Abstract：
UNASSIGNED: Patients presenting with cardiogenic shock (CS) are at risk of developing mixed shock (MS), characterized by distributive-inflammatory phenotype. However, no objective definition exists for this clinical entity.
UNASSIGNED: We assessed the frequency, predictors, and prognostic relevance of MS complicating CS, based on a newly proposed objective definition. MS complicating CS was defined as an objective shock state secondary to both an ongoing cardiogenic cause and a distributive-inflammatory phenotype arising at least 12 hours after the initial CS diagnosis, as substantiated by predefined longitudinal changes in hemodynamics, clinical, and laboratory parameters.
UNASSIGNED: Among 213 consecutive patients admitted at 2 cardiac intensive care units with CS, 13 with inflammatory-distributive features at initial presentation were excluded, leading to a cohort of 200 patients hospitalized with pure CS (67±13 years, 96% Society of Cardiovascular Angiography and Interventions CS stage class C or higher). MS complicating CS occurred in 24.5% after 120 (29-216) hours from CS diagnosis. Lower systolic arterial pressure (P=0.043), hepatic injury (P=0.049), and suspected/definite infection (P=0.013) at CS diagnosis were independent predictors of MS development. In-hospital mortality (53.1% versus 27.8%; P=0.002) and hospital stay (21 [13-48] versus 17 [9-27] days; P=0.018) were higher in the MS cohort. At logistic multivariable analysis, MS diagnosis (odds ratio [OR], 3.00 [95% CI, 1.39-6.63]; Padj=0.006), age (OR, 1.06 [95% CI, 1.03-1.10] years; Padj<0.001), admission systolic arterial pressure <100 mm Hg (OR, 2.41 [95% CI, 1.19-4.98]; Padj=0.016), and admission serum creatinine (OR, 1.61 [95% CI, 1.19-2.26]; Padj=0.003) conferred higher odds of in-hospital death, while early temporary mechanical circulatory support was associated with lower in-hospital death (OR, 0.36 [95% CI, 0.17-0.75]; Padj=0.008).
UNASSIGNED: MS complicating CS, objectively defined leveraging on longitudinal changes in distributive and inflammatory features, occurs in one-fourth of patients with CS, is predicted by markers of CS severity and inflammation at CS diagnosis, and portends higher hospital mortality.
UNASSIGNED: We assessed the frequency, predictors, and prognostic relevance of MS complicating CS, based on a newly proposed objective definition. MS complicating CS was defined as an objective shock state secondary to both an ongoing cardiogenic cause and a distributive-inflammatory phenotype arising at least 12 hours after the initial CS diagnosis, as substantiated by predefined longitudinal changes in hemodynamics, clinical, and laboratory parameters.
UNASSIGNED: Among 213 consecutive patients admitted at 2 cardiac intensive care units with CS, 13 with inflammatory-distributive features at initial presentation were excluded, leading to a cohort of 200 patients hospitalized with pure CS (67±13 years, 96% Society of Cardiovascular Angiography and Interventions CS stage class C or higher). MS complicating CS occurred in 24.5% after 120 (29-216) hours from CS diagnosis. Lower systolic arterial pressure (P=0.043), hepatic injury (P=0.049), and suspected/definite infection (P=0.013) at CS diagnosis were independent predictors of MS development. In-hospital mortality (53.1% versus 27.8%; P=0.002) and hospital stay (21 [13-48] versus 17 [9-27] days; P=0.018) were higher in the MS cohort. At logistic multivariable analysis, MS diagnosis (odds ratio [OR], 3.00 [95% CI, 1.39-6.63]; Padj=0.006), age (OR, 1.06 [95% CI, 1.03-1.10] years; Padj<0.001), admission systolic arterial pressure <100 mm Hg (OR, 2.41 [95% CI, 1.19-4.98]; Padj=0.016), and admission serum creatinine (OR, 1.61 [95% CI, 1.19-2.26]; Padj=0.003) conferred higher odds of in-hospital death, while early temporary mechanical circulatory support was associated with lower in-hospital death (OR, 0.36 [95% CI, 0.17-0.75]; Padj=0.008).
UNASSIGNED: MS complicating CS, objectively defined leveraging on longitudinal changes in distributive and inflammatory features, occurs in one-fourth of patients with CS, is predicted by markers of CS severity and inflammation at CS diagnosis, and portends higher hospital mortality.
摘要：
■出现心源性休克（CS）的患者有发生混合性休克（MS）的风险，以分布炎症表型为特征。然而,该临床实体没有客观定义.
■我们评估了频率，预测因子,和MS合并CS的预后相关性，基于新提出的目标定义。MS并发CS被定义为在初始CS诊断后至少12小时出现的持续心源性原因和分布性炎症表型继发的客观休克状态。如血液动力学的预定义纵向变化所证实，临床,和实验室参数。
■在2个心脏重症监护病房收治的连续213例CS患者中，排除了13例初始表现时具有炎症分布特征的患者，导致200例纯CS住院患者（67±13年，96％的心血管造影和介入学会CS阶段C级或更高）。在CS诊断后120（29-216）小时后，MS并发CS的发生率为24.5％。收缩压降低（P=0.043），肝损伤（P=0.049），CS诊断时的可疑/明确感染（P=0.013）是MS发展的独立预测因子。MS队列中住院死亡率（53.1%vs27.8%;P=0.002）和住院时间（21[13-48]vs17[9-27]天;P=0.018）较高。在逻辑多变量分析中，MS诊断（比值比[OR]，3.00[95%CI，1.39-6.63]；Padj=0.006)，年龄（或，1.06[95%CI，1.03-1.10]年；Padj<0.001)，入院收缩压<100mmHg（OR，2.41[95%CI，1.19-4.98]；Padj=0.016)，和入院血清肌酐（OR，1.61[95%CI，1.19-2.26]；Padj=0.003）赋予了更高的院内死亡几率，而早期临时机械循环支持与较低的住院死亡率相关(OR，0.36[95%CI，0.17-0.75]；Padj=0.008）。
■MS使CS复杂化，客观定义的利用分布和炎症特征的纵向变化，发生在四分之一的CS患者中，在CS诊断时通过CS严重程度和炎症的标志物来预测，并预示着更高的医院死亡率。
■我们评估了频率，预测因子,和MS合并CS的预后相关性，基于新提出的目标定义。MS并发CS被定义为在初始CS诊断后至少12小时出现的持续心源性原因和分布性炎症表型继发的客观休克状态。如血液动力学的预定义纵向变化所证实，临床,和实验室参数。
■在2个心脏重症监护病房收治的连续213例CS患者中，排除了13例初始表现时具有炎症分布特征的患者，导致200例纯CS住院患者（67±13年，96％的心血管造影和介入学会CS阶段C级或更高）。在CS诊断后120（29-216）小时后，MS并发CS的发生率为24.5％。收缩压降低（P=0.043），肝损伤（P=0.049），CS诊断时的可疑/明确感染（P=0.013）是MS发展的独立预测因子。MS队列中住院死亡率（53.1%vs27.8%;P=0.002）和住院时间（21[13-48]vs17[9-27]天;P=0.018）较高。在逻辑多变量分析中，MS诊断（比值比[OR]，3.00[95%CI，1.39-6.63]；Padj=0.006)，年龄（或，1.06[95%CI，1.03-1.10]年；Padj<0.001)，入院收缩压<100mmHg（OR，2.41[95%CI，1.19-4.98]；Padj=0.016)，和入院血清肌酐（OR，1.61[95%CI，1.19-2.26]；Padj=0.003）赋予了更高的院内死亡几率，而早期临时机械循环支持与较低的住院死亡率相关(OR，0.36[95%CI，0.17-0.75]；Padj=0.008）。
■MS使CS复杂化，客观定义的利用分布和炎症特征的纵向变化，发生在四分之一的CS患者中，在CS诊断时通过CS严重程度和炎症的标志物来预测，并预示着更高的医院死亡率。
