Version May 2024
INTRODUCTION — Patients with ST-elevation myocardial infarction (STEMI) should undergo risk stratification soon after presentation. This process has two components:
●Early in-hospital identification of patients at increased risk for recurrent ischemic events.
●Identification of patients after a myocardial infarction (MI) who are at increased risk for arrhythmic or nonarrhythmic death.
The individual risk factors that influence prognosis will be discussed here. The use of these risk factors in risk prediction models and the prognosis of patients after MI are discussed separately. (See "Risk stratification after acute ST-elevation myocardial infarction", section on 'Early risk stratification' and "Prognosis after myocardial infarction".)
Although there is significant overlap in the risk factors for acute non-ST-elevation coronary syndrome (NSTEACS) and STEMI, they are presented separately, in part because the risk prediction models for STEMI and NSTEACS differ in their components. (See "Risk factors for adverse outcomes after non-ST elevation acute coronary syndromes".)
FACTORS PRESENT BEFORE MI
Number of CHD risk factors — The four modifiable coronary heart disease (CHD) risk factors (hypertension, smoking, dyslipidemia, and diabetes), as well as a family history of premature CHD, predict the development of atherosclerosis and its clinical consequences (including STEMI) in a high percentage of patients. (See "Overview of established risk factors for cardiovascular disease", section on 'Established risk factors for atherosclerotic CVD'.)
The relationship between the number of these risk factors and in-hospital mortality was evaluated in a study of 542,008 patients with first MI and without prior cardiovascular disease from the National (United States) Registry of Myocardial Infarction (NRMI) [1]. Over 85 percent of patients had at least one CHD risk factor. After adjustment for age and other clinical risk factors, there was a statistically significant inverse increase in risk between the number of CHD risk factors and in-hospital mortality (odds ratios of 1.54, 1.39, 1.30, 1.10, 1.09, and 1.00 with 0, 1, 2, 3, 4, and 5 risk factors, respectively). The explanation for this surprising finding is unknown. Patients who continue to smoke after an MI are at particularly high risk for recurrent MI and/or death.
Chronic kidney disease — Patients with chronic renal failure as well as those with end-stage kidney disease have a higher risk for and a worse outcome after MI. (See "Chronic kidney disease and coronary heart disease" and "Risk factors and epidemiology of coronary heart disease in end-stage kidney disease (dialysis)".)
The magnitude of this effect has been examined in several studies [2-5]:
●In a review of over 130,000 older adults hospitalized with an acute MI, the one-year mortality was 24, 46, and 66 percent in patients with a serum creatinine of <1.5, 1.5 to 2.4, and 2.5 to 3.9 mg/dL (<132, 132 to 212, and 221 to 345 micromol/L), respectively [2]. After adjustment for patient and treatment characteristics, the hazard ratios for mild and moderate renal insufficiency were greatest at one month and gradually declined, no longer being significant at one year.
●Similar observations were made in an analysis from the VALIANT trial of 14,527 patients with an acute MI (two-thirds with STEMI) complicated by heart failure (HF), left ventricular (LV) dysfunction, or both [3]. At three years, the mortality rates for patients with an estimated glomerular filtration rate (GFR) of ≥75, 60 to 74.9, 45 to 59.9, and <45 mL/min per 1.73 m2 were 14.1, 20.5, 28.9, and 45.5 percent. After adjustment for other risk factors, the risk of death or nonfatal cardiovascular complications increased significantly with declining GFR (hazard ratio 1.10 for each 10-unit decrease in GFR below 81.0 mL/min per 1.73 m2).
A potential limitation of these studies is that only baseline serum creatine values were used. This can be a source of error because the formulas used for calculation of the creatinine clearance and the estimated GFR require stable values over time, which might not be present in patients with an acute coronary syndrome. (See "Assessment of kidney function".)
Peripheral artery disease — The presence of intermittent claudication appears to predict worse outcomes in patients with an STEMI. This was illustrated in a study of 1045 patients (52 percent with a known STEMI) evaluated two months after an acute MI in which 78 (7 percent) had intermittent claudication [6]. At 26 months of follow-up, those with claudication were five times more likely to have a fatal cardiac event than those without claudication (19.2 versus 3.6 percent). The patients with claudication were older and more likely to have a history of diabetes, a prior MI, a stroke, or diminished LV function. Even when these comorbidities were taken into account, patients with claudication had a significantly higher incidence of cardiac death (hazard ratio 6.57).
Low BMI — Multiple studies have identified low body mass index (BMI) as a predictor of poor outcome after MI. As an example, a cohort study of over 57,000 patients with MI found that underweight patients had a significant 13 percent higher adjusted risk of 30-day death [7], possibly as the result of concomitant frailty. This increased risk persisted as long as 17 years.
HEART FAILURE — Evidence of HF on physical examination or chest radiograph on hospital arrival indicates extensive LV systolic and/or diastolic dysfunction and is associated with a worse prognosis compared with no pulmonary congestion [8].
Killip class — The Killip classification categorizes patients with an acute MI based upon the presence or absence of simple physical examination findings that suggest LV dysfunction (table 1) [9]. Patients presenting with Killip class II or III HF complicating an acute MI tend to be older and are more often female; they also have higher rates of comorbidities, including hypertension and diabetes [10,11]. Patients with HF are also less likely to receive therapies of known efficacy in acute MI, including aspirin, heparin, beta blockers, statins, fibrinolytic agents, and angioplasty, despite evidence that these therapies are beneficial in this patient subset [10,11].
The higher the Killip class on presentation, the greater the subsequent mortality [8-17]. A study from the Second National Registry of Myocardial Infarction (NRMI-2) included 190,518 patients with acute MI, of whom 36,303 (19 percent) had Killip class II or III HF on admission [10]. These patients had a significantly higher in-hospital mortality than those without HF (21.4 versus 7.2 percent). Similar findings were noted in an analysis of international data on 4830 patients with STEMI from the GRACE registry [11]. Sixteen percent had Killip class II or III HF on admission; patients with HF had increased mortality in-hospital (17 versus 4 percent) as well as from discharge to six months (20 versus 3 percent). In this report, HF developing after admission was associated with an even higher in-hospital mortality (18 percent).
The Killip class is prognostically important in patients who undergo fibrinolysis [8,12,13] or primary percutaneous coronary intervention (PCI) (angioplasty with or without stenting) [14-17]. In one series of 1548 patients undergoing primary angioplasty, increasing Killip class was associated with increasing mortality at one year, an association that appears to have been due to a higher incidence of suboptimal myocardial perfusion [17]. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction".)
Hypotension — Hypotension (systolic pressure <100 mmHg) or frank shock is associated with a poor prognosis. This is especially true in the patient with an anterior MI in whom hypotension is the result of extensive myocardial damage and markedly reduced LV ejection fraction (LVEF) [8]. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)
In comparison, hypotension in the presence of an inferior MI may be the result of increased vagal activity, the so-called Bezold-Jarisch reflex. This tends to be a transient phenomenon that is often reversed with atropine and/or intravenous volume administration. The prognosis for these patients is usually good.
Tachycardia — Although heart rate may be elevated soon after the patient arrives in the CCU, heart rate usually declines thereafter to a level that reflects the degree of activation of the sympathetic nervous system. Patients with sustained heart rates >90 beats/min usually have larger and more often anterior infarcts, marked impairment of LV function, and therefore a poor prognosis [8,18]. (See "Sinus tachycardia: Evaluation and management", section on 'Management in patients with acute coronary syndrome'.)
ELECTROCARDIOGRAM — Worse outcomes after STEMI are seen with the following electrocardiogram (ECG) findings, which usually indicate a larger infarction:
●Anterior compared to inferior infarcts
●The presence of Q waves
●A greater number of leads showing ST elevation
●Lack of ST elevation resolution at 90 to 180 minutes after fibrinolysis or of ST depression in leads without ST elevation
The prognostic role of the ECG is discussed in detail elsewhere. (See "Electrocardiogram in the prognosis of myocardial infarction or unstable angina".)
CONDUCTION SYSTEM DISEASE — New left bundle branch block or atrioventricular block after acute MI are associated with worse outcomes. These occur less often with active reperfusion. (See "Conduction abnormalities after myocardial infarction", section on 'Prognosis'.)
ATRIAL FIBRILLATION — Atrial fibrillation (AF) is the most common supraventricular arrhythmia after an MI and its development at any time is associated with increased mortality. The reported incidence of new onset (no prior history) AF within 48 hours of MI is 6.7 to 7.8 percent in large series [19]. The discussion of AF developing shortly after MI is found elsewhere. (See "Supraventricular arrhythmias after myocardial infarction", section on 'Atrial fibrillation'.)
The best available information on the relationship between AF and long-term mortality after MI comes from a community-based study of 3220 patients with first MI cared for between 1983 and 2007 [20]. AF developed in 729 (218 within two days, 119 between days 3 and 30, and 392 after 30 days) with a cumulative incidence of 19 percent at five years (incidence rate of 42 per 1000 person-years). During a mean follow-up of 6.6 years, the development of AF was independently associated with an increased risk of death (hazard ratio [HR] 3.77, 95% CI 3.37-4.21). The magnitude of this risk was associated with the time of development of AF (HR 1.63 for AF within two days, 1.81 for AF between 3 and 30 days, and 2.58 for AF >30 days). An increased risk of long-term mortality was also noted in a study of more than 2300 patients with acute coronary syndrome (37 percent with STEMI; 19 percent with AF) cared for between 1995 and 2001 [21]. The risk of all-cause mortality was increased significantly at 10 years.
VENTRICULAR ARRHYTHMIAS — The occurrence of ventricular tachycardia (VT) in the peri-MI period (ie, within the first 48 hours after the MI) is presumably due to transient ischemia. The prognosis after either early VT or ventricular fibrillation (VF) is discussed elsewhere. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features", section on 'Prognosis after early VF'.)
RECURRENT ISCHEMIA — Recurrent ischemia, either symptomatic (ie, angina at rest or with minimal exertion) or silent, markedly worsens the prognosis [22-26]. The following observations from GUSTO-I and GUSTO-IIb illustrate the range of findings.
The GUSTO-I trial evaluated 40,484 patients with a STEMI who were treated with fibrinolysis. Recurrent ischemia occurred in 8131 patients (20 percent), including 4488 who had angina only, 3021 with angina and ST segment changes, 337 with angina and hemodynamic abnormalities, and 285 patients with angina, ST segment changes, and hemodynamic abnormalities [22].
●Patients with recurrent ischemia were more often female, had more cardiovascular risk factors, less often received intravenous heparin, and had more extensive and severe coronary disease.
●The 30-day reinfarction rate was higher in patients with recurrent ischemia, particularly when associated with ST segment changes or hemodynamic abnormalities (figure 1). In comparison, 30-day mortality was higher only in those patients who had hemodynamic abnormalities (figure 2). This pattern was maintained at one year.
Similar findings were noted in the GUSTO-IIb trial, which included 4125 patients with an STEMI: 23 percent had recurrent ischemia, which responded to medical therapy in 78 percent [23]. Compared to those without ischemia, those with responsive or refractory ischemia had a higher rate of reinfarction at 30 days (2.7 versus 11 and 28 percent, respectively) and at six months (4.6 versus 13 and 30 percent, respectively). The patients without ischemia had a lower mortality at 30 days and at one year (9 versus 10.7 and 16.4 percent, respectively).
A report from the GISSI-3 trial, in which 14 percent of patients had recurrent angina after fibrinolytic therapy, also evaluated the setting and timing of ischemia [24]. Angina occurred at rest in 94 percent of patients; one-third of episodes occurred within 72 hours of the MI and between 6 and 10 AM.
The clinical features and management of recurrent angina after STEMI are discussed separately. (See "Overview of the nonacute management of ST-elevation myocardial infarction", section on 'Recurrent chest pain' and "Diagnosis and management of failed fibrinolysis or threatened reocclusion in acute ST-elevation myocardial infarction".)
Silent ischemia after STEMI is associated with a two- to four-fold increase in cardiac event rates during follow-up compared to those without evidence of ischemia [25,26]. The management of silent ischemia after STEMI is discussed separately. (See "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis", section on 'Revascularization'.)
A number of biomarkers have been correlated with risk in patients with STEMI.
TROPONIN — Troponin I (cTnI) and T (cTnT) are regulatory proteins found in cardiac myocytes; they are sensitive and specific markers of myocardial necrosis and elevated levels have prognostic importance. (See "Troponin testing: Clinical use".)
The potent prognostic value of elevated troponins, obtained within 24 hours of admission or even three or four days after the MI, has been demonstrated in patients with STEMI, even when a percutaneous coronary intervention is performed [27-30]. The higher the peak level of troponin following acute MI, the worse the prognosis, presumably because this reflects more extensive myocardial necrosis. This issue is discussed in detail elsewhere. (See "Troponin testing: Clinical use", section on 'Prognosis'.)
B-TYPE NATRIURETIC PEPTIDE — Concentrations of B-type natriuretic peptide (BNP) and N-terminal-pro-BNP (NT pro-BNP) are useful in the diagnosis and prognosis of HF. (See "Natriuretic peptide measurement in heart failure".)
BNP and NT pro-BNP also appear to have predictive value in STEMI [31-37]. Elevated values are associated with increased mortality, even in patients without clinical HF and after adjustment for age and LV ejection fraction [32-36]. It has been suggested that NT pro-BNP drawn within 24 hours of the onset of chest pain is more accurate than the TIMI risk score in predicting mortality at nine months [37]. (See "Risk stratification after acute ST-elevation myocardial infarction", section on 'TIMI risk score'.)
The clinical role of BNP and NT pro-BNP in risk stratification in patients with STEMI remains to be determined.
SERUM POTASSIUM — Studies performed before the routine use of beta blockers, statins, and aggressive antithrombotic therapy, in addition to urgent reperfusion in many patients, demonstrated a relationship between low serum potassium levels and the risk of ventricular arrhythmias. These early studies led to specific recommendations for the serum potassium level in patients with acute MI. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features", section on 'Ventricular fibrillation'.)
The relationship between serum potassium level and in-hospital mortality in patients with acute MI and managed with recommended therapies was evaluated in a study of nearly 40,000 patients enrolled in a United States database between 2000 and 2008 [38]. After multivariate analysis, a U-shaped relationship between mean post-admission serum potassium level and in-hospital mortality was found. Using a mean post-admission serum potassium level of 3.5 to <4.0 mEq/L as the reference, the adjusted odds ratio for mortality for those with serum potassium levels of <3.0, 3.0 to <3.5, 4.0 to <4.5, 4.5 to <5.0, 5.0 to <5.5, and ≥5.5 mEq/L were 8.11, 1.45, 1.25, 1.96, 3.27, and 6.44, respectively. It is important to note that patients with a serum potassium between 4.5 and 5.0 mEq/L, a range that has previously considered “within normal limits,” had a nearly twofold greater risk of death compared to those with levels between 3.5 to <4.0 mEq/L. The findings of this study pertaining to the secondary composite outcome of ventricular fibrillation or cardiac arrest are presented separately. The relationship between hyperkalemia and mortality in patients with acute MI was confirmed in a 2016 report [39]. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features", section on 'Ventricular fibrillation'.)
GLYCEMIC CONTROL — Patients with diabetes are at increased risk of adverse events after an acute MI compared with patients without diabetes (figure 3).
WHITE BLOOD CELL COUNT — Patients with a higher baseline white blood cell (WBC) count, which is a marker of inflammation and the extent of infarction, have an increased risk for an adverse events and short- and long-term mortality after an acute ST elevation [40-45]. In a report from the Cooperative Cardiovascular Project of over 150,000 patients ≥65 years of age with an acute MI (40 percent with ST elevation or left bundle branch block), patients in the highest quintile of WBC were significantly more likely to die at 30 days than those in the lowest quintile (10.3 versus 30.2 percent, adjusted odds ratio 2.37) [43].
Similar findings were noted in the TIMI 10A and B trials in which the mortality at 30 days was higher in patients with a WBC count >15,000/µL (10.4 versus 0 to 4.9 for a count <15,000 /µL) [41]. In addition, patients with a closed artery at 60 and 90 minutes, those with evidence of thrombus, and those with poorer TIMI myocardial perfusion grades had a significantly higher WBC count than those without these findings [41]. The increase in mortality associated with an elevated baseline WBC persists for as long as 10 months [42].
ANEMIA — The presence of anemia appears to be an adverse predictor of prognosis in patients with a STEMI. In a review of clinical trials that included over 25,000 patients with STEMI, there was an adjusted odds ratio (OR) for cardiovascular mortality at 30 days of 1.21 for each 1 g/dL decline in hemoglobin below 14 g/dL [46]. The risk was also significantly increased (adjusted OR 1.79) in patients with hemoglobin values above 17 g/dL.
There also may be a graded increase in late (up to 24 months) mortality in patients with anemia on admission or at discharge [47].
PLASMA ALDOSTERONE — Although the plasma aldosterone concentration is not routinely measured in patients with acute MI, there is evidence that it is a predictor of patient outcomes. The relationship between the plasma aldosterone concentration at the time of presentation of STEMI and subsequent cardiovascular morbidity and mortality was evaluated in an observational study of 356 patients treated with primary percutaneous coronary intervention (PCI) [48]. Patients were divided into four quartiles of plasma aldosterone and evaluated for in-hospital events and six-month mortality. There was a stepwise significant increase in the risk of in-hospital death; HF; ventricular fibrillation or resuscitated cardiac arrest. After adjusting for age, Killip class (table 1) and reperfusion status, compared with patients in the first aldosterone quartile, patients in the highest quartile were at a significantly higher risk of death at six months.
The adverse outcomes associated with hyperaldosteronism may be explained by at least two mechanisms: Hyperaldosteronism is a secondary event, being a marker of reduced peripheral perfusion, and/or high levels of aldosterone have direct cardiovascular toxicity. Support for the latter hypothesis comes from studies of patients with primary hyperaldosteronism and from the survival benefit associated with aldosterone antagonists in selected patients with HF and MI. (See "Overview of the nonacute management of ST-elevation myocardial infarction", section on 'Discharge medications' and "Pathophysiology and clinical features of primary aldosteronism", section on 'Cardiovascular risk' and "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Evidence'.)
FINDINGS AT THE TIME OF ANGIOGRAPHY AND PCI
Coronary artery patency — A patent-infarct-related artery, established as early as possible after coronary artery occlusion, is associated with lower mortality in patients who have received fibrinolytic therapy [49-58]. Similarly, spontaneous reperfusion is associated with lower mortality [59,60], while persistent occlusion of the infarct-related artery is associated with increased morbidity and mortality.
Abnormal myocardial perfusion — Angiographic (myocardial blush or perfusion grade and TIMI frame count) signs of abnormal myocardial perfusion predict a worse outcome after both fibrinolysis and primary percutaneous coronary intervention (PCI). The definition of the angiographic variables and their predictive value are discussed separately. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy" and "Diagnosis and management of failed fibrinolysis or threatened reocclusion in acute ST-elevation myocardial infarction", section on 'Primary failure'.)
Age of aspirated thrombus — Thrombus aspiration is performed in many patients who undergo primary PCI for STEMI. The short-term outcomes of thrombus aspiration and the possible prognostic importance of thrombus age are discussed separately. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'Thrombectomy'.)
"Wrap around" LAD — An infarct-related, left anterior descending coronary artery that wraps around the LV apex is a predictor of adverse clinical outcomes at three years in patients with STEMI [61].
PSYCHOSOCIAL FACTORS — The role of psychosocial factors as triggers for and determinants of outcome with acute MI are discussed separately. Specifically, psychologic stress has been associated with both stress (Takotsubo) cardiomyopathy and spontaneous coronary artery dissection. (See "Psychosocial factors in acute coronary syndrome" and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Role of catecholamines' and "Spontaneous coronary artery dissection", section on 'Triggers'.)
SOCIOECONOMIC STATUS — Socioeconomic Status (SES) has been investigated as a determinant of outcomes in patients with STEMI. Among more than 5000 Australian registry participants, lower SES was associated with greater prevalence of diabetes mellitus, smoking, and initial presentation to non-percutaneous coronary intervention (PCI)-capable hospitals, leading to a slightly greater time to reperfusion and less frequent drug-eluting stents during the interval of 2005 to 2015. Lower SES was not associated with worse survival 12 months after PCI [62]. In another study, STEMI patients in the lower SES groups were more likely to be smokers, have diabetes, and to have previously had coronary heart disease, but no significant differences in survival with 30-day, one-, or three-year follow-up were observed [63]. In a third study of more than 6.6 million United States patients with MI in the National Inpatient Sample study from 2004 to 2014, STEMI patients in the lowest SES quartile, estimated by residential income geocoding, were slightly less likely to undergo coronary angiography or PCI and experienced mildly greater risk for clinical atherosclerotic cardiovascular disease outcomes [64].
REHOSPITALIZATION WITHIN 30 DAYS — For patients with acute MI, the rehospitalization rate within 30 days ranges between 10 and 30 percent and readmission often occurs within two to four days [65-67]. Women have a higher rate than men. Poor baseline quality of life and depression, as well as longer index hospital length of stay, are predictive of rehospitalization.
SUMMARY
●All patients with an acute coronary syndrome should undergo risk stratification to predict those who are at high risk for short- and long-term adverse outcomes. Risk stratification should begin soon after hospitalization. (See "Risk stratification after acute ST-elevation myocardial infarction".)
●Although many risk factors for adverse events after ST-elevation myocardial infarction (STEMI) have been identified, only a few are used in the risk prediction models:
•For patients who receive fibrinolytic therapy, the most important risk factors are age >65 years, Killip class II to IV, blood pressure <100 mmHg or hypotension, heart rate >100 beats per minute (bpm), elevated serum creatinine, anterior myocardial infarction (MI), and cardiac arrest during presentation. (See "Risk stratification after acute ST-elevation myocardial infarction", section on 'Early risk stratification'.)
•For patients who receive primary percutaneous coronary intervention (PCI), the most important risk factors are reduced left ventricular (LV) ejection fraction, Killip class, elevated serum creatinine, anemia, reduced TIMI flow grade, triple vessel disease, and age >65 years. (See "Risk stratification after acute ST-elevation myocardial infarction", section on 'Late risk stratification'.)
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