Comparison of the GRACE, HEART and TIMI score to predict major adverse cardiac events in chest pain patients at the emergency department.

BACKGROUND: The performance of the GRACE, HEART and TIMI scores were compared in predicting the probability of major adverse cardiac events (MACE) in chest pain patients presenting at the emergency department (ED), in particular their ability to identify patients at low risk. METHODS: Chest pain patients presenting at the ED in nine Dutch hospitals were included. The primary outcome was MACE within 6weeks. The HEART score was determined by the treating physician at the ED. The GRACE and TIMI score were calculated based on prospectively collected data. Performance of the scores was compared by calculating AUC curves. Additionally, the number of low-risk patients identified by each score were compared at a fixed level of safety of at least 95% or 98% sensitivity. RESULTS: In total, 1748 patients were included. The AUC of GRACE, HEART, and TIMI were 0.73 (95% CI: 0.70-0.76%), 0.86 (95% CI: 0.84-0.88%) and 0.80 (95% CI: 0.78-0.83%), respectively (all differences in AUC highly statistically significant). At an absolute level of safety of at least 98% sensitivity, the GRACE score identified 231 patients as "low risk" in which 2.2% a MACE was missed; the HEART score identified 381 patients as "low risk" with 0.8% missed MACE. The TIMI score identified no "low risk" patients at this safety level. CONCLUSIONS: The HEART score outperformed the GRACE and TIMI scores in discriminating between those with and without MACE in chest pain patients, and identified the largest group of low-risk patients at the same level of safety.

Medical consumption compared for TIMI and HEART score in chest pain patients at the emergency department: a retrospective cost analysis.

OBJECTIVE: To investigate which risk score (TIMI score or HEART score) identifies the largest population of low-risk patients at the emergency department (ED). Furthermore, we retrospectively calculated the corresponding expected decrease in medical consumption if these patients would have been discharged from the ED. METHODS: We performed analyses in two hospitals of the multicentre prospective validation study of the HEART score, executed in 2008 and 2009. Patients with chest pain presenting to the ED were included and information was collected on major adverse cardiac events (MACEs) and on hospital admissions and diagnostic procedures within 6 weeks. The TIMI and HEART score were calculated for each patient. RESULTS: We analysed 640 patients (59% male, mean age of 60, cumulative incidence of MACE 17%). An estimated total of €763 468 was spent during follow-up on hospital admission and diagnostic procedures. In total, 256 (40%) patients had a HEART score of 0-3 and were considered low risk (miss rate 1.6%), a total of €64 107 was spent on diagnostic procedures and hospital admission after initial presentation in this group. In comparison, 105 (16%) patients with TIMI score of 0 were considered low risk (miss rate 0%), with a total of €14 670 spent on diagnostic procedures and initial hospital admission costs. With different cut-offs for low risk, HEART 0-2 (miss rate 0.7%), would have resulted in a total of €25 365 in savings, compared with €71 905 when an alternative low risk cut-off for TIMI of TIMI≤1 would be used (miss rate 3.0%). CONCLUSIONS: The HEART score identifies more patients as low risk compared with the TIMI score, which may lead to a larger reduction in diagnostic procedures and costs in this low-risk group. Future studies should prospectively investigate whether adhering to the HEART score in clinical practice and early discharge of low-risk patients is safe and leads to a reduction in medical consumption.

A prospective validation of the HEART score for chest pain patients at the emergency department.

BACKGROUND: The focus of the diagnostic process in chest pain patients at the emergency department is to identify both low and high risk patients for an acute coronary syndrome (ACS). The HEART score was designed to facilitate this process. This study is a prospective validation of the HEART score. METHODS: A total of 2440 unselected patients presented with chest pain at the cardiac emergency department of ten participating hospitals in The Netherlands. The HEART score was assessed as soon as the first lab results and ECG were obtained. Primary endpoint was the occurrence of major adverse cardiac events (MACE) within 6 weeks. Secondary endpoints were (i) the occurrence of AMI and death, (ii) ACS and (iii) the performance of a coronary angiogram. The performance of the HEART score was compared with the TIMI and GRACE scores. RESULTS: Low HEART scores (values 0-3) were calculated in 36.4% of the patients. MACE occurred in 1.7%. In patients with HEART scores 4-6, MACE was diagnosed in 16.6%. In patients with high HEART scores (values 7-10), MACE occurred in 50.1%. The c-statistic of the HEART score (0.83) is significantly higher than the c-statistic of TIMI (0.75)and GRACE (0.70) respectively (p<0.0001). CONCLUSION: The HEART score provides the clinician with a quick and reliable predictor of outcome, without computer-required calculating. Low HEART scores (0-3), exclude short-term MACE with >98% certainty. In these patients one might consider reserved policies. In patients with high HEART scores (7-10) the high risk of MACE may indicate more aggressive policies.

Consumption of diagnostic procedures and other cardiology care in chest pain patients after presentation at the emergency department.

OBJECTIVE: The HEART score serves risk stratification of chest pain patients at the emergency department (ED). Quicker and more solid decisions may be taken in these patients with application of this score. An analysis of medical consumption of 122 acute chest pain patients admitted before the introduction of this score may be indicative of possible savings. METHODS: Numbers of cardiology investigations and clinical admission days were counted. Charged cost of medicine was divided into three categories: ED, in-hospital, and outpatient clinic. RESULTS: The total cost of care was 469,631, with an average of 3849 per patient. Seventy-five percent of this cost was due to hospitalisation under the initial working diagnosis of acute coronary syndrome (ACS). This diagnosis was confirmed in only 29/122 (24 %) of the patients. The low-risk group (41 patients with HEART scores 0-3) included one patient with a previously scheduled CABG. In the remaining 40 patients, hospitalisation occurred in 12/40 (30 %) patients and 30/40 (75 %) patients visited the outpatient clinic. The total cost of medical care after presentation of these 40 patients was 37,641; there were no cases where a new diagnosis of coronary artery disease was made. When medical care in this subgroup is declared redundant, major savings on national medical care budgets could be made. CONCLUSION: If the HEART score were to be routinely applied, diagnostic pathways could be shortened and costs reduced, in particular in low-risk patients.

Risk scores for patients with chest pain: evaluation in the emergency department.

Chest pain is a common reason for presentation to the emergency department (ED). Absolute criteria for Acute Coronary Syndrome without ST elevation (NSTE-ACS) are lacking. An acute coronary syndrome (ACS) needs to be distinguished from a variety of other cardiac and non-cardiac diseases that may cause chest pain.For patients with confirmed ACS, several scoring methods can be applied in order to distinguish patients in the coronary care unit who may benefit most from therapies. The PURSUIT, TIMI, GRACE and FRISC risk scores are well validated with this respect. However, none of these risk scores has been used in the identification of an ACS in the emergency setting. The vast majority of patients with chest pain due to causes other than ACS were not evaluated in these trials. An evidence-based systematic stratification and policy for these patients does not currently exist.The more recently developed HEART score is specifically designed to stratify all chest pain patients in the ED. The HEART score was validated in a retrospective multicenter study and proved to be a strong predictor of event free survival on one hand and potentially life threatening cardiac events on the other hand. The HEART score facilitates risk stratification of chest pain patients in the ED.

Chest pain in the emergency room: value of the HEART score.

BACKGROUND: Chest pain is one of the most common causes of presentation to the emergency room. The diagnosis of non-ST-elevation acute coronary syndrome typically causes uncertainty. Classical considerations for risk stratification are History, ECG, Age, Risk factors and Troponin (HEART). Each can be scored with zero, one or two points, depending on the extent of the abnormality. The HEART score is the sum of these five considerations. Methods. Clinical data from 122 patients referred to the emergency room for chest pain were analysed. The predictive value of the HEART score for reaching an endpoint was evaluated in 120/122 patients. RESULTS: Twenty-nine patients reached one or more endpoints: an acute myocardial infarction was diagnosed in 16 patients, 20 underwent revascularisation and two died. The HEART score in the patients with and without an endpoint was 6.51+/-1.84 and 3.71+/-1.83 (p<0.0001) respectively. A HEART score of 0-3 points holds a risk of 2.5% for an endpoint and supports an immediate discharge. With a risk of 20.3%, a HEART score of 4-6 points implies admission for clinical observation. A HEART score >/=7points, with a risk of 72.7%, supports early invasive strategies. CONCLUSION: The HEART score facilitates accurate diagnostic and therapeutic choices. The HEART score is an easy, quick and reliable predictor of outcome in chest pain patients. (Neth Heart J 2008;16:191-6.).

Long term follow up after elective percutaneous coronary intervention for unprotected non-bifurcational left main stenosis: is it time to change the guidelines?

BACKGROUND: According to the American College of Cardiology/American Heart Association guidelines, percutaneous coronary intervention (PCI) for left main coronary artery (LMCA) stenosis is contraindicated and coronary artery bypass graft surgery (CABG) is preferred. However, PCI of the LMCA is performed under exceptional circumstances. OBJECTIVE: To analyse the data of patients who underwent PCI of the unprotected LMCA in St Antonius Hospital, Nieuwegein, Netherlands. RESULTS: In a database of 17 683 PCI procedures, 71 patients (0.4%) were found with non-bifurcational LMCA stenosis who underwent an elective PCI between 1991 and 2001. Ages ranged from 26.7-86.5 years. Severe concomitant disease was the most frequent argument in favour of PCI instead of CABG. PCI consisted of only balloon angioplasty in 23 cases (32.4%). A stent was used in 46 cases (64.4%). Average follow up was 43 months (range 0-121 months). One patient died one day after the procedure. The total one year survival rate was 98.6% (70/71). Seven patients died during the follow up period, mostly because of non-cardiac reasons. The annual mortality rate was 2.5%. Recurrent elective percutaneous transluminal coronary angioplasty for restenosis of the LMCA was performed in one patient (1.4%) six weeks after the initial procedure. CABG was required in 13 patients (18.3%) throughout the follow up period. CONCLUSION: These results suggest that at highly experienced centres, elective PCI of the non-bifurcational LMCA can be performed safely where the anatomy is suitable.

Predictive value of ventricular arrhythmias for patency of the infarct-related coronary artery after thrombolytic therapy.

In animal studies reperfusion of coronary arteries is commonly accompanied by ventricular arrhythmias. It is not certain, however, whether ventricular arrhythmias can be used as a reliable non-invasive marker of reperfusion in humans. Two-channel Holter recordings were obtained from the start of an intravenous infusion of streptokinase until coronary angiography (2.8 (2.7) hours (mean SD)) afterwards) in 57 patients with acute myocardial infarction of less than four hours who were generally not treated with antiarrhythmic drugs. Ventricular arrhythmias occurred in 21 (37%) of the 57 patients: accelerated idioventricular rhythm in 13 patients and non-sustained ventricular tachycardia in 15 patients. Seven patients had both accelerated idioventricular rhythm and non-sustained ventricular tachycardia. Coronary angiography showed a patent infarct-related vessel in 12 (92%) of the 13 patients with accelerated idioventricular rhythm (95% confidence interval 66 to 99%), in 22 (50%) of the 44 patients without accelerated idioventricular rhythm (95% CI 34 to 66%), in 11 (73%) of the 15 patients with non-sustained ventricular tachycardia (95% CI 45 to 92%), and in 23 (55%) (95% CI 39 to 71%) of the 42 patients who did not have non-sustained ventricular tachycardia. Seventeen (81%) of the 21 patients with accelerated idioventricular rhythm, or non-sustained ventricular tachycardia, or both, had a patent infarct-related vessel (95% CI 58 to 94%) as did 17 (47%) of the 36 patients with no ventricular arrhythmia (95% CI 29 to 65%). In patients with accelerated idioventricular rhythm after thrombolysis the infarct-related vessel is almost certain to be patent; but the infarct-related coronary artery can still be patent when no arrhythmia is seen.

The influence of coronary angiography and angioplasty on parameters of hemostasis and fibrinolysis.

The influence of invasive investigations on parameters of hemostasis and fibrinolysis is generally unknown, although this has consequences for the design of prospective studies on the association between those parameters and regression or progression of atherosclerosis. We therefore determined hemostatic and fibrinolytic factors in 12 patients who were admitted to the hospital for coronary angiography (CAG; n = 5) or percutaneous transluminal coronary angioplasty (PTCA; n = 7). Blood samples were drawn under basal circumstances on the day before, the day of and the day after CAG or PTCA. Significant changes occur in the concentrations of platelets and white blood cells, hematocrit (Ht), von Willebrand factor antigen (vWF:ag), antithrombin III-activity (AT III-ag), antithrombin III-antigen (AT III-ant), fibrinogen, plasminogen, alpha2-antiplasmin (alpha2-AP), histidine-rich glycoprotein (HRG), and plasminogen activator inhibitor (PAI)-activity. Mean values of beta-thromboglobulin, platelet factor 4, factor VIII:C, tissue-type plasminogen activator activity (t-PA act) and euglobulin clot lysis time (ECLT) do not differ significantly. After correction for Ht, no significant differences exist between the day before and the day of the procedure; but on the day after CAG and PTCA significant differences occur in white blood cells, factor VIII:C, AT III-ag, alpha2-AP and PAI-act. It is concluded that principally blood samples for investigations on fibrinolysis may be taken on the day before or the day of CAG or PTCA without a loss of quality, if the values are corrected for Ht. Samples taken on the day after the procedure are not useful for such purposes.

Plasmin inhibitors in the prevention of systemic effects during thrombolytic therapy: specific role of the plasminogen-binding form of alpha 2-antiplasmin.

To delineate the role of plasmin inhibitors, especially the two molecular forms of alpha 2-antiplasmin (that is, the plasminogen-binding and the nonplasminogen-binding forms), in the control of systemic effects during thrombolytic therapy, the consumption of plasmin inhibitors and the degree of fibrinogen breakdown were studied in 35 patients with acute myocardial infarction treated with recombinant tissue-type plasminogen activator (rt-PA) or streptokinase. At a low degree of plasminogen activation (in six patients treated with rt-PA), plasminogen-binding alpha 2-antiplasmin was consumed first. At a higher degree of plasminogen activation (in 20 patients), plasminogen-binding alpha 2-antiplasmin became exhausted (less than 20%) and other plasmin inhibitors (that is, nonplasminogen-binding alpha 2-antiplasmin and alpha 2-macroglobulin) were consumed. After extensive plasminogen activation (in nine patients treated with streptokinase), plasminogen-binding alpha 2-antiplasmin consumption was complete and nonplasminogen-binding alpha 2-antiplasmin and alpha 2-macroglobulin were consumed to about 30% to 50% of the pretreatment level. No significant C1-inactivator consumption occurred, even at extreme degrees of plasminogen activation. Fibrinogen breakdown as a marker for systemic effects correlated strongly with consumption of plasminogen-binding alpha 2-antiplasmin. Fibrinogen breakdown did occur, but only when the amount of plasminogen-binding alpha 2-antiplasmin was decreased to less than 20% of the pretreatment level. The other plasmin inhibitors could not prevent fibrinogen breakdown. These results were confirmed by in vitro studies. It is concluded that plasminogen-binding alpha 2-antiplasmin is the most important inhibitor of plasmin in the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

A double-blind randomized multicenter dose-ranging trial of intravenous streptokinase in acute myocardial infarction.

Intravenous streptokinase administration is now a widely applied therapy for patients in the early hours of acute myocardial infarction (AMI). The dosages used do not appear to be based on comparative clinical investigations. Therefore a double-blind randomized trial was carried out to establish the optimal dose of streptokinase. A total of 189 patients who had symptoms of AMI for less than 4 hours were treated with 200,000, 750,000, 1,500,000 or 3,000,000 IU streptokinase intravenously. At coronary angiography 2.8 +/- 2.7 hours (mean +/- standard deviation) after the start of streptokinase infusion, patency of the infarct-related coronary artery was observed in 38, 75, 60 and 82% of the patients, respectively, in the 4 groups. The result of the dosage of 200,000 IU was significantly poorer than that of the other dosages (p less than 0.01). The result of a dosage of 3,000,000 IU was significantly better than that of 1,500,000 IU (p less than 0.05), but the differences with 750,000 IU were not significant. Blood transfusion was required in 4 patients (2%), distributed over the 4 groups in 0, 2, 1 and 1 of the patients. One patient had major bleeding; this patient had been treated with 750,000 IU. The 3-month mortality-rate in the whole study population was 5%. Thus, of the 4 doses of streptokinase tested, 750,000 IU is the minimal therapeutic dosage, and the arguments for 1,500,000 IU as standard therapy for comparison with other fibrinolytic drugs are poor. The best results in this study were achieved with 3,000,000 IU, but further research will be needed to establish the efficacy and safety of this new regimen.

Activation of the fibrinolytic system during intracoronary streptokinase administration.

Serial biochemical studies were performed in 12 patients treated with intracoronary streptokinase infusion for acute myocardial infarction, in order to study the method of activation of the fibrinolytic system during local administration of a relatively low dose of this drug and to determine correlations between systemic effects and reperfusion. Plasma samples were obtained before and every 15 minutes during the infusion of streptokinase and after completion of the therapy. Streptokinase dosage in this study was 211,000 +/- 88,000 IU (+/- SD). The average time from the onset of symptoms to the start of infusion was 2 hours 50 minutes (range 1 hour 10 minutes to 3 hours 30 minutes). Reperfusion occurred in six patients and temporary recanalization in three; in three patients no recanalization was achieved. Fibrinolytic assays of pretreatment plasma samples revealed elevated levels of plasminogen activators, presumably caused by the release of tissue-type plasminogen activator after a condition of stress. Plasminogen concentrations decreased from 94 +/- 17% to 44 +/- 30%. Alpha 2-antiplasmin fell from 84 +/- 27% to 12 +/- 19%; in seven patients no plasmin inhibitor activity was measurable at the completion of the infusion. Free plasmin occurred in samples only when this inhibitor had disappeared. This resulted in a lytic state leading to degradation of fibrinogen, the levels of which fell from 2.9 +/- 0.7% to 1.5 +/- 1.1%. Fibrinogen degradation products, measured in plasma with monoclonal antibodies, increased exponentially during streptokinase infusion in at least four patients.(ABSTRACT TRUNCATED AT 250 WORDS)