# Higher vasoactive usage despite hemodynamic goals is associated with higher mortality in acute myocardial infarction-related cardiogenic shock

**Authors:** Jorge A. Ortega-Hernández, Héctor González-Pacheco, Diego Araiza-Garaygordobil, Rodrigo Gopar-Nieto, Daniel Sierra-Lara-Martínez, Daniel Manzur-Sandoval, José Luis Briseño-De-La-Cruz, Salvador Mendoza-García, Álvaro Montañez-Orozco, Arturo Arzate-Ramírez, José Omar Arenas-Díaz, César A. Gómez-Rodríguez, Hector Antonio Santos-Alfaro, Jaime Hernández-Montfort, Alexandra Arias-Mendoza

PMC · DOI: 10.3389/fcvm.2025.1461714 · Frontiers in Cardiovascular Medicine · 2025-02-13

## TL;DR

Using more vasoactive drugs in patients with heart attack-related cardiogenic shock is linked to higher death rates, even when hemodynamic goals are met.

## Contribution

This study reveals that higher vasoactive drug use correlates with increased mortality in AMI-related cardiogenic shock despite achieving hemodynamic goals.

## Key findings

- Patients using more than two vasoactive drugs had significantly higher mortality rates.
- Vasopressin and levosimendan showed time-dependent associations with mortality.
- Hemodynamic goals did not reduce mortality in patients with higher vasoactive use.

## Abstract

Cardiogenic shock (CS) is a severe complication of acute myocardial infarction (AMI) with high mortality. Few studies have examined the selection and subsequent choice of vasoactive agents in CS. This study investigates the impact of vasoactive drug use and in-hospital outcomes among AMI-CS.

A total of 309 patients who underwent pulmonary artery catheterization between 2006 and 2021 were categorized by the number of vasoactive drugs used (0–1, 2, or >2). Clinical and 24 h hemodynamic data were analyzed. Primary outcomes explored the correlation between vasoactive use and in-hospital mortality. Secondary analyses assessed hemodynamic changes and estimated mortality probabilities at different intervals using logistic regression.

In total, 57 patients received 0–1, 76 received 2, and 176 received >2 vasoactive drugs. The median age was 61 years; most were men (82%), and 82.8% had ST-segment elevation myocardial infarction. End-organ function showed progressive deterioration with escalating vasoactive use. Survival analysis revealed an increased mortality in the >2 vasoactive group [HRadj = 4.62 (2.07–10.32)], achieving ≥5/6 hemodynamic goals that did not mitigate mortality [HRadj = 7.18 (1.59–32.39)]. Subgroup analyses within patients who reached different hemodynamic goals reiterated adverse outcomes associated with >2 vasoactives (P < 0.05). Further analysis showed that vasopressin was associated with the highest mortality in a time-dependent fashion [HRDay1, 8.77 (6.04–12.75) → HRDay30, 1.23 (0.8–1.87)], and levosimendan had similar behavior [HRDay1, 2.67 (1.82–3.91) → HRDay30, 0.66 (0.42–1.03)].

A significant association between the number of vasoactives and in-hospital mortality was found in AMI-CS, which requires future long-term studies to explore the role of vasoactive drug therapies and early temporary mechanical circulatory support.

In 309 cases with acute myocardial infarction-related cardiogenic shock (AMI-CS) with pulmonary artery catheter, the higher utilization of vasoactive agents, even in the attainment of defined hemodynamic goals, emerges as a predictor of elevated mortality in the context of AMI-CS. This intriguing association is further underscored by a parallel escalation in organ dysfunction, imparting clinical significance to the delicate balance between vasoactive usage and patient outcomes.

## Linked entities

- **Chemicals:** vasopressin (PubChem CID 8230), levosimendan (PubChem CID 3033825)
- **Diseases:** acute myocardial infarction (MONDO:0004781), cardiogenic shock (MONDO:0800175)

## Full-text entities

- **Diseases:** AMI (MESH:D009203), CS (MESH:D012770)
- **Chemicals:** levosimendan (MESH:D000077464), vasoactive (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC11865078/full.md

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Source: https://tomesphere.com/paper/PMC11865078