Artemisinin resistance or tolerance in human malaria patients

Malaria is a major cause of morbidity and mortality in the developing world. This situation is mainly due to emergence of resistance to most antimalarial drugs currently available. Artemisinin-based combination treatments are now first-line drugs for Plasmodium falciparum (P. falciparum) malaria. Artemisinin (qinghaosu) and its derivatives are the most rapid acting and efficacious antimalarial drugs. This review highlights most recent investigations into the emergence of artemisinin resistance in falciparum malaria patients on the Thai-Cambodian border, a historical epicenter for multidrug resistance spread spanning over 50 years. The study presents the first evidence that highlights the parasites reduced susceptibility to artemisinin treatment by prolonged parasite-clearance times, raising considerable concern on resistance development. Although the exact mechanism of action remains unresolved, development of resistance was proposed based from both in vitro experiments and human patients. Lines of evidence suggested that the parasites in the patients are in dormant forms, presumably tolerate to the drug pressure. The World Health Organization has launched for prevention and/or containment of the artemisinin-resistant malaria parasites. Taken together, the emergence of artemisinin resistance to the most potent antidote for falciparum malaria, poses a serious threat to global malaria control and prompts renewed efforts for urgent development of new antimalarial weapons.     

Thoracocardiography: Noninvasive monitoring of left ventricular stroke volume

Thoracocardiography noninvasively monitors global stroke volume by inductive plethysmographic recording of ventricular volume curves as previously validated by thermodilution. Our purpose was to investigate the potential of thoracocardiography to individually assess stroke volume of the left ventricle. We hypothesized that curves predominantly reflecting left ventricular volume could be obtained by recording waveforms from thoracocardiographic transducers placed at various levels around the chest, and by identifying their origin as the left ventricle if mean expiratory exceeded mean respiratory stroke volumes during spontaneous breathing. Stroke volumes obtained by thoracocardiography in normal subjects were compared beat by beat with estimates derived from simultaneous measurements of left ventricular cavity stroke area by echocardiography with automatic boundary detection. Changes in respiratory variations of stroke volumes were analyzed during spontaneous breathing at fixed rate and tidal volume, during mechanical ventilation, and resistive loaded breathing. In 170 comparisons of beat-by-beat stroke volumes, 89% of thoracocardiographic fell within ±20% of echocardiographic estimates. Changes in tidal volume, resistive loaded breathing, and mechanical ventilation induced respiratory variations of thoracocardiographic derived stroke volumes consistent with the known effect of respiratory changes in intrapleural pressure on left ventricular stroke volumes. The results suggest that thoracocardiography noninvasively tracks changes in left ventricular stroke volumes. Their absolute value may also be monitored if an initial calibration by an independent technique, such as echocardiography, is performed.