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European Journal of Heart Failure 2008 10(8):780-785; doi:10.1016/j.ejheart.2008.06.004
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© 2008 European Society of Cardiology

Acute heart failure in patients with acute myocardial infarction treated with primary percutaneous coronary intervention

Giovanni M. Santoro, Nazario Carrabba*, Angela Migliorini, Guido Parodi and Renato Valenti

Division of Cardiology, Careggi Hospital Florence, Italy

* Corresponding author. Division of Cardiology, Careggi Hospital, Viale Morgagni 85; 50134 Firenze, Italy. Tel.: +39 055 7947221; fax: +39 055 7947625. E-mail address: carddept{at}tin.it (N. Carrabba).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: Scanty data exist about the relation between acute heart failure (HF) and acute myocardial infarction (AMI).

Aim: To assess the impact of HF on outcome in AMI patients treated with primary percutaneous coronary intervention (PCI).

Methods and results: Out of 2089 AMI patients, 82% did not present HF, 17% presented HF on admission and 1% developed HF after hospitalisation. Predictors of HF on admission were age, diabetes, prior MI, time delay to admission, anterior location, and TIMI grade 0–1 in the culprit vessel. Predictors of HF during hospitalisation were age and peak creatine kinase. The 1- and 6-month mortalities were 1.1% and 2.2%, 8% and 12%, 26% and 33% in patients without HF, with HF on admission and after hospitalisation, respectively. The risk of death was higher in patients with HF than in patients without HF (HR 3.47), as well as in patients with HF after admission (HR 5.19) than in patients with HF on admission (HR 2.44).

Conclusions: In a primary PCI setting, the incidence of HF on hospital admission remains high, but mortality is lower when compared with historical patient series. Primary PCI may prevent the development of HF during hospitalisation; however, when HF develops, the prognosis remains severe.

Key Words: Heart failure • Myocardial infarction • Angioplasty • Prognosis

Received January 31, 2008; Revised April 29, 2008; Accepted June 10, 2008


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
The occurrence of acute heart failure (HF) in patients with acute myocardial infarction (AMI) is recognized as a significant predictor of increased morbidity and mortality [1-9]. Since abrupt myocyte loss is considered the key determinant of HF complicating AMI, timely reperfusion treatment, preventing the progression of myocardial necrosis and limiting the extent of the final myocardial damage, could reduce the incidence and improve the prognosis of this severe complication. Primary percutaneous coronary intervention (PCI) has recently been indicated as the first choice reperfusion strategy, because it reduces the mortality and the complication rates of ST-segment elevation AMI in comparison with fibrinolytic treatment [10,11]. There are limited data about the incidence and clinical significance of HF in patients with AMI treated with primary PCI [12], but these data, derived from the analysis of patients enrolled in randomised clinical trials, cannot be generalized to all patients with AMI, since these trials enrolled mainly populations with a low incidence of HF. Furthermore, there is little information about the relation between patient characteristics and timing of HF development, or about the prognostic relevance of HF according to onset time.

The goals of this study were: 1. to evaluate the incidence of HF on admission in patients scheduled to undergo primary PCI as well as the incidence of HF which developed after PCI during the initial hospitalisation; 2. to compare differences in demographic, clinical and angiographic characteristics between patients without HF and patients with HF on hospital admission or during hospitalisation; 3. to evaluate in-hospital and 6-month outcome. The present data were obtained from a 10-year database of a single tertiary centre in which the only reperfusion treatment adopted was primary PCI.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Patients, data collection and definitions
The registry of ST-segment elevation AMI of the Division of Cardiology of the Careggi Hospital in Florence, includes all patients hospitalised with a diagnosis of AMI who were treated with primary PCI since January 1995. The diagnosis of ST-segment elevation AMI was based on the presence of chest pain lasting 20 min or longer combined with typical electrocardiographic changes (≥0.1 mV of ST-segment elevation in ≥2 limb leads or ≥2 mV in ≥2 contiguous precordial leads, presumed new complete left bundle branch block). Primary PCI was proposed systematically to all patients, without any restriction based on age or clinical status if hospital admission had occurred within 6 h of symptom onset (12 h in case of continuing ischaemia) and a culprit lesion could be identified at coronary angiography. All these patients were followed up according to a prospectively defined protocol to which they had given informed consent. The collection of hospital data and performance of clinical follow-up for research purposes was approved by the institutional ethics committee.

For the purposes of this study, patients with cardiogenic shock on admission or patients who developed cardiogenic shock during hospitalisation were excluded. Cardiogenic shock was defined as the presence of systolic blood pressure <90 mm Hg for >30 min, unresponsive to fluid replacement and associated with signs of peripheral and end-organ hypoperfusion (cold extremities, cyanosis, oliguria or decreased mentation).

Patients with HF at the time of hospital admission were identified if they presented with bibasilar rales or pulmonary oedema at the initial clinical evaluation (classes II and III according to the Killip classification [2]). Patients who developed HF during hospitalisation were identified when the indicated signs of HF appeared for the first time after the initial clinical evaluation. Left ventricular ejection fraction (LVEF) was available for 1483 patients at admission, on the basis of the left ventricular angiography performed immediately after the diagnostic coronary angiography before PCI.

Time from symptom onset to treatment was defined as the time from the symptom onset to the first balloon inflation. PCI failure was defined as the inability to restore Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow in the culprit vessel at the end of the procedure. ST-segment monitoring (12 leads) was performed, starting before PCI and continuing until 30 min after the end of the procedure. ST-segment elevation resolution of more than 50% in the single lead with the most prominent ST-segment elevation at baseline was considered indicative of successful reperfusion at myocardial tissue level [13].

2.2. Statistical analysis
Categorical variables (presented as absolute values and percentages) and continuous variables (presented as mean±standard deviation) were compared by {chi}2 test (or Fischer exact test, when indicated) and Student's t test, respectively. All tests were two-sided, and statistical significance was defined as p<0.05. Survival curves were constructed using the Kaplan-Meier method, and differences in survival were assessed with the log rank test. Stepwise, multivariate regression analyses (forward method, with p<0.10 for entrance into, and p>0.15 for removal from the model) were used to identify factors independently associated with acute HF on admission and after hospital admission. The considered variables were: age as a continuous variable, sex, diabetes, hypertension, previous infarction, anterior infarct location, time from symptom onset to treatment as a continuous variable, multivessel coronary disease, and TIMI grade 0-1 flow in the culprit vessel at initial angiography. The same variables, plus PCI failure and peak creatine kinase as a continuous variable, were included in the analysis of the predictors of the development of HF after hospital admission. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated. In addition, Cox adjusted regression analysis was used to assess the prognostic effect of HF at any time, HF on admission and HF after hospital admission on 6-month mortality. The considered variables were: age, sex, diabetes, previous infarction, anterior infarct location, time from symptom onset to treatment, multivessel coronary disease, TIMI grade 0-1 flow in the culprit vessel at initial angiography, PCI failure, and peak creatine kinase. To this purpose, hazard ratios (HR) and 95% CI were calculated. All analyses were carried out using Statistica 4.5 for Windows (Statsoft, INC., Tulsa, OK), and SPSS 11.5 for Windows (SPSS, INC., Chicago, IL, USA).


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
Out of 2372 patients enrolled in the registry between January 1995 and April 2005, 283 patients were excluded because they presented cardiogenic shock at admission or during hospitalisation. Therefore 2089 patients met the criteria for the present analysis. Of these, 1705 (81.7%) did not present HF at any time, 357 (17%) presented HF on admission and 27 (1.3%) developed signs of HF during hospitalisation.

3.1. Patient characteristics and predictors of HF
In comparison with patients without HF (Table 1), patients with HF on admission were older, more frequently females and had higher rates of diabetes and previous myocardial infarction. They were more likely to have anterior infarct location and longer time delay from symptom onset to admission. At baseline angiography, patients with HF had multivessel disease more frequently and showed a trend towards a higher rate of TIMI grade 0-1 flow in the culprit vessel. LVEF before PCI was significantly lower in patients with HF on admission (data available in 221 patients, 64%) than in patients without HF (data available in 1247 patients, 73%) (41±11% vs 49±11%, p<0.001, respectively). The rate of primary PCI failure was low in both groups, but significantly higher in patients with HF. A higher peak creatine kinase was observed in patients with HF. At multivariate analysis significant predictors of HF on admission were age (HR 1.05, 95% CI 1.04-1.06), diabetes (HR 1.62, 95% CI 1.19-2.20), previous myocardial infarction (HR 1.60, 95% CI 1.13-2.26), time delay to admission (HR 1.07, 95% CI 1.01-1.12), anterior infarct location (HR 2.42, 95% CI 1.89-3.11), and TIMI grade 0-1 in the culprit vessel at initial angiography (HR 1.57, 95% CI 1.15-2.13).


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  		Table 1 Patient demographics and clinical characteristics according to absence of HF, HF on admission and HF after admission hospital

 
In comparison with patients without HF (Table 1), patients who developed HF during hospitalisation were older and more likely to have anterior infarct location. LVEF before PCI was significantly lower in patients with HF during hospitalisation (data available in 15 patients, 55%) than in patients without HF (38±11% vs 49±11%, p<0.001, respectively). Peak creatine kinase was significantly higher in comparison with that observed not only in patients without HF, but also in patients with HF on admission (p<0.0001). At multivariate analysis, the only significant predictors of the development of HF during hospitalisation were age (HR 1.05, 95% CI 1.01-1.09) and peak creatine kinase (HR 1.00, 95% CI 1.000-1.001).

In the 1366 patients in whom ST-segment monitoring was available, a significantly higher rate of ST resolution ≥50% was observed in patients without HF (964/1155, 83%), in comparison with patients with HF on admission (142/198, 72%; p<0.0001) and patients who developed HF during hospitalisation (8/13, 65%; p=0.035).

Treatment during hospital stay has been systematically recorded in our database since 2003 and was available for 610 patients. ACE inhibitors were frequently prescribed in patients without HF and in patients with HF on admission and during hospitalisation (88%, 89% and 75%, respectively, p=ns comparing both groups of patients with HF vs patients without HF), while beta blockers were less frequently prescribed (36%, 48%, 50%, respectively, p=ns comparing both groups of patients with HF vs patients without HF).

3.2. Mortality
The survival curves, estimated according to the Kaplan-Meier method and stratified according to the presence and timing of HF, are reported in Fig. 1. In comparison to patients without HF, both patients with HF on admission and those with HF occurring during hospitalisation showed a significantly lower survival curve (log rank test, p<0.0001 for both). Among patients with HF, those who developed HF during hospitalisation had a significantly lower survival curve than those with HF on admission (log rank test, p<0.001). The in-hospital and 6-month case mortality rates were 1.1% and 2.2% in patients without HF, 8% and 12% in patients with HF on admission and 26% and 33% in patients with HF during hospitalisation. At Cox multivariate analysis, the hazard of 6-month mortality for patients with HF at any time was significantly higher than that of patients without HF (HR 3.47, 95% CI 2.14-5.62), but the risk of death was substantially higher in patients who developed HF during hospitalisation (HR 5.19, 95% CI 2.44-11.0) than in patients with HF on admission (HR 2.44, 95% CI 1.51-3.93).


Figure 01
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  		Fig. 1 Cumulative survival (Kaplan-Meier) probability by the presence and time of heart failure development, from index acute myocardial infarction to 6-month follow-up. N° = number of patients; HF = heart failure; adm = admission; hosp = hospitalisation. Log rank test: comparison no HF-HF on admission and no HF-HF after admission, p<0.0001 for both.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
In this study of patients treated with primary PCI, the incidence of HF at the time of hospital admission (17.3%) was consistent with other studies [6,7,9,12]. In the National Registry of Myocardial Infarction (NRMI) -2 and -3, 20.4% of the patients showed clinical signs of HF at hospital admission [6]. In the Global Registry of Acute Coronary Events (GRACE), the incidence of HF on hospital admission was 15.6% [9]. These percentages are much lower than the incidence of 40-50% reported in earlier studies [3] and confirm a reduction in the incidence of HF complicating AMI [4]. In contrast, the incidence of HF which occurred during hospitalisation observed in our study (1.3%) was much lower than that reported in previous analyses [6,9]. In the study by Spencer et al. [6], based on the data of the NRMI-2 and -3, HF during hospitalisation was observed in 8.6% of the patients. In the GRACE registry [9] 10.4% of the patients with ST-segment elevation AMI developed HF during hospitalisation. The lower incidence of HF, which was not present on admission and occurred during hospitalisation, was probably related to the reperfusion treatment by primary PCI, which was applied to all patients included in our registry. In the study by Spencer et al. [6] PCI or coronary artery by-pass grafting was performed in about 40% of AMI patients without HF but only 20% of those with HF at the time of presentation and 36% of those who developed HF after admission underwent revascularization. In the GRACE registry [9], including also patients with non-ST-segment elevation AMI and unstable angina, coronary revascularization, by either PCI or by-pass, was performed in 38.4% of the patients without HF and in 31.9% of the patients who had HF on admission or developed HF thereafter. Primary PCI, when performed promptly, has been shown to reduce infarct size and preserve left ventricular function [14,15]. The extremely low rate of HF which occurred during hospitalisation in our patient series may have been related to the systematic use of primary PCI. The early restoration of TIMI grade 3 flow in the culprit vessel may have had a crucial role in reducing myocardial damage and preventing the occurrence of HF [16]. In addition, the extensive use of stents may have reduced the occurrence of HF at a later time by preventing recurrent ischaemia [17].

In agreement with previous studies [3-9], patients with HF at the time of admission were older and more likely to have a history of myocardial infarction and diabetes in comparison with patients without HF. Furthermore, in patients with HF on admission, an anterior location of AMI was more frequent, time delay to treatment was longer, and baseline coronary angiography showed multivessel disease and TIMI grade 0-1 flow in the culprit vessel in a higher percentage of patients. These data confirm that HF on admission may be facilitated by pre-existing conditions which limit the ability of the left ventricle to compensate the acute dysfunction induced by a long-lasting severe ischaemia [6]. On the other hand, patients who developed HF during hospitalisation had a much higher peak creatine kinase in comparison not only to patients without HF but also to those patients with HF on admission, suggesting a more extensive infarct size. Age and peak creatine kinase were the only significant predictors of the development of HF during hospitalisation in our analysis. These data confirm that the extent of the final myocardial damage is the key determinant of HF which occurs after admission [6]. These patients were unlikely to have had benefited from primary PCI, probably due to an intervention which, although performed promptly and capable of restoring TIMI grade 3 flow in the great majority of cases, had been less effective in salvaging myocardium. ST-segment resolution ≥50% was observed less frequently in patients with HF, suggesting that in these patients the recanalization of the culprit coronary vessel was more likely to be ineffective in achieving myocardial tissue reperfusion [13,18].

In our study, HF on hospital admission was associated with a 2- to 3-fold increase in in-hospital and 6-month mortality rates in comparison to those observed in patients without HF. However, although differences in the demographic and clinical characteristics of patients included in our study limit the validity of the comparison with previous studies, it is noteworthy that the in-hospital mortality observed in our registry was much lower than that reported in previous studies [3,4,6,7,9]. The in-hospital mortality rate of patients with HF enrolled in the Worcester Heart Attack was 18% [4], that of patients with HF on admission included in the NRMI-2 and -3 was 20.9% [6], and that of patients with ST-segment elevation AMI and HF on admission enrolled in the GRACE registry was 16.5% [9]. The in-hospital mortality rate of 8% observed in our study deserves some comment. Although primary PCI obviously cannot reduce the incidence of HF already present on hospital admission, our data suggest that an early intervention to restore flow in the occluded coronary vessel and to reperfuse the myocardium may improve the outcome of patients presenting with HF, achieving a beneficial effect which is similar to that observed in patients presenting with cardiogenic shock [19].

As in previous studies [6,9] the development of HF during hospitalisation was associated with a worse outcome in comparison not only to patients without HF but also to patients with HF on hospital admission. The in-hospital mortality rate of 26% observed in our study is not far from the 31.5% reported by Spencer et al. [6]. In this group of patients, primary PCI was probably ineffective at salvaging myocardium and limiting the final left ventricular damage. The high mortality rate was due to the large extent of necrosis, as suggested by the high peak creatine kinase, and the consequent severe left ventricular dysfunction.

This study has some limitations. Although the study was an observational analysis, patients were prospectively enrolled and data prospectively collected, and no patient was excluded. Therefore the present cohort is representative of the patient population referred to a tertiary centre for primary PCI in the real world. The diagnosis of HF was based on a clinical evaluation, which is considered of limited reliability and may have missed a portion of patients with HF due to low sensitivity [20,21]. However, the results of our study show that the diagnosis of HF used in the present analysis is of prognostic value and confirm previous studies in demonstrating the persisting validity of this simple method to stratify the risk of patients [22,23]. In our analysis we excluded patients with cardiogenic shock, these patients have the most severe degree of HF. However the impact of primary PCI in patients with cardiogenic shock has already been studied in detail. Lastly patients included in this analysis were enrolled over a period of ten years, during this time primary PCI, adjunctive therapy, and treatment of HF have changed. Our study was not designed to evaluate possible variations in incidence and outcome of HF in relation to changes in strategy of intervention and pharmacological treatment. Finally, previous histories of HF and renal dysfunction, both strong predictors of adverse prognosis, were not systematically recorded in our database. Thus, we were unable to test the relevance of these variables as predictors of HF and survival in our model.

In conclusion, this study shows that in the era of primary PCI, the characteristics of HF complicating ST-segment elevation AMI have changed. Although the incidence of HF, which is present on hospital admission, is similar to that reported in previous studies, primary PCI appears to improve the prognosis of these patients. Furthermore, the systematic application of primary PCI may prevent the subsequent development of HF, but, when HF develops, the prognosis remains severe. Therefore, an aggressive strategy should be recommended particularly in patients who have clinical signs of HF on admission or who have an AMI with a large risk area susceptible to evolve in an extensive myocardial necrosis conditioning HF.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

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