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To evaluate the cause and prognosis of hyperdynamic left ventricular ejection fraction in critically ill patients with sepsis.

Summary Unsupervised clustering methods of transthoracic echocardiography variables have not been used to characterise circulatory failure mechanisms in patients with COVID‐19 pneumonitis. We conducted a retrospective, single‐centre cohort study in ICU patients with COVID‐19 pneumonitis whose lungs were mechanically ventilated and who underwent transthoracic echocardiography between March 2020 and May 2021. We performed latent class analysis of echocardiographic and haemodynamic variables. We characterised the identified subphenotypes by comparing their clinical parameters, treatment responses and 90‐day mortality rates. We included 305 patients with a median (IQR [range]) age 59 (49–66 [16–83]) y. Of these, 219 (72%) were male, 199 (65%) had moderate acute respiratory distress syndrome and 113 (37%) did not survive more than 90 days. Latent class analysis identified three cardiovascular subphenotypes: class 1 (52%; normal right ventricular function); class 2 (31%; right ventricular dilation with mostly preserved systolic function); and class 3 (17%; right ventricular dilation with systolic impairment). The three subphenotypes differed in their clinical characteristics and response to prone ventilation and outcomes, with 90‐day mortality rates of 22%, 42% and 73%, respectively (p < 0.001). We conclude that the identified subphenotypes aligned with right ventricular pathophysiology rather than the accepted definitions of right ventricular dysfunction, and these identified classifications were associated with clinical outcomes.

Cardiovascular Subphenotypes in Acute Respiratory Distress Syndrome*OBJECTIVES: To use clustering methods on transthoracic echocardiography (TTE) findings and hemodynamic parameters to characterize circulatory failure subphenotypes and potentially elucidate underlying mechanisms in patients with acute respiratory distress syndrome (ARDS) and to describe their association with mortality compared with current definitions of right ventricular dysfunction (RVD).

was 74 [95% CI [67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82] for plasmepsin 2 and 42 [37][38][39][40][41][42][43][44][45][46] for plasmepsin 3-1) than with MDR1 inhibition for plasmepsin 2 and 29 [24][25][26][27][28][29][30][31][32][33][34] for plasmepsin 3-1; appendix pp 2, 4).In the previous studies, crt mutations associated with piperaquine resistance arose on a genetic background of amplified plasmepsin genes. 1,2 Together with our data, this finding suggests that although initial selection of plasmepsin and mdr1 copy number variations does not cause a resistant phenotype in itself, it generates a favourable P falciparum genetic background for crt mutations to arise.Altogether, our results recapitulate in vitro a complementary mechanism between plasmepsins, mdr1, and crt involved in piperaquine resistance, supporting the molecular epidemiological data in southeast Asia 1,2 and furthering understanding of how piperaquine drug resistance evolves.