Subgroups of monocytes predict cardiovascular events in patients with coronary heart disease. The PHAMOS trial (Prospective Halle Monocytes Study).

Background: Monocytes can be differentiated by the presence of CD14 and CD16 (CD14++CD16-, classical; CD14++CD16+, intermediate and CD14 + CD16++, non-classical monocytes). Recent studies have reported conflicting results regarding an association between subtypes of monocytes as defined by the expression of these two surface markers in atherosclerosis.

Methods: We investigated subtypes of monocytes in n = 994 patients with angiographically documented coronary artery disease (CAD).

Ischemic and endotoxin pre-conditioning reduce lung reperfusion injury-induced surfactant alterations.

Background: Pulmonary ischemia/reperfusion injury represents a common clinical phenomenon after lung transplantation, pulmonary embolism, and cardiac surgery with extracorporeal circulation. We investigated the influence of ischemic and endotoxin pre-conditioning on gas exchange and surfactant properties in a canine model of ischemia/reperfusion injury.

Methods: Twenty-six foxhounds underwent 3 hours of warm ischemia of the left lung, followed by 8 hours of reperfusion.

Bronchoscopic surfactant administration preserves gas exchange and pulmonary compliance after single lung transplantation in dogs.

Background: Surfactant abnormalities have been implicated in reperfusion injury and respiratory failure in lung transplantation.

Methods: We investigated the efficacy of bronchoscopic administration of a bovine natural lung surfactant extract (Alveofact) to improve gas exchange and lung mechanics after heterologous left lung transplantation in foxhounds (+4 degrees C ischemia for 24 hours, conservation with Euro-Collins solution). Animals received either no surfactant therapy (untreated controls, n = 6) or 50 mg/kg body weight (prior to explantation, only graft) and 200 mg/kg body weight Alveofact (immediately after reperfusion, both lungs, n = 6).

Cardio-protective determinants are conserved in aged human myocardium after ischemic preconditioning.

Ischemic preconditioning (IPrec) improves post-ischemic dysfunctions of the myocardium along with activation of protein kinase C isozymes including PKCdelta. Moreover, expression of cardio-protective determinants can reduce ischemic damages. Because IPrec is limited in aged hearts, we assessed in an experimental model the impact of aging on PKCdelta and selected protective proteins in the preconditioned myocardium from adult (< or =55) and older (> or =70 years) humans.

Ischemic preconditioning is not cardioprotective in senescent human myocardium.

Background: Cellular and functional changes secondary to aging could impair myocardial tolerance to ischemia and affect the heart's response to ischemic preconditioning.

Methods: We investigated the impact of cardiac aging on preconditioning in right atrial trabeculae of adult patients (< or = 55 years) and senescent patients (> or = 70 years) with coronary artery disease. Specimens were subjected to 30 minutes of simulated ischemia (hypoxic substrate-free superfusion) with and without 5 minutes of ischemic pretreatment.

Dysfunction of mitochondrial respiratory chain complex I in human failing myocardium is not due to disturbed mitochondrial gene expression.

Objectives: Activity of mitochondrial respiratory chain complexes with and without mitochondrially encoded subunits was assessed in failing human myocardium together with parameters of mitochondrial gene expression.

Background: Mutations and deletions in mitochondrial genome (mtDNA) sporadically accumulate in the aging myocardium. In experimental heart failure, they are discussed to be a generalized problem resulting in disturbances of mitochondrial gene expression and mitochondrial function.

Age-dependent changes of cardiac neuronal noradrenaline reuptake transporter (uptake1) in the human heart.

Objectives: The purpose of this study was to elucidate whether the neuronal noradrenaline reuptake transporter (uptake1) undergoes age-dependent regulation in the human heart.

Background: Aging is associated with various alterations in cardiovascular function.

Methods: We determined uptake1 density (by [3H]-nisoxetine binding to membranes) and activity (by accumulation of [3H]-noradrenaline into tissue slices) in the right atria (RA) of 42 patients (age range 3 months to 76 years) undergoing open-heart surgery without apparent heart failure.

The systemic inflammatory response syndrome following cardiac surgery: different expression of proinflammatory cytokines and procalcitonin in patients with and without multiorgan dysfunctions.

Cardiopulmonary bypass is associated with an injury that may cause pathophysiological changes in the form of systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS). In the present study, we investigated the inflammatory response of patients with multiple organ dysfunctions following open-heart surgery. Plasma levels of cytokines (IL-1beta, IL-6, IL-8, IL-18) and procalcitonin (PCT) were measured on the first four postoperative days in 12 adult male patients with SIRS and two or more organ dysfunctions after myocardial revascularization (MODS group), and 15 patients without organ dysfunctions (SIRS group).

Apoptotic pathway activation from mitochondria and death receptors without caspase-3 cleavage in failing human myocardium: fragile balance of myocyte survival?

Objectives: Activation of the caspase cascade through the mitochondrial and/or death receptor pathway was investigated in the failing human myocardium, in which the mode and extent of the cascade activation are unknown.

Background: In terminal heart failure, a loss of cardiomyocytes by overload-induced apoptosis is an attractive mechanism, explaining the progressive character of the disease. However, its relevance is unclear, because the specificity of probes for apoptotic deoxyribonucleic acid damage is under debate.