Detection of a broad variety of molecular signatures in all CHD specimens suggests that diverse bacterial colonization may be more important than a single pathogen. Our observation does not allow us to conclude that bacteria are the causative agent in the etiopathogenesis of CHD. However, bacterial agents could have secondarily colonized atheromatous lesions and could act as an additional factor accelerating disease progression.

"Dilated coronaropathy" is an entity of nonobstructive, ischemic coronary artery disease. Nitroglycerin is of no therapeutic benefit but leads to an aggravation of exercise-induced CI.

Excimer laser angioplasty with adjunctive balloon angioplasty is a safe and efficient technology to treat in-stent restenoses. These data justify a randomized comparison with balloon angioplasty.

No abstract

No abstract

Abstract. Acute stress results in activation of the hypothalamic-pituitary-adrenal (HPA) axis. ACTH and cortisol secretion is stimulated by corticotropinreleasing hormone (CRH). It has also been shown that activation of the HPA axis during stress is accompanied by changes in the immune response. However, little is known about the influence of acute stress on the release of cytokines such as inteleukin-1 (IL-1) or interleukin-2 (IL-2). In this study, we determined serum IL-1 a and IL-2 levels in 19 patients undergoing the acute stress of angioplasty for coronary artery disease. A second protocol was devised to determine serum IL-1 a and IL-2 concentrations as well as lymphocyte subpopulations in 10 normal volunteers receiving 1 pg kg-' human CRH intravenously. Finally, IL-1 a concentrations were measured in CRH-incubated mononuclear cell (MNC) and monocyte cultures.In response to the stress of angioplasty, ACTH and cortisol as well as IL-1 a and IL-2 concentrations were clearly above baseline levels (IL-1 a, mean f SEM, baseline: 1.39 f 0-34 ngml-l, after angioplasty: 2.64 f 0.73 ng ml-l, P < 0.05; IL-2, baseline: 1.2f 0.13 ng ml-I , after angioplasty: 2,8 f 1.14 ng ml, P < 0-05). A similar pattern was obtained in normal subjects in response to CRH (11-1 a, baseline: 0.8 f 0.2 ng ml-l, after angioplasty: 3.7 f 1.4ngml-I, P < 0.05; IL-2, baseline: 1-9 f 0.4 ngml-l, after angioplasty: 5.4 f 2.2 ng ml-', P < 0.02). The percentage of IL-2 receptor-positive lymphocytes rose from 3.9 f 1.2% to 6.2 f 1.6% (P < 0.05), the relative number of CD-3 lymphocytes rose from 74.5 f 1.6% to 78.3 f 2.0% (P < concentrations in cultures containing CRH were not significantly different from control cultures. Our data demonstrate significant activation of the HPA axis and secretion of IL-1 a and IL-2 in response to both angioplasty and CRH. Furthermore, CRH administration resulted in activation of the cellular immune system (indicated by an increase in IL-2 receptor positive lymphocytes). Our in vitro data suggest that CRH may not directly act on blood mononuclear cells to induce IL-1 a release or, alternatively, sources other than blood mononuclear cells may account for the elevated IL-1 a levels observed in vivo. We conclude that CRH may play a major role in neuroendocrineimmune interactions during acute stress.0

No abstract

Parathyroid hormone (PTH) influences the calcium metabolism of many different mammalian cell types; indeed, hypertension due to changes in muscle tone is a frequent symptom of hypercalcemic hyperparathyroidism. In a blind study of 81 patients with various forms of heart disease undergoing coronary angiography, the plasma concentrations of the midcarboxyl regional PTH immunoreactivity were determined. PTH concentrations were elevated in 26 of the 56 patients exhibiting organic coronary artery disease (CAD). The plasma PTH levels were highest in those patients with CAD affecting three vessels and in patients with evidence of myocardial infarction. PTH levels were not influenced by previous drug treatments, and did not correlate to stress hormone levels. We propose that increased PTH levels may be a marker for initiation or potentiation of calcium-dependent changes in vascular smooth muscle behavior inducing coronary functional and anatomic lesions typical of CAD.