Zeitschrift für Kardiologie
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Despite numerous experimental and clinical investigations, the exact mechanisms involved in the development of cardiac pain are not completely understood. Sensory receptors for painful stimuli, presumably sympathetic sensory nerve endings, are located in the atria, the ventricles, and in the walls of the coronary arteries. These receptors fire at a background rate under normal hemodynamic conditions. ⋯ Still unknown is the role of the afferent vagal fibers in pain perception; however, a modulating influence on pain threshold and characteristics seems possible. Two main mechanisms may be responsible for cardiac pain during ischemic periods: a) chemical excitation of free sensory nerve endings by substances such as bradykinin, PGE2, adenosine, histamine, serotonin, or K+; b) abnormal motion of ischemic segments (dyskinesia, bulging) during systole and excitation of mechanical receptors by passive stretching, and probably a combination of a) and b): the release of chemical substances sensitizes mechanical receptors and lowers their threshold for nociceptive stimuli. These can be suppressed at various spinal or supraspinal levels.
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Cardiac nociceptive afferences are mainly transmitted by sympathetic nervous tracts. After passing the ganglion stellatum and neighbouring ganglia, the nerves enter the dorsal horn of the spinal cord at C8-Th9 (especially Th2-Th6). Here the nerve synapses for the first time, mainly to neurons which run up to the thalamus contralaterally by the tractus spinothalamicus. ⋯ Patients with silent myocardial ischemia have higher beta-endorphin levels compared to symptomatic patients at the same exercise level. This can be interpreted as expressing quantitative differences in a superior pain regulation system. Myocardial ischemia is experienced as angina pectoris pain when the peripheral nociceptive impulse rate is so pronounced that the prevailing inhibitory pain threshold can be overcome and when the pain pathways are intact.
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To obtain good results in cardiac valve reconstruction surgery it is necessary to assess intraoperatively the efficiency of mitral or tricuspid valve repair. In 15 patients (three with mitral stenosis, 12 with mitral insufficiency) the mitral valve, in eight patients the tricuspid valve and in two patients both av-valves were reconstructed individually by commissurotomy and/or annulorrhaphy. During cardiac arrest, the valves were tested by filling the left or right ventricle with saline solution. ⋯ An intraoperative decision for valve replacement was made. Our results show that transesophageal contrast echocardiography is a simple and accurate method of assessing the efficiency of valve reconstruction procedures. In some cases it gives more information than testing during cardiac arrest.
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Comparative Study
[Central and regional vascular hemodynamics of milrinone in experimental heart failure: comparison with captopril and dobutamine].
The present study was designed to evaluate the regional vascular profile of milrinone in the setting of experimental heart failure. Utilizing the rat model of myocardial infarction and failure (average infarct size 28%), we measured cardiac output (CO), arterial pressure (MAP), LVEDP, heart rate and systemic vascular resistance, as well as regional blood flow (radioactive microspheres 15 +/- 5 microns) before and after milrinone i.v. (20 microns/kg bolus, 3 micrograms/kg/min infusion) in the conscious state (LVEDP 22 mm Hg versus 10 mm Hg in the sham-operated group, p less than 0.01). Similarly, central hemodynamics and regional blood flow were determined before and after dobutamine or captopril, administering equipotent doses. ⋯ In contrast to captopril, the effects of milrinone on renal perfusion were modest. These results demonstrate the potent vasodilator activity of milrinone, which is independent of its direct-positive inotropic effects, being most prominent in the splanchnic, coronary and skeletal muscle circulation. The latter might have clinical relevance since improved muscular flow during exercise is likely to improve exercise capacity in heart failure after long-term treatment.
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This report presents a case of penetrating chest trauma leading to pericardial tamponade and ventricular septum defect successfully resuscitated by surgery in 1968 in an 11-year-old boy. 10 years later a first-size calcified hematoma was removed. However the 30% left to right intracardiac shunt flow as established by complete heart catheterization prior to surgery was not corrected. Non-invasive methods were used to assess cardiac function 18 years after the initial event including physical examination, chest X-ray, thoracic computer tomography, ECG, 24 h Holter monitoring and exercise testing, combined with myocardial scintigraphy and radionuclide angiography and echocardiographic techniques using the transthoracic and the transoesophageal approach. The diagnostic value of echocardiographic examinations is emphasized with special reference to contrast- and Doppler-echocardiography including the color-coded Doppler-flow-imaging technique.