Der Internist
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Between 10 and 20% of patients with histologically proven inflammatory disease of the heart muscle develop a chronic disorder after acute myocarditis which results in dilated cardiomyopathy with increasing cardiac insufficiency. Viral infections are a frequent cause of inflammatory heart muscle diseases and thus also responsible for myocardial damage in the initial phase. In the past, evidence for enterovirus, adenovirus, and cytomegalovirus was in the focus of attention. ⋯ While the virus is still being eliminated, the second phase of the disease begins, which is characterized by autoimmune phenomena and often a cardiac inflammatory response which likewise correlates with a worsening prognosis. The transition to the third and final phase with development of dilated cardiomyopathy occurs gradually and can take years. The goal of every diagnostic and therapeutic intervention must be to eradicate the virus and eliminate the inflammatory response to prevent the disease from progressing to terminal cardiac insufficiency.
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Sleep disordered breathing, especially obstructive sleep apnea, are common in cardiovascular disease. Negative hemodynamic effects are mediated by nocturnal ischemia and intrathoracal pressure swings. ⋯ Further on, clinical course of coronary artery disease seems to be influenced by nocturnal breathing disorders. Application of continuous positive airway pressure (CPAP) is effective in most of the patients and attenuates cardiodepressive hemodynamic effects of obstructive sleep apnea.
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In patients suffering from severe sepsis an impairment of cardiac function is seen constantly. Patients with septic shock often show a transient reduction of cardiac ejection fraction. Besides, a tremendous impairment of heart rate variability corresponding to a poor prognosis is often found. ⋯ The method of choice to quantify the degree of septic cardiomyopathy at the intensive care unit certainly is to determine cardiac output in relation to systemic vascular resistance. Unfortunately, clinical trials aiming to influence the causal pathogenesis of septic cardiomyopathy (inhibition of excess formation of nitric oxide, suppression of cytokine release etc.) were rather disappointing so far. Positive effects might be assumed for the administration of activated protein C thereby underlining the role of microcirculatory alterations in the development of septic cardiomyopathy.
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Case Reports
[Withdrawal in a patient with an implantable drug delivery system in spite of continuation of opiate therapy].
A male patient with severe chronic pain has been treated with a combined drug therapy scheme of morphine and clonidine. After cessation of clonidine the patient reported opiate-withdrawal symptoms with agitation, polyuria, diarrhea, and hyperalgesia. It is known that the combination of these two substances causes synergistic analgetic effects. The abrupt cessation of clonidine after a combined administration with morphine seems to lead to a relative decrease in opiate effects and furthermore excite opiate-withdrawal symptoms.