Antecedent hypertension and myocardial injury in patients with reperfused ST-elevation myocardial infarction

As a consequence of its well established role as a major cardiovascular risk factor [1], antecedent HTN is a frequent finding in MI patients. In our analysis, history of HTN was present in 68 % of STEMI patients. These results fit well with recent prospective STEMI registry studies which reported a prevalence between 60 and 70 % [23, 24]. Antecedent HTN has been acknowledged as significant risk factor for adverse outcome in survivors of acute MI for many years [4‐6]. For instance, Thune et al. found that antecedent HTN at the time of MI was strongly associated with an increased risk of future heart failure, stroke, cardiovascular death and a composite endpoint consisting of death, myocardial infarction, heart failure, stroke, or cardiac arrest in more than 14.000 patients included in the VALIANT trial (Valsartan in Myocardial Infarction Trial) [4]. Nevertheless, over the last years, reperfusion strategies and pharmacological interventions were significantly refined and consequently improved the outcome of patients presenting with acute MI [25]. These advances might have modified the relationship between HTN and the clinical course after STEMI [26]. Indeed, in a meta-analysis performed by Chen et al. the strength of the association between antecedent HTN and poor clinical outcome has decreased over time [11]. However, antecedent HTN was still associated with increased MACE and mortality rates at 12-month follow-up in our study. This was also observed after adjustment for confounding variables. Therefore, our findings highlight that even in the contemporary era of PPCI the simple information of HTN history can be used to identify patients at risk for adverse prognosis post-STEMI. This high risk group might also benefit from more intensified medical treatment strategies including aggressive antihypertensive treatment. Contrary to the information on antecedent HTN, HTN at the time of the acute event was not related with MACE in our study. Consequently, antecedent HTN seems of greater importance as compared with HTN at the time of STEMI.

It is well established that MI patients with a history of HTN show a distinctive baseline risk profile, irrespective of STEMI or non-STEMI presentation. Studies consistently observed that hypertensive patients with MI were older, more often female, had a higher body mass index, and higher rates of other cardiovascular risk factors including diabetes or hypercholesterolemia [6‐10]. Our data confirm these previous findings and it is likely that these factors might at least partly explain the higher risk of hard clinical events of hypertensive STEMI patients. Further observations from our and other studies are the higher incidence of a previous cardiac disease and the greater extent of coronary artery disease [4, 7, 9, 10]. Since both have been proved to be associated with adverse clinical outcome in STEMI patients [27], these factors might also contribute to the increased risk of infarction patients with antecedent HTN. Recent studies could also disclose that diffuse myocardial fibrosis, measured by T1 mapping, is increased in patients with hypertension and previous infarction [28].

It has been speculated that coronary occlusion in patients with pre-existing HTN might be associated with more extensive myocardial damage, greater myocardial dysfunction, and consequently adverse clinical outcome [11, 26]. Contrary, one might argue that a higher diastolic pressure could enhance coronary perfusion and collateral circulation with subsequently improved efficacy of reperfusion and limited expansion of myocardial necrosis. Studies investigating the impact of antecedent HTN on myocardial damage are very limited so far [29]. In particular, there is no study answering these questions by using the current reference standard technique, which is CMR [12]. CMR not only enables exact infarct sizing but also detailed tissue characterization of the jeopardized and infarcted myocardium [12]. These additional assessed parameters, primarily microvascular obstruction, but also myocardial salvage index provide strong prognostic information that is incremental to clinical, biomarker, electrocardiographic, and angiographic risk markers [15, 30]. To the best of our knowledge, the study by De Luca et al. [29]. is the first and only study that evaluated the impact of HTN on infarct size in 830 STEMI patients undergoing PPCI. The authors found that HTN was not associated with larger infarcts as determined by scintigraphy at 1 month after infarction. Nevertheless, some important limitations of this study have to be mentioned. The authors used a scintigraphic technique to assess infarct size, which is less accurate compared to CMR, especially for the detection of subendocardial infarcts [31]. Secondly, De Luca et al. were also not able to assess the association of antecedent HTN with myocardial salvage and microvascular dysfunction. Our study therefore complements and extends the previous literature by showing for the first time that the adverse outcome of reperfused STEMI patients with antecedent HTN is not associated with differences in reperfusion success or more pronounced myocardial injury.

Our study has some important limitations. Based on the in- and exclusion criteria of this multicenter clinical trial as well as the treatment of patients in specialized high-volume centers, our results might not be generalizable to all STEMI populations. Although AIDA STEMI was designed as all-comers trial to represent a “real-world” STEMI population [18, 20], further confirmation of our findings in other studies would be important. It is, however, important to note that the power of our study to exclude a 3 % difference in infarct size or LV ejection fraction between groups was approximately 95 %. Information on HTN was based on patient history and data on the duration of HTN as well as patients adherence to medication and effectiveness of HTN treatment, which could have prognostic implications as well, was not available. Nevertheless, our study shows that the simple assessment of antecedent HTN by anamnesis or during hospitalization has strong prognostic implications in STEMI patients treated with PPCI. Forty-eight patients (6 %) had a previous myocardial infarction. Chronic infarcts were not included in infarct size measurements and thus the “true volume” of the infarcted myocardium is not represented in the reported values. On the other hand, omitting those patients from statistical analysis did not significantly change the results.