Sildenafil as adjunct therapy to high-dose epoprostenol in a patient with pulmonary veno-occlusive disease.

Pulmonary veno-occlusive disease is refractory to medical treatment and is generally associated with a poor prognosis. Treatment with vasodilators, such as prostacyclin, of patients with PVOD is controversial because of concerns regarding hemodynamic deterioration. Although a preferential pulmonary vasodilatory effect of a specific phosphodiesterase-5 inhibitor, sildenafil, has recently been reported in patients with primary pulmonary hypertension, little information is available regarding the effect of sildenafil on patients with pulmonary veno-occlusive disease.

Cross-talk between bone morphogenetic protein 2 and leukemia inhibitory factor through ERK 1/2 and Smad1 in protection against doxorubicin-induced injury of cardiomyocytes.

The survival of cardiomyocytes is regulated by growth factors and cytokines such as bone morphogenetic protein (BMP) 2 and leukemia inhibitory factor (LIF). BMP2 and LIF induce distinct signal transduction pathways that each activate a different transcription factor [Smad1 and signal transducing activating transcriptional factor (Stat) 3, respectively] and common signal pathway [mitogen-activated protein kinase (MAPK)]. We previously demonstrated that BMP2 and LIF protect cardiomyocytes via Smad1 and STAT3 signaling pathways, respectively.

Smad1 protects cardiomyocytes from ischemia-reperfusion injury.

Background: We previously reported that bone morphogenetic protein 2 (BMP2) protected against apoptosis of serum-deprived cardiomyocytes via induction of Bcl-xL through the Smad1 pathway. To investigate whether Smad1 signaling promotes cell survival in the adult heart, we subjected transgenic mice with cardiac-specific overexpression of smad1 gene (Smad1TG) to ischemia-reperfusion (I/R) injury.

Methods And Results: The effects of BMP2 or adenovirus-mediated transfection of smad1 on cardiomyocyte survival in hypoxia-reoxygenation were examined using rat neonatal cardiomyocytes.

Hemodynamics of microvascular dysfunction in patients with anterior wall acute myocardial infarction.

This study investigated whether the no-reflow phenomenon in acute myocardial infarction (AMI) is associated with an increase in coronary zero flow pressure (ZFP), a decrease in coronary arterial conductance, or both phenomena. Coronary blood flow velocity and pressure were measured with a Doppler guidewire and a pressure wire, respectively, during vasodilation with adenosine triphosphate after coronary intervention. The data indicate that the no-reflow phenomenon is not necessarily associated with a decrease in coronary arterial conductance but with an increase in ZFP.

Solitary right ventricle metastasis by renal cell carcinoma.

A 57-year-old man with a history of renal cell carcinoma presented with presyncope. He underwent nephrectomy years earlier followed by HLA-matched allogeneic peripheral-blood stem-cell transplantation. Echocardiographic investigation revealed a solitary right ventricle mass without contiguous vena caval or right atrial involvement.

Specific cardiomyopathy caused by multisystemic lipid storage in Jordans' anomaly.

Multisystemic lipid storage disease is a rare disorder of lipid metabolism. We report one case of a Japanese man with systemic lipid storage in skeletal muscle and heart as well as in leukocytes (Jordans' anomaly). Positron emission tomography (PET) using 18F-fluoro-2-deoxyglucose (FDG) clearly revealed an abnormal increase of uptake during fasting in the left ventricle, suggesting changes in the energy metabolism in the heart.

Activation of gp130 transduces hypertrophic signal through interaction of scaffolding/docking protein Gab1 with tyrosine phosphatase SHP2 in cardiomyocytes.

Grb2-associated binder-1 (Gab1) is a scaffolding/docking protein and contains a Pleckstrin homology domain and potential binding sites for Src homology (SH) 2 and SH3 domains. Gab1 is tyrosine phosphorylated and associates with protein tyrosine phosphatase SHP2 and p85 phosphatidylinositol 3-kinase on stimulation with various cytokines and growth factors, including interleukin-6. We previously demonstrated that interleukin-6-related cytokine, leukemia inhibitory factor (LIF), induced cardiac hypertrophy through gp130.

Effect of plaque debulking before stent implantation on in-stent neointimal proliferation: a serial 3-dimensional intravascular ultrasound study.

Background: Recent intravascular ultrasound (IVUS) studies have suggested that plaque burden has a role in promoting intimal hyperplasia after stenting. We report on volumetric assessments of in-stent neointimal formation with 3-dimensional IVUS analysis, comparing directional coronary atherectomy (DCA) plus stenting (DCA/stenting) to stenting without DCA.

Methods: Twenty-four patients (24 lesions) treated with DCA before stenting were matched to 24 patients (24 lesions) receiving stenting without DCA.

A Single-Center, Open-Label, Randomized, Parallel-Group Study Assessing the Differences Between an Angiotensin II Receptor Antagonist and an Angiotensin-Converting Enzyme Inhibitor in Hypertensive Patients with Congestive Heart Failure: The Research for Efficacy of Angiotensin II Receptor Antagonist in Hypertensive Patients with Congestive Heart Failure Study.

Background: Angiotensin II receptor blockers (ARBs) and angiotensin-converting enzyme inhibitors (ACEIs) have been used to treat congestive heart failure (CHF). According to a MEDLINE search, however, few studies are available on the clinical differences between ARBs and ACEIs in CHF.

Objective: To examine the clinical differences between an ARB (candesartan cilexetil) and an ACEI (lisinopril) in the treatment of CHF, we investigated exercise capacity, ventricular function, and neurohormonal levels in hypertensive patients with CHF before and after treatment with these agents.