[Typical laboratory constellation of a non-ST-segment elevation myocardial infarction in polymyositis].

History And Admission Findings: a 80-year-old women was admitted with a hypertensive crisis. Laboratory tests showed elevated cardiac enzymes (CK, CK-MB and troponin T). She was treated for suspected non-ST segment elevation myocardial infarction.

The PPAR-gamma agonist rosiglitazone facilitates Akt rephosphorylation and inhibits apoptosis in cardiomyocytes during hypoxia/reoxygenation.

Background And Aim: Results on the cardiovascular effects of PPAR-gamma agonists are conflicting. On one hand, it was suggested that the PPAR-gamma agonist rosiglitazone may increase the risk of cardiovascular events. On the other hand, PPAR-gamma agonists reduce myocardial infarct size and improve myocardial function during ischemia/reperfusion in animal studies in vivo.

The cardiac effects of prolonged vitamin B12 and folate deficiency in rats.

In the recent past, hyperhomocysteinemia (HHCY) has been linked to chronic heart failure. Folate and vitamin B12 deficiencies are the common causes of HHCY. The impact of these vitamins on cardiac function and morphology has scarcely been investigated.

[Update cardiology 2006/2007].

This article reviews advances in cardiovascular medicine published last year. The following issues are reported in detail: (1) risk factors and lifestyle, (2) computed tomography in coronary artery disease, (3) revascularization in cardiogenic shock, (4) long-term anticoagulation in venous thrombosis, (5) anemia in heart failure, (6) optimism and cardiovascular death, (7) mortality after drug-eluting stents, (8) diabetes and cardiovascular disease, (9) new guidelines atrial fibrillation, (10) dopamine agonists and cardiac valve regurgitation, (11) beta-blockers and hypertension, (12) angiotensin-converting enzyme inhibitors and aortic rupture, (13) statin therapy, (14) adherence to pharmacotherapy.

Hyperhomocysteinemia and myocardial expression of brain natriuretic peptide in rats.

Background: Hyperhomocysteinemia (HHcy) has been linked to impaired left ventricular function and clinical class in patients with chronic heart failure. We hypothesized that HHcy stimulates myocardial brain natriuretic peptide (BNP) expression and induces adverse left ventricular remodeling.

Methods: We randomized 50 rats into 5 groups.

Hepatocyte growth factor (HGF) enhances cardiac commitment of differentiating embryonic stem cells by activating PI3 kinase.

Hepatocyte growth factor (HGF) is a pleiotropic cytokine promoting proliferation, migration and survival in several cell types. HGF and its cognate receptor c-Met are expressed in cardiac cells during early cardiogenesis, but data concerning its role in cardiac differentiation of embryonic stem cells (ESCs) and the underlying molecular mechanisms involved are limited. In the present study we show that HGF significantly increases the number of beating embryoid bodies of differentiating ESCs without affecting beating frequency.

Association of RhoGDIalpha with Rac1 GTPase mediates free radical production during myocardial hypertrophy.

Objective: Reactive oxygen species (ROS) contribute to the pathogenesis of myocardial hypertrophy. NADPH oxidase is a major source of ROS production. The small GTPase Rac1 mediates the activation of NADPH oxidase; however, the mechanism of Rac1 activation is incompletely understood.

c-Jun N-terminal kinases mediate reactivation of Akt and cardiomyocyte survival after hypoxic injury in vitro and in vivo.

Akt is a central regulator of cardiomyocyte survival after ischemic injury in vitro and in vivo, but the mechanisms regulating Akt activity in the postischemic cardiomyocyte are not known. Furthermore, although much is known about the detrimental role that the c-Jun N-terminal kinases (JNKs) play in promoting death of cells exposed to various stresses, little is known of the molecular mechanisms by which JNK activation can be protective. We report that JNKs are necessary for the reactivation of Akt after ischemic injury.

[Characteristics of patients with coronary ectasias with and without stenotic coronary artery disease].

Background And Objective: The term "coronary ectasia" describes the dilatation of one or more coronary artery segments with the signs of an impaired coronary blood flow. The prevalence, clinical significance and necessity of treatment of such a lesion is unclear.

Patients And Methods: Diagnostic coronary angiographies of 7101 patients (2131 women and 4970 men) were retrospectively evaluated for the presence of dilated coronary segments.

[Systolic heart failure in the elderly].

Aging is associated with changes in cardiac and vascular structure, promoting the development of heart failure. An increase in vascular stiffness leads to an increase of systolic arterial pressure and pulse wave velocity. This augments the afterload of the heart, which contributes to cardiac hypertrophy and neuroendocrine activation in the elderly.

[From hypertension to heart failure-a pathophysiological continuum].

The heart failure syndrome is one the most common chronic diseases in western countries with poor prognosis. In view of the estimated aging of our society, it will gain further importance. Hypertension and/or myocardial infarction are the main causes of chronic heart failure, accounting for about three quarters of the cases.

Glycogen synthase kinase-3beta regulates growth, calcium homeostasis, and diastolic function in the heart.

Glycogen synthase kinase (GSK) 3beta is a negative regulator of stress-induced cardiomyocyte hypertrophy. It is not clear, however, if GSK-3beta plays any role in regulating normal cardiac growth and cardiac function. Herein we report that a transgenic mouse expressing wild type GSK-3beta in the heart has a dramatic impairment of normal post-natal cardiomyocyte growth as well as markedly abnormal cardiac contractile function.

Oxygen free radical release in human failing myocardium is associated with increased activity of rac1-GTPase and represents a target for statin treatment.

Background: Reactive oxygen species (ROS) contribute to the development of heart failure. A potential source of myocardial ROS is the NADPH oxidase, which is regulated by the small GTP-binding protein rac1. Isoprenylation of rac1 can be inhibited by statin therapy.

Deletion of cytosolic phospholipase A2 promotes striated muscle growth.

Generation of arachidonic acid by the ubiquitously expressed cytosolic phospholipase A2 (PLA2) has a fundamental role in the regulation of cellular homeostasis, inflammation and tumorigenesis. Here we report that cytosolic PLA2 is a negative regulator of growth, specifically of striated muscle. We find that normal growth of skeletal muscle, as well as normal and pathologic stress-induced hypertrophic growth of the heart, are exaggerated in Pla2g4a-/- mice, which lack the gene encoding cytosolic PLA2.

Stabilization of beta-catenin by a Wnt-independent mechanism regulates cardiomyocyte growth.

beta-Catenin is a transcriptional activator that regulates embryonic development as part of the Wnt pathway and also plays a role in tumorigenesis. The mechanisms leading to Wnt-induced stabilization of beta-catenin, which results in its translocation to the nucleus and activation of transcription, have been an area of intense interest. However, it is not clear whether stimuli other than Wnts can lead to important stabilization of beta-catenin and, if so, what factors mediate that stabilization and what biologic processes might be regulated.

Stretch-activated pathways and left ventricular remodeling.

Stretch of cardiomyocytes in vivo occurs in response to a number of stimuli, including pressure or volume overload, but it is most clearly seen following relatively large, acute myocardial infarctions. It is in this setting that stretch is most clearly related to the pathogenesis of heart failure. Stretch of the remote, noninfacted myocardium leads to the activation of a large number of cellular signal transduction pathways, which sets into motion a series of what are designed to be compensatory responses to the increased wall stress on the surviving myocardium.

Alterations of beta-adrenergic signaling and cardiac hypertrophy in transgenic mice overexpressing TGF-beta(1).

Transforming growth factor-beta(1) (TGF-beta(1)) promotes or inhibits cell proliferation and induces fibrotic processes and extracellular matrix production in numerous cell types. Several cardiac diseases are associated with an increased expression of TGF-beta(1) mRNA, particularly during the transition from stable cardiac hypertrophy to heart failure. In vitro studies suggest a link between TGF-beta(1) signaling and the beta-adrenergic system.

Impact of HMG CoA reductase inhibition on small GTPases in the heart.

Objective: Members of the Rho GTPase family, Rac1 and RhoA have been suggested to be mediators of cardiac hypertrophy in mice. Rho proteins are posttranslationally isoprenylated. In addition to cholesterol-lowering, statins inhibit the isoprenylation of small G proteins.

Congenital dyserythropoietic anemia type III associated with congenital atrioseptal defect has led to severe cardiac problems in a 32-year-old patient.

We report the case of a 32-year-old woman who was admitted at hospital because of ortho-dyspnea, arrhythmia, and paleness. Clinical examination showed continuous arrhythmia, systolic heart murmur, enlargement of spleen and liver, and pathologic hematological parameters, thus indicating an intravasal hemolysis (elevated HBDH, bilirubin, and reticulocytes; reduced hemoglobin and haptoglobin levels), and bone-marrow-smears showed a typical cytomorphology of CDA III. The patient's diagnosis was heart failure caused by mitral valve insufficiency due to congenital atrioseptal defect associated with congenital dyserythropoietic anemia type III (CDA III).

Effects of endotoxin on human myocardial contractility involvement of nitric oxide and peroxynitrite.

Objectives: This study examined the effects of endotoxin on cardiac contractility in human myocardium.

Background: In animal myocardium, endotoxin and cytokine treatment led to enhanced inducible nitric oxide synthase (iNOS) expression and contractile dysfunction. Effects in human myocardium are unknown.

Overexpression of the Na(+)-Ca2+ exchanger leads to enhanced inotropic responsiveness to Na(+)-channel agonist without sarcoplasmic reticulum protein changes in transgenic mice.

The present study investigated the influence of over-expression of the cardiac Na(+)-Ca2+ exchanger on myocardial force of contraction and alterations in sarcoplasmic reticulum (SR) Ca(2+)-handling proteins in a transgenic mouse model. Inotropic effects of Na+ channel agonist BDF 9148 and isoprenaline were determined in isolated electrically driven atria. Protein levels of key SR Ca(2+)-handling proteins were determined by Western blot analysis.

Functional coupling of overexpressed beta 1-adrenoceptors in the myocardium of transgenic mice.

To assess functional and cellular effects of myocardial beta 1-adrenoceptor overexpression, alterations of the beta-adrenergic signal transduction pathway and contractile function in transgenic mice with atrial overexpression of the human beta 1-adrenoceptor were investigated. Radioligand binding experiments confirmed a 5- to 6-fold increase in beta-adrenoceptor density and a 2.7-fold increase in high-affinity binding sites in atria of transgenic mice.

Acute effects of nitric oxide and cyclic GMP on human myocardial contractility.

Evidence that the activity of nitric oxide synthase and the generation of nitric oxide (NO) within the myocardium are enhanced in several cardiovascular disorders is increasing. Findings whether NO exerts a direct effect on cardiac contractility are contradictory. Therefore, the direct effect of the NO donor sodium nitroprusside (SNP) on isometric force of contraction of human atrial and ventricular myocardium was investigated, and the question was addressed whether the effects of NO on cardiac contractility are mediated via cGMP.