To test feasibility of myocardial T1 mapping of the right ventricle (RV) at systole when myocardium is more compact and to determine the most appropriate imaging plane. 20 healthy volunteers (11 men; 33 ± 8 years) were imaged on a 1.5T scanner (MAGNETOM Avanto, Siemens AG, Erlangen, Germany). A modified look-locker inversion-recovery sequence was acquired at mid-ventricular short axis (SAX), as horizontal long-axis view and as transversal view at systole (mean trigger time 363 ± 37 ms). Myocardial T1 time of the left-ventricular and RV myocardium was measured within a region of interest (ROI) on generated T1-maps. The most appropriate imaging plane for the RV was determined by the ability to draw a ROI including the largest amount of myocardium without including adjacent tissue or blood. At systole, when myocardium is thicker, measurements of the RV myocardium were feasible in 18/20 subjects. Average size of the ROI was 0.42 ± 0.28 cm(2). In 10/18 subjects, short axis was the most appropriate imaging plane to obtain measurements (p = 0.034). Average T1 time of the RV myocardium was 1,016 ± 61 ms, and average T1 of the left-ventricular (LV) was 956 ± 25 ms (p < 0.001). T1 mapping of the RV myocardium is feasible during systole in the majority of healthy subjects but with a small ROI only. SAX plane was the optimal imaging plane in the majority of subjects. Native myocardial T1 time of the RV is significantly longer compared to the LV, which might be explained by the naturally higher collagen content of the RV.
Malaria parasites rely on specialized stages, called gametocytes, to ensure human-to-human transmission. The formation of these sexual precursor cells is initiated by commitment of blood stage parasites to the sexual differentiation pathway. Plasmodium falciparum, the most virulent of six parasite species infecting humans, employs nutrient sensing to control the rate at which sexual commitment is initiated, and the presence of stress-inducing factors, including antimalarial drugs, has been linked to increased gametocyte production in vitro and in vivo. These observations suggest that therapeutic interventions may promote gametocytogenesis and malaria transmission. Here, we engineered a P. falciparum reporter line to quantify sexual commitment rates after exposure to antimalarials and other pharmaceuticals commonly prescribed in malaria-endemic regions. Our data reveal that some of the tested drugs indeed have the capacity to elevate sexual commitment rates in vitro. Importantly, however, these effects are only observed at drug concentrations that inhibit parasite survival and only rarely result in a net increase of gametocyte production. Using a drug-resistant parasite reporter line, we further show that the gametocytogenesis-promoting effect of drugs is linked to general stress responses rather than to compound-specific activities. Altogether, we did not observe evidence for mechanistic links between the regulation of sexual commitment and the activity of commonly used pharmaceuticals in vitro. Our data hence does not support scenarios in which currently applied therapeutic interventions would promote the spread of drug-resistant parasites or malaria transmission in general.
Dissolution of a saphenous vein graft thrombus with systemic glycoprotein IIb/IIIa receptor inhibition prior to percutaneous coronary interventionA 60-year-old man with known coronary artery disease was admitted to the hospital with severe retrosternal pain persisting over two hours. In the week before admission he had suffered from short episodes of chest pain but the symptoms always had resolved spontaneously. The patient had undergone coronary artery bypass grafting of the proximal left anterior descending coronary artery (LAD) and the first diagonal branch 21 years ago, and had suffered from a myocardial infarction ten years ago, but no coronary angiography had been performed at that time. On admission, the ECG showed a non-significant infero-lateral ST segment depression without elevation of the cardiac enzymes. Anti-ischaemic therapy with aspirin, beta-blockers, and a weightadapted abciximab bolus with subsequent continuous infusion was started, and the chest pain resolved. The next day cardiac troponin I was raised to 103 µ g/l and creatine kinase to 504 U/l. Due to a sudden recurrence of chest pain the patient was urgently transferred to the cardiac catheterisation laboratory. Coronary angiography revealed severe three-vessel disease without high-grade stenoses of the right coronary and circumflex artery, but a chronic proximal occlusion of the LAD with an open saphenous vein graft (SVG) on the mid part and an occluded SVG on the first diagonal branch with a large thrombus in the distal part ( fig. 1A.). Due to the high periprocedural risk of embolisation the intervention was postponed and treatment with abciximab was continued for another 48 hours in combination with half-dose low molecular weight heparin, followed by full-dose low molecular weight heparin for another seven days. The subsequent clinical course was uneventful without recurrence of symptoms. Ten days after admission a repeated coronary angiography revealed a high-grade proximal stenosis of the SVG on the first diagonal branch with a total dissolution of the thrombus (fig. 1B.). Percutaneous transluminal coronary angioplasty of the culprit lesion was performed with insertion of a 3.5/18 mm bare stent ( fig. 1C.). Heparin therapy was stopped, and clopidogrel was started for six months. Before discharge, the patient underwent a clinically negative exercise stress test without any significant ECG alterations.Percutaneous coronary intervention (PCI) is the treatment of choice in acute coronary syndromes. However, PCI in thrombotic SVG occlusions remains an unresolved issue because of technical difficulties, distal embolisation, high restenosis rate, and a poor outcome with low event-free survival rates [1]. The use of distal embolisation protection devices reduces major adverse events after stenting of stenotic SVG [2], and intracoronary application of glycoprotein (GP) IIb/IIIa blockers during angioplasty reduces thrombus burden [3]. GP IIb/IIIa receptor inhibitors prevent platelet aggregation, have a great potential to diminish formation of ...
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