Abstract
Dear Editor,
We thank Su and Li for their thoughtful comments regarding our study, “Effect of Invasive Hemodynamic Monitoring on the Outcomes of Cardiogenic Shock in Patients with Acute Myocardial Infarction.”1,2 We appreciate their recognition of the ongoing uncertainty surrounding the role of invasive hemodynamic monitoring in acute myocardial infarction complicated by cardiogenic shock (AMI-CS); we agree that this remains an important area requiring more rigorous prospective evaluation.3,4
The central message of our study was not that invasive hemodynamic monitoring lacks clinical value. Rather, our findings suggest that, in a real-world retrospective registry of patients with AMI-CS, invasive monitoring as used across multiple centers was not independently associated with lower in-hospital mortality after adjustment for measured baseline differences. 2 This distinction is important. Invasive hemodynamic monitoring is not a therapeutic intervention by itself; it is a diagnostic and management-enabling tool. Its potential benefit depends on timing, completeness of data acquisition, clinician interpretation, and whether the information leads to actionable changes in therapy, including vasoactive medication titration, volume management, recognition of right ventricular or biventricular failure, and selection, escalation, or weaning of mechanical circulatory support.5-7
We agree with Su and Li 1 that confounding by indication is a major consideration. In our unmatched cohort, patients selected for invasive monitoring had more severe clinical presentations, including more frequent cardiac arrest, bradyarrhythmia, and advanced Society for Cardiovascular Angiography and Interventions (SCAI) shock stages.2,8,9 After propensity score matching, in-hospital mortality was similar between groups, supporting the interpretation that baseline disease severity likely contributed to the excess mortality observed before adjustment. 2 However, as with all observational analyses, propensity matching cannot eliminate residual confounding from variables not captured in the registry, including neurologic status after arrest, infarct size, timing of revascularization, vasoactive-inotropic score trajectory, lactate clearance, institutional shock protocols, and operator- or center-level differences in the use of temporary mechanical circulatory support.4,6,7
Another important limitation is the heterogeneity of “invasive monitoring.” In our study, most patients underwent right heart catheterization; only a smaller subset had Swan-Ganz catheter placement. 2 Therefore, our analysis should not be interpreted as a definitive evaluation of continuous pulmonary artery catheter-guided shock management. A single or limited hemodynamic assessment may not have the same clinical impact as early, complete, serial hemodynamic profiling embedded within a standardized multidisciplinary shock algorithm.5-7 This distinction may help explain why prior observational studies have reported potential benefit from invasive monitoring, particularly when hemodynamic data were obtained early and used to guide advanced heart failure therapies or mechanical circulatory support decisions.5-7,10
We also agree that the longer hospital stay observed among patients receiving invasive monitoring requires cautious interpretation.1,2 It may reflect greater illness severity, more complex care pathways, prolonged intensive care support, or survivorship bias rather than a direct adverse effect of invasive monitoring. Similarly, the lack of association between cardiac index, pulmonary capillary wedge pressure, right atrial pressure, or Swan-Ganz use and mortality in our invasive-monitoring subgroup should not be interpreted as evidence that these physiological variables are unimportant. 2 AMI-CS outcomes are determined by multiple dynamic factors, including timely reperfusion, cardiac arrest, shock stage progression, acidosis, renal dysfunction, right ventricular involvement, and response to pharmacologic and mechanical support.3,4,8,9 Hemodynamic measurements obtained at variable time points may incompletely capture this trajectory.
Future studies should move beyond the binary question of invasive versus noninvasive monitoring and instead evaluate when, in whom, and how invasive hemodynamic data should be used. Particularly relevant subgroups include patients with persistent hypoperfusion after revascularization, suspected right ventricular infarction or biventricular shock, escalating vasopressor or inotrope requirements, unclear volume status, mixed shock physiology, and patients being considered for temporary mechanical circulatory support.5-7,10 Prospective studies should also capture the timing of catheter placement relative to shock onset, revascularization, and device implantation; the completeness of hemodynamic profiling; protocol-driven therapeutic responses; and outcomes beyond mortality, including organ failure-free days, renal replacement therapy, bleeding or vascular complications, device escalation, length of intensive care, and cost.
In summary, our findings support a selective, early, and purposeful approach to invasive hemodynamic monitoring in AMI-CS rather than indiscriminate routine use or complete avoidance.2,5-7 We agree with Su and Li that refined patient selection and prospective investigation are needed to determine whether invasive monitoring can improve outcomes in specific AMI-CS phenotypes when integrated into standardized, multidisciplinary shock-care pathways.1,4,10
