Tissue resident C reactive protein in degenerative aortic valves: correlation with serum C reactive protein concentrations and modification by statins.

Objective: To assess aortic valve probes for valvar C reactive protein (CRP) presence, the relation between valvar and serum CRP, and a possible modification of CRP by statin medication.

Setting: Tertiary referral centre.

Patients And Design: End stage, degenerative valve tissue was taken from 81 patients, 57 with non-rheumatic aortic valve stenosis (AS) and 24 with degenerative aortic valve bioprosthesis (BP).

Cells of primarily extra-valvular origin in degenerative aortic valves and bioprostheses.

Aims: We assessed aortic valves from patients with non-rheumatic aortic valve stenosis (AS) and with degenerative aortic valve bioprostheses (BP) for the presence of progenitor cell and leukocyte subtype-specific markers.

Methods And Results: Diseased valve probes from a total of 87 patients (60 AS and 27 BP) were studied. We assessed presence and localization of endothelial progenitor cells (EPCs: CD34, CD133), dendritic cells (DCs: S100), T-lymphocytes (CD3), and macrophages (CD68) by immunohistochemical and morphometric analyses.

Transit time flow measurement in on-pump and off-pump coronary artery surgery.

Objective: Transit time flow measurement is frequently used during coronary artery bypass with and without cardiopulmonary bypass to detect graft dysfunction resulting from technical errors.

Methods: Intraoperative transit time flow measurement measurements of 896 patients requiring surgery for double- or triple-vessel disease were reviewed retrospectively. Six-hundred and ninety-five patients were operated on-pump (Group A: coronary artery bypass with cardiopulmonary bypass), and 201 patients off-pump (Group B: coronary artery bypass without cardiopulmonary bypass).

Do we still need CK-MB in coronary artery bypass grafting surgery?

Aim: The aim of this study was to evaluate the role of cardiac Troponin I (cTnI) and CK-MB for early prediction of outcome of patients undergoing coronary artery bypass grafting (CABG) surgery.

Methods: In 134 consecutive patients undergoing CABG-surgery blood samples were analyzed for cTnI concentration and CK-MB activity. ECG, hemodynamic parameters and the need for inotropic support, were continuously registered.

Persistence of Chlamydia pneumoniae in degenerative aortic valve stenosis indicated by heat shock protein 60 homologues.

Background And Aims Of The Study: Based on the concept of chronic persistent infections with Chlamydia pneumoniae among variable stressors for aortic valve degeneration, the study aim was to assess the presence of chlamydial heat shock protein (cHSP) 60 and its human homologue (hHSP60) in diseased valvular tissue.

Methods: Surgical specimens of high-grade stenosed, native (n = 33) and bioprosthetic (n = 10) aortic valves were examined immunohistochemically for the localization of cHSP60, hHSP60 and macrophages (CD68), supplemented by polymerase chain reaction (PCR) and electron microscopy to prove microbial presence.

Results: Degenerated valves showed specific immunostaining of cHSP60 in 27 cases (65%), of hHSP60 in 26 (63%), and of CD68 in 36 (84%).

[Chlamydia pneumoniae and cytomegalovirus in degenerative aortic valve stenoses].

Recent evidence suggests a causal relationship between inflammatory as well as infectious pathomechanisms and valvular degeneration. Based on the concept of chronic Chlamydia pneumoniae and cytomegalovirus (CMV) infections, and of variable stressors working on valvular microecology, the present study sought to assess the presence of the specific chlamydial heat shock protein (cHSP) 60, of CMV, of macrophages and of the human homologue hHSP60. Serial sections of high-grade degenerated native (n = 16) and prosthetic (n = 6) aortic valves were analyzed by immunohistochemistry for the presence of these determinants.

Species-specific pharmacological properties of human alpha(2A)-adrenoceptors.

On the basis of data obtained in rabbits, the imidazoline receptor ligand rilmenidine has been suggested to decrease blood pressure in humans by activating central alpha(2A)-adrenoceptors. A prerequisite for this hypothesis was the unproved assumption that rabbit and human alpha(2A)-adrenoceptors are equally activated by rilmenidine. Because alpha(2A)-adrenoceptors in the brain and on cardiovascular sympathetic nerve terminals are identical, the latter were used as a model for the former to confirm or disprove this assumption.

Are microbubbles free flowing tracers through the Myocardium? Comparison of indicator-dilution curves obtained from dye dilution and echo contrast using harmonic power Doppler imaging.

Background: Harmonic power Doppler imaging (H-PDI) has been introduced into the field of contrast echocardiography as a contrast-specific imaging modality. However, there has been considerable skepticism as to whether H-PDI would be quantifiable, because it depends on the destruction of microbubbles and has more complex signal processing than gray scale imaging. The aim of the present study was to evaluate the relationship between the concentration of microbubbles and the resulting H-PDI signals even under conditions where bubble destruction is most likely.

N-Type calcium channels control sympathetic neurotransmission in human heart atrium.

Background: Because knowledge about the type of calcium channels involved in action potential-induced norepinephrine release from the human peripheral sympathetic nervous system is sparse, we investigated which types of calcium channels are functionally important in the sympathetic nerves of human cardiac tissue.

Methods And Results: In superfused segments of human right atrial appendages, the type of calcium channels that control [(3)H]norepinephrine release evoked by transmural electrical stimulation was determined. [(3)H]norepinephrine release was almost abolished by 0.

[Persistence of Chlamydia pneumoniae in coronary plaque tissue. A contribution to infection and immune hypothesis in unstable angina pectoris].

Background And Objective: There is an increasing number of pointers towards a causative connection between Chlamydia pneumoniae and atherosclerosis. But the pathogenetic mechanism and intimal structures that are involved remain unclear. Starting with the hypothesis of a chronic infection, as demonstrated by the presence of the chlamydial stress (heat-shock) protein 60 (HSP 60), the presence and localization of these bacterial products in coronary atheromas was investigated.

Presynaptic cannabinoid and imidazoline receptors in the human heart and their potential relationship.

Segments of human right atrial appendages preincubated with [3H]noradrenaline and superfused with physiological salt solution containing desipramine and corticosterone were used to examine whether the cardiac sympathetic nerves are endowed with cannabinoid receptors and to further study pharmacological properties of presynaptic imidazoline receptors. The cannabinoid CB1 receptor agonists CP55,940, HU210 and anandamide inhibited evoked [3H]noradrenaline release. The inhibition by CP55,940 and anandamide was abolished by the CB1 receptor antagonists SR141716A (1 microM) and LY320135 (1 microM).

[Chlamydia pneumoniae in coronary plaques: Increased detection with acute coronary syndrome].

Background And Objective: There is seroepidemiologic and experimental evidence for a link between Chlamydia (C.) pneumoniae and arteriosclerosis. However, the clinical importance and the pathogenic pathways implicated remain unclear.

Modulation of noradrenaline release from the sympathetic nerves of human right atrial appendages by presynaptic EP3- and DP-receptors.

Strips of human right atrial appendages were preincubated with [3H]noradrenaline and then superfused with physiological salt solution containing inhibitors of uptake1 and uptake2. Tritium overflow was evoked by transmural electrical stimulation (standard frequency: 2 Hz). Prostaglandin E2 (PGE2) inhibited the electrically evoked tritium overflow; at the highest concentration investigated, tritium overflow was reduced by about 80% and the pIC50% value was 7.

[Spiral CT and MRT of the operated Stanford-type-A aortic dissection: its course and complications].

Purpose: To demonstrate normal postoperative spiral CT and MRI findings and typical complications in patients with aortic repair after Stanford type A aortic dissection.

Methods: 24 patients with aortic repair after Stanford type A aortic dissection were followed up by spiral CT and MRI (0.5 Tesla).

Effects of selective h5-HT1B (SB-216641) and h5-HT1D (BRL-15572) receptor ligands on guinea-pig and human 5-HT auto- and heteroreceptors.

Human cerebral cortical slices and synaptosomes, guinea-pig cerebral cortical slices and human right atrial appendages were used to study the effects of SB-216641, a preferential h5-HT1B receptor ligand, and of BRL-15572, a preferential h5-HT1D receptor ligand, on the presynaptic h5-HT1B and h5-HT1B-like autoreceptors in the human and guinea-pig brain preparations, respectively, and on the presynaptic h5-HT1D heteroreceptors in the human atrium. The brain preparations, preincubated with [3H]serotonin ([3H]5-HT), and the segments of atrial appendages, preincubated with [3H]noradrenaline, were superfused with modified Krebs' solution and tritium overflow was evoked electrically (human and guinea-pig cerebral cortex slices and human atrial appendages) or by high K+ (human cerebral cortex synaptosomes). The electrically evoked tritium overflow from guinea-pig cerebral cortex slices was reduced by the 5-HT receptor agonist 5-carboxamidotryptamine (5-CT).

Presynaptic imidazoline receptors and non-adrenoceptor [3H]-idazoxan binding sites in human cardiovascular tissues.

1 In segments of human right atrial appendages and pulmonary arteries preincubated with [3H]-noradrenaline and superfused with physiological salt solution containing desipramine and corticosterone, the involvement of imidazoline receptors in the modulation of [3H]-noradrenaline release was investigated. 2 In human atrial appendages, the guanidines aganodine and DTG (1,3-di(2-tolyl)guanidine) which activate presynaptic imidazoline receptors, inhibited electrically-evoked [3H]-noradrenaline release. The inhibition was not affected by blockade of alpha 2-adrenoceptors with 1 microM rauwolscine, but antagonized by extremely high concentrations of this drug (10 and/or 30 microM; apparent pA2 against aganodine and DTG: 5.

Presynaptic imidazoline receptors and alpha 2-adrenoceptors in the human heart: discrimination by clonidine and moxonidine.

The involvement of presynaptic alpha 2-autoreceptors and imidazoline receptors in the modulation of noradrenaline release was investigated in strips from human atrial appendages preincubated with [3H]noradrenaline and superfused with medium containing desipramine and corticosterone. Electrical impulses were applied transmurally at 2 Hz. The imidazoline derivatives moxonidine and clonidine reduced to evoked tritium overflow in a concentration-dependent manner.

Inhibition of noradrenaline release via presynaptic 5-HT1D alpha receptors in human atrium.

In segments of human right atrial appendages preincubated with [3H]noradrenaline and superfused with physiological salt solution containing desipramine and corticosterone, we determined the effects of 5-hydroxytryptamine (5-HT) receptor agonists and antagonists on tritium overflow evoked by transmural electrical stimulation (2 Hz). Tritium overflow was inhibited by 5-HT, 5-carboxamidotryptamine (5-CT), 5-methoxytryptamine (5-MeOT), 5-methoxy-3(1,2,3,6-tetrahydro-4-pyridinyl)-1H indole succinate (RU 24969) and sumatriptan. Yohimbine and oxymetazoline (in the presence of idazoxan) also inhibited tritium overflow.

Presynaptic 5-HT auto- and heteroreceptors in the human central and peripheral nervous system.

In view of the potential pathophysiological and therapeutic implications, presynaptic 5-HT auto- and heteroreceptors have been identified and characterized in isolated human tissues and their functional role has been determined. Such investigations have been carried out in different laboratories including that of the authors. Basic evidence for the involvement of inhibitory 5-HT receptors in modulation of 5-HT release in the cerebral cortex was obtained in slices: exogenous 5-HT inhibited 5-HT release in a manner susceptible to blockade by methiothepin, which given alone facilitated 5-HT release, probably by preventing endogenous 5-HT from activating the inhibitory receptors.

Modulation of noradrenaline release from the sympathetic nerves of the human saphenous vein and pulmonary artery by presynaptic EP3- and DP-receptors.

1. Spirally cut strips of the human saphenous vein and pulmonary artery were used to determine the pharmacological properties of the presynaptic prostanoid receptors involved in the modulation of sympathetic [3H]-noradrenaline release. Strips preincubated with [3H]-noradenaline were superfused with physiological salt solution containing inhibitors of uptake1 and uptake2 and rauwolscine to eliminate involvement of presynaptic alpha 2-adrenoceptors.

[The influence of the new phosphodiesterase inhibitor enoximone in patients with an acute catecholamine-refractory heart insufficiency during open-heart surgery].

19 patients in whom cardiopulmonary bypass (cpb) was performed during different types of cardiac operations, developed myocardial failure which remained refractory to inotropic support with increasing doses of adrenaline, dopamine and dobutamine, so that it was impossible to discontinue cpb. After changing the therapeutic approach to a new regime consisting of adrenaline, dopamine and enoximone, low-output syndrome (LCOS) could be successfully reversed in 12 of the 19 patients. In the 7 remaining patients blood pressure dropped in a clinically relevant way under treatment with enoximone.

Inhibition of noradrenaline release from the sympathetic nerves of the human saphenous vein by presynaptic histamine H3 receptors.

The human saphenous vein was used to examine whether presynaptic histamine receptors can modulate noradrenaline release and, if so, to determine their pharmacological characteristics. Strips of this blood vessel were incubated with [3H]noradrenaline and subsequently superfused with physiological salt solution containing desipramine and corticosterone. Electrically (2 Hz) evoked 3H overflow was inhibited by histamine and the H3 receptor agonist R-(-)-alpha-methylhistamine.

[Scintigraphy with 123I-labelled fatty acids in coronary heart disease].

Forty-two patients (6 women, 36 men; mean age 55 [39-69] years), with one-, two- or three-vessel disease on coronary angiography, were studied using single-photon emission computer tomography with 15-p-123I-iodophenyl-pentadecanoic acid (IPPA), in order to evaluate this new method of demonstrating abnormalities of myocardial perfusion. The reference range for fatty acid turnover was determined in eleven controls (4 women, 7 men; mean age 41 [20-51] years) with no coronary stenosis. 185 MBq (5 mCi) of IPPA was administered intravenously during submaximal stress on a bicycle ergometer.

Single photon emission tomography imaging of myocardial oxidative metabolism with 15-(p-[123I]iodophenyl) pentadecanoic acid in patients with coronary artery disease and aorto-coronary bypass graft surgery.

A total of 29 patients with coronary artery disease (CAD) were investigated with 15-(p-[123I] iodophenyl)pentadecanoic acid (123I-IPPA) and sequential single photon emission tomography (SPET). Of these, 19 were studied after aorto-coronary bypass graft surgery. Some 13 patients without evidence of CAD served as a control group.

IMA-graft patency control by thermal coronary angiography during coronary bypass surgery.

Thermal coronary angiography (TCA) was evaluated for the intraoperative assessment of graft patency and flow in internal mammary artery (IMA) bypass grafts. TCA was performed in 210 patients undergoing 460 vein and 153 IMA bypass grafts after completion of the distal anastomoses. The IMA grafts and the recipient coronary arteries were delineated by the temperature differential between a cold epimyocardium and the perfusing warm blood after bulldog clamp release.