Key result
Non-invasive monitoring detects ~184 mmHg/s rise in dP/dt at guidewire crossing during primary PCI.
Why the study?
Haemodynamic assessment during primary PCI for STEMI is mostly limited to arterial blood pressure monitoring, and the feasibility of continuous non-invasive haemodynamic monitoring using the volume-clamp method had not been evaluated.
Is continuous non-invasive haemodynamic monitoring using the volume-clamp method feasible and capable of detecting haemodynamic changes during and up to 24 hours after primary PCI in patients with STEMI?
Cohort (n=33)
Is continuous non-invasive haemodynamic monitoring using the volume-clamp method feasible and capable of detecting haemodynamic changes during and up to 24 hours after primary PCI in patients with STEMI?
Continuous non-invasive haemodynamic monitoring via the volume-clamp method is feasible during primary PCI for STEMI and detects immediate improvements in dP/dt and cardiac index upon guidewire crossing that are not reflected by standard arterial blood pressure or pulse rate.
Transient dP/dt rise at guidewire crossing may reflect acute response; leaves open utility of volume-clamp monitoring in primary PCI.
Background/Objectives: Haemodynamic assessment during primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) is mostly restricted to continuous monitoring of arterial blood pressure. The volume-clamp method provides continuous non-invasive arterial pressure monitoring without the need for vascular access, together with simultaneous estimation of stroke volume, cardiac output and other haemodynamic variables, but its feasibility during primary PCI has not been evaluated. Methods: In this prospective observational study, 33 patients with STEMI undergoing primary PCI were monitored continuously (Acumen IQ, HemoSphere) at seven pre-specified timepoints: baseline, guidewire crossing of the culprit lesion, stent implantation, end of procedure, and after 1, 6 and 24 h. Patients with cardiogenic shock, ongoing cardiopulmonary resuscitation or symptom onset more than 24 h before admission were excluded. Cardiac index (CI), stroke volume index (SVI), systemic vascular resistance index (SVRI), pulse rate, dP/dt, mean arterial pressure (MAP) and the Hypotension Prediction Index (HPI) were analysed using linear mixed models with Holm correction within families of related tests. Results: Patients were aged 65.4 ± 12.7 years and 25 (76%) were men. The culprit vessel was the left anterior descending artery in 15 patients (45%), and ST-segment resolution exceeding 50% was achieved in 25 patients (76%). The overall time effect was significant for six of seven variables, all except pulse rate. At guidewire crossing, dP/dt rose by 183.7 mmHg/s (95% CI 87–276) in 25 of 29 patients (86%; corrected p = 0.008), with a concurrent rise in CI (corrected p = 0.042) and no change in pulse rate or MAP. At 24 h, CI, SVI and dP/dt were indistinguishable from baseline, whereas MAP (−13.7 mmHg) and SVRI (−427 dyn·s·cm−5·m2) were lower. SVI and MAP were unrelated (r = +0.057; p = 0.431) across 227 measurements, while SVI and pulse rate were inversely coupled (r = −0.434) in 28 of 33 patients. Increasing age was associated with lower CI and MAP and higher HPI values, but not with the change in arterial dP/dt at guidewire crossing. Patients with TIMI 0 flow had higher SVRI by 510 dyn·s·cm−5·m2. Baseline pulse rate and its changes were different depending on the culprit vessel. Conclusions: Continuous non-invasive haemodynamic monitoring was feasible during primary PCI for STEMI. Given the small sample, the absence of a control group and the lack of validation against a reference method, the findings are exploratory and their clinical value remains to be established.
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Klatt et al. (2026) conducted a cohort in ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) (n=33). Continuous non-invasive haemodynamic monitoring via the volume-clamp method (Acumen IQ, HemoSphere) was evaluated on Haemodynamic changes during and up to 24 hours after primary PCI ( specifically dP/dt at guidewire crossing) (MD 183.7 mmHg/s, 95% CI 87-276, p=0.008). Continuous non-invasive monitoring during primary PCI detected a 183.7 mmHg/s rise in dP/dt at guidewire crossing (95% CI 87-276; p=0.008) in 86% of STEMI patients.
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