29 research outputs found
Past and future aspects of clinical electrophysiology
The diagnosis and treatment of clinical electrophysiology has a long and fascinating history.
From the earliest time, no clinical symptom impressed the patient (and the physician) more
than an irregular heart beat. Although ancient Chinese pulse theory laid the foundation for the
study of arrhythmias and clinical electrophysiology in the 5th century BC, the most significant
breakthrough in the identification and treatment of cardiac arrhythmias first occurred in this
century. In the last decades, our knowledge of electrophysiology and pharmacology has increased
exponentially. The enormous clinical significance of cardiac rhythm disturbances has
favoured these advances. On the one hand, patients live longer and thus are more likely to
experience arrhythmias. On the other hand, circulatory problems of the cardiac vessels have
increased enormously, and this has been identified as the primary cause of cardiac rhythm
disorders. Coronary heart disease has become not just the most significant disease of all, based
on the statistics for cause of death. Arrhythmias are the main complication of ischemic heart
disease, and they have been directly linked to the frequent arrhythmogenic sudden death
syndrome, which is now presumed to be an avoidable “electrical accident” of the heart.
A retrospective look - often charming in its own right - may not only make it easier to sort
through the copious details of this field and so become oriented in this universe of important
and less important facts; it may also assist the observer in a chronological vantage point of the
subject. The study of clinical electrophysiology is no dry compendium of facts and figures, but
rather a dynamic field of study evolving out of the competition between various ideas, intentions
and theories. (Cardiol J 2008; 15: 293-297
Pathogen burden, inflammation, proliferation and apoptosis in human in-stent restenosis - Tissue characteristics compared to primary atherosclerosis
Pathogenic events leading to in-stent restenosis (ISR) are still incompletely understood. Among others, inflammation, immune reactions, deregulated cell death and growth have been suggested. Therefore, atherectomy probes from 21 patients with symptomatic ISR were analyzed by immunohistochemistry for pathogen burden and compared to primary target lesions from 20 stable angina patients. While cytomegalovirus, herpes simplex virus, Epstein-Barr virus and Helicobacter pylori were not found in ISR, acute and/or persistent chlamydial infection were present in 6/21 of these lesions (29%). Expression of human heat shock protein 60 was found in 8/21 of probes (38%). Indicated by distinct signals of CD68, CD40 and CRP, inflammation was present in 5/21 (24%), 3/21 (14%) and 2/21 (10%) of ISR cases. Cell density of ISR was significantly higher than that of primary lesions ( 977 +/- 315 vs. 431 +/- 148 cells/mm(2); p < 0.001). There was no replicating cell as shown by Ki67 or PCNA. TUNEL+ cells indicating apoptosis were seen in 6/21 of ISR specimens (29%). Quantitative analysis revealed lower expression levels for each intimal determinant in ISR compared to primary atheroma (all p < 0.05). In summary, human ISR at the time of clinical presentation is characterized by low frequency of pathogen burden and inflammation, but pronounced hypercellularity, low apoptosis and absence of proliferation. Copyright (C) 2004 S. Karger AG, Basel