Mitogen-activated protein kinases (p38 and c-Jun NH2-terminal kinase) are differentially regulated during cardiac volume and pressure overload hypertrophy.

Chronic pressure overload (PO) and volume overload (VO) result in morphologically and functionally distinct forms of myocardial hypertrophy. However, the molecular mechanism initiating these two types of hypertrophy is not yet understood. Data obtained from different cell types have indicated that the mitogen-activated protein kinases (MAPKs) comprising c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 play an important role in transmitting signals of stress stimuli to elicit the cellular response.

Revisiting the surgical creation of volume load by aorto-caval shunt in rats.

Cardiac hypertrophy is an early landmark during the clinical course of heart failure, and is an important risk factor for subsequent morbidity and mortality. The hypertrophy response to different types of cardiac overload is distinguished both at the molecular and cellular levels. These changes have been extensively characterized for pressure load hypertrophy; however, similar information for volume load hypertrophy is still needed.

Intermediate results of the anatomic repair for congenitally corrected transposition.

Background: Anatomic repair of congenitally corrected transposition of the great arteries has several advantages over the traditional approach but lacks long-term evaluation.

Methods: The data on 12 patients who had the procedure between January 1989 and June 2000 were retrospectively reviewed. Associated lesions included ventricular septal defect in 12 patients, pulmonary stenosis in 10 patients, and moderate to severe tricuspid valve regurgitation in 4 patients.