Previously the subject of much debate, there is now consensus that diastolic heart failure (DHF) represents a distinct form of heart failure. Epidemiologic data indicate that DHF is common. Indeed, there is evidence that, among elderly persons, DHF is more common than systolic heart failure (SHF). Like SHF, DHF is associated with significant morbidity, mortality, and cost; however, few clinical trials focusing on isolated DHF have been completed. Much of the treatment of DHF is based on current concepts of the pathophysiology of DHF, small clinical studies, and experience gained from treating patients with SHF. The diagnosis of DHF is clinical; data supporting the establishment of a diagnosis of DHF are limited. Differences exist in prognosis and treatment between diastolic and systolic heart failure. This article reviews diastolic heart failure with emphasis on evidence-based management, aimed at primary care physicians who routinely provide care to patients with DHF. (J Am Board Fam Pract 2005;18:189 -98.)

Background: PM exposure can lead to myocardial hypertrophy, with a potential contribution via DNA methylation. Myocardial lipotoxicity is closely related to myocardial hypertrophy. But, myocardial lipotoxicity caused by PM has not been reported. PDGFRβ, a platelet-derived growth factor receptor, is also essential for normal cardiovascular development. However, It is unclear the role of PM-induced PDGFRβ methylation in myocardial hypertrophy and myocardial lipotoxicity. We investigated the effect of PDGFRβ methylation induced by PM on myocardial hypertrophy and myocardial lipotoxicity. Results: PDGFRβ methylation caused by PM decreased PDGFRβ mRNA and protein expression in C57BL/6J mouse hearts. Thus inhibiting gene expression in its downstream pathway, ultimately leading to cardiac hypertrophy. Disturbances of myocardial lipid metabolism caused by PM in AC16 cells and C57BL/6J mouse hearts were also observed. High expression of PDGFRβ in neonatal rat primary cardiomyocytes was found to activate its downstream pathway and ameliorate the effects of PM-induced cardiac hypertrophic activity. At the same time, adenovirus was used to induce high expression of PDGFRβ in C57BL/6J mice. It was found that PDGFRβ not only improved PM-induced cardiac hypertrophy, but also alleviated PM-induced myocardial lipotoxicity. Conclusions: PDGFRβ gene methylation may be one of the potential biomarkers of myocardial hypertrophy induced by PM exposure. And high expression of PDGFRβ may be a potential way to prevent myocardial hypertrophy and cardiac lipid metabolism disorder caused by PM exposure in mice.