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European Journal of Heart Failure 2008 10(7):668-674; doi:10.1016/j.ejheart.2008.04.015
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© 2008 European Society of Cardiology

Percutaneous coronary intervention for acute MI does not prevent in-hospital development of cardiogenic shock compared to fibrinolysis

Matias G. Lindholma,*, Søren Boesgaarda, Jens Jakob Thunea, Henning Kelbaeka, Henning Rud Andersenb, Lars Kobera DANAMI-2 investigators

a Medical Department B, Division of Cardiology, Rigshospitalet, University Hospital of Copenhagen Denmark
b Department of Cardiology, Skejby Hospital, University Hospital of Aarhus Denmark

* Corresponding author. Medical Department B72, Hospital of Roskilde, Kogevej 7-13, DK-4000 Roskilde, Denmark. Tel.: +45 25 38 36 01; fax: +45 35 45 25 13. E-mail address: Matiasgl{at}dadlnet.dk (M.G. Lindholm).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: It has been speculated that invasive revascularization prevents development of cardiogenic shock. Data from randomised trials comparing angioplasty with fibrinolysis on the development of cardiogenic shock are lacking.

Aims: To elucidate the effect of angioplasty on in-hospital development of cardiogenic shock compared to fibrinolysis.

To evaluate whether mortality in patients who develop cardiogenic shock after treatment is dependent on revascularization strategy.

Methods and results: DANAMI-2 randomly assigned 1572 STEMI patients to fibrinolysis (782 patients) or angioplasty (790 patients). Data on patients with in-hospital development of cardiogenic shock after randomisation were included. Of the 103 patients (6.6%) patients developing cardiogenic shock 57% were randomised to angioplasty with an unadjusted odds ratio of 1.39 (0.92–2.11, p=0.14). During the three year follow-up 58% of the total mortality was due to cardiogenic shock, and treatment strategy did not influence the risk associated with shock (hazard ratio of 1.05 (0.67–1.64) for angioplasty vs. fibrinolysis).

Conclusions: Angioplasty does not prevent the in-hospital development of cardiogenic shock complicating acute MI compared to fibrinolysis. Cardiogenic shock is still the leading cause of death in patients hospitalised for acute MI. There was no difference in mortality, with regards to treatment strategy in patients developing cardiogenic shock after the initial treatment.

Key Words: Acute heart failure • Cardiogenic shock • Angioplasty • Revascularization • Acute myocardial infarction

Received July 13, 2007; Revised April 8, 2008; Accepted April 28, 2008


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
In patients with ST-elevation myocardial infarction (STEMI) restoration of coronary flow in the infarct-related artery can be achieved by fibrinolysis or angioplasty. Studies show that time from symptom onset to restoration of flow and magnitude of coronary flow correlates with short- and long-term outcomes regardless of whether reperfusion is accomplished by fibrinolysis or angioplasty [1].

Studies show that angioplasty is superior to fibrinolysis with regard to restoration of epicardial flow and subsequent blood flow to the ischaemic area [2]. In consequence, invasive revascularization with angioplasty is preferred to fibrinolysis in high volume centres when treating patients with STEMI [3,4].

The incidence of cardiogenic shock among the total infarction population is approximately 7%, with 75% developing cardiogenic shock after admission to the hospital and initiation of treatment. Several important risk factors like previous myocardial infarction (MI), infarction size and location have been identified as predictors of cardiogenic shock [5].

Long-term data from the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) Trial show a mortality benefit from invasive revascularization compared to fibrinolysis in patients with cardiogenic shock [6]. The European guidelines on treatment of acute heart failure (AHF) state that angioplasty improves or prevents AHF and reduces mortality from AHF complicating acute coronary syndromes [7]. It is tempting to speculate whether invasive revascularization prevents the in-hospital development of cardiogenic shock compared to fibrinolysis, but data from randomised trials comparing angioplasty with fibrinolysis on the development of cardiogenic shock are lacking. Focusing on the subpopulation of STEMI patients who developed in-hospital cardiogenic shock in the Danish Multicenter Randomised Study on Fibrinolytic Therapy versus Acute Coronary Angioplasty in Acute Myocardial Infarction (DANAMI-2) trial, the present study investigates the incidence of cardiogenic shock and the subsequent mortality in patients treated with either angioplasty or fibrinolysis.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Study population and design
DANAMI-2 randomly assigned 1572 patients with ST-elevation myocardial infarctions (STEMI) to fibrinolysis (782 patients) or primary angioplasty (790 patients). Randomisation took place from December 1997 to October 2001 at 24 referral hospitals without angioplasty facilities and 5 high volume invasive revascularization centres. Each patient was only included once using first MI of the study period. Patients with cardiogenic shock and severe heart failure (sustained systolic blood pressure less than 65 mm Hg) at the time of randomisation were excluded. No patients developed cardiogenic shock during transfer.

The investigation conformed with the principles outlined in the declaration of Helsinki and was carried out in accordance with the local ethics committee.

The rationale, design, and baseline characteristics have been published previously [8].

2.2. Definitions
Index MI was defined as typical chest pain for more than 30 min and ST-elevation in 2 or more leads with a total of 4 mm. Cardiogenic shock was defined primarily by clinical criteria. The criteria were 1) hypotension (a systolic blood pressure of <90 mm Hg for at least 30 min or the need for supportive measures to maintain a systolic blood pressure of >90 mm Hg) and 2) end-organ hypoperfusion (cool extremities, a urine output of <30 ml per hour, a heart rate of >60 beats per min). Both hypotension and end-organ hypoperfusion had to be present. This corresponds to the definition of cardiogenic shock used in the SHOCK trial. Pulmonary-artery catheterization was not required. Data on how many patients had right heart pressures measured and on whether cardiogenic shock was due to a mechanical complication, were not available. Heart failure without cardiogenic shock during hospitalisation was registered as Killip class 2 or 3. Time to treatment was defined as time from onset of symptoms to fibrinolysis or first injection of contrast in the catheterization laboratory, respectively.

For each patient, the Thrombolysis in Myocardial Infarction (TIMI) risk score for ST-elevation myocardial infarction (TIMI STEMI score) was calculated as the arithmetic sum of the following variables obtained at admission: age ≥75 years=3 points; age 65 to 74 years=2 points; systolic blood pressure<100 mm Hg=3 points; heart rate>100 bpm=2 points; Killip class 2 to 4=2 points; weight<67 kg=1 point; anterior ST-segment elevation=1 point; time from symptom onset to treatment>4 h=1 point; and a history of angina, diabetes, or hypertension=1 point, for a possible score of 0 to 14 [9].

2.3. Follow-up
The primary endpoint of the present study was all cause mortality. Follow-up was carried out via the Danish Central Person Register. No patients were lost to follow-up.

Data on patients with in-hospital development of cardiogenic shock after randomisation were analyzed in the present study. Data on cardiogenic shock and development of cardiogenic shock were collected prospectively and thus collected and analysed blinded to the final outcome.

2.4. Statistics
Characteristics of the study population were analysed using the chi-square test for discrete variables and the rank sum test for continuous variables. Discrete variables are presented as percentages and continuous variables as median values with 5th to 95th percentiles. Univariate and multivariable analyses of predictors of cardiogenic shock were done by logistic regression. In the multivariable analyses a result is presented for a model including all variables (without model building) and a result after exclusion of all non-significant predictors of cardiogenic shock. Mortality curves were generated by means of Kaplan-Meier estimates and compared by log-rank test. Hazard ratio (HR) of all cause mortality was estimated by a Cox proportional-hazards regression model including variables with prognostic importance (p-value<0.05) in univariate analyses. All variables were included with the baseline value except ventricular fibrillation and cardiogenic shock (that occurred within the first 5 days). We were not able to perform time-dependent Cox analysis as date of shock or ventricular fibrillation was not registered. Supporting analyses excluding early death showed similar results as those presented. Interaction analyses were conducted by including an interaction term in the proportional hazard models. The proportional hazard assumption and linearity of continuous variables were checked and found valid. No adjustments for multiple comparisons were made. Calculations were made with SAS 9.1 (SAS Institute, Cary, NC). For all analyses a p-value<0.05 was considered significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
In the present study all information from randomisation during in-hospital stay to 3 years follow-up was included. Information on cardiogenic shock was missing in 1 patient resulting in 1571 patients participating in this substudy.

3.1. Baseline characteristics
Of the 1571 patients, a total of 103 (6.6%) developed cardiogenic shock after randomisation. No difference in incidence was noted according to whether patients were randomised in a referral hospital (incidence 6.4%) or an invasive revascularization centre (incidence 7.0%, p=0.66). When comparing the cardiogenic shock group to the patients without cardiogenic shock, most of the known risk factors such as high age, female sex, previous MI, large infarction, late presentation at the hospital and subsequently delayed treatment, and Killip class>1 were more prevalent in the cardiogenic shock group as shown in Table 1. The incidence of cardiogenic shock complicating acute MI in the high-risk group with a TIMI STEMI score >5 was 13.2% as compared to 4.7% in the low risk group (p-value<0.0001).


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  		Table 1 Baseline characteristics of 103 patients who developed in-hospital cardiogenic shock and 1468 patients without in-hospital cardiogenic shock in the Danish Multicenter Randomised Study of Fibrinolytic Therapy versus Acute Coronary Angioplasty in Acute Myocardial Infarction (DANAMI-2) trial

 
Low blood pressure, increased heart rate, supraventricular and ventricular arrhythmias were all significantly more often present at randomisation in those who developed cardiogenic shock. There was a significantly more frequent use of intra-aortic balloon counterpulsation (IABP) and ventilator in the cardiogenic shock population. Left ventricular ejection fraction (LVEF) was assessed prior to discharge and therefore data are missing for patients who died during the index admission. Table 1 shows that patients with in-hospital development of cardiogenic shock who survived to discharge had a significantly lower ejection fraction at time of discharge compared to patients without cardiogenic shock during admission.

3.2. Characteristics according to treatment strategy
When subdividing patients with cardiogenic shock by treatment strategy only the use of Angiotensin-Converting Enzyme (ACE) inhibitors was significantly more prevalent in the fibrinolytic group at admission (Table 1).

The use of specialized intensive treatments during the hospital stay, such as IABPs and ventilators, was higher in patients who were treated with primary angioplasty. Time from symptoms to treatment was almost 50% longer in the angioplasty group with cardiogenic shock compared to the fibrinolytic group. In the angioplasty group, time from symptom onset to treatment was significantly longer in the cardiogenic shock population compared to patients without cardiogenic shock, with a time to treatment of 4.0 h and 3.4 h, respectively. Patients who developed cardiogenic shock had significantly higher rates of reocclusions, multiple vessel disease and TIMI flow <3 of the culprit lesion. Forty three percent of patients in cardiogenic shock had reocclusion of the infarct-related artery and 60% had a TIMI flow less than 3 after angioplasty (data not shown).

3.3. Predictors of cardiogenic shock
When comparing the incidence of cardiogenic shock in the fibrinolysis group to the angioplasty group in an unadjusted analysis a statistically non-significant odds ratio of 1.39 (0.92-2.11, p=0.14) was found. However, when adjusting for all other risk factors as listed in Table 1 we found an odds ratio of 1.91 (1.09-3.36), p=0.03. The result of a logistic regression of significant predictors of cardiogenic shock in the total population is shown in Table 2. In addition to primary angioplasty, predictors of the development of cardiogenic shock after admission to the hospital were advanced age, female sex, previous acute MI, heart rate, and low blood pressure at the time of admission.


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  		Table 2 Predictors of development of in-hospital cardiogenic shock in a multivariable logistic regression model

 
3.4. Predictors of mortality at long-term follow-up
Predictors of mortality in multivariable analyses were age, history of diabetes, congestive heart failure, intermittent claudication, heart rate and cardiogenic shock (Table 3). We found that 58% of the three year mortality in the DANAMI-2 trial was due to cardiogenic shock.


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  		Table 3 Predictors of mortality at long-term follow-up in a Cox regression model

 
The 30-day mortality rate (Fig. 1) was 3% in the non-shock and 65% in the cardiogenic shock group (p-value=0.01). Long-term follow-up showed that patients surviving cardiogenic shock had a mortality rate similar to patients without cardiogenic shock during the index admission. When subdividing the cardiogenic shock patients by treatment strategy, no differences were seen with regard to three year mortality with a hazard ratio of 1.05 (0.67-1.64) for angioplasty vs. fibrinolysis. (Fig. 2; p-value for interaction=0.25). The significantly higher rate of reinfarctions in patients randomised to fibrinolysis found in the DANAMI-2 trial was replicated in our substudy. We found that 9 patients treated with fibrinolysis had a reinfarction, 77% of which occurred during the first 6 days. Only 4 patients in the angioplasty group developed a reinfarction and 3 of these did so more than 18 days after the index MI. When looking at NYHA classification after one year, we found a significantly higher proportion of patients with NYHA class 1 in the cardiogenic shock population randomised to angioplasty compared to patients treated with fibrinolysis, 47% versus 7% (p=0.01), respectively.


Figure 01
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  		Fig. 1 Short and long-term mortality in patients with ST-elevation myocardial infarctions (STEMI) depending on in-hospital development of cardiogenic shock (n=103) or not (n=1468).

 


Figure 02
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  		Fig. 2 Short and long-term mortality in patients with ST-elevation myocardial infarctions (STEMI) treated with either angioplasty or fibrinolysis depending on in-hospital development of cardiogenic shock.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
The main findings of the present study are 1) that invasive treatment strategies do not seem to prevent the development of cardiogenic shock after acute myocardial infarction compared to fibrinolysis, 2) cardiogenic shock is still the leading cause of death in patients hospitalised for acute myocardial infarction and 3) cardiogenic shock following primary angioplasty is as prognostically detrimental as cardiogenic shock following fibrinolysis.

4.1. Data supporting use of angioplasty for STEMI
The first meta-analysis of randomised trials comparing thrombolytic treatment with angioplasty for acute MI, was conducted in 1995(4). Michels et al. indicated that PTCA may be more beneficial than thrombolytic therapy in acute MI and that PTCA was related to a reduction in 6-week mortality. A later meta-analysis on acute MI patients, by Keeley et al. concluded that angioplasty was better than thrombolytic therapy at reducing overall short and long-term mortality, non-fatal reinfarction, stroke and the combined endpoint of death, non-fatal reinfarction and stroke [3]. A pooled analysis by Boersma et al. of 25 randomised trials testing the efficacy of angioplasty compared to fibrinolysis, concluded that despite treatment delay, angioplasty was associated with significantly lower 30-day mortality [10] in patients with acute MI. In the DANAMI-2 trial, only the combined endpoint was significant, with no obvious effect on mortality [8]. A post-hoc analysis of data from the DANAMI-2 trial demonstrated that the benefit of primary angioplasty was most prevalent in patients at high risk according to the TIMI STEMI score [11]. Currently the suggested acceptable time delay from first medical contact to the angioplasty procedure is 90 min [12].

4.2. Cardiogenic shock incidence
Cardiogenic shock is a serious complication of acute MI and the incidence does not seem to have changed over the last 30 years [5,13]; 75% of patients developing cardiogenic shock do so after admission to the hospital [5]. In the TRACE-registry, 59% of patients developed cardiogenic shock within 48 h [14]. In this medically treated population of acute MI patients in Denmark, a total of 443 developed cardiogenic shock with an incidence of 6.7%. In the present study, we found an incidence of 6.6%, indicating that the incidence of cardiogenic shock in Denmark has not changed over time.

Our data suggest that angioplasty most likely does not protect against development of in-hospital cardiogenic shock compared to fibrinolysis, but additional information about the relationship between primary angioplasty and cardiogenic shock is sparse. Data from the Global Use of Strategies to Open Coronary Arteries in Acute Coronary Syndromes (GUSTO IIb) trial show an incidence of shock within 30 days which is 1.3 times higher in the angioplasty group [15]. In Europe, Bonnefoy et al. reported a similar trend towards an increase in development of cardiogenic shock from randomisation to hospital discharge in the angioplasty arm [16]. Reasons for this overrepresentation of cardiogenic shock in the invasive arm compared to the non-invasively treated MI patients have not previously been addressed.

There is strong evidence that patients treated with angioplasty have more effective ST-resolution, higher infarct vessel patency, less residual stenosis and a reduction in infarct size compared to fibrinolysis [17]. Despite current myocardial reperfusion strategies and ancillary antithrombotic and antiplatelet therapies, the morbidity and mortality of an AMI remain significant, with the number of patients developing cardiac failure increasing, necessitating the development of novel strategies for cardioprotection which can be applied at the time of myocardial reperfusion to reduce reperfusion injury and myocardial stunning. Most of the clinical studies to evaluate PCI have focused on the mechanical techniques and outcomes of opening the stenosed or occluded coronary artery and maintaining vessel patency. However, PCI-related injury leading to myonecrosis associated with stent-related side-branch flow impairment/occlusion or associated with atherosclerotic debris plugging the downstream coronary microcirculation as well as ischaemia/reperfusion injury associated with revascularization of occluded coronary vessels has not been fully emphasized. There is good clinical evidence to support the concept that all patients undergoing invasive revascularization have varying degrees of myocardial stunning, occasionally requiring inotropic support [18,19]. No data on the incidence of cardiogenic shock in relation to the use of new protective devices or therapy to reduce reperfusion injury and stunning are available.

The impact of abciximab therapy on the efficacy of myocardial reperfusion in patients with acute myocardial infarction (AMI) undergoing primary infarct-related artery (IRA) stenting remains uncertain. Completed randomised trials comparing infarct artery stenting alone with stenting plus abciximab have produced conflicting results [20,21]. A study by Kastrati et al. compared the extent of myocardial salvage in patients with acute MI treated with abciximab and coronary stenting or fibrinolysis. They showed a significant reduction in infarct size associated with coronary stenting [22]. The only study reporting on the incidence of cardiogenic shock showed a significant effect of stenting in combination with abciximab in reducing the subsequent development of cardiogenic shock compared to stenting alone [23].

Patients in cardiogenic shock had a highly significant increased max CKMB at baseline in our study. We also found a significantly longer time to treatment and increased max CKMB in the angioplasty patients in cardiogenic shock. When including these data into a multivariable analysis, the trend towards an increased incidence of cardiogenic shock in the invasive arm decreases, indicating that a longer time to treatment and perhaps therefore a larger infarction in patients treated with angioplasty may partly explain the trend towards a higher incidence of cardiogenic shock in the invasive arm.

4.3. Long-term follow-up
Cardiogenic shock remains the leading cause of death in patients hospitalised with myocardial infarction in the reperfusion era [16,24,25]. We found that 58% of the total mortality up to three years in the DANAMI-2 trial was due to cardiogenic shock. Babaev et al. showed an overall in-hospital mortality that decreased from 60.3% in 1995 to 47.9% in 2004 in the NRMI registry. This paralleled the increasing frequency of revascularization. Furthermore, the mortality rate decreased over time for patients who underwent primary angioplasty for cardiogenic shock. Multivariable analysis of in-hospital mortality adjusted for demographics, medical history, clinical presentation, hospital characteristics, year of discharge, and procedures demonstrated that primary angioplasty remained strongly independently associated with a lower in-hospital mortality rate [5].

In our study, no difference in short or long-term mortality was seen when comparing treatment strategies. There is limited data available on the association between the post-treatment development of cardiogenic shock and mortality in relation to treatment strategy [26]. When looking at NYHA classification after one year, we found a significantly higher proportion of patients with NYHA class 1 in the cardiogenic shock population randomised to angioplasty. These data confirm previous results from the SHOCK trial [6,27]. During the last few years the traditional pathophysiology of cardiogenic shock has been questioned. Data indicate that systemic inflammation might constitute part of the explanation, indicating that it may primarily be a universal inflammatory response and not only infarct size that predicts cardiogenic shock [28-30]. This could explain some of the unresolved questions in our present study.

Some limitations must be mentioned. A possible confounder in our analysis is the survival bias problem as some time is necessary for patients to develop and be diagnosed with cardiogenic shock. Thus patients who died very early might be included in the non-cardiogenic shock group simply because they did not live long enough to be diagnosed with cardiogenic shock. However, this would only diminish the difference in mortality between patients with and without cardiogenic shock. Also in our analysis of predictors of cardiogenic shock we cannot exclude a competing risk problem as any variable that increases survival indirectly increases the risk of cardiogenic shock. However, as mortality during the first three days was equally high in both subgroups we believe that both the survival bias problem and competing risk problem are likely to have very little influence on our results. Due to the number of events, the present substudy was not powered to show a difference in the incidence of cardiogenic shock with respect to treatment modality. With a cardiogenic shock incidence of 5.6% in the thrombolysis arm, the corresponding incidence in the PCI arm would need to have been 2.7% or 9.4% or more to detect a difference with 80% power and a two-sided significance level of 5%.

With regard to 30-day mortality, we would have had 90% power to detect a difference with a two-sided significance level of 5% if the absolute difference had been 8%. With an absolute difference of 5% we had a power of 54%. Finally, given the post-hoc nature of the study and the multiple comparisons, all results are hypothesis generating.

Our main finding in the present study is that angioplasty does not protect against in-hospital development of cardiogenic shock compared to fibrinolysis. In addition, we found that cardiogenic shock is still the leading cause of death in patients hospitalised for acute MI and that there was no difference in mortality, with regards to treatment strategy, when comparing patients who developed cardiogenic shock after the initial treatment. After one year a significantly higher proportion of patients in the cardiogenic shock population randomised to angioplasty were in NYHA class I compared to patients treated with fibrinolysis.


   Acknowledgements
 
This study was supported by grants from the Jørgen Møller Foundation.


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

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