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Baseline Q wave predicts PCI outcome in STEMI patients

Baseline Q waves independently predict clinical outcome in ST-elevation myocardial infarction (STEMI) patients treated with primary percutaneous coronary intervention (PCI), shows research.

Paul Armstrong (University of Alberta, Edmonton, Canada) and colleagues evaluated baseline Q waves and ST-segment resolution 30 minutes after PCI electrocardiograms (ECGs) in 4530 STEMI patients enrolled in the APEX-AMI (Assessment of Pexelizumab in Acute MI) trial, who presented within 6 hours of symptom onset.

Their findings show that patients who exhibited Q waves on their baseline ECG were those with clinical profiles suggesting more advanced disease, eg, older men with diabetes, a more advanced Killip class, more frequent noninferior MI, greater baseline ST-segment deviation, and delayed presentation.

As reported in the Journal of the American College of Cardiology, patients with baseline Q waves had greater mortality and a higher composite rate of death, heart failure (HF), or cardiogenic shock at 90 days compared with those without, at rates of 5.3% versus 2.1% and 12.1% versus 4.8%, respectively (both p<0.001).

Similarly, patients who underwent PCI within 3 hours had better 90-day outcomes than those undergoing PCI later, evident both for mortality (3.1 vs 4.5%, p=0.018) and the composite death, HF, or shock (6.7 vs 10.3%, p<0.0001).

Further analysis showed that, among patients with noninferior MIs, those with Q-wave at baseline had significantly higher mortality than those without (5.8 vs 2.3%, p<0.001), whereas the relationship was somewhat attenuated in those with inferior MIs (4,2 vs 1,9%, p=0.004). A similar pattern was seen for the composite outcome, the authors note.

Finally, after multivariable adjustment, baseline Q-wave, but not time from symptom onset to PCI, was associated with a significant 78% relative increase in the risk for 90-day mortality and 90% relative increase in the risk for 90-day death, HF, or shock.

“Of note, baseline Q-wave had a greater contribution to the prediction of the composite than time from symptom onset to PCI (8.8 vs 3.2%, respectively),” Armstrong and team highlight.

“Because baseline Q waves seem to provide a window into the stage of evolution of infarction, it might be useful to incorporate them into the design and evaluation of future clinical trials aimed at salvaging ischemic myocardium,” comment the researchers.

“Moreover, the use of baseline Q waves might prove to be of assistance to frontline clinicians evaluating STEMI patients (similar to those enrolled in the APEX-AMI trial) for triage and potential transfer to a tertiary center for planned PCI as well as the substantial proportion of patients in whom the history of symptom onset is unclear or unavailable.”

"What we found was that a single brief nitrite treatment elicited persisting changes in the heart's oxidation status together with lasting alterations to numerous proteins involved in the heart's energy metabolism, redox regulation, and signaling," said David H. Perlman, a post-doctoral research associate in the Cardiovascular Proteomics Center at Boston University School of Medicine, and lead author of the study. "These alterations were particularly striking because they persisted at least 24 hours after the actual nitrite levels had returned back to normal, and they were correlated strongly with the improvements in heart function observed at the same time."

He noted that this type of protection, called 'cardiac preconditioning', is a recently discovered phenomenon shown to be caused by numerous pharmacological agents.

"The proteins we have implicated include some key proteins, such as mitochondrial aldehyde dehydrogenase, that have been shown by others to be critical to cardiac protection afforded by other agents and triggers," added Perlman. "This is exciting because it ties nitrite-triggered cardioprotection into the broader preconditioning field. Our study complements and extends other work, and identifies new players of potential importance for protection of the heart."

Perlman explained that nitrite levels in our bodies change under a number of circumstances, such as when we run up a flight of stairs or eat a big serving of salad.

"For years, the resulting bursts in nitrite were considered to be of little if any physiological relevance. Now we have good reason to believe that even small spikes in nitrite concentration can alter protein function in the heart in ways that afford protection," noted Perlman.

"We are intrigued by the breadth and magnitude of the proteomic changes in heart mitochondria elicited by a single, short-lasting elevation in nitrite concentration and believe that our findings will have broad implications for mitochondrial signalling and cardiac energetics," commented Martin Feelisch, senior author of the study. "It looks as though nitrite is triggering an ancient program aimed at fine-tuning mitochondrial function. Although the present study focussed on the heart, our observations may extend to other tissues and translate into relevant changes in muscle function elsewhere. If true, this may help explain, for example, the training effects of very short periods of exercise, which are known to be associated with elevations in circulating nitrite concentrations."

Interestingly, only low and high doses of nitrite, but not those in-between, were found to be protective. Although further studies will be needed to fully delineate the mechanisms of nitrite-induced cardioprotection, this study informs ongoing basic and translational studies by highlighting the importance of the dose-effect relationship for nitrite and the broad array of downstream targets possibly involved in its cardioprotective efficacy, the researchers concluded.