin phosphorylation, and extracellular matrix remodeling, with echocardiography serving as the primary diagnostic modality.
Reinforces echocardiography as the clinical standard for detecting diastolic dysfunction; extends mechanistic understanding of.
Diastolic dysfunction is a condition in which ventricular fi lling is impaired, regardless of the presence of symptoms and irrespective of whether the ejection fraction is normal or reduced. Left ventricular diastolic dysfunction results from complex and interconnected biochemical and cellular mechanisms. Among them, impaired myocardial relaxation due to calcium dysregulation, altered titin phosphorylation affecting the passive elasticity of the myocardium, and extracellular matrix remodeling with the development of fi brosis mediated by signalling pathways such as TGF-β/SMAD and MAPK play a leading role. Additional contributing factors include oxidative stress and mitochondrial dysfunction, chronic infl ammation and activation of cytokine cascades, metabolic disturbances such as diabetes and obesity, as well as protein dysfunction related to endoplasmic reticulum stress and impaired proteolysis. All these processes in complex lead to impaired diastolic fi lling of the left ventricle, i.e., diastolic dysfunction. Due to its broad availability and proven clinical value, echocardiography is the primary method for diagnosing diastolic dysfunction. Invasive and other imaging modalities offer complementary information in complex or borderline cases, or when echocardiographic evaluation is diffi cult or impossible.
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Ivanov et al. (2025) conducted a review in Left ventricular diastolic dysfunction. Left ventricular diastolic dysfunction results from complex biochemical and cellular mechanisms including impaired myocardial relaxation, increased myocardial stiffness due to fibrosis, oxidative stress, inflammation, and metabolic disturbances such as diabetes and obesity, with echocardiography as the primary diagnostic method.
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