Multimodality Imaging for Diagnosis and Characterization of a Cardiac Hydatid Cyst.

Here, we report the case of a young patient admitted to the emergency department because of abdominal pain. Computed tomography revealed a mass within her right heart. Through serial multimodality imaging testing, including computed tomography, three-dimensional (2D)- and three-dimensional echocardiography, as well as cardiac magnetic resonance, the diagnosis of cardiac involvement in the course of Echinococcus granulosus infection was hypothesized.

Hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin prevents cardiac hypertrophy induced by pressure overload and inhibits p21ras activation.

BACKGROUND: Patients with cardiac hypertrophy are at increased cardiovascular risk. It has been hypothesized that hydroxymethylglutaryl coenzyme A reductase inhibitors may exert beneficial effects other than their cholesterol-lowering actions. The aims of the study were to assess the in vivo effects of simvastatin (SIM) on cardiac hypertrophy and on Ras signaling in rats with ascending aorta banding. METHODS AND RESULTS: Wistar rats were randomized to receive either treatment with SIM or placebo, and then short-term (group I) and long-term (group II) left ventricular pressure overload was performed by placing a tantalum clip on ascending aorta. At the end of treatment period, left and right ventricular weight, body weight, and tibial length were measured and echocardiographic evaluations were performed. Ras signaling was investigated by analyzing Ras membrane localization and activation, ERK2 phosphorylation, and p27(kip1) and cdk4 levels. In SIM-treated rats, a significant reduction of left ventricular weight/body weight, echocardiographic left ventricular mass, and left ventricular end-diastolic diameter and end-diastolic pressure was found. In rats with pressure overload, SIM treatment significantly reduced Ras membrane targeting, Ras in vivo activation, ERK2 phosphorylation, and the ratio cdk4/p27(kip1). CONCLUSIONS: HMG CoA inhibitor SIM inhibits in vivo Ras signaling and prevents left ventricular hypertrophy development in aortic-banded animals.

Is Left Ventricular Noncompaction Only a Morphological Feature? A Case of Disappearance of Noncompaction after Surgical Correction of Aorto-Right Ventricular Fistula, Interventricular Septal Defect and Aortic Stenosis.

A 55-year-old man complaining of worsening dyspnea on exertion was diagnosed with restrictive interventricular septal defect, left ventricular noncompaction (LVNC), mild aortic valve stenosis and aorto-right ventricular fistula. He underwent surgical aortic valve replacement with a mechanical bileaflet valve (St. Jude n. 23) and contextual direct suture of interventricular septal defect and closure of aorto-right ventricular fistula. At 2 years of follow-up, the patient was in good general condition. A complete echocardiographic examination showed normalization of left ventricular dimensions and ejection fraction. Furthermore, left ventricular trabeculations became less evident and no longer met the diagnostic criteria for noncompaction. In our case, the expected left ventricular reverse remodeling after cardiac surgery was associated with a significant reduction in LVNC features. In conclusion, physicians should be careful in avoiding overdiagnosis of LVNC, whose features may indeed reflect only the hypertrabeculated morphology of a normal or pathological heart.