Response Response

To the Editor,

We appreciate the interest shown by Martínez Sellés et al in our article dealing with acute myocardial infarction without ST segment elevation and coronary arteries with no significant stenoses.¹ In the first part of their letter, they express their surprise to the fact that we did not include the characteristics of the chest pain as predictors and refer to a predictive clinical model described by their group.² Several studies of our group have analyzed the prognostic value of the clinical data in patients who come to the emergency departament with chest pain.^3-6 However, both these studies and those of Martínez Sellés et al have been carried out in patients with chest pain of uncertain origin and normal troponin T levels, and their objective was to optimize the clinical history to aid in making the difficult decision as to whether to admit or discharge the patient. This scenario is very different from that of the patients dealt with in our article, all of whom were admitted to the hospital with elevated troponin levels. Thus, the clinical models designed for populations with normal troponin T levels are not applicable to patients with elevated troponin. On the other hand, the index described by Martínez Sellés et al can not be considered a predictor of normal coronary arteries since coronary angiography was not performed in their study.

The introduction of troponins has revolutionized the diagnosis of myocardial infarction to such an extent that two consensus documents have been published on its definition.^7,8 Still, as demonstrated by Laraudogoitia Zaldumbide et al,⁹ cardiac magnetic resonance can identify diagnoses other than infarction in patients with elevated troponin levels. This, however, does not imply that it can be generalized to the extent to state that chest pain with troponin elevation and coronary arteries without significant lesions "is not usually an infarction." In fact, we think this has not been the case in the majority of the patients in our series for the following reasons; a) all the patients had suggestive chest pain and the diagnosis of infarction was established by a cardiologist on the basis of the in-hospital study; b) no patient had ST segment elevation indicative of acute pericarditis; c) the troponin T level showed a pattern of elevation and reduction, as indicated in the document defining infarction; d) although coronary angiography did not detect significant stenoses, this fact does not imply the absence of arteriosclerosis; and e) the incidence of coronary arteries with no significant stenoses (13%) coincides with that reported in other larger series.¹⁰ We have not recorded the incidence of possible coronary spasm, nor was the ergonovine test performed; thus, some patients may have had coronary spasm, but this would support the diagnosis of myocardial infarction and could be one of the mechanisms.

Sensitive troponins will reach our hospitals in the near future and will increase the number of diagnoses of infarction. We are convinced that this will generate a debate that will result in a new consensus document for the redefinition of infarction. In this respect, the letter of Martínez Sellés et al is very timely. However, according to the criteria currently accepted by the scientific societies, we suggest a modulation of their message, since "suggestive chest pain and increased troponin levels is usually a myocardial infarction."