Alpha-CGRP as a specific response mediator during acute myocardial infarction in humans: findings from an observational longitudinal study

TL;DR

This study found that alpha-CGRP levels rise during heart attacks in humans and return to normal after recovery, suggesting a possible protective role.

Contribution

The study provides new human evidence that alpha-CGRP is elevated during acute myocardial infarction and normalizes post-recovery.

Findings

Alpha-CGRP levels were significantly higher in AMI patients compared to healthy controls.

Alpha-CGRP levels normalized in most patients six months after AMI.

Patients with poor outcomes had lower alpha-CGRP levels, though not statistically significant.

Abstract

Calcitonin gene-related peptide (CGRP), particularly its alpha isoform, might play a role in restoring physiological cardiovascular functioning. While its involvement in acute myocardial infarction (AMI) pathophysiology has been suggested, human data remain scarce. This study analyzed circulating alpha-CGRP levels during AMI, comparing them to healthy controls (HC) and post-AMI resolution levels.

A total of 26 AMI patients and 26 age- and sex-matched HC were recruited. Blood samples were collected from patients within four hours of AMI onset and, when possible, six months post-event. Alpha-CGRP serum concentrations were measured using a validated ELISA assay.

Alpha-CGRP levels were significantly higher in AMI patients at admission (mean ± SD: 96.0 ± 77.4 pg/ml) compared to HC (42.0 ± 25.8 pg/ml, p < 0.0001), with an average increase of 129%. Among nine patients available for follow-up, levels normalized to the HC range (45.1 ± 26.7 pg/ml, p = 0.011). Patients with poor outcomes had numerically lower alpha-CGRP levels (72.6 ± 37.2 pg/ml) than those with a satisfactory resolution (100.3 ± 82.5 70.6 pg/ml; p = 0.241).

Alpha-CGRP is acutely elevated during AMI, likely as a compensatory vasodilator response to ischemia. Its post-AMI normalization suggests a transient protective mechanism. Further research is needed to explore its role in AMI-related pathophysiology and usefulness as a therapeutic agent.

Figures