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J Am Coll Cardiol, 2000; 36:1084-1090
© 2000 by the American College of Cardiology Foundation
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CLINICAL STUDY

Implications of the timing of onset of cardiogenic shock after acute myocardial infarction: a report from the SHOCK Trial Registry

John G. Webb, MD, FACCa, Lynn A. Sleeper, ScD{dagger}, Christopher E. Buller, MD, FACC{ddagger}, Jean Boland, MD§, Angela Palazzo, MD||, Elizabeth Buller, RNa, Harvey D. White, DSc, Judith S. Hochman, MD, FACC|| for the SHOCK Investigators

a St. Paul’s Hospital, Vancouver, British Columbia, Canada
{dagger} New England Research Institutes, Watertown, Massachusetts, USA
{ddagger} Vancouver General Hospital, Vancouver, British Columbia, Canada
§ CHR Citadelle, Liège, Belgium
|| St. Luke’s–Roosevelt Hospital Center, New York, New York, USA
Green Lane Hospital, Auckland, New Zealand

Manuscript received February 16, 2000; revised manuscript received June 2, 2000, accepted June 7, 2000.

Reprint requests and correspondence: Dr. John Webb, St. Paul’s Hospital, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6
webb{at}providencehealth.bc.ca


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES

We sought to examine the implications of the timing of onset of cardiogenic shock (CS) after acute myocardial infarction (MI).

BACKGROUND

Little information is available about the relationships between timing, clinical substrate, management and outcomes of shock.

METHODS

The multinational SHOCK Trial Registry enrolled MI patients with CS from 1993 to 1997. Cardiogenic shock was predominantly attributable to left ventricular (LV) failure in 815 Registry patients for whom temporal data were available. We examined factors related to the timing of shock onset and the relation of temporal onset to in-hospital outcomes.

RESULTS

Overall, shock developed a median of 6.2 h after MI symptom onset. Shock onset varied by culprit artery: left main, median 1.7 h; right, 3.5 h; circumflex, 3.9 h; left anterior descending (LAD), 11.0 h; saphenous vein graft, 10.9 h (p = 0.025). Early shock (<24 h) occurred in 74.1% and was associated with chest pain at shock onset, ST-segment elevation in two or more leads, multiple infarct locations, inferior MI, left main disease and smoking. Late shock (≥24 h) was associated with recurrent ischemia, Q waves in two or more leads and LAD culprit vessel. Mortality was higher in patients with early versus late shock (62.6% vs. 53.6%, p = 0.022).

CONCLUSIONS

Shock onset after acute MI occurred within 24 h in 74% of the patients with predominant LV failure. Mortality was slightly higher in patients developing shock early rather than later. Many factors influence when shock develops, which has implications for its management.

Abbreviations and Acronyms
  AMI = acute myocardial infarction
  CS = cardiogenic shock
  CK-MB = creatine kinase (-MB fraction)
  ECG = electrocardiogram, electrocardiographic
  LAD = left anterior descending (artery)
  LV = left ventricular, left ventricle
  PTCA = percutaneous transluminal coronary angioplasty
  RV = right ventricular, right ventricle
  SHOCK = SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?

Cardiogenic shock (CS) is the major cause of mortality among patients hospitalized for acute myocardial infarction (AMI) (1–4). Yet, most patients who develop shock are not in shock when they first arrive at the hospital (1–3). Little information is available with respect to the timing of shock onset, and less is available about the relationships between timing, clinical substrate, management and outcome. What data are available are based on highly selected cohorts of shock patients (3,5).

The SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) Trial Registry was a prospective, multicenter registry of patients with known or suspected CS complicating AMI. Using this Registry, we sought to describe the temporal and clinical patterns of shock onset due to predominant left ventricular (LV) failure in a large and relatively unselected population.


   Methods
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 Abstract
 Methods
Results
 Discussion
 References
 
Patient sample.   Thirty-six multinational centers prospectively enrolled patients with suspected CS complicating AMI into the SHOCK Trial Registry and the SHOCK Trial from 1993 to 1997 and from 1993 to 1998, respectively (6). Of the 1,190 patients enrolled in the Registry, 306 patients were excluded because shock was attributable to mechanical causes, clinically diagnosed "isolated" right ventricular (RV) infarction or factors other than predominant LV failure. A total of 884 patients (74%) were classified with CS due to predominant LV failure, 69 of whom were excluded from analysis because of inadequate information about the timing of MI or shock onset. Data were thus available on 815 patients with post-MI CS primarily due to LV failure. This cohort constitutes the basis of this report. Results from the 302 patients in the concurrent randomized SHOCK Trial are reported for comparison.

Data collection.   Coordinators prospectively identified patients who had a clinical diagnosis of suspected CS complicating MI. Local discharge diagnoses of AMI and of CS (DRGs 410 combined with 785.51) constituted criteria for being registered. Patients randomized in the SHOCK Trial were excluded from the Registry (6,7). Data were abstracted from the medical record by study coordinators who were centrally trained to complete standard report forms. Right-heart catheterization was performed in 523 patients, the pulmonary capillary wedge was recorded in 490, and the cardiac index in 441. Left ventricular ejection fraction was measured during hospitalization in 311 patients by LV angiography (37%), by echocardiogram (59%) or by gated blood-pool scan (5%). The following variables were on revised data forms and were available for a maximum of 583 patients: ejection fraction, pulmonary-artery and RV pressures, chest pain at shock onset, history of elevated lipids, peripheral vascular disease, inotropic agent usage, and re-infarction/recurrent ischemia.

Definitions.   Three temporal groups were identified. Early shock was defined as shock developing <24 h after MI onset. Late shock was defined as shock developing ≥24 h after MI onset. A third group with very early shock was identified, consisting of patients who developed shock <6 h after MI onset. The early (<24 h) versus late (≥24 h) groups were compared.

Predominant LV failure was considered to be the cause of CS in the absence of isolated RV infarction, acute severe mitral regurgitation, ventricular rupture, tamponade, severe valvular disease, excess beta or calcium-channel blockade or shock resulting from a complication of cardiac catheterization. Re-infarction was defined as: 1) recurrent chest pain or ischemic symptoms for ≥30 min with recurrent ST-segment elevation, new Q waves, or new left bundle branch block; 2) a total creatine kinase (CK) at least twice the upper limit of normal and ≥25% or 200 U/mL over the previous value, with an elevated CK-MB; or 3) increase in CK-MB to above the upper limit of normal after a reversion to normal. Recurrent ischemia was defined as rest angina or ischemic symptoms for ≥5 min with ST-segment depression, T-wave inversion, or both, without cardiac enzyme elevation.

Statistical analysis.   Comparisons of the early and late shock groups were conducted using the Fisher exact test for unordered categorical variables, the Mantel-Haenszel test for linear trend for ordered categorical variables (8), the Wilcoxon rank-sum test for ordinal or non-normally distributed variables, and the Student t-test for all other continuous variables. Logistic regression was used to determine whether early (vs. late) shock was an independent predictor of mortality, adjusted for differences in patient and treatment characteristics. All variables with a univariate p value <0.20 for early versus late shock were considered, except for the use of inotropic agents and right heart catheterization measurements (because of incomplete data). Results with a p value <0.05 were considered statistically significant. Analyses were conducted using Statistical Analysis, version 6.12 (SAS Institute; Cary, North Carolina).


   Results
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 Abstract
 Methods
 Results
Discussion
 References
 
Timing of shock onset.   Most patients presented to the hospital early after the onset of MI. The median delay from MI symptom onset to hospital admission was 1.25 h (25th and 75th percentiles, 0.17 h and 4.17 h, respectively) and from admission to shock onset, 4.6 h (25th and 75th percentiles, 0.2 h and 28.4 h, respectively). The median time from MI symptom onset to shock onset was 6.2 h (25th and 75th percentiles, 1.7 h and 20.1 h, respectively) in the Registry; similar to the 5.5 h (25th and 75th percentiles, 2.3 h and 14.1 h, respectively) in the randomized SHOCK Trial (p = 0.103) (9). Very early shock (shock onset <6 h after MI onset) was identified in 46.6% of Registry patients, early shock (onset <24 h) in 74.1% and late shock (onset ≥24 h) in 25.9%. Shock was diagnosed at presentation in 9% of the Registry patients and 14% of the Trial patients (9).

Relationship between clinical characteristics and the timing of shock onset.   The demographic, historical, clinical, hemodynamic and MI management characteristics of the temporal groups were similar (Tables 1–3). Early shock was more often associated with chest pain at shock onset, ST-segment elevation in two or more leads, multiple locations of MI (by electrocardiogram [ECG]), inferior MI, smoking, mechanical ventilation, hypotension, coronary angiography and percutaneous transluminal coronary angioplasty (PTCA) after shock onset, and in-hospital death. Late shock (≥24 h) was more often associated with recurrent ischemia, the presence of new Q waves in two or more leads, the use of inotropic agents and transfer to a tertiary care center.


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  		Table 1 Baseline Characteristics and Timing of Shock Due to Predominant LV Failure

 

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  		Table 2 Myocardial Infarction Characteristics and Timing of Onset of Shock Due to Predominant LV Failure

 

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  		Table 3 Clinical Characteristics and Timing of Onset of Shock Caused by Predominant Left Ventricular Failure

 
Recurrent ischemia.   Chest pain was reported in 83.8% of all patients and occurred at shock onset in 55.9% (Table 3). Chest pain at the time of shock onset was more common with early shock than with late shock (62.3% vs. 35.9%, p < 0.0001). Recurrent ischemia after the initial MI and before shock onset was more common in the late shock group (38% vs. 13.2%, p < 0.0001). Re-infarction after the initial MI and before shock onset was diagnosed in 8.3% of patients, with no difference between temporal groups.

Angiographic findings.   Coronary angiographic data are presented in Table 4. Most patients had multivessel disease (78%). Shock developed earlier after MI with left main diameter stenosis ≥50% (median 5.9 h), single-vessel disease (5.5 h), or double-vessel disease (4.6 h), compared with triple-vessel disease (7.8 h), but these differences were not significant. The distributions of the number of diseased vessels did not differ significantly between the early- and late-shock groups. Although the left anterior descending (LAD) artery was the most common culprit vessel for both groups for patients, late shock patients were even more likely to have the LAD artery as the culprit (56%) than early shock patients (40.6%), while the right coronary artery was more often the culprit in early shock patients (30.3%), compared with late shock patients (20%, p = 0.025). The median time to shock onset was shortest when the culprit artery was the left main (1.7 h), shorter in the case of the right coronary (3.5 h) or circumflex (3.9 h) and longest in the case of the LAD (11 h) and saphenous vein grafts (10.9 h). Over two thirds of the patients in both groups had Thrombolysis In Myocardial Infarction flow grade 0/1 in the culprit artery; vessel patency was not associated with timing of shock (p = 0.699).


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  		Table 4 Angiographic Characteristics and Timing of Onset of Shock Due to Predominant LV Failure

 
Revascularization and mortality.   Overall in-hospital mortality was 60.3% (Table 5). Mortality was significantly higher in patients with early shock versus late shock (62.6% vs. 53.6%, p = 0.022). This higher mortality with early shock was most evident in the 58% of patients admitted directly to a SHOCK Registry hospital (mortality 69.6% vs. 58.8%, p = 0.043). Although the interaction of shock timing and transfer status was not significant (p = 0.288), a survival advantage for late shock patients was not evident in the 41% of patients selected for and surviving transfer to a SHOCK Registry hospital (51.7% for early shock vs. 48.6% for late shock, p = 0.644). The in-hospital mortality rates for patients with shock at presentation in the Registry and Trial were similar (64.3% vs. 74.8%, p = 0.178) (9).


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  		Table 5 Revascularization and In-hospital Mortality in Relation to Timing of Shock Onset

 
Multivariate analysis was conducted to determine whether timing of shock was an independent predictor of mortality after adjustment for patient and treatment factors associated with shock timing (transfer status, systolic blood pressure, revascularization and ventilator use). This analysis did not support a relationship between timing of shock post-MI and mortality (late vs. early shock odds ratio for death = 0.86, 95% confidence interval, 0.59–1.25; p = 0.430).


   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
The timing of shock.   According to retrospective studies (2,5,6), from 1% of 5% of patients with AMI arrive at the hospital in CS, while another 5% to 7% develop shock during hospitalization. Our large, prospective, multicenter study confirms that a small minority of patients (9%) were in shock at arrival, while the majority developed shock after presentation. Nevertheless, about half of our patients (46.6%) who developed CS did so within 6 h of infarct onset. This raises speculation that the diagnosis of severe pump failure or pre-shock may be missed at presentation or that early therapy, including use of agents that may induce hypotension, may cause iatrogenic shock in marginally compensated patients (10). By 24 h, almost three quarters (74.1%) of those who would eventually develop shock had done so. By implication, then, there is often a therapeutic window that could allow for intervention either before CS develops or early in its course. The median time from hospital admission to shock onset was only 4.6 h, however, indicating that the window is relatively narrow for many patients.

Early shock.   It is intuitive to suspect that shock might occur early after MI due to occlusion of a major coronary artery and very extensive myocardial damage. Not surprisingly, early shock was more often associated with ST-segment elevation in multiple leads and with multiple ECG infarct locations. The LAD coronary artery was the most common culprit vessel regardless of the time of shock onset. Nevertheless, patients in whom the right coronary artery was the culprit, or who had inferior MI on clinical grounds, were relatively more likely to develop shock early. Mortality in these patients may be reduced with aggressive medical support and reperfusion strategies (11–13). Although patients clinically diagnosed with "isolated" RV MI were excluded from analysis, RV involvement may have been a significant factor in many patients thought to suffer primarily from LV involvement. Excessive vagal tone may play a role in this setting by limiting the compensatory tachycardia, inotropy and vasoconstriction otherwise associated with myocardial dysfunction (11,12).

Late shock.   More than 25% of patients who developed shock did so relatively late (≥24 h) after MI. With a median delay of 51 h after MI onset in this group, the implications for etiology and treatment may differ from those for patients developing shock early (16). Several factors may favor the delayed appearance of shock. Infarct expansion may progressively reduce mechanical efficiency, particularly after large anterior MIs (3,13). This relationship may underlie the frequent association between a culprit LAD artery, multiple new Q waves and late shock.

Infarct extension may follow thrombotic reocclusion of a temporarily patent infarct artery, propagation of intracoronary thrombus, occlusion of a remote artery, reduced coronary perfusion pressure or increased myocardial oxygen demand. Shock patients are more likely to have persistently elevated cardiac enzymes, myocardium in varying stages of necrosis and clinical re-infarction, suggesting an important role for ongoing or recurrent ischemia (3,4). The greater incidence of recurrent ischemia in patients with late shock suggests that measures that reduce recurrent ischemia also may reduce the incidence of late shock.

In patients with multivessel disease, reduced systemic arterial pressure may exacerbate ischemia that is remote from the infarct region and compromise non–infarct zone myocardial function (3,15). Metabolic derangements may impair the contractility of non-infarcted myocardium (3,14). Although most shock patients undergoing angiography had an identifiable culprit artery (possibly amenable to thrombolysis or PTCA), most also had multivessel disease (77.5%), suggesting that more complete revascularization (13,15) with multivessel PTCA or bypass surgery might be desirable in the setting of late shock.

Mortality and timing of shock.   Regardless of the time of shock onset, mortality remains high. In-hospital mortality was higher in patients presenting with early shock (<24 h) versus late shock (≥24 h) (62.6% vs. 53.6%). Almost half of the patients admitted to SHOCK tertiary-care hospitals were transferred from other institutions, and their mortality was lower than that of patients admitted directly to tertiary hospitals. This may reflect a selection bias, considering that late shock patients had a higher transfer rate than early shock patients: patients with a higher risk of early mortality are excluded from the transferred cohort, and the patients most likely to benefit from aggressive management may be selected for transfer. The similar outcome seen with early and late shock in transferred patients may reflect this selection process. Among relatively unselected patients (those admitted directly to a SHOCK Trial Registry hospital), a worse outcome with early shock was particularly evident (mortality 69.6% vs. 58.8%). This relationship was supported by multivariate analysis.

Reperfusion therapy in shock.   Reperfusion therapy can improve outcome in CS (3,9,13,16–21). Unfortunately, thrombolysis results in relatively low rates of reperfusion in patients in whom shock is already established (22,23). The randomized SHOCK Trial found a significant reduction in six-month mortality with revascularization, with a 20.1% absolute reduction in six-month mortality in patients age <75 years (9). The likelihood of sustained reperfusion is higher with PTCA and may be improved further when combined with stenting, intra-aortic balloon pumping and newer antiplatelet regimens (13,21,26). It seems reasonable to expect that early reperfusion would be the most beneficial (13,25), but even late reperfusion may be desirable (3, 11–13,18–20,26–32). Although this is speculative, reperfusion therapy with thrombolysis or PTCA may be particularly desirable in patients with early shock, which more often may reflect occlusion of a single major coronary artery and ongoing infarction.

Study limitations.   Information is lacking with regard to patients who die before they can be admitted to a hospital or who are not selected for transfer from referral hospitals.

Conclusions.   Most patients who develop CS do so relatively early after MI. Shock developed within 6 h in about 50%, and within 24 h in 75%, of those who eventually developed shock during hospitalization. Mortality is slightly higher in patients with early shock. A therapeutic window is often present, allowing for intervention before CS develops or early during its course. Many factors appear to influence the timing of shock onset, which probably has implications for its management. 24


   Footnotes
 
Supported by RO1 grants HL50020 and HL49970, 1994–1999, from the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland.


   References
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 Abstract
 Methods
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 Discussion
 References
 

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