902

INTERVENTIONAL CARDIOLOGY AND SURGERY

Renal function and long term mortality after unstable

angina/non-ST segment elevation myocardial infarction
treated very early and predominantly with percutaneous
coronary intervention
C Mueller, F-J Neumann, A P Perruchoud, H J Buettner
...............................................................................................................................

Heart 2004;90:902–907. doi: 10.1136/hrt.2003.021741

Objectives: To quantify the impact of baseline renal function on in-hospital and long term mortality in
patients with unstable angina/non-ST elevation acute myocardial infarction (UA/NSTEMI) treated with a
very early invasive strategy.
Design: Prospective cohort study of 1400 consecutive patients with UA/NSTEMI undergoing coronary
See end of article for angiography and subsequent coronary stenting of the culprit lesion as the primary revascularisation
authors’ affiliations strategy within 24 hours of admission. Patients were stratified according to calculated glomerular filtration
....................... rate (GFR) on admission.
Correspondence to: Results: In-hospital mortality was 0% among patients with a GFR > 130 ml/min/1.73 m2, 0.4% with a
Dr Christian Mueller, GFR of 90–129 ml/min/1.73 m2, 2.6% with a GFR of 60–89 ml/min/1.73m2, and 5.1% with a GFR of
Department of Internal , 60 ml/min/1.73 m2. Cumulative three year survival rates were 92.6%, 95.5%, 91.9%, and 76.8%,
Medicine, University respectively. Patients with a GFR of , 60 ml/min/1.73 m2 were four times more likely to die in hospital
Hospital, Petersgraben 4,
CH-4031 Basel, (hazard ratio (HR) 4.0, 95% confidence interval (CI) 1.8 to 9.1; p = 0.001) and four times more likely to
Switzerland; die during long term follow up (HR 4.0, 95% CI 2.5 to 6.4; p , 0.001). After adjusting for potential
[email protected] confounders, a GFR of , 60 ml/min/1.73 m2 remained a strong independent predictor of long term
Accepted mortality (HR 2.6, 95% CI 1.5 to 4.5; p = 0.001).
12 November 2003 Conclusions: Baseline renal function is a strong independent predictor of in-hospital and long term
....................... mortality after UA/NSTEMI treated with very early revascularisation.

A
bout four million patients attend emergency depart- is both safe and efficacious for patients presenting with renal
ments in Europe each year with chest pain and dysfunction.
suspected unstable angina/non-ST segment elevation
myocardial infarction (UA/NSTEMI).1 However, risk stratifi-
METHODS
cation is often particularly challenging in UA/NSTEMI. Early
Patient population
coronary angiography and revascularisation has been pro-
From January 1996 to December 1999, consecutive patients
posed as a novel potentially superior management strategy
admitted to our centre with UA/NSTEMI were treated with a
for these patients.2–5 Current practice guidelines for the
very early invasive strategy. Patients undergoing coronary
management of patients with UA/NSTEMI recommend an
early invasive strategy for most patients.2 6 Predictors of long angiography for symptoms of myocardial ischaemia occur-
term mortality in UA/NSTEMI treated with an early invasive ring at rest (Braunwald class IIIB unstable angina) were
strategy remain to be established. eligible for inclusion in this study.13 We excluded patients
The implications of chronic kidney disease for cardiovas- with de novo angina pectoris on exertion or worsening
cular outcomes have attained increasing recognition.7 8 Large angina during exertion only (Braunwald class 1A–C),
registries including predominantly patients with ST elevation patients with persistent ST elevation, and patients with
myocardial infarction treated with thrombolytic agents postinfarction angina (Braunwald class 1C, 2C, or 3C),
suggested that baseline renal function measured as serum patients in whom angiography was not performed because
creatinine or estimated creatinine clearance is a predictor of of patient refusal (n = 6) or extremely severe concomitant
mortality.9–11 McCullough and colleagues12 confirmed this disease (n = 9 with severe dementia or advanced malig-
observation among patients admitted to a single coronary nancy), and patients with no serum creatinine determined on
care unit. In these studies, patients were primarily treated admission (n = 50). Therefore, this study included 96%
conservatively with anti-ischaemic and antithrombotic med- (1400 of 1465) of the total number of consecutive patients
ication unless ST elevation was evident on the admission with UA/NSTEMI admitted to our centre and 99% of those
ECG. Coronary angiography was performed only after ‘‘cool- with serum creatinine available. These include patients with
ing down’’ with medical treatment and was restricted to end stage renal disease on dialysis, high bleeding risks, and
patients with recurrent ischaemia.
Thus, the present study had two aims: firstly, to explore Abbreviations: BARI, bypass angioplasty revascularisation
the association between baseline renal function and investigation; CABG, coronary artery bypass grafting; CI, confidence
interval; CK, creatine kinase; GFR, glomerular filtration rate; PCI,
mortality after UA/NSTEMI in a large cohort of consecutive
percutaneous coronary intervention; TACTICS-TIMI 18, treat angina with
unselected patients treated uniformly very early and pre- Aggrastat and determine cost of therapy with an invasive or conservative
dominantly with percutaneous coronary intervention (PCI); strategy–thrombolysis in myocardial infarction 18; UA/NSTEMI,
and secondly, to test whether this latest, aggressive treatment unstable angina/non-ST segment elevation myocardial infarction

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Renal function and long term mortality after ACS 903

prior stroke. The study was carried out according to the reaching at least three times the upper limit of normal.
principles of the Declaration of Helsinki and was approved by ECGs were recorded for all patients directly after PCI or
the institutional review board. Informed consent was CABG and in the following morning. In addition, cardiac
obtained from all participating patients. At hospital discharge markers (CK and CK-MB) were determined 8–24 hours after
all patients were prescribed a low cholesterol diet and statins the intervention and additionally whenever ischaemic symp-
were recommended to achieve a low density lipoprotein toms developed.
cholesterol concentration below 3.0 mmol/l during follow up. The statistical analyses were done with the SPSS/PC
Angiotensin converting enzyme inhibitors were given to all (version 11.0, SPSS Inc, Chicago, Illinois, USA) software
patients with renal dysfunction, diabetes, or prior myocardial package. Discrete variables were expressed as percentage
infarction unless they were considered hypovolaemic. (95% confidence interval (CI)) and continuous variables as
mean (95% CI). A significance level of 0.05 was used.
Renal function and glomerular filtration rate Comparisons were made by analysis of variance for indepen-
The glomerular filtration rate (GFR) is the best measure of dent samples and x2 tests as appropriate. All hypothesis
overall kidney function.14–16 We calculated GFR with the use testing was two tailed. Cox proportional hazards regression
of the abbreviated modification of diet in renal disease study analysis was used as the appropriate multivariate method for
equation14–16: GFR (in ml/min/1.73 m2 of body surface adjustment throughout. Multivariate Cox regression analysis
area) = 186 6 (serum creatinine in mg/dl)21.154 6 (age in was performed to identify independent predictors of death.
years)20.203 6 0.742 for female patients and 6 1.210 for All baseline clinical, laboratory, and angiographic variables
black patients. This equation is based on data from Levey were entered into the model. The cumulative survival curves
and colleagues15 on 1628 patients with 558 in the validation were constructed with the use of the Kaplan-Meier method.
set.
A venous blood specimen for serum creatinine determina- RESULTS
tion was drawn on admission. All samples were analysed in a Baseline characteristics
central laboratory with the use of an enzymatic kit (CREA GFR was estimated for 1400 consecutive patients. The
plus, Boehringer Mannheim Systems, Mannheim, Germany). median GFR was 88 ml/min/1.73 m2 of body surface area
Patients were divided into groups according to their renal (mean 89 ml/min/1.73 m2). Table 1 describes the baseline,
function as assessed by GFR (National Kidney Foundation demographic, clinical, angiographic, and procedural charac-
kidney disease outcomes quality initiative stages).14–16 teristics of the cohort, divided into groups according to their
renal function as assessed by GFR (National Kidney
Very early revascularisation Foundation kidney disease outcomes quality initiative
Patients with persistent chest pain underwent immediate stages).14–16
coronary angiography. Among patients asymptomatic while Table 1 shows the differences in baseline characteristics
taking medical treatment, coronary angiography was per- between these groups. Patients with a GFR , 60 ml/min/
formed within 24 hours of admission. Whenever possible, 1.73 m2 of body surface area (kidney disease outcomes
coronary stenting of the culprit lesion was done immediately quality initiative stage 3–5) were older, more often had prior
after angiography. Stenting was not restricted to patients myocardial infarction, diabetes, and hypertension, and less
with one and two vessel disease but was also favoured for often were smokers. In addition, these patients more often
patients with three vessel disease with suitable lesions. The required mechanical cardiopulmonary resuscitation or
median time interval from admission to PCI was five hours. If defibrillation before admission and more often had new ST
revascularisation was indicated but PCI was not considered segment depression, increased troponin T, and increased
the optimal treatment option (unprotected left main disease, white blood cell count on admission than did patients in
diffuse three vessel disease), patients were scheduled for the other GFR ranges. Coronary angiography was per-
urgent coronary artery bypass grafting (CABG). formed in all 1400 patients and showed that the extent of
coronary artery disease was significantly more advanced in
Follow up patients with a GFR , 60 ml/min/1.73 m2 of body surface
All patients were scheduled for outpatient visits at six area.
months. In addition, patients were contacted by question-
naire in September 2000, nearly five years after enrolment of Revascularisation
the first patient. For patients reporting cardiac symptoms, at PCI was the predominant revascularisation procedure applied
least one clinical and ECG examination was performed in the in all ranges of GFR. About 70% of patients actually
outpatient clinic or by the referring physician. All informa- underwent revascularisation. The overall PCI to CABG ratio
tion derived from contingent hospital readmission records or was 4:1, with the highest CABG rate among patients with a
provided by the referring physician or by the outpatient clinic GFR , 60 ml/min/1.73 m2 of body surface area.
was reviewed and entered on to the computer database.
Outcome
End points and statistical analysis Eighty two deaths and 59 non-fatal myocardial infarctions
The pre-specified primary end point was defined as death occurred during a mean follow up of 20 months (95% CI 19 to
from all causes occurring in hospital or during follow up. As 21 months). The mean interval until last patient contact or
secondary end points we assessed non-fatal myocardial patient death was 21 months in the groups with GFR
infarction and the composite of death and non-fatal > 130 ml/min/1.73 m2 (2177 person-months) and GFR 90–
myocardial infarction. Myocardial infarction was defined as 129 ml/min/1.73 m2 (11293 person-months), 20 months
typical chest pain at rest followed by an increase in creatine with GFR 60–89 ml/min/1.73 m2 (11443 person-months),
kinase concentration (CK and CK-MB beyond twice the and 16 months with GFR , 60 ml/min/1.73 m2 (2886
upper limit of normal and five times the upper limit of person-months). The majority of deaths were from cardiac
normal after CABG) or new Q waves on the ECG. To meet causes. In-hospital mortality was significantly higher among
this end point criterion, patients who had initially presented patients with a GFR , 60 ml/min/1.73 m2 of body surface
with myocardial infarction had to have new ST segment area than among patients with higher GFR (table 2). The rate
changes and an increase in CK of at least 50% over the was 0% with GFR > 130 ml/min/1.73 m2, 0.4% with GFR 90–
previous trough concentration in at least two samples 129 ml/min/1.73 m2, 2.6% with GFR 60–89 ml/min/1.73 m2,

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904 Mueller, Neumann, Perruchoud, et al

Table 1 Baseline patient and procedural characteristics according to glomerular filtration rate (GFR) on admission
Group by GFR (ml/min/1.73 m2)
All patients
(n = 1400) >130 (n = 106) 90–129 (n = 548) 60–89 (n = 570) ,60 (n = 176) p Value*
2
GFR (ml/min/1.73 m ) 89 (27) 146 (15) 105 (10) 77 (8) 46 (13)
Age (years) 65 (11) 58 (11) 61 (11) 67 (9) 71 (8) ,0.001
Female sex (%) 29 (27 to 32) 22 (14 to 30) 28 (25 to 32) 29 (25 to 33) 35 (28 to 42) 0.135
Prior MI (%) 33 (31 to 36) 22 (14 to 30) 28 (25 to 32) 36 (32 to 40) 45 (38 to 53) ,0.001
Prior coronary bypass grafting (%) 14 (12 to 16) 13 (7 to 20) 12 (9 to 14) 15 (12 to 18) 15 (10 to 21) 0.291
Prior coronary angioplasty (%) 22 (20 to 24) 17 (10 to 24) 22 (19 to 26) 24 (20 to 27) 21 (15 to 27) 0.471
Diabetes (%) 19 (17 to 21) 17 (10 to 24) 16 (13 to 20) 18 (15 to 22) 30 (23 to 36) 0.001
Hypercholesterolaemia (%) 66 (63 to 68) 64 (55 to 73) 65 (61 to 69) 68 (64 to 72) 63 (55 to 70) 0.476
Hypertension (%) 62 (60 to 65) 55 (45 to 64) 56 (52 to 60) 67 (63 to 70) 71 (64 to 78) ,0.001
Smoking (%) 23 (20 to 25) 41 (31 to 50) 27 (23 to 30) 18 (15 to 21) 14 (9 to 19) ,0.001
Angina pectoris at rest .48 h (%) 16 (14 to 18) 11 (5 to 17) 14 (11 to 17) 19 (16 to 22) 17 (11 to 23) 0.073
Angina pectoris at rest ,48 h (%) 69 (67 to 72) 67 (58 to 76) 70 (66 to 74) 68 (64 to 72) 72 (65 to 78) 0.714
Non-Q wave MI (%) 15 (13 to 17) 22 (14 to 30) 16 (13 to 19) 13 (10 to 16) 11 (7 to 16) 0.060
Mechanical CPR (%) 1.4 (0.8 to 2.0) 0.9 (0 to 2.8) 0.7 (0 to 1.4) 1.2 (0.3 to 2.1) 4.0 (1.1 to 6.9) 0.013
Defibrillation (only) (%) 1.7 (1.0 to 2.4) 1.9 (0 to 4.5) 1.3 (0.3 to 2.2) 1.2 (0.3 to 2.1) 4.6 (1.4 to 7.7) 0.020
Cardiogenic shock (%) 0.9 (0.4 to 1.4) 0 0.6 (0 to 1.2) 1.2 (0.3 to 2.1) 1.7 (0 to 3.6) 0.313
New ST depression >1 mm (%) 10 (8 to 11) 4 (1 to 7) 9 (7 to 12) 9 (7 to 11) 15 (9 to 20) 0.021
New T wave inversion >1 mm (%) 29 (26 to 31) 38 (28 to 47) 31 (27 to 35) 25 (22 to 29) 27 (21 to 34) 0.029
Troponin T >0.01 mg/l (%) 56 (53 to 59) 52 (42 to 62) 55 (50 to 60) 53 (48 to 58) 72 (64 to 80) 0.002
White cell count (6109/l) 8.9 (7.4) 9.1 (2.7) 8.7 (3.0) 8.5 (3.7) 10.6 (18.9) 0.010
Platelet count (6109/l) 235 (75) 232 (62) 235 (66) 234 (79) 241 (92) 0.661
Coronary vessels with >50% stenosis (%) 0.001
0 13 (12 to 15) 18 (10 to 25) 15 (12 to 18) 12 (9 to 15) 10 (5 to 15)
1 25 (23 to 27) 31 (22 to 40) 29 (25 to 33) 22 (18 to 25) 18 (12 to 24)
2 23 (21 to 25) 23 (14 to 31) 23 (19 to 27) 24 (20 to 28) 18 (12 to 24)
3 39 (36 to 41) 29 (20 to 38) 33 (29 to 37) 42 (38 to 46) 53 (45 to 61)
Percutaneous coronary intervention (%) 56 (53 to 58) 58 (48 to 67) 58 (54 to 62) 55 (51 to 59) 51 (43 to 58) 0.372
With stent (%) 80 (77 to 83) 83 (73 to 93) 78 (73 to 83) 80 (76 to 85) 80 (71 to 89) 0.810
With Gp IIb/IIIa antagonists (%) 12 (9 to 14) 9 (1 to 16) 11 (7 to 14) 11 (7 to 15) 21 (12 to 30) 0.060
Coronary artery bypass grafting (%) 14 (12 to 16) 9 (4 to 15) 12 (10 to 15) 15 (12 to 18) 21 (15 to 27) 0.016
Medical treatment (%) 30 (28 to 32) 33 (24 to 42) 30 (26 to 34) 30 (26 to 34) 28 (22 to 35) 0.877

Data are expressed as mean (SD) or percentage (95% confidence interval (CI)).
*Comparison between groups.
CPR, cardiopulmonary resuscitation; Gp, glycoprotein; MI, myocardial infarction.

and 5.1% with GFR , 60 ml/min/1.73 m2 (hazard ratio (HR) Subgroup analysis
4.0, 95% CI 1.8 to 9.1; p = 0.001). The incidence of in- The predictive value of GFR was irrespective of the presence
hospital non-fatal myocardial infarction was low and not or absence of diabetes (fig 2). The cumulative three year
different between the GFR ranges. survival rates among non-diabetic and diabetic patients with
During total follow up, mortality was significantly higher GFR , 60 ml/min/1.73 m2 were 78.9% and 74.7%, respec-
among patients with a GFR , 60 ml/min/1.73 m2 of body tively (HR for diabetes 2.0, 95% CI 0.9 to 4.4; p = 0.09).
surface area than among patients with higher GFR (table 2). Non-diabetic patients with GFR , 60 ml/min/1.73 m2 were
Relative to patients in the higher GFR ranges, patients with at higher risk of death than were diabetic patients with GFR
GFR , 60 ml/min/1.73 m2 were four times more likely to die . 60 ml/min/1.73 m2 (HR 1.9, 95% CI 1.0 to 3.8; p = 0.058).
during follow up (HR 4.0; p , 0.001). The incidence of non- Renal function was predictive of long term mortality
fatal myocardial infarction during total follow up was not irrespective of the revascularisation method applied.
different between the GFR ranges. Kaplan-Meier survival Patients with a GFR , 60 ml/min/1.73 m2 of body surface
analysis showed cumulative three year survival rates of 92.6% area had an HR of 3.6 (95% CI 1.7 to 7.6; p = 0.001) if
with GFR > 130 ml/min/1.73 m2, 95.5% with GFR 90– receiving PCI and an HR of 3.9 (95% CI 1.9 to 8.1; p , 0.001)
129 ml/min/1.73 m2, 91.9% with GFR 60–89 ml/min/ if receiving CABG. HR was 2.9 (95% CI 0.9 to 8.8; p = 0.065)
1.73 m2, and 76.8% with GFR , 60 ml/min/1.73 m2 for those being managed without revascularisation and
(p , 0001 by log rank) (fig 1). The cumulative three year with medical treatment only. Among patients without a
survival rate was 96.9% among patients with creatinine > 50% stenosis in the epicardial segments of the coronary
concentrations on admission not available. vessels (n = 173) and therefore presumably with either

Table 2 Association between glomerular filtration rate on admission and outcome

Group by GFR (ml/min/1.73 m2)
Hazard ratio
>130 (n = 106) 90–129 (n = 548) 60–89 (n = 570) ,60 (n = 176) (95% CI)* p Value*

In-hospital (%)
Death 0 0.4 (0 to 0.9) 2.6 (1.3 to 4.0) 5.1 (1.8 to 8.4) 4.0 (1.8 to 9.1) 0.001
Non-fatal MI 0 2.7 (1.4 to 4.1) 3.3 (1.9 to 4.8) 2.3 (0.1 to 4.5) 1.0 (0.4 to 2.9) 0.984
Total follow up (%)
Death 3.8 (0.1 to 7.5) 2.6 (1.2 to 3.9) 6.5 (4.5 to 8.5) 15.4 (10.0 to 20.8) 4.0 (2.5 to 6.4) ,0.001
Non-fatal MI 6.6 (1.8 to 11.4) 3.1 (1.7 to 4.6) 5.1 (3.3 to 6.9) 3.4 (0.7 to 6.2) 1.0 (0.4 to 2.3) 0.983
Combined end point of death or
non-fatal MI 10.4 (4.5 to 16.3) 5.5 (3.6 to 7.4) 11.2 (8.6 to 13.8) 17.7 (12.0 to 23.4) 2.5 (1.7 to 3.7) ,0.001

Data are expressed as percentage (95% CI).

*GFR ,60 ml/min versus GFR >60 ml/min.

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Renal function and long term mortality after ACS 905

Figure 1 Cumulative survival in

relation to glomerular filtration rate on
admission.

thromboembolic, vasospastic, microvascular, or non-cardiac p = 0.001) (table 3). Of note, diabetes fell out of the
disease, the event rate during follow up was very low. Only predictive model when renal function was considered.
four patients died or experienced non-fatal myocardial
infarction. Therefore, this study did not have sufficient DISCUSSION
statistical power to assess the predictive value of renal This large study of 1400 consecutive patients with UA/
function in this subset of patients. NSTEMI treated uniformly very early and predominantly
with PCI confirmed baseline renal function as a strong
Multivariate analysis independent predictor of in-hospital and long term mortality
Together with calculated GFR, all baseline, demographic, and thereby extends this important finding to this latest
clinical, and angiographic variables shown in table 1 were revascularisation strategy. With its universal availability,
entered into a multivariate Cox regression analysis. After calculated GFR may serve as an inexpensive new tool for
adjustment for these cofounders, a GFR , 60 ml/min/ risk stratification in UA/NSTEMI. The increased risk of death
1.73 m2 of body surface area was found to be a strong with chronic kidney disease was independent of and additive
independent predictor of long term mortality (HR 2.6; to the risk associated with diabetes, in full agreement with an
observation in CABG patients reported by the BARI (bypass
angioplasty revascularisation investigation) investigators.17
Moreover, when diabetes and renal function were taken into
consideration together, chronic kidney disease was the
dominant risk factor. The adjusted HR for long term
mortality was 2.6 for those with a GFR of , 60 ml/min/
1.73 m2, whereas diabetes was no longer an independent
predictor.

Table 3 Independent predictors of long term mortality in

multivariate analysis
HR (95% CI) p Value

GFR ,60 ml/min/1.73 m2 2.55 (1.46 to 4.46) 0.001

Cardiogenic shock 5.05 (1.77 to 14.45) 0.003
White cell count .106109/l 3.10 (1.82 to 5.28) ,0.001
Troponin T >0.01 mg/l 2.46 (1.25 to 4.84) 0.010
Coronaries with >50% stenosis 1.59 (1.12 to 2.26) 0.010
Age (continuous) 1.07 (1.04 to 1.10) ,0.001
T wave inversion 0.44 (0.21 to 0.92) 0.030

For the comparison of GFR ,60 ml/min versus >60 ml/min,

cardiogenic shock versus no cardiogenic shock, white cell count
.106109/l versus white cell count (106109/l, troponin T >0.01 mg/l
versus troponin T ,0.01 mg/l, for one additional coronary artery with
>50% stenosis, for an increase in age of one year, and T wave inversion
Figure 2 Cumulative survival in relation to the presence of diabetes versus no T wave inversion.
mellitus (DM) and chronic kidney disease (CKD). CKD was defined as a CI, confidence interval; HR, hazard ratio.
glomerular filtration rate , 60 ml/min/1.73 m2.8

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906 Mueller, Neumann, Perruchoud, et al

Among the explanations for why chronic kidney disease is Renal function in patients undergoing elective PCI
such a potent risk factor for adverse outcomes in UA/ Recent studies have extended the correlation between renal
NSTEMI, excess co-morbidity, less use of beneficial treat- insufficiency and clinical outcome to patients undergoing
ments for patients with chronic kidney disease, excess elective PCI.25–27 Chronic kidney disease was independently
toxicity from conventional treatments used, and the unique associated with mortality and other adverse events during
pathobiology of the chronic kidney disease state seem to be and after PCI, in a dose dependent manner. Risk increased
the most decisive.8 Given the importance of the under use even when renal insufficiency was mild, with a doubling of
of cardioprotective treatments for patients with chronic mortality at one year.25
kidney disease and the finding that low utilisation of
reperfusion strategies contributed significantly to the poor Unique risks and benefits of revascularisation among
prognosis of these patients in previous studies,10 this study patients with chronic kidney disease
appears particularly strong in that it is based on a pro- Coronary angiography, PCI, and CABG are associated with
spective, consecutive, and unselected patient cohort and that increased morbidity and mortality among patients with
a uniform revascularisation strategy was applied to all chronic kidney disease.7 17 25–29 This excess in risk is at least
patients. These factors eliminate selection bias and ease partly explained by the patients’ baseline characteristics.
the extrapolation of findings into clinical practice. However, patients with chronic kidney disease are a high risk
Therefore, our data support the findings of the TACTICS- subgroup of patients with UA/NSTEMI and that is exactly the
TIMI 18 (treat angina with Aggrastat and determine cost subset of patients who derive the maximum benefit from
of therapy with an invasive or conservative strategy– early revascularisation.2–6 Randomised trials specifically
thrombolysis in myocardial infarction 18) trial, where including patients with chronic kidney disease are lacking
patients with a serum creatinine concentration of more than but would be highly desirable. The cumulative three year
2.5 mg/dl (221 mmol/l), a history of PCI or CABG within the survival rate was 76.8% among patients with GFR , 60 ml/
preceding six months, factors associated with an increased min/1.73 m2 in this study. This compares favourably with
risk of bleeding, cardiogenic shock, or severe systemic cohorts treated primarily medically.9–11 Although any com-
disorders were excluded.18 Moreover, the median time parison with historical controls has important limitations,
interval from admission to PCI was five hours in this study our data along with those of others suggest that patients with
as compared with 25 hours in the invasive strategy of the chronic kidney disease fair better with early revascularisa-
TACTICS-TIMI 18 trial.18 Other particular features of the tion.2 3 5 6 18 This is further supported by recent registry data
present study are the long term follow up and that the extent suggesting that coronary stenting, which was used in our
of coronary artery disease was quantified for all patients and study as the predominant revascularisation procedure, has
entered into the multivariate analysis as a potential significantly improved procedural success rates and long term
confounder. outcome for patients with chronic kidney disease.29

Rationale for renal function as a predictor of outcome Limitations

Our results extend renal function as a powerful prognostic Firstly, serum creatinine was used for the calculation of GFR.
factor to an increasingly common disease treated with the This measure has limitations, as it may not be in a stable
latest revascularisation strategy. Very early revascularisation state and may reflect hydration status. Secondly, any
with predominantly PCI does not ameliorate the negative equation for the calculation of GFR inherently includes age,
prognostic impact of renal function. The excess risk in and age has been a consistent factor in predicting cardiac
patients with chronic kidney disease observed in previous outcome.
studies can therefore not be sufficiently explained by lower
efficacy and greater adverse events associated with thrombo- Conclusion
lytic treatment or extended periods of conservative anti- Renal function is a strong independent predictor of in-
thrombotic and anti-ischaemic treatment. Our data support hospital and long term mortality in UA/NSTEMI treated with
the importance of excess co-morbidities8 contributing to the very early revascularisation. With its universal availability,
inferior outcome for patients with impaired renal function. GFR may serve as an inexpensive new tool for risk
Firstly, patients with a GFR , 60 ml/min/1.73 m2 were older, stratification in UA/NSTEMI.
they were more often diabetic, and coronary artery disease
was more advanced with high rates of prior myocardial
ACKNOWLEDGEMENTS
infarction and three vessel disease. Secondly, UA/NSTEMI This study was supported by research grants from the Novartis
was more severe in patients with a GFR , 60 ml/min/ Foundation, the Krokus Foundation, and the University of Basel (to
1.73 m2, as cardiopulmonary resuscitation, defibrillation, ST Dr Mueller).
segment depression, and increased troponin T were seen
more often than among patients in the higher GFR ranges. .....................
However, even after adjustment for these differences, the Authors’ affiliations
presence of a GFR , 60 ml/min/1.73 m2 was still predictive C Mueller*, F-J Neumann, H J Buettner, Herz-Zentrum, Bad Krozingen,
Germany
of long term mortality. Therefore, the unique pathobiology of
André P Perruchoud, University Hospital Basel, Department of Internal
the chronic kidney disease state8 seemed to contribute Medicine, Basel, Switzerland
additionally to mortality during follow up.
*Also at the University Hospital Basel
This study was not designed to clarify the causal mediators
of renal risk. Candidate mechanisms may include the
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IMAGES IN CARDIOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
doi: 10.1136/hrt.2003.029488
Free floating thrombus in left atrium

A
78 year old male patient presented
with dyspnoea (New York Heart
Association functional class III) with
past history of left sided hemiparesis two
years previously with atrial fibrillation on
ECG. Chest x ray showed evidence of
enlargement of the left atrium, right ven-
tricle, and right atrium with redistribution of
blood flow toward the lung apices.
M mode echocardiography showed multi-
ple dense lines over the mitral valve area
(thickened valve), reduced E-F slope of
mitral valve (15 mm/s), with erratically
moving multiple lines in an enlarged left
atrium (73 mm).
Two dimensional echocardiography showed
thickened, non-pliable leaflets, and a calci-
fied valve annulus with a mitral valve area
of approximately 0.7 cm2.
A globular, hyperechoic mass (thrombus)
of 3 6 2 cm was detected in an enlarged left
atrium. It was moving freely from the upper
part of the left atrium to the lower part and
was bouncing back after striking the mitral
valve leaflets. The mass was unable to find
its way through the mitral valve as it was
larger than the mitral valve orifice. The mass
was a dislodged thrombus that had failed to
embolise.

P Vaid
[email protected]

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