Evaluation of heart failure by Killip classification has been an important adjunct in prognostic evaluation since first described by Killip and Kimball in the early 1960’s . It’s clinical usefulness has been demonstrated several times, most recently by DeGeare et al., in a modern post-revascularization setting in 2001 . The present study extends these observations, and demonstrates that even in patients with AMI presenting with Killip class II and III, lactate levels ≥ 2.5 mmol/L confers a worse prognosis.
In our material, lactate analysed as a continuous variable was significantly related both to short- and long term mortality in patients with acute coronary syndrome and signs of heart failure.
Further, in patients presenting with clinical light to moderate heart failure, defined as Killip class II and III, we found that an increased blood lactate level analysed as a dichotomous parameter with threshold ≥2.5 mmol/L, was associated with increased mortality at both 30 and 365 days even when excluding patients with known negative prognostic factors such as overt cardiogenic shock, hypotension, and out of hospital cardiac arrest, patients seeking care more than 24 h after symptom debut and undergoing rescue PCI.
A control sample of 20 patients classified as Killip class I was analysed, from which 4 patients presented with blood lactate > 2.5 mmol/L. Three of these patient had MI, while one healthy individual underwent a coronary angiography on behalf of suspected unstable angina pectoris with normal result. All where alive after 365 days. Even though several patients classified as Killip I had lactate levels above normal, the mortality of the group as a whole remained as low as 3% after 30 days. This could suggest that an elevated lactate level can be used a predictor of mortality, only when clinical signs of heart failure is present, a question that lies beyond the scope of this study.
It is established that patients presenting with acute coronary syndrome but without overt signs of congestive heart failure (Killip class I) have a relatively favourable outcome (mortality 3% at 30-days in our material, and 2.4% in De Geare and colleagues’ material from 2001) . On the other hand, mortality in cardiogenic shock remains high in spite of historical efforts to improve outcome with means such as inotrope agents,  intra-aortic balloon pumps , ventricular assist devices  and extra corporeal membrane oxygenation (ECMO) . Our data showed a 30-day mortality of 50% in patients with ACS and cardiogenic shock. This level is consistent with comparable international data .
Earlier studies on blood lactate have proved its role in risk stratification regarding patients in need of intensive care in general [14, 15] and specifically in patients suffering of sepsis [12, 13, 16]. In patients suffering of acute coronary disease, data have been more inconsistent. Lazzeri and colleagues  showed in 2010 that an increased lactate was associated with early mortality in patients presenting with STEMI and advanced Killip class, but could not identify a relationship in patients in Killip class I and II. To the best of our knowledge, though, this study did not separate patients with no signs of heart failure from those with low-grade heart failure, and lactate level was tested as a continuous variable, and not as a dichotomous parameter with a low cut-of point. The same year, Vermeulen et al  demonstrated a relationship between blood lactate and short-term mortality in STEMI, but did not exclude patients with advanced Killip class (however, intubated patients were excluded).
Blood pressure analysed as a semi-continuous variable (by steps of 10mHg), was statistically associated with mortality only when including patients classified as Killip class IV. When excluding patients with overt shock or hypotension with signs of peripheral vasoconstriction (Killip class IV), this association was no longer seen. The same result was seen when analysing systolic blood pressure as a dichotomous parameter with threshold 90 mmHg.
The relationship between systolic blood pressure and mortality in the case of acute heart failure has been established previously , and lack of significance in this study may have several explanations. Mainly, one could suspect it to be type I error due to few hypotensive patients. Among 77 patients in Killip class II and higher only 6 (8%) were hypotensive at arrival. This number is lower than expected from previous studies, but might be attributed to relatively short transport times and well-developed infrastructure in southern Sweden, and hence relatively short time from symptom debut to arrival at the hospital. Secondly, when analysing blood pressure as a dichotomous parameter, we disregard any differences between moderate and more severe hypotension.
The main limitation of this study is the relatively small number of available subjects from a single centre. The SCAAR registry consists of data manually recorded by the responsible angiography operator, and for a total of 46 (4%) patients were excluded from the study on ground of missing Killip classification. All data were reviewed retrospectively. Data on blood pressure and blood lactate were derived from first recorded values in the patient journal on arrival, but the exact time of measurement or sampling relating to the angiographic procedure cannot accurately be decided retrospectively. In addition, time from symptom debut could possibly affect lactate levels, but is not available in our data. Collecting peak lactate and lactate development could have given additional information. Furthermore, lactate levels are possibly affected by presence of diabetes. Analysing this relationship would have been interesting to analyse further, if not limited by our data number.
Compared with equivalent data from earlier studies [3, 23], the data in our material included relatively few patients presenting with signs of heart failure as a whole, as well as far developed heart failure. Notably, the mortality in patients in Killip class II was higher than those in Killip class III. This difference is probably due to few available data, but could also be a result of imprecise classification. Despite this, the mortality rates in both Killip class IV and Killip classes II/II when assessed together, are in parity or even lower than similar data from previous studies [3, 23].
Patients with acute coronary syndrome and evaluated heart failure in Killip class IV or hypotension have a high mortality rate. In this material, we have identified patients with clinical heart failure without affected hemodynamics, which despite adequate blood pressure have high mortality rates. Rising lactate in these patients could be a marker of tissue hypoxia as a result of peripheral vasoconstriction, as adrenergic compensation still maintains the blood pressure despite an increase in pre-load and falling cardiac output (CO). Could lactate in these cases in fact be a marker of insipient but still compensated cardiogenic shock? Mortality in established cardiogenic shock is still severe. If lactate indeed is an early marker, it might be a useful adjunct in early detection and initiation of treatment to prevent escalation into overt cardiogenic shock.