Sympathetic hyperactivity induces adverse effects in myocardial. Recent studies have shown that exercise training induces cardioprotection against sympathetic overload; however, relevant mechanisms of this issue remain unclear. We analyzed whether exercise can prevent pathological hypertrophy induced by sympathetic hyperactivity with modulation of the kallikrein-kinin and angiogenesis pathways....

ALTHOUGH TWO NINETEENTH CENTURY French pathologists1 2 and an early twentieth century German pathologist3 described cardiac pathological findings compatible with what we know today as "6asymmetrical hypertrophy of the heart," it remained for Donald Teare to bring attention to this entity in 1958.4 In nine cases of sudden death, Teare described a marked hypertrophy and thickening of the interven...

Background Recently, basal left ventricular hypertrophy has been suggested as a new form of hypertrophic cardiomyopathy. However, we have noticed that substantial focal basal hypertrophy often occurs in patients with mitral valve prolapse (Figure 1). Our objective was to characterize the extent and distribution of focal basal left ventricular hypertrophy in patients with MVP and assess the corr...

Hypertrophy is undoubtedly the most important problem in the structural adaptation of heart muscle. It stands at the centre of medical discussion because it is just the hypertrophic heart muscle that, after performing efficiently for a long time, finally fails. For this reason structural researches into hypertrophy include those of myocardial failure (Buchner, I950, I96I). According to the macr...

OBJECTIVES We examined whether the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel openers (KCOs) block myocardial hypertrophy and whether the 70-kDa S6 kinase (p70S6K) or extracellular signal-regulated kinase (ERK)-dependent pathway is involved. BACKGROUND Long-term inhibition of nitric oxide (NO) synthesis induces cardiac hypertrophy independent of blood pressure, by incre...

Background Cushing’s disease (CD) has demonstrated subclinical myocardial involvement such as left ventricular (LV) hypertrophy and both diastolic and systolic impairment. Although myocardial fibrosis may play an important role in such myocardial alterations, the new T1 mapping techniques have not yet been used in CD to characterize the myocardium at baseline and to evaluate the effect of treat...

Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness par...

Myocardial hypertrophy is a common feature of numerous diseases. It is important to distinguish between these diseases in order to enable accurate diagnosis and the administration of appropriate therapy. Using whole‑exome sequencing, the present study aimed to identify a pathogenic mutation in a Chinese family, which may lead to cardiac hypertrophy and Wolff‑Parkinson‑White syndrome. The proban...

BACKGROUND Previous studies have shown that hypertrophy of surviving myocytes after myocardial infarction (MI) is limited. Progressive ventricular dilatation after MI may occur when compensatory hypertrophy cannot restore left ventricular (LV) wall stress to normal. METHODS AND RESULTS To test whether induction of additional myocyte hypertrophy might prevent pathological LV remodeling after l...

The pathways inducing the critical transition from compensated hypertrophy to cardiac dilation and failure remain poorly understood. The goal of our study is to determine the role of Rac-induced signaling in this transition process. Our previous results showed that Thyroxin (T4) treatment resulted in increased myocardial Rac expression in wild-type mice and a higher level of expression in Zea m...