STEMI Patients with Preinfarction Angina Show Fewer Signs of Myocardial Damage

Angina experienced shortly before ST-segment elevation myocardial infarction (STEMI) may predispose to smaller infarct size and better heart function after percutaneous coronary intervention (PCI). The benefits of preinfarction angina likely stem from preconditioning, according to a paper published online January 22, 2013, ahead of print in Circulation: Cardiovascular Interventions.

The findings were previously presented as an abstract at the 2011 American Heart Association Scientific Sessions in Orlando, FL.

For the single-center study, Jay H. Traverse, MD, and colleagues at Abbott Northwestern Hospital (Minneapolis, MN) reviewed the records of 245 patients with occluded arteries who underwent PCI for a first-time STEMI between 1 and 6 hours after symptom onset. Among them, 79 had documented chest pain within 24 hours prior to STEMI. Baseline characteristics and procedural factors did not differ between patients with and without angina.

Chest Pain Equals Lower Biomarkers

Patients showed similar ischemic times (185 ± 5 minutes vs. 181 ± 5 minutes; P = 0.67) and angiographic areas at risk (24.1 ± 1.2% vs. 25.3 ± 0.9%; P = 0.43) regardless of whether they did or did not have chest pain. Yet preinfarction angina was associated with lower peak values of creatinine kinase—indicating smaller infarct size—and troponin T up to 48 hours after reperfusion (table 1). Creatinine kinase area under the curve also was reduced in the angina group.

Table 1. Peak Values Within 48 Hours of PCI

Moreover, in an echocardiographic subanalysis (n = 220), patients with angina before STEMI showed better LVEF compared with those who did not experience chest pain (51.4 ± 1.1% vs. 47.4 ± 1.0%; P < 0.02). Angina appeared to be protective of LVEF regardless of infarct size.

The data also suggest that timing matters more in the absence of angina. “Although myocardial damage increased with ischemic duration in patients without preinfarction angina, no such correlation was observed in [those with chest pain],” the investigators note, adding that angina’s protective effect “may last for at least 6 hours. This also implies that the benefit of late PCI may be greater in patients with preinfarction angina because more myocardium can be salvaged.”

More than Preconditioning?

According to the paper, several mechanisms may explain the protective effects of preinfarction angina, “including accelerated thrombolysis, opening of pre-existing collateral vessels, reduced microvascular obstruction, and a myocardial conditioning effect similar to [ischemic preconditioning].”

But “the truth is, we don’t know,” Dr. Traverse told TCTMD in a telephone interview. “It has [always been thought of] as the clinical correlate to ischemic preconditioning, which is supposedly the most powerful endogenous myocardial protective mechanism that’s ever been discovered.”

Though the phenomenon is widely known among cardiologists, he said, “I think it’s underappreciated and could have ramifications in a lot of the clinical trials [on novel therapies to limit] infarct size.” Dr. Traverse estimated that 30% to 40% of STEMI patients have experienced recent chest pain. According to the paper, this could explain why clinical trials on interventions to reduce myocardial damage have been largely negative despite positive preclinical studies. Perhaps the inclusion of patients with preinfarction angina has been masking a treatment effect, they suggest.

No Direct Impact on Practice

Stephen G. Ellis, MD, of the Cleveland Clinic (Cleveland, OH), told TCTMD in an e-mail communication that the relationship between chest pain and subsequent infarct size may be better recognized among researchers than among clinicians. He characterized the change in creatinine kinase observed by Traverse et al as “very” clinically relevant, noting that the effect on LVEF was “more than I would have expected.”

In a telephone interview with TCTMD, Sorin J. Brener, MD, of Weill Cornell Medical College (New York, NY), said that the current study is “very nice, because they selected a very pure group of patients. In that respect it helps [clarify things].”

The biomarker changes “are very convincing,” he commented, suggesting that assessment of regional wall motion abnormalities might also be more informative than LVEF.

Dr. Brener emphasized that, while the study does not speak to patient management, it importantly provides “verification of the concept. [In the real world, of course,] we can’t control who has angina and who doesn’t, but maybe we can learn from this how to do preconditioning well.”

One implication, Dr. Ellis added, is that preinfarction angina “would widen the time wherein one would expect benefit” from primary PCI.

Dr. Traverse reported that the next step will be to analyze extended follow-up on the same group of patients. As to the clinical relevance of the findings, an absolute improvement of 4% in LVEF “is not huge but may have a bearing in the long term,” he said, adding that there could be possible differences in remodeling over time. “As far as I know, there’s no good long-term data on this, and that would be important to see. That would really determine how clinically relevant [preinfarction angina] is.”

Study Details

A total of 1,031 patients were screened for study enrollment. Exclusion criteria included previous MI, infarct artery patency before PCI, and visible collateral blood flow to the infarct region.

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