Risk factors for adverse outcomes after non-ST elevation acute coronary syndromes

Authors:: Michael Simons, MD; Joseph S Alpert, MD; Peter WF Wilson, MD; Jeffrey A Breall, MD, PhD; Pamela S Douglas, MD
Section Editors:: Christopher P Cannon, MD; Allan S Jaffe, MD; Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC; Juan Carlos Kaski, DSc, MD, DM (Hons), FRCP, FESC, FACC, FAHA; Patricia A Pellikka, MD, FACC, FAHA, FASE
Deputy Editor:: Todd F Dardas, MD, MS

Literature review current through: Jan 2024.

This topic last updated: May 31, 2023.

INTRODUCTION — Patients with an acute coronary syndrome (ACS) should undergo risk stratification to predict those who are at high risk for short- and long-term adverse outcomes. Among patients with non-ST-elevation acute coronary syndrome (NSTEACS), which includes non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA), risk stratification begins soon after presentation to detect patients at high risk during the early hospital phase. Subsequent risk stratification is aimed at predicting which patients are at increased risk after discharge.

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 myocardial infarction (MI) are discussed separately. (See "Risk stratification after non-ST elevation acute coronary syndrome" and "Prognosis after myocardial infarction".)

Although we recognize that there is significant overlap in the risk factors for NSTEACS and ST-elevation MI (STEMI), the latter are presented separately. (See "Risk factors for adverse outcomes after ST-elevation myocardial infarction".)

FACTORS PRESENT BEFORE MYOCARDIAL INFARCTION

Number of coronary heart disease 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 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 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.

Older age — Age is one of the most important risk factors for diffuse coronary disease and for a poorer outcome in hospitalized patients with unstable angina (UA) or NSTEMI [2,3]. In the TIMI III registry, patients over the age of 75 with UA/NSTEMI had more diffuse and severe coronary disease and more adverse outcomes both in hospital and within the first six weeks after discharge than those less than 75 years of age [3].

Sex — Most [4-11], but not all [12], studies report higher in-hospital and 30-day mortality after MI in females compared with males. This effect is primarily seen in younger females (less than 55 years), and differences between the sexes progressively decline with age [6,11]. It is thought that the higher early mortality in females may be accounted for by differences in symptoms at presentation. With regard to long-term mortality, most studies have suggested comparable [13] or better [14-16] outcomes in females and, in particular, those with NSTEMI, as long as the outcomes are adjusted for other risk factors such as age [5,9,15,17,18].

Prior MI — Among patients with an acute MI, those with a past history of MI have an increased risk for complications and mortality when compared with those with a first MI [19-21].

Peripheral artery disease — The presence of intermittent claudication, a prominent complaint of patients with peripheral artery disease, appears to predict worse outcomes in patients with an NSTEMI [22-24]. This was illustrated in a study of 1045 patients (35 percent with a known NSTEMI) who were evaluated two months after an acute MI in which 78 (7 percent) had intermittent claudication [22]. 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). When comorbidities were taken into account, patients with claudication had a significantly higher incidence of cardiac death (hazard ratio [HR] 6.57). A similar increase in risk and in underlying comorbidities in patients with peripheral artery disease has been noted in other studies [23,24].

COPD — Chronic obstructive pulmonary disease (COPD) and coronary artery disease are frequently present in the same patient. (See "Management of the patient with COPD and cardiovascular disease".)

The impact of COPD on outcomes of patients with acute MI was evaluated in a 10-year retrospective, single site study of nearly 6300 patients (17 percent with a history of COPD) cared for between 1997 and 2007 [25]. Short-term mortality was higher for those with COPD both during hospitalization (13.5 versus 10.0 percent) and within 30 days of discharge (18.7 versus 13.2). After multivariable adjustment, the adverse effects of COPD on 30-day post-discharge all-cause mortality persisted (OR 1.31, 95% CI 1.10-1.58). There was a similar trend for in-hospital mortality.

Obstructive sleep apnea — Obstructive sleep apnea has been associated with MI and may be a marker for worse cardiovascular outcomes. This issue is discussed separately. (See "Obstructive sleep apnea and cardiovascular disease in adults".)

Chronic kidney disease — Patients with end-stage kidney disease have a much higher risk for and a worse outcome after MI. However, lesser degrees of renal dysfunction also predict an adverse prognosis in patients with an acute 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 [26-28]:

●In an analysis of three major trials of over 19,000 patients with a NSTEACS, the patients with impaired renal function (estimated baseline creatinine clearance below 70 mL/min) had increased mortality at both 30 days and six months (approximately 10.5 versus 3.4 percent at six months) [26]. They were also older and had more baseline risk factors. After accounting for these differences, the adjusted HR for death or MI at six months was significantly increased in patients with reduced renal function (1.23 and 1.08, respectively, for each 10 mL/min decrement in creatinine clearance). The increase in risk was most pronounced in patients with the lowest creatinine clearances (median 45 mL/min).

●Similar observations were made in an analysis from the VALIANT trial of 14,527 patients with an acute MI (one-third with an NSTEMI) complicated by heart failure, left ventricular dysfunction, or both [27]. The glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Disease (MDRD) equation. After adjustment for other risk factors, the risk of death or nonfatal cardiovascular complications increased significantly with declining GFR (HR 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 creatinine values were used. 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 ACS. (See "Assessment of kidney function".)

Prior stroke — In an analysis of older patients treated in routine practice in the large CRUSADE registry of patients with NSTEMI, a history of stroke was a significant predictor of long-term mortality (HR approximately 1.35) [29].

HEART FAILURE — Overt heart failure (HF; both preexisting and developing consequent to MI) and severe left ventricular (LV) dysfunction are features that identify patients at very high short- and long-term risk. Several factors contribute individually and in concert to increase HF risk after NSTEACS. Mechanisms include persistent ischemia, severity of ventricular dysfunction, and fluid overload. Higher Killip classification of acute MI (table 1), brain natriuretic peptide levels, and troponin levels, as well as decreased estimated glomerular filtration rate, help to characterize and identify persons at greater risk. (See "Natriuretic peptide measurement in heart failure", section on 'Plasma BNP'.)

In a study of 46,519 NSTEACS patients enrolled in clinical trials between 1994 and 2008, 10.6 percent had HF at presentation and 2.9 percent developed HF during hospitalization [30,31]. Patients with HF were older, more often female, and had a higher risk of death at 30 days (odds ratio 1.74, 95% CI 1.35-2.26).

Ischemic MR — Ischemic mitral regurgitation (MR), which often presents with severe left heart failure, is associated with increased mortality [32]. (See "Chronic secondary mitral regurgitation: General management and prognosis".)

Killip class — The Killip classification categorizes patients with an acute MI based upon the presence or absence of physical examination findings that suggest LV dysfunction and heart failure (table 1) [33-35].

The higher the Killip class on presentation, the greater the subsequent mortality [36,37]. In an analysis of data from 26,090 patients enrolled in the GUSTO IIb, PURSUIT, PARAGON A, and PARAGON B trials, survival was analyzed by Killip class; those in classes III and IV were combined into a single category [37]. Compared to those in Killip class I, those in class II and III/IV had significantly higher mortality rates at 30 days (3 versus 9 and 14 percent) and six months (5 versus 15 and 23 percent).

Similar findings were noted in an analysis of international data on 3917 patients with NSTEMI and 4960 patients with unstable angina (UA) from the GRACE registry [36].

ARRHYTHMIAS

Sustained ventricular arrhythmias — The prognostic relevance of ventricular arrhythmias early after MI is discussed elsewhere. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

Atrial fibrillation — Atrial fibrillation (AF) is associated with increased mortality. In an analysis from the PURSUIT trial, 6.4 percent of patients with an NSTEACS developed AF during hospitalization [38]. These patients had a higher mortality at 30 days (adjusted hazard ratio [HR] 4.4) and at six months (adjusted HR 3). Similar findings were noted in a study of more than 2300 patients with ACS (73 percent unstable angina or NSTEMI; 19 percent with AF) cared for between 1995 and 2001 [39]. The risk of all-cause mortality was significantly increased at 30 days and 10 years. However, a large part of this association is probably related to the presence of concurrent heart failure. (See "Supraventricular arrhythmias after myocardial infarction" and 'Heart failure' above.)

ELECTROCARDIOGRAM — Components of the electrocardiogram obtained early after acute MI can provide prognostic information in patients with NSTEACS. This issue is discussed in detail elsewhere. (See "Electrocardiogram in the prognosis of myocardial infarction or unstable angina", section on 'ECG for prognosis in unstable angina and NSTEMI'.)

SILENT ISCHEMIA — Continuous ST-segment monitoring can identify patients with silent ischemia after a MI or an episode of unstable angina (UA); silent ischemia has been associated with an adverse clinical outcome in such patients [40]. There was a direct relationship between the number of ischemic episodes per 24 hours and the risk of a cardiac event (death or MI) at 5 or 30 days. (See "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis".)

The presence of silent ischemia on continuous monitoring early after NSTEMI also adversely affects long-term prognosis. (See "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Continuous electrocardiography'.)

Silent ischemia also may be detected at stress testing performed prior to discharge in patients who have not undergone revascularization (see "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Stress testing').

BIOMARKERS — A number of biomarkers can be measured to assist in risk stratification of patients with unstable angina (UA)/NSTEMI. The most commonly used is troponin. Other biomarkers, such as myoglobin, C-reactive protein (CRP), and brain natriuretic peptide (BNP), also have prognostic significance. However, we do not recommend that they be measured for either diagnostic or prognostic purposes.

Troponin — Cardiac troponin I (cTnI) and T (cTnT) are sensitive and specific markers of myocardial necrosis. Elevations in troponins are associated with a graded adverse effect in early, mid-term, and long-term prognosis in males and females with NSTEMI. The data supporting this relationship are described in detail elsewhere. (See "Troponin testing: Clinical use".)

The largest experience on the magnitude of the predictive value of troponin T comes from the GUSTO IV ACS trial of over 7000 patients who did not undergo early revascularization [41]. The patients were stratified by quartiles of troponin T (≤0.01, 0.01 to 0.12, 0.12 to 0.47, and 0.47). The 30-day mortality rate increased from 1.1 to 7.4 percent from the first to fourth quartiles of cTnT. There was also a significant increase in the 30-day rate of MI from the first to second quartiles of cTnT (2.5 versus 6.7 percent), but no further increase between the upper three quartiles. Troponin T and CRP had independent and complementary prognostic significance.

Elevations in troponins are considered indications for an early invasive strategy [42]. Ensuing revascularization in many of these patients may alter the adverse predictive value of elevated cardiac enzymes noted in many of the studies mentioned below. (See "Non-ST-elevation acute coronary syndromes: Selecting an approach to revascularization".)

BNP and NT-proBNP — B-type natriuretic peptide (BNP) is a neurohormone synthesized in the left ventricular myocardium and released into circulation in response to ventricular dilatation and pressure overload. Elevated concentrations of BNP, which can be measured by a rapid bedside assay, are of prognostic importance for both early and late outcomes in patients with an NSTEACS, a presumed reflection of left ventricular dysfunction [43-49]. (See "Natriuretic peptide measurement in heart failure".)

The predictive value of BNP was best illustrated in a study of 2525 such patients in whom BNP was measured at a mean of 40 hours after the onset of symptoms [43]. After adjusting for other predictors of risk, the odds ratios for death at 10 months were 3.8, 4, and 5.8 for concentrations in the second, third, or fourth quartiles compared to those in the lowest quartile; higher BNP was also associated with an increased risk of new or recurrent MI and new or worsening heart failure.

N-terminal pro-BNP (NT-proBNP) has similar predictive value [44,50-55]. The largest study of this issue is an analysis of data on 6809 patients from the GUSTO IV ACS trial [50]. Blood samples obtained within 24 hours of symptom onset in patients with an NSTEACS were retrospectively assayed for NT-proBNP. Patients in the lowest decile of NT-proBNP (≤98 ng/L) had a significantly lower mortality rate at one year than those in the highest decile (>4634 ng/L) (0.4 versus 27.1 percent). NT-proBNP had a stronger correlation with mortality than any other marker studied, including cTnT and CRP.

Some studies suggest prognostic benefit from serial measurements [47,55,56].

The role of BNP or NT-proBNP monitoring in patients with an NSTEACS remains to be determined.

GLYCEMIC CONTROL — Patients with diabetes have a higher risk of adverse outcomes after an NSTEACS than those without diabetes (figure 1) [57].

ANEMIA AND MAJOR BLEEDING — Anemia appears to be an adverse predictor of prognosis in patients with an NSTEACS. In a review of clinical trials that included over 14,500 patients with a NSTEACS, the likelihood of cardiovascular mortality, nonfatal MI, or recurrent ischemia at 30 days was increased in patients with a hemoglobin below 11 g/dL compared to those with a hemoglobin of 15 to 16 g/dL [58]. After adjustment for baseline characteristics, a hemoglobin below 11 g/dL was an independent predictor of the combined end point (adjusted odds ratio [OR] 1.45 per each 1 g/dL decrement in hemoglobin).

There also may be a graded increase in late (up to 24 months) mortality in patients with anemia on admission or at discharge [59].

Many of the patients with anemia described above have had major bleeding during their hospitalization. The relationship between major bleeding and long-term death or ischemic events was evaluated in a study of over 34,000 patients with NSTEACS enrolled in the OASIS registry and the OASIS-2 and CURE trials [60]. The likelihood of death in patients who bled compared to those who did not was significantly increased at 30 days and between 30 days and six months (adjusted hazard ratio 5.37, 95% CI 3.97-7.26 and 1.54, 95% CI 1.01-2.36, respectively). A similar significant association existed between bleeding and MI.

One possible explanation for these observations is that patients who have significant bleeding during their hospitalization are not discharged on guideline recommended antiplatelet therapy [61]. In addition, there may be a delay in starting dual antiplatelet therapy long after the major bleed has come under control.

This theory was evaluated using data in the PREMIER registry of 2498 patients with acute MI [61]. Patients with in-hospital bleeding (n = 301) were significantly less likely to be receiving aspirin or thienopyridine at discharge (adjusted OR 0.45, 95% CI 0.31-0.54 and 0.62, 95% CI 0.52-0.91, respectively). At one month, patients were significantly less likely to be receiving aspirin (OR 0.68, 95% CI 0.50-0.92) and there was a non-significant decreased likelihood of receiving thienopyridine.

PSYCHOSOCIAL AND OTHER SOCIAL FACTORS — The role of psychosocial factors as triggers for and determinants of outcome with acute MI are discussed separately. (See "Psychosocial factors in acute coronary syndrome".)

MI WITHOUT CHEST PAIN — Up to 33 percent of patients with MI have atypical symptoms such as dyspnea alone, nausea and/or vomiting, palpitations, syncope, or cardiac arrest. In one series of 2096 patients with a first confirmed MI, the 20 percent who presented without chest pain had higher mortality at 30 days (49 versus 18 percent with chest pain) and one year (61 versus 26 percent) [62]. These patients were less likely to receive treatment strategies of proven benefit, which may partly account for worse outcomes. (See "Overview of the acute management of ST-elevation myocardial infarction".)

MI WITH NORMAL CORONARY ARTERIES — Among patients with a NSTEACS, coronary angiography in major trials revealed either normal vessels or no vessel with ≥50 percent stenosis in 12 to 14 percent [63,64]. A somewhat lower rate (7.5 percent) has been noted in patients with STEMI. These patients have a lower mortality than those with an identifiable culprit lesion. (See "Acute coronary syndrome: Terminology and classification", section on 'Absence of significant coronary disease' and "Microvascular angina: Angina pectoris with normal coronary arteries", section on 'Epidemiology' and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Exclusion of coronary artery disease'.)

CLINICIAN AND HOSPITAL EXPERIENCE — The experience of the clinician caring for patients with an acute MI affects patient survival [65,66]. In a review of almost 100,000 Canadian patients with an acute MI treated by over 5300 clinicians, the risk-adjusted mortality was significantly higher when the admitting clinician cared for ≤5 cases per year (lowest quartile) compared with those who cared for >24 cases per year (highest quartile) at both 30 days (15.3 versus 11.8 percent) and one year (24.2 versus 19.6 percent) [65]. In this study, clinician subspecialty was not an independent predictor after adjusting for clinician volume. However, other studies have suggested that patients cared for by a cardiologist have a lower mortality than those cared for by a nonspecialist [66-69].

The experience of the hospital may be another determinant of outcome. The magnitude of this effect was examined in an analysis of 98,898 Medicare patients admitted with an acute MI [68]. The patients in the quartile admitted to hospitals with the lowest acute MI volume were more likely to die within 30 days than patients in the quartile admitted to hospitals with the highest acute MI volume (hazard ratio 1.17, 95% CI 1.09-1.26).

SUMMARY

●All patients with an acute coronary syndrome (ACS) 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 non-ST elevation acute coronary syndrome".)

●Many individual risk factors are independently associated with a poor prognosis. The following risk factors carry the greatest weight in the risk prediction models:

•Overt heart failure or severe left ventricular dysfunction (see 'Heart failure' above)

•Chronic kidney disease (see 'Chronic kidney disease' above)

•Prior stroke (see 'Prior stroke' above)

•Increasing age (see 'Older age' above)

Canto JG, Kiefe CI, Rogers WJ, et al. Number of coronary heart disease risk factors and mortality in patients with first myocardial infarction. JAMA 2011; 306:2120.
Goldberg RJ, McCormick D, Gurwitz JH, et al. Age-related trends in short- and long-term survival after acute myocardial infarction: a 20-year population-based perspective (1975-1995). Am J Cardiol 1998; 82:1311.
Stone PH, Thompson B, Anderson HV, et al. Influence of race, sex, and age on management of unstable angina and non-Q-wave myocardial infarction: The TIMI III registry. JAMA 1996; 275:1104.
Greenland P, Reicher-Reiss H, Goldbourt U, Behar S. In-hospital and 1-year mortality in 1,524 women after myocardial infarction. Comparison with 4,315 men. Circulation 1991; 83:484.
Gottlieb S, Harpaz D, Shotan A, et al. Sex differences in management and outcome after acute myocardial infarction in the 1990s: A prospective observational community-based study. Israeli Thrombolytic Survey Group. Circulation 2000; 102:2484.
Vaccarino V, Parsons L, Every NR, et al. Sex-based differences in early mortality after myocardial infarction. National Registry of Myocardial Infarction 2 Participants. N Engl J Med 1999; 341:217.
Gan SC, Beaver SK, Houck PM, et al. Treatment of acute myocardial infarction and 30-day mortality among women and men. N Engl J Med 2000; 343:8.
Stone GW, Grines CL, Browne KF, et al. Comparison of in-hospital outcome in men versus women treated by either thrombolytic therapy or primary coronary angioplasty for acute myocardial infarction. Am J Cardiol 1995; 75:987.
Malacrida R, Genoni M, Maggioni AP, et al. A comparison of the early outcome of acute myocardial infarction in women and men. The Third International Study of Infarct Survival Collaborative Group. N Engl J Med 1998; 338:8.
Mak KH, Kark JD, Chia KS, et al. Ethnic variations in female vulnerability after an acute coronary event. Heart 2004; 90:621.
Vaccarino V, Parsons L, Peterson ED, et al. Sex differences in mortality after acute myocardial infarction: changes from 1994 to 2006. Arch Intern Med 2009; 169:1767.
Berger JS, Elliott L, Gallup D, et al. Sex differences in mortality following acute coronary syndromes. JAMA 2009; 302:874.
Hochman JS, McCabe CH, Stone PH, et al. Outcome and profile of women and men presenting with acute coronary syndromes: a report from TIMI IIIB. TIMI Investigators. Thrombolysis in Myocardial Infarction. J Am Coll Cardiol 1997; 30:141.
Roger VL, Farkouh ME, Weston SA, et al. Sex differences in evaluation and outcome of unstable angina. JAMA 2000; 283:646.
Chang WC, Kaul P, Westerhout CM, et al. Impact of sex on long-term mortality from acute myocardial infarction vs unstable angina. Arch Intern Med 2003; 163:2476.
Hochman JS, Tamis JE, Thompson TD, et al. Sex, clinical presentation, and outcome in patients with acute coronary syndromes. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes IIb Investigators. N Engl J Med 1999; 341:226.
Vaccarino V, Krumholz HM, Berkman LF, Horwitz RI. Sex differences in mortality after myocardial infarction. Is there evidence for an increased risk for women? Circulation 1995; 91:1861.
Køber L, Torp-Pedersen C, Ottesen M, et al. Influence of gender on short- and long-term mortality after acute myocardial infarction. TRACE study group. Am J Cardiol 1996; 77:1052.
Wagner S, Burczyk U, Schiele R, et al. The 60 Minutes Myocardial Infarction Project. Characteristics on admission and clinical outcome in patients with reinfarction compared to patients with a first infarction. Eur Heart J 1998; 19:879.
Shotan A, Gottlieb S, Goldbourt U, et al. Prognosis of patients with a recurrent acute myocardial infarction before and in the reperfusion era--a national study. Am Heart J 2001; 141:478.
Dönges K, Schiele R, Gitt A, et al. Incidence, determinants, and clinical course of reinfarction in-hospital after index acute myocardial infarction (results from the pooled data of the maximal individual therapy in acute myocardial infarction [MITRA], and the myocardial infarction registry [MIR]). Am J Cardiol 2001; 87:1039.
Narins CR, Zareba W, Moss AJ, et al. Relationship between intermittent claudication, inflammation, thrombosis, and recurrent cardiac events among survivors of myocardial infarction. Arch Intern Med 2004; 164:440.
Cotter G, Cannon CP, McCabe CH, et al. Prior peripheral arterial disease and cerebrovascular disease are independent predictors of adverse outcome in patients with acute coronary syndromes: are we doing enough? Results from the Orbofiban in Patients with Unstable Coronary Syndromes-Thrombolysis In Myocardial Infarction (OPUS-TIMI) 16 study. Am Heart J 2003; 145:622.
Januzzi JL Jr, Buros J, Cannon CP, Tactics TIMI 18 Investigators. Peripheral arterial disease, acute coronary syndromes, and early invasive management: the TACTICS TIMI 18 trial. Clin Cardiol 2005; 28:238.
Stefan MS, Bannuru RR, Lessard D, et al. The impact of COPD on management and outcomes of patients hospitalized with acute myocardial infarction: a 10-year retrospective observational study. Chest 2012; 141:1441.
Al Suwaidi J, Reddan DN, Williams K, et al. Prognostic implications of abnormalities in renal function in patients with acute coronary syndromes. Circulation 2002; 106:974.
Anavekar NS, McMurray JJ, Velazquez EJ, et al. Relation between renal dysfunction and cardiovascular outcomes after myocardial infarction. N Engl J Med 2004; 351:1285.
Freeman RV, Mehta RH, Al Badr W, et al. Influence of concurrent renal dysfunction on outcomes of patients with acute coronary syndromes and implications of the use of glycoprotein IIb/IIIa inhibitors. J Am Coll Cardiol 2003; 41:718.
Roe MT, Chen AY, Thomas L, et al. Predicting long-term mortality in older patients after non-ST-segment elevation myocardial infarction: the CRUSADE long-term mortality model and risk score. Am Heart J 2011; 162:875.
Becker RC, Burns M, Gore JM, et al. Early assessment and in-hospital management of patients with acute myocardial infarction at increased risk for adverse outcomes: a nationwide perspective of current clinical practice. The National Registry of Myocardial Infarction (NRMI-2) Participants. Am Heart J 1998; 135:786.
Bahit MC, Lopes RD, Clare RM, et al. Heart failure complicating non-ST-segment elevation acute coronary syndrome: timing, predictors, and clinical outcomes. JACC Heart Fail 2013; 1:223.
Bursi F, Enriquez-Sarano M, Nkomo VT, et al. Heart failure and death after myocardial infarction in the community: the emerging role of mitral regurgitation. Circulation 2005; 111:295.
Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol 1967; 20:457.
Zhang Q, Zhou L, Cai HL, Lu HH. Relationship of the ORBIT and HAS-BLED scores with Killip class 3-4 in patients with ST-segment elevation myocardial infarction. Medicine (Baltimore) 2019; 98:e14578.
Vicent L, Velásquez-Rodríguez J, Valero-Masa MJ, et al. Predictors of high Killip class after ST segment elevation myocardial infarction in the era of primary reperfusion. Int J Cardiol 2017; 248:46.
Steg PG, Dabbous OH, Feldman LJ, et al. Determinants and prognostic impact of heart failure complicating acute coronary syndromes: observations from the Global Registry of Acute Coronary Events (GRACE). Circulation 2004; 109:494.
Khot UN, Jia G, Moliterno DJ, et al. Prognostic importance of physical examination for heart failure in non-ST-elevation acute coronary syndromes: the enduring value of Killip classification. JAMA 2003; 290:2174.
Al-Khatib SM, Pieper KS, Lee KL, et al. Atrial fibrillation and mortality among patients with acute coronary syndromes without ST-segment elevation: results from the PURSUIT trial. Am J Cardiol 2001; 88:A7, 76.
Poçi D, Hartford M, Karlsson T, et al. Role of the CHADS2 score in acute coronary syndromes: risk of subsequent death or stroke in patients with and without atrial fibrillation. Chest 2012; 141:1431.
Akkerhuis KM, Klootwijk PA, Lindeboom W, et al. Recurrent ischaemia during continuous multilead ST-segment monitoring identifies patients with acute coronary syndromes at high risk of adverse cardiac events; meta-analysis of three studies involving 995 patients. Eur Heart J 2001; 22:1997.
James SK, Armstrong P, Barnathan E, et al. Troponin and C-reactive protein have different relations to subsequent mortality and myocardial infarction after acute coronary syndrome: a GUSTO-IV substudy. J Am Coll Cardiol 2003; 41:916.
Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014; 130:2354.
de Lemos JA, Morrow DA, Bentley JH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes. N Engl J Med 2001; 345:1014.
Richards AM, Nicholls MG, Espiner EA, et al. B-type natriuretic peptides and ejection fraction for prognosis after myocardial infarction. Circulation 2003; 107:2786.
Tapanainen JM, Lindgren KS, Mäkikallio TH, et al. Natriuretic peptides as predictors of non-sudden and sudden cardiac death after acute myocardial infarction in the beta-blocking era. J Am Coll Cardiol 2004; 43:757.
Mega JL, Morrow DA, De Lemos JA, et al. B-type natriuretic peptide at presentation and prognosis in patients with ST-segment elevation myocardial infarction: an ENTIRE-TIMI-23 substudy. J Am Coll Cardiol 2004; 44:335.
Morrow DA, de Lemos JA, Blazing MA, et al. Prognostic value of serial B-type natriuretic peptide testing during follow-up of patients with unstable coronary artery disease. JAMA 2005; 294:2866.
Blankenberg S, McQueen MJ, Smieja M, et al. Comparative impact of multiple biomarkers and N-Terminal pro-brain natriuretic peptide in the context of conventional risk factors for the prediction of recurrent cardiovascular events in the Heart Outcomes Prevention Evaluation (HOPE) Study. Circulation 2006; 114:201.
Kistorp C. Risk stratification in secondary prevention: advances in multimarker profiles, or back to basics? Circulation 2006; 114:184.
James SK, Lindahl B, Siegbahn A, et al. N-terminal pro-brain natriuretic peptide and other risk markers for the separate prediction of mortality and subsequent myocardial infarction in patients with unstable coronary artery disease: a Global Utilization of Strategies To Open occluded arteries (GUSTO)-IV substudy. Circulation 2003; 108:275.
Jernberg T, Stridsberg M, Venge P, Lindahl B. N-terminal pro brain natriuretic peptide on admission for early risk stratification of patients with chest pain and no ST-segment elevation. J Am Coll Cardiol 2002; 40:437.
Omland T, Persson A, Ng L, et al. N-terminal pro-B-type natriuretic peptide and long-term mortality in acute coronary syndromes. Circulation 2002; 106:2913.
Jernberg T, Lindahl B, Siegbahn A, et al. N-terminal pro-brain natriuretic peptide in relation to inflammation, myocardial necrosis, and the effect of an invasive strategy in unstable coronary artery disease. J Am Coll Cardiol 2003; 42:1909.
Bazzino O, Fuselli JJ, Botto F, et al. Relative value of N-terminal probrain natriuretic peptide, TIMI risk score, ACC/AHA prognostic classification and other risk markers in patients with non-ST-elevation acute coronary syndromes. Eur Heart J 2004; 25:859.
Heeschen C, Hamm CW, Mitrovic V, et al. N-terminal pro-B-type natriuretic peptide levels for dynamic risk stratification of patients with acute coronary syndromes. Circulation 2004; 110:3206.
Lindahl B, Lindbäck J, Jernberg T, et al. Serial analyses of N-terminal pro-B-type natriuretic peptide in patients with non-ST-segment elevation acute coronary syndromes: a Fragmin and fast Revascularisation during In Stability in Coronary artery disease (FRISC)-II substudy. J Am Coll Cardiol 2005; 45:533.
Donahoe SM, Stewart GC, McCabe CH, et al. Diabetes and mortality following acute coronary syndromes. JAMA 2007; 298:765.
Sabatine MS, Morrow DA, Giugliano RP, et al. Association of hemoglobin levels with clinical outcomes in acute coronary syndromes. Circulation 2005; 111:2042.
Aronson D, Suleiman M, Agmon Y, et al. Changes in haemoglobin levels during hospital course and long-term outcome after acute myocardial infarction. Eur Heart J 2007; 28:1289.
Eikelboom JW, Mehta SR, Anand SS, et al. Adverse impact of bleeding on prognosis in patients with acute coronary syndromes. Circulation 2006; 114:774.
Wang TY, Xiao L, Alexander KP, et al. Antiplatelet therapy use after discharge among acute myocardial infarction patients with in-hospital bleeding. Circulation 2008; 118:2139.
Dorsch MF, Lawrance RA, Sapsford RJ, et al. Poor prognosis of patients presenting with symptomatic myocardial infarction but without chest pain. Heart 2001; 86:494.
Invasive compared with non-invasive treatment in unstable coronary-artery disease: FRISC II prospective randomised multicentre study. FRagmin and Fast Revascularisation during InStability in Coronary artery disease Investigators. Lancet 1999; 354:708.
Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 2001; 344:1879.
Tu JV, Austin PC, Chan BT. Relationship between annual volume of patients treated by admitting physician and mortality after acute myocardial infarction. JAMA 2001; 285:3116.
Casale PN, Jones JL, Wolf FE, et al. Patients treated by cardiologists have a lower in-hospital mortality for acute myocardial infarction. J Am Coll Cardiol 1998; 32:885.
Jollis JG, DeLong ER, Peterson ED, et al. Outcome of acute myocardial infarction according to the specialty of the admitting physician. N Engl J Med 1996; 335:1880.
Thiemann DR, Coresh J, Oetgen WJ, Powe NR. The association between hospital volume and survival after acute myocardial infarction in elderly patients. N Engl J Med 1999; 340:1640.
Ayanian JZ, Landrum MB, Guadagnoli E, Gaccione P. Specialty of ambulatory care physicians and mortality among elderly patients after myocardial infarction. N Engl J Med 2002; 347:1678.

Topic 77 Version 34.0

خرید پکیج

Risk factors for adverse outcomes after non-ST elevation acute coronary syndromes

References