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(Chest. 2000;117:1286-1290.)
© 2000 American College of Chest Physicians

Hemodynamic Classification in Acute Myocardial Infarction*

Has Anything Changed in the Last 3 Decades?

Eftychios Siniorakis, MD; Spyridon Arvanitakis, MD; Giannis Voyatzopoulos, MD; Petros Hatziandreou, MD; Giannis Plataris, MD; Athanasios Alexandris, MD and Petros Bonoris, MD

* From the Department of Cardiology, Coronary Care Unit, Elpis Municipal General Hospital, Athens, Greece.

Correspondence to: Eftychios Siniorakis, MD, Pallini Post Office, Box 67591, 15302 Athens, Greece


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Objective: Current mortality (M1) in hemodynamic subgroups of patients with acute myocardial infarction (AMI) was compared to that observed 30 years ago (M0), when hemodynamic classification was established. The prognostic value of oxyhemodynamic indexes in predicting M1 for patients receiving right heart catheterization (RHC) was investigated.

Patients and methods: We assigned 393 patients with AMI (mean age, 72 ± 10 years) to four Killip categories. A fiberoptic reflectance catheter was inserted in the pulmonary artery (PA) in 136 patients. Cardiac index (CI), PA wedge pressure (PWP), PA mixed venous blood oxygen saturation (SvO2), oxygen extraction ratio (O2ER), and normalized CI (NCI; CI/O2ER) were measured. Catheterized patients were classified into four Forrester groups, and M1 and M0 were compared. Survivors (group S) were compared to nonsurvivors (group NS), and the prognostic value of oxyhemodynamic parameters in predicting M1 was estimated.

Results: A significant decline in total mortality was observed (M1 of 8% vs M0 of 34%; p < 0.0001). In catheterized patients, total M1 was also decreased (M1 of 15% vs M0 of 26%; p < 0.05). Compared with group S, group NS had lower (mean ± SD) CI (1.8 ± 0.4 L/min/m2 vs 2.4 ± 0.6 L/min/m2; p < 0.01), SvO2 (46.1 ± 10.6% vs 59.9 ± 10.0%; p < 0.01), NCI (4.2 ± 1.4 vs 7.4 ± 4.1 L/min/m2; p < 0.01), and higher PWP (22.7 ± 6.8 mm Hg vs 14.4 ± 4.7 mm Hg; p < 0.01). NCI presented the best sensitivity (81%), specificity (78%), and predictive value (40%), in predicting M1.

Conclusions: The historical AMI hemodynamic classification has lost its semiquantitative value, since mortality has decreased. RHC does not compromise the outcome. NCI has a high prognostic value in predicting early mortality.

Key Words: acute myocardial infarction • cardiac index • Killip classification • oxyhemodynamics • right heart catheters • risk stratification


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
In 1967, Killip1 classified patients with acute myocardial infarction (AMI) into four subsets, depending on the clinical manifestations of cardiac failure on admission. In 1977, Forrester et al2 3 proposed the use of right heart catheterization (RHC) in AMI and classified patients into four invasive subsets based on cardiac index (CI) and pulmonary artery wedge pressure (PWP) values. Threshold values for PWP and CI were 18 mm Hg and 2.2 L/min/m2, heralding imminent pulmonary edema and cardiogenic shock, respectively.3 With both classifications, each subgroup demonstrated a concrete mortality rate, which increased with advancing cardiac failure.1 3 The term hemodynamic has been applied on the Killip and Forrester classifications somewhat arbitrarily. It should be used for the study of the motion of blood (Greek hema) through cardiac chambers and vessels, and the forces (Greek dynamis) developing. Killip’s classification aspires to predict the patients’ invasive status through clinical signs only. On the other hand, Forrester’s classification takes into account parameters such as the CI, which are not explained solely from the flow of blood. Despite their etymologic weakness, both classifications, invasive and noninvasive, are characterized today as hemodynamic. They became, and still remain very popular because they predicted the in-hospital mortality independently of the patient’s age, gender, precipitating factors, and AMI location.1 2 3 4 5

Since the first description of the hemodynamic classification, AMI management has changed dramatically, and mortality has decreased.6 7 Moreover, RHC has been optimized to estimate the satisfaction of the global tissue oxygen demand for a specific cardiac output.8 9 Despite this, it is remarkable that most major cardiology textbooks refer to the old mortality figures when describing hemodynamics in AMI, without specifying if these rates have actual or only historical value.10 11 The question was thus raised whether hemodynamic criteria of the past 3 decades still maintain both their qualitative and quantitative values. This prospective study was organized on the traces of the original Killip and Forrester observations, in order to check their credibility in time.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Three hundred ninety-three nonreperfused consecutive patients with AMI (male/female, 295/98; mean age, 72 ± 10 years; 58% anterior wall infarction) were enrolled between May 1996 and November 1997. Killip and Forrester methodology in recruitment of patients was reproduced as faithfully as possible, in order to ensure the comparability of data. Thus, patients receiving thrombolysis, coronary angioplasty, or bypass grafting were excluded. Only new Q wave AMI patients were recruited, depending on the presence of two of the following three criteria: (1) typical ischemic pain lasting > 15 min and unrelieved by nitrates; (2) evolutionary ST-T wave changes; and (3) elevation of both serum creatine kinase and glutamic oxaloacetic transaminase above the upper limits of normal. The reasons for not administering thrombolysis were as follows: active peptic ulcer (n = 99), hemorrhagic diabetic retinopathy (n = 21), chronic anticoagulant therapy (n = 42), laborious cardiopulmonary resuscitation (n = 14), persistent hypertension (n = 33), age > 80 years (n = 50), stroke within 3 months (n = 44), recent noncardiac operation (n = 12), and other (n = 24). Fifty-four patients with inferior AMI without involvement of other locations were not thrombolyzed. Pure inferior AMI are considered of good prognosis, and the benefit derived from thrombolysis, when weighted against the risk of stroke, is uncertain.12 13

Admission Killip class was determined as follows: Killip I, no heart failure; Killip II, S3 and/or basal lung crepitations; Killip III, acute pulmonary edema; and Killip IV, cardiogenic shock. Clinical assessment was performed by two authors, and in case of discordance, the opinion of a third doctor, blinded to the study, was sought.

One hundred thirty-six patients (male/female, 89/47; mean age, 74 ± 5 years) with suspected (systolic BP < 90 mm Hg, unexplained tachycardia, insufficient diuresis) or overt heart failure, not responding to empirical treatment, received RHC (35%) within the first 24 h (mean time, 6 ± 4 h after admission). Fiberoptic reflectance thermodilution catheters (Opticath; Abbott; North Chicago, IL) were used. These catheters, apart from measuring intracardiac pressures and CI, also measure the oxygen saturation of mixed venous blood (SvO2; normal value, 60 to 80%) in the pulmonary artery, and the oxygen extraction ratio (O2ER): the fraction of delivered oxygen that is actually consumed by tissue (oxygen consumption/delivered oxygen). A rise in O2ER is a compensatory mechanism employed when supply is inadequate for the level of metabolic activities.14 Tissue avid for oxygen elicits a high O2ER and a consequently low SvO2. A combination of a high O2ER and a low SvO2, if untreated, heralds an imminent cardiogenic shock regardless of CI values.15 In this study, CI, PWP, SvO2, and O2ER were measured after catheterization, with all patients in a steady hemodynamic state, breathing room air, prior to drastic pharmacologic manipulations. For each parameter, five measurements were taken, and the average value was considered as the indicative one. Values should not fluctuate by > 5%. RHC remained in situ for a maximum of 24 h to avoid complications.

Catheterized patients were classified into four hemodynamic subsets as described by Forrester et al3 : in the Forrester I group, patients had PWP < 18 mm Hg and CI >= 2.2 L/min/m2. Forrester II group had PWP >= 18 mm Hg and CI >= 2.2 L/min/m2. Forrester III group was comprised of patients with CI < 2.2 L/min/m2 and PWP < 18 mm Hg, whereas Forrester IV group patients had PWP >= 18 mm Hg and CI < 2.2 L/min/m2. A composite parameter, namely the normalized CI (NCI), the CI/O2ER, was calculated. It was hypothesized that NCI would confer more objectivity to classical CI by matching CI with global tissue oxygen consumption.

In previous observations (E. Siniorakis, MD; unpublished data; December 1995) from our institution, it was seen that in 18 catheterized AMI patients who died of heart failure, 15 had an NCI < 5 L/min/m2. Twelve of them had a normal CI.

As far as management was concerned, oxygen, nitrates, diuretics, and inotropic drugs were administered until an NCI value >= 5 L/min/m2 was obtained according to our previous observations. Two blood specimens were sent for cultures the day after the removal of the catheter, to rule out possible catheter-related bacteremias.

In-hospital stay lasted for 12 ± 4 days. Outcome was recorded for each individual. Deaths occurring in the emergency department were not considered as in-hospital. For each clinical or invasive subset, the actual mortality rate (M1) was compared with the historical mortality rate (M0) of the corresponding subset in Killip and Forrester studies, by using the {chi}2 test. Catheterized patients were classified into two groups: survivors (S) and nonsurvivors (NS). Student’s t test was used for the comparison of the two group hemodynamic parameters. Sensitivity, specificity, and predictive value (PV) of PWP, CI, SvO2, and NCI concerning in-hospital deaths were estimated for various cutoff values, with receiver operating characteristics curves.16 Mortality rates of catheterized patients for various cutoff values of the measured parameters were compared by the {chi}2 test. Multivariate logistic regression analysis was used to analyze data (SPSS Version 7.5; SPSS; Chicago, IL). Killip and Forrester classifications, as well as CI, PWP, SvO2, and NCI were used as independent variables. Survival was the binary dependent variable. A p value < 0.05 was considered as statistically significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Killip’s classification of patients, with their respective M1 and M0 values are shown in Table 1 . Forty-four percent of patients demonstrated some degree of cardiac failure (equal to or greater than Killup II) on admission. Total M1 was significantly lower than in Killip’s original study (mortality rate reduction by 76%; p < 0.0001). All deaths were of cardiac origin: pump failure (93%), arrhythmic deaths (7%). For each Killip subset, M1 was significantly lower than M0. The lowest M1 was observed in patients with no cardiac failure, whereas the highest M1 was in patients with cardiogenic shock. A class greater than Killip I presented sensitivity of 97%, specificity of 61%, and PV of 18% in predicting mortality.


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  		Table 1. M1 and M0 Values According to Killip’s Classification in Patients With AMI

 
Invasive classification of catheterized patients was as shown in Table 2 . Patients in Forrester I, II, and IV subgroups had similar mortality to the original Forrester groups. On the contrary, those belonging to Forrester III subgroup demonstrated a fall in mortality, thus reducing total mortality compared to 1977 figures. A class greater than Forrester I had sensitivity of 95%, specificity of 44%, and PV of 24% in predicting M1 in our study. No catheter complications were noted. Blood culture results were negative for all patients.


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  		Table 2. Invasive Classification and Mortality Rates in Catheterized Patients

 
Table 3 shows the correlation between Forrester and admission Killip classifications in catheterized patients. Clinical and hemodynamic status did not always coincide. In 57 of 136 patients (42%), the two classifications correlated precisely. A comparison of the proposed oxyhemodynamic classification with the clinical status and the Forrester classification is shown in Table 4 . For simplification, low-risk subgroups I and II are shown combined, in Killip and Forrester classifications. The same applies for high-risk subgroups III and IV. Concurrence of Killip I/II class with NCI >= 5 L/min/m2 and of Killip III/IV class with NCI < 5 L/min/m2 was observed in 111 of 136 patients (82%). NCI >= 5 L/min/m2 was associated with Forrester I/II and NCI < 5 L/min/m2 with Forrester III/IV, in 98 of 136 patients (72%).


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  		Table 3. Clinical and Hemodynamic Comparison (No. of Catheterized Patients)

 

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  		Table 4. Comparison Between Old Forrester, Clinical, and Proposed Oxyhemodynamic Classification (No. of Catheterized Patients)

 
In the subgroup of catheterized patients, 115 survived and 21 died. The measured hemodynamic parameters and their values (mean ± SD) in relation to the outcome appear in Table 5 . Group NS had lower CI, SvO2, and NCI, and higher PWP values in relation to group S. Sensitivity, specificity, and PV of invasive parameters in predicting M1 appears in Table 6 . CI and PWP had a high sensitivity but low specificity and PV in M1 prognosis. NCI at a cutoff value < 5 L/min/m2 presented equally high sensitivity with the other parameters in predicting M1, while its specificity and PV were the highest.


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  		Table 5. Comparison of Hemodynamic Parameters Between S and NS*

 

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  		Table 6. Prognostic Value of Hemodynamic Parameters in Predicting In-Hospital Mortality*

 
The most advantageous cutoff points for in-hospital survival are presented in Table 7 . There was a sevenfold increase in mortality among patients with a CI < 2.2 L/min/m2 compared to those with a CI >= 2.2 L/min/m2. Patients with a PWP >= 18 mm Hg had an in-hospital mortality three times higher than those with a PWP < 18 mm Hg. Patients with SvO2 < 60% or NCI < 5 L/min/m2 had a 10-fold increase in mortality compared to patients with SvO2 >= 60% and NCI >= 5 L/min/m2.


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  		Table 7. Invasive Parameters and Mortality Rates at Cutoff Values

 
Multivariate analysis showed that only NCI (p < 0.001), followed by CI (p < 0.01), were powerful independent variables in predicting the outcome.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Mortality trends listed in the original Killip study1 are still qualitatively accurate, but quantitative estimates are grossly inflated compared with what would be observed in contemporary coronary care unit patients receiving the benefits of 3 decades of advances in coronary care medicine. Mortality has decreased for each Killip subgroup, and we believe that new figures should be incorporated into texts reciting only the historical rates.10 11

Catheterized patients retain a constant mortality rate throughout time, except subgroup Forrester III, where a significant reduction in mortality was noted. We can only speculate about this stability of the mortality rate of Forrester subgroups and the apparent failure of RHC to reduce mortality by focusing on the cause of deaths in our study. Two of three deaths in Forrester I and II groups were arrhythmogenic (ventricular fibrillation) and occurred 3 to 5 days after catheter withdrawal. Forrester’s classification cannot yield useful information concerning arrhythmogenic deaths. Deaths unrelated to heart failure cannot be prevented by using exclusively invasive data. On the other hand, Forrester IV patients were in a critical condition, as 71% of them were in cardiogenic shock with pulmonary edema, resistant to empirical therapy. It is known that mortality in this subgroup ranges from 65 to 85%, despite the progress in modern medicine.17

Forrester III subgroup demonstrated a significant drop in mortality. These patients were found during catheterization to have a low CI, and a low PWP, which allowed a careful titration of fluid loading until an appropriate preload was achieved. The fact that these patients did not need inotropes and vasoactive drugs suggests a lesser degree of heart failure, resulting in lower mortality.

There have been recent reports18 19 on patients who underwent RHC, noting excessive mortality rates, much higher than in the original Forrester study. The suspicion was raised that these fatalities were due to catheter-related complications and overtreatment. Cautious use of RHC from skillful personnel should be beneficial for critically ill patients.20 21 22 Catheter-related complications were not observed in our study, perhaps due to the short period RHC remained in situ. Concerning the hypothesis of overtreatment, we believe that estimating NCI in conjunction with the other classic hemodynamic parameters, we avoided the use of potentially toxic drugs, such as inotropes, in patients who did not really need them. In the present study, patients presenting an apparently low CI after correction of PWP, and an NCI >= 5 L/min/m2 with a good clinical status were closely monitored, while inotropic support was withheld.

A classic hemodynamic parameter, PWP, did not confirm its prognostic value in this study. Similarly, CI, despite its significant correlation with survival emerging from multivariate analysis, demonstrated low specificity in predicting mortality.

NCI was shown to be the independent variable best predicting outcome. We believe that NCI opens a new perspective in evaluating hemodynamic findings by normalizing CI with respect to global tissue oxygen consumption.

A numerically low CI may be adequate for tissue demands, whereas an apparently normal CI may not guarantee fulfillment of global tissue needs. In our study, patients with NCI >= 5 L/min/m2 were unlikely to develop signs of low perfusion, irrespective of CI values. Similarly, patients with NCI < 5 L/min/m2 were prone to develop cardiogenic shock, even though initial values of CI were apparently normal.

Remarkable disparity between clinical and classical hemodynamic findings was noted in this study. This discrepancy had also been observed by Forrester et al2 and was then attributed to a phase lag between clinical and hemodynamic evaluation, administration of drugs, and the occurrence of various compensatory mechanisms, which allowed an apparently good clinical picture despite an unfavorable hemodynamic status. Although the above may be true, we believe that the main reason for this discrepancy is an intrinsic weakness of CI, and this was overcome in the present study by "normalizing" CI. After reclassifying patients based on NCI and comparing the new oxyhemodynamic status with the clinical one, a substantial concurrence was achieved.

Concluding, we would like to refer again to the title of this study. Has anything changed in the hemodynamics of AMI the last 30 years? We believe the answer is yes. Neither Killip nor Forrester classifications are independent predictors of outcome. Historical Killip mortality rates appear to be exaggerated today. Current texts are out of date by quoting historical figures. Despite suggestions to the contrary, mortality in AMI patients receiving RHC was not increased, and in certain subgroups, it dropped drastically. Maybe the time has come for the adoption of official guidelines on the use of newer RHC-incorporating oxyhemodynamics in AMI. So far, there has not been a systematic comparison of those newer catheters to the usual catheters.23

The classic CI has room for improvement on its prognostic value and therapeutic implications. NCI constitutes an attempt toward achieving this goal.


   Footnotes
 
Abbreviations: AMI = acute myocardial infarction; CI = cardiac index; M0 = historical mortality rate; M1 = actual mortality rate; NCI = normalized CI; NS = nonsurvivors; O2ER = oxygen extraction ratio; PV = predictive value; PWP = pulmonary artery wedge pressure; RHC = right heart catheterization; S = survivors; SvO2 = oxygen saturation of mixed venous blood

Received for publication November 17, 1999. Accepted for publication November 29, 1999.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Killip, T, Kimball, J (1967) Treatment of myocardial infarction in a coronary care unit: a two year experience with 250 patients. Am J Cardiol 20,457-465[CrossRef][ISI][Medline]
  2. Forrester, J, Diamond, G, Chatterjee, K, et al (1976) Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts). N Engl J Med 295,1356-1362[ISI][Medline]
  3. Forrester, J, Diamond, G, Swan, H (1977) Correlative classification of clinical and hemodynamic function after acute myocardial infarction. Am J Cardiol 39,137-145[CrossRef][ISI][Medline]
  4. . The Multicentre Postinfarction Research Group. (1983) Risk stratification and survival after myocardial infarction. N Engl J Med 309,331-336[Abstract]
  5. Sahasakul, Y, Chaithiraphan, S, Panchavinnin, P, et al (1990) Multivariate analysis in the prediction of death in hospital after myocardial infarction. Br Heart J 64,182-185[Abstract/Free Full Text]
  6. Ferrieres, J, Cambon, JP, Ruidavets, JB, et al (1995) Trends in acute myocardial infarction prognosis and treatment in southwestern France between 1985 and 1990 (the Monica Project-Toulouse). Am J Cardiol 75,1202-1205[CrossRef][ISI][Medline]
  7. Widdershoven, J, Gorgels, A, Vermeer, F, et al (1997) Changing characteristics and in-hospital outcome in patients admitted with acute myocardial infarction: observations from 1982 to 1994. Eur Heart J 18,1073-1080[Abstract/Free Full Text]
  8. Krouskop, R, Cabatu, E, Chelliah, B, et al (1983) Accuracy and clinical utility of an oxygen saturation catheter. Crit Care Med 11,744-749[ISI][Medline]
  9. Gore, J, Sloan, K (1984) Use of continuous monitoring of mixed venous saturation in the coronary care unit. Chest 86,757-761[Abstract/Free Full Text]
  10. Pasternak, R, Braunwald, E, Sobel, B (1992) Acute myocardial infarction. Braunwald, E eds. Heart disease: a textbook of cardiovascular medicine ,1249-1251 W.B. Saunders Philadelphia, PA.
  11. Antman, E (1995) General hospital management. Julian, D Braunwald, E eds. Management of acute myocardial infarction ,39-43 W.B. Saunders London, UK.
  12. Gruppo Italiano per lo Studio della Streptochinasi nell’ Infarto Miocardico (GISSI). Lancet 1986; 1:397–401
  13. . Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group (1994) Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results of all randomized trials of more than 1000 patients. Lancet 343,311-322[CrossRef][ISI][Medline]
  14. Bryan-Brown, C, Gutierrez, G (1989) Gas transport and delivery. Shoemaker, W Ayres, S Grenvik, Aet al eds. Textbook of critical care ,491-496 W.B. Saunders Philadelphia, PA.
  15. Vincent, J (1990) The relationship between oxygen demand, oxygen uptake, and oxygen supply. Intensive Care Med 16(suppl2),145-148
  16. McNeil, B, Keeler, E, Adelstein, J (1975) Primer on certain elements of medical decision making. N Engl J Med 293,211-215[Abstract]
  17. Goldberg, R, Gore, J, Alpert, J, et al (1991) Cardiogenic shock after acute myocardial infarction: incidence and mortality from a community-wide perspective, 1975 to 1988. N Engl J Med 325,1117-1122[Abstract]
  18. Gore, J, Goldberg, R, Spodick, D, et al (1987) A community-wide assessment of the use of pulmonary artery catheters in patients with acute myocardial infarction. Chest 92,721-727[Abstract/Free Full Text]
  19. Zion, M, Balkin, J, Rosenmann, D, et al (1990) Use of pulmonary artery catheters in patients with acute myocardial infarction: analysis of experience in 5841 patients in the SPRINT Registry. Chest 98,1331-1335[Abstract/Free Full Text]
  20. Clinical competence in hemodynamic monitoring: a statement for physicians from the ACP/ACC/AHA task force on clinical privileges in cardiology. J Am Coll Cardiol 1990; 15:1460–1464
  21. . Coalition For Critical Care Excellence. (1995) Consensus Conference on Physiologic Monitoring Devices. Standards of evidence for the safety and effectiveness of critical care monitoring devices and related interventions. Crit Care Med 23,1756-1763[CrossRef][ISI][Medline]
  22. Ryan, T, Anderson, J, Antman, E, et al (1996) ACC/AHA guidelines for the management of patients with acute myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice. J Am Coll Cardiol 28,1328-1428[CrossRef][ISI][Medline]
  23. Mueller, H, Chatterjee, K, Davis, K, et al (1998) Present use of bedside right heart catheterization in patients with cardiac disease. J Am Coll Cardiol 32,840-864[Free Full Text]



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