1,721,045 research outputs found
Acute heart failure. What doctors in clinical practice need to know
No full textHeart failure is a highly prevalent disease in the adult population. Patients suffering from decompensated heart failure are often acutely admitted to hospital where this potentially life-threatening situation requires immediate therapy. The clinical picture of heart failure can be unspecific, especially as the major symptom, respiratory insufficiency (dyspnea) is also seen in patients suffering from various lung disorders. Therefore, it is essential to assess the patient's acute problems in form of a careful physical examination and also by a detailed medical history. During medical examination a careful auscultation of the lungs as well as the assessment of potential peripheral edema is recommended. Importantly, signs of cardiogenic shock must not be overlooked. A standard 12-lead electrocardiogram (ECG) and an echocardiographic assessment of cardiac function represent two essential technical investigations. Heart rhythm, frequency and potential abnormalities of the ECG may be informative with respect to the specific disease entity. Similarly, cardiac performance, dimensions and more specific aspects, such as valve function can be evaluated using echocardiography and can help to initiate an appropriate therapy. These specific cardiac investigations should be combined with X-ray imaging of the lungs and specific blood parameters. Acute heart failure is a very common and acutely life-threatening clinical picture. Every physician working in emergency medicine or in an intensive care unit should be able to recognize it as soon as possible and to treat the patient accordingly
Pro-thrombotic condition in a woman with peripartum cardiomyopathy treated with bromocriptine and an Impella LP 2.5 heart pump
No full textInhibition of ERK-MAPK signalling via BRCA1 associated protein 2 (BRAP) leads to heart failure in transgenic mice
No full textECHOCARDIOGRAPHIC ESTIMATION OF MEAN PULMONARY ARTERY PRESSURE: A COMPARISON OF DIFFERENT APPROACHES TO PREDICT PULMONARY HYPERTENSION
No full textDual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A is a NFAT Kinase Mediating Negative Feedback on Calcineurin/NFAT Signaling.
No full textDual-specificity tyrosine phosphorylation-regulated kinase 1A is a NFAT kinase mediating negative feedback on Calcineurin/NFAT signaling in cardiac myocytes
No full textDual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A (DYRK1A) Strongly Antagonizes Calcineurin/NFAT Signaling but Can Be Prohypertrophic on Overexpression
No full textCelecoxib, a cycloxygenase-2 inhibitor, prevents hypertrophic response in cardiomyocytes through inhibition of Akt/GSK-3beta signaling
No full textExercise intolerance and systemic manifestations of pulmonary emphysema in a mouse model
Full text linkBackground: Systemic effects of chronic obstructive pulmonary disease (COPD) significantly contribute to severity and mortality of the disease. We aimed to develop a COPD/emphysema model exhibiting systemic manifestations of the disease. Methods: Female NMRI mice were treated 5 times intratracheally with porcine pancreatic elastase (emphysema) or phosphate-buffered saline (control). Emphysema severity was quantified histologically by mean linear intercept, exercise tolerance by treadmill running distance, diaphragm dysfunction using isolated muscle strips, pulmonary hypertension by measuring right ventricular pressure, and neurohumoral activation by determining urinary norepinephrine concentration. Results: Mean linear intercept was higher in emphysema (260.7 +/- 26.8 mu m) than in control lungs (24.7 +/- 1.7 mu m). Emphysema mice lost body weight, controls gained weight. Running distance was shorter in emphysema than in controls. Diaphragm muscle length was shorter in controls compared to emphysema. Fatigue tests of muscle strips revealed impaired relaxation in emphysema diaphragms. Maximum right ventricular pressure and norepinephrine were elevated in emphysema compared to controls. Linear correlations were observed between running distance changes and intercept, right ventricular weight, norepinephrine, and diaphragm length. Conclusion: The elastase mouse model exhibited severe emphysema with consecutive exercise limitation, and neurohumoral activation. The model may deepen our understanding of systemic aspects of COPD
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