Effects of telmisartan and losartan on cardiovascular protection in Japanese hypertensive patients.

The Telmisartan and Losartan Cardiac Evaluation Trial, a multicenter, prospective, randomized, open-labeled, blinded-endpoint trial, was designed to compare the effects of two angiotensin II receptor blockers (ARBs), telmisartan and losartan, on cardiovascular protection in Japanese patients with mild to moderate essential hypertension. We compared the effects of telmisartan and losartan on left ventricular (LV) hypertrophy, cardiac function, atherosclerosis of carotid arteries and surrogate markers related to the actions of peroxisome proliferator-activated receptor-γ. A total of 58 patients were enrolled in the present trial and the follow-up period was 1 year.

Abdominal aortic pseudoaneurysm caused by prolonged methicillin-resistant Staphylococcus aureus sepsis.

The mechanism of pseudoaneurysm formation caused by prolonged sepsis is thought to be related to the vascular endothelium being directly invaded and broken by bacteria. Moreover, matrix metalloproteinases (MMPs) which are up-regulated by chronic inflammation have been reported to be implicated in the pathogenesis of aneurysm development through increased proteolysis of extracellular matrix proteins. An effective treatment for infected pseudoaneurysm remains unsettled.

Transferring images via the wireless messaging network using camera phones shortens the time required to diagnose acute coronary syndrome.

Background: Clear images can be sent via e-mail using camera phones. We examined whether camera phones are useful to transmit electrocardiogram (ECG) images.

Methods And Results: ECG images were taken of 20 patients suspected to have acute coronary syndrome.

Takayasu arteritis evaluated by multi-slice computed tomography in an old man.

In the case of patients with Takayasu arteritis (TA), they consult a doctor for the first time when they have a slight fever, shoulder pain, chest pain, back pain, or headache, or when they are pointed out to have high CRP or anemia by chance in medical check-up. In TA, they are usually young women. In our case, the very old patient had bilateral massive pleural effusion and aortic aneurysm with a 64-slice computed tomography (CT).

Coronary aneurysm reduced after coronary stenting.

We describe as case of a 70-year-old man who underwent a percutaneous coronary intervention with stenting, for a severe stenosis complicated by a coronary aneurysm just distal to the stenotic site. Notably, coronary angiogram showed an immediate and progressive reduction in the size of coronary aneurysm. Curved planar reconstruction images of the enhanced CT showed no thrombus and no dissection of the coronary aneurysm.

G-CSF prevents the progression of atherosclerosis and neointimal formation in rabbits.

Granulocyte colony-stimulating factor (G-CSF) prevents left ventricular remodeling after myocardial infarction, but its effect on atherosclerosis is unknown. We examined two kinds of rabbit atherosclerosis models. Myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHL-MI) rabbits were treated with G-CSF or saline for 7 days from 14 months old.

Granulocyte colony stimulating factor directly inhibits myocardial ischemia-reperfusion injury through Akt-endothelial NO synthase pathway.

Objective: Granulocyte colony stimulating factor (G-CSF) has been reported recently to prevent cardiac remodeling and dysfunction after acute myocardial infarction through signal transducer and activator of transcription 3 (STAT3). In this study, we examined acute effects of G-CSF on the heart against ischemia-reperfusion injury.

Methods And Results: Rat hearts were subjected to global 35-minute ischemia and 120-minute reperfusion in Langendorff system with or without G-CSF (300 ng/mL).

Cardioprotective effects of granulocyte colony-stimulating factor in swine with chronic myocardial ischemia.

Objectives: The aim of this study was to investigate the effect of granulocyte colony-stimulating factor (G-CSF) on chronic myocardial ischemia in swine.

Background: We recently have reported that G-CSF prevents cardiac remodeling and dysfunction after acute myocardial infarction in mice and swine. It remains unclear whether G-CSF has beneficial effects on chronic myocardial ischemia.

Effects of G-CSF on left ventricular remodeling and heart failure after acute myocardial infarction.

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic cytokine that promotes proliferation and differentiation of neutrophil progenitors. G-CSF also possesses immunomodulatory properties. G-CSF-induced hematopoietic stem cell mobilization is widely used clinically for transplantation.

G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes.

Granulocyte colony-stimulating factor (G-CSF) was reported to induce myocardial regeneration by promoting mobilization of bone marrow stem cells to the injured heart after myocardial infarction, but the precise mechanisms of the beneficial effects of G-CSF are not fully understood. Here we show that G-CSF acts directly on cardiomyocytes and promotes their survival after myocardial infarction. G-CSF receptor was expressed on cardiomyocytes and G-CSF activated the Jak/Stat pathway in cardiomyocytes.

Effects of G-CSF on cardiac remodeling after acute myocardial infarction in swine.

We examined whether granulocyte colony-stimulating factor (G-CSF) prevents cardiac dysfunction and remodeling after myocardial infarction (MI) in large animals. MI was produced by ligation of left anterior descending coronary artery in swine. G-CSF (10 microg/kg/day, once a day) was injected subcutaneously from 24h after ligation for 7 days.

Forefront of Na+/Ca2+ exchanger studies: role of Na+/Ca2+ exchanger--lessons from knockout mice.

We used Na+/Ca2+ exchanger (NCX) knockout mice to evaluate the effects of NCX in cardiac function and the infarct size after ischemia/reperfusion injury. The contractile function in NCX KO mice hearts was significantly better than that in wild type (WT) mouse hearts after ischemia/reperfusion and the infracted size was significantly smaller in NCX KO mice hearts compared with that in WT mice hearts. NCX is critically involved in the development of ischemia/reperfusion-induced myocardial injury, and therefore the inhibition of NCX function may contribute to cardioprotection against ischemia/reperfusion injury.

Cytokine therapy prevents left ventricular remodeling and dysfunction after myocardial infarction through neovascularization.

Pretreatment with a combination of granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) has been reported to attenuate left ventricular (LV) remodeling after acute myocardial infarction (MI). We here examined whether the cytokine treatment started after MI has also beneficial effects. Anterior MI was created in the recipient mice whose bone marrow had been replaced with that of transgenic mice expressing enhanced green fluorescent protein (GFP).

Role of Na+-Ca2+ exchanger in myocardial ischemia/reperfusion injury: evaluation using a heterozygous Na+-Ca2+ exchanger knockout mouse model.

We used Na(+)-Ca(2+) exchanger (NCX) knockout mice to evaluate the effects of NCX in cardiac function and the infarct size after ischemia/reperfusion injury. The contractile function in NCX KO mice hearts was significantly better than that in wild type (WT) mice hearts after ischemia/reperfusion and the infarct size was significantly small in NCX KO mice hearts compared with that in WT mice hearts. NCX is critically involved in the development of ischemia/reperfusion-induced myocardial injury and therefore the inhibition of NCX function may contribute to cardioprotection against ischemia/reperfusion injury.

Pleiotropic effects of cytokines on acute myocardial infarction: G-CSF as a novel therapy for acute myocardial infarction.

Many cytokines have been reported to be increased in human and animal models with cardiovascular diseases. Myocardial infarction (MI) is accompanied with an inflammatory reaction which induces cardiac dysfunction and remodeling. The inflammatory reaction has been investigated in animal models of MI or myocardial ischemia-reperfusion injury.

[Gene therapy for heart failure].

Pharmacological, device, and surgical therapies can be used in the management of heart failure. Because those conventional therapies are not effective in patients with the most severe heart failure, gene therapy is expected to become a viable alternative. The molecular pathways that contribute to the development of heart failure have been clarified in recent years.