Heart failure complicating acute myocardial infarction. Does the time of presentation matter?

Heart failure complicating acute myocardial infarction. Does the time of presentation matter?

International Journal of Cardiology 204 (2016) 48–50 Contents lists available at ScienceDirect International Journal of Cardiology journal homepage:...

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International Journal of Cardiology 204 (2016) 48–50

Contents lists available at ScienceDirect

International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard

Correspondence

Heart failure complicating acute myocardial infarction. Does the time of presentation matter? Luciano Consuegra-Sánchez a,⁎, Leticia Jaulent-Huertas a, Marta Vicente-Gilabert b, German Escudero-García a, Ángela Díaz-Pastor a, José Galcerá-Tomás b, Antonio Melgarejo-Moreno a a b

Hospital Universitario Santa Lucía de Cartagena, Murcia, Spain Hospital Clínico Universitario Virgen de la Arrixaca de Murcia, Murcia, Spain

a r t i c l e

i n f o

Article history: Received 15 November 2015 Accepted 22 November 2015 Available online 23 November 2015 Keywords: Myocardial infarction Heart failure Prognosis

Previous studies have shown evidence about the prognostic significance of heart failure (HF) complicating an acute myocardial infarction (MI) [1]. Recently, we read with interest the manuscript of Greco et al. [2] about the patients of the Italian National Registry. These authors reported that the identification of HF is a relevant complication subsequent to acute MI that deeply affects both short- and long-term prognosis. These findings are consistent with those recently published of Desta et al. [3] about the patients of the Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapies (SWEDEHEART) registry. This study emphasized that HF is steadily decreasing but remains a factor that dramatically impacts adversely the outcome after MI. However, in our view, both studies had a major limitation [2,3] in that patients who presented with clinical HF on admission could not be distinguished from those who developed HF during hospital stay. In this line, it has been suggested that the distinction of both forms of HF is of paramount importance since they are related to different physiopathological pathways [4,5]. It has been reported that HF at the time of admission is mainly related to a higher age and prevalence of previous comorbidities and cardiovascular risk factors [4,5]. On the other side, that form of HF appeared during hospital stay (and not present at the time of admission) is related to the size of MI and/or mechanical complications. ⁎ Corresponding author at: Coronary Care Unit, University Hospital Santa Lucia, Paraje Los Arcos s/n, 30201 Cartagena, Murcia, Spain. E-mail address: [email protected] (L. Consuegra-Sánchez).

http://dx.doi.org/10.1016/j.ijcard.2015.11.145 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.

Thus, in the present study, we aimed to investigate the baseline characteristics and prognosis associated with HF stratifying by the time of appearance in patients with acute MI. This was a prospective observational study that recruited all consecutive patients with acute MI from January 1998 to March 2014. The exclusion criteria were (1) acute MIs occurring during revascularization and (2) acute MI diagnosis later invalidated in favor of another diagnosis. HF at admission was defined as Killip class N 1 [6]. HF during hospitalization was defined as Killip class N 1 beyond the initial 24 h and Killip class = 1 at the time of admission. The study protocol was approved by the Clinical Investigation Committee, informed consent was obtained from each patient and the study protocol conforms to the Declaration of Helsinki. The primary end point was the occurrence of in-hospital and postdischarge long-term all-cause mortality. This was confirmed either by review of medical records and/or telephone contact. The relative risk of in-hospital and long-term death was derived from multivariable regression analyses. Variables considered as covariates were those that have shown a potential impact upon mortality in previous studies and were independently associated with mortality (p b 0.05): baseline variables (age, gender, hypertension, diabetes mellitus, current smoker, dyslipidemia, preexisting myocardial infarction, heart failure, stroke, peripheral arterial disease, atrial fibrillation, cancer, chronic renal disease, chronic obstructive pulmonary disease, ST segment elevation), additional procedural variables (reperfusion, including coronary revascularization) and heart rate, systolic blood pressure, glycemia on admission, peak CK-MB and left ventricular ejection fraction. In order to test the robustness of the data, we performed 3000 iterations of bootstrap validation analyses. All was performed using SPSS, version 20.0 (IBM, USA). Among 7647 patients admitted to hospitalization, 1865 (24.4%) presented with HF at admission and 511 (6.7%) developed HF during hospitalization. Patients with HF during hospitalization showed (compared to those with HF at admission) significantly a lower prevalence of cardiovascular risk factors and comorbidities (Table 1). They further showed a better previous New York Heart Association (NYHA) functional class compared to those HF at admission. A STEMI diagnosis was significantly more frequent in patients with HF during hospitalization. Peak mass CK-MB and ∑ ST segment elevation were also significantly higher. Both HF at admission and during hospitalization showed similar inhospital mortality but substantially higher compared to patients without HF (Fig. 1). However, long-term mortality (median = 5.5 years,

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Table 1 Baseline characteristics and complications stratified by the presence of heart failure.

Age mean ± SD, years Female, n (%) BMI, kg/m2 Diabetes, n (%) Hypertension, n (%) Dyslipidemia, n (%) Current smoker, n (%) P. arteriopathy, n (%) Previous CVD, n (%) Previous IHD, n (%) CRF, n (%) COPD, n (%) Cancer, n (%) NYHA ≥2, n (%) Previous AF, n (%) Delay to admission, mean ± SD, minutes No chest pain, n (%) STEMI, n (%) Heart rate, mean ± SD, bpm Systolic BP, mean ± SD, mmHg Glycemia at admission, mean ± SD, mg/dL Peak mass CKMB, ng/mL ∑ST segment elevation, mm Reperfusion,b n (%) LVEF, %, mean ± SD Cardiac catheterization, n (%) Number of diseased coronary vessels, mean ± SD Mechanical complications,c n (%) Angor/reinfarction, n (%) Major bleeding,d n (%) In-hospital mortality, n (%) Long-term mortality, IR (95% CI), per 100 patients-year.

No HF (n = 5271, 68.9%)

HF at admission (n = 1865, 24.4%)

HF during hospitalization (n = 511, 6.7%)a

p value

64 ± 13 1184 (22.5) 27.9 ± 4.3 1642 (31.2) 2836 (53.8) 2005 (38.1) 2220 (42.1) 322 (6.1) 355 (6.7) 2450 (46.5) 178 (3.4) 420 (8.0) 211 (4.0) 662 (12.6) 133 (2.5) 207 ± 310 410 (7.8) 4061 (77.0) 76 ± 20 138 ± 27 166 ± 79 137 ± 158 7±7 4286 (81.3) 52 ± 8 3621 (68.7) 1.5 ± 0.8 52 (1.0) 427 (8.1) 101 (1.9) 136 (2.6) 3.0 (2.9–3.3)

73 ± 11 673 (36.1) 28.0 ± 4.3 1020 (54.7) 1203 (64.7) 670 (36.2) 438 (23.5) 276 (14.8) 282 (15.1) 1091 (58.6) 286 (15.4) 278 (14.9) 122 (6.5) 916 (49.2) 139 (7.5) 255 ± 451 584 (31.4) 1279 (68.6) 95 ± 28 130 ± 38 237 ± 119 165 ± 203 8±8 1232 (66.1) 40 ± 11 1115 (59.8) 1.9 ± 1.1 88 (4.7) 142 (7.7) 89 (4.8) 583 (31.3) 11.3 (10.5–12.2)

72 ± 11 186 (36.4) 27.8 ± 4.4 214 (41.9) 281 (55.0) 156 (30.5) 137 (26.8) 50 (9.8) 53 (10.4) 260 (50.9) 39 (7.6) 70 (13.7) 35 (6.8) 135 (26.5) 27 (5.3) 296 ± 797 84 (16.5) 410 (80.2) 81 ± 24 128 ± 27 209 ± 114 220 ± 226 9±9 418 (81.8) 41 ± 10 362 (70.8) 1.8 ± 1.0 41 (8.0) 102 (20.4) 36 (7.0) 143 (28.0) 7.0 (6.0–8.3)

b0.001 b0.001 0.696 b0.001 b0.001 0.002 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001 b0.001

AF = Atrial fibrillation, BMI = Body mass index, BP = Blood Pressure, BPM = beats per minute, CI = Confidence Interval, CKMB = creatine kinase MB isoform, COPD = chronic obstructive pulmonary disease, CVD = cerebrovascular disease, CRF = chronic renal failure, IHD = ischemic heart disease, IR = incident rate, LVEF = left ventricular ejection fraction, NYHA = New York Heart Association, SD = standard deviation, STEMI = ST segment elevation myocardial infarction, ∑ST segment elevation = sum of millimeters of J-point elevation in each derivation. a Defined as HF that appears during hospitalization and it is not present at the time of admission. b Defined as fibrinolysis, primary angioplasty, rescue angioplasty, next-day angioplasty after successful revascularization, any angioplasty during hospitalization and surgical coronary artery bypass graft. c Defined as rupture of the septum or free ventricular wall or papillary muscle. d Defined as retroperitoneal, intracranial or severe gastrointestinal bleeding or need a blood transfusion.

Fig. 1. Kaplan–Meier survival method showing mortality differences according to the presence of heart failure (HF).

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interquartile range = 1.8–8.6) was higher in patients with HF at admission compared to those with HF during hospitalization. The rate of mechanical and ischemic complications was also higher in patients with HF during hospitalization (Table 1). In a multivariable setting, both HF at admission (odds ratio = 4.88, 95% CI = 3.62–6.58) and HF during hospitalization (odds ratio = 6.20, 95% CI = 4.38–8.78) were independent predictors of in-hospital mortality. At long-term (after discharge), HF at admission (hazard ratio = 1.36, 95% CI = 1.19–1.55) remained as an independent predictor of mortality but HF during hospitalization did not (hazard ratio = 1.22, 95% CI = 0.97–1.50). Our findings indicate the following: First, clinical baseline characteristics of patients with HF during hospitalization are different compared to those with HF at admission. Second, the crude inhospital mortality is similar between HF during hospitalization and HF at admission. Third, HF at admission is associated with higher crude long-term mortality compared to patients with HF during hospitalization. Fourth, our study confirms that both forms of HF are clinically relevant predictors of short-term mortality. Fifth, at long-term follow-up, only HF at admission remained as an independent predictor.

Conflict of interest The authors have nothing to disclose. References [1] F. Najafi, A.J. Dobson, M. Hobbs, K. Jamrozik, Temporal trends in the frequency and longer term outcome of heart failure complicating myocardial infarction, Eur. J. Heart Fail. 9 (2007) 879–885. [2] C. Greco, S. Rosato, P. D'Errigo, G.F. Mureddu, E. Lacorte, F. Seccareccia, Trends in mortality and heart failure after acute myocardial infarction in Italy from 2001 to 2011, Int. J. Cardiol. 184 (2015) 115–121. [3] L. Desta, T. Jernberg, I. Löfman, et al., Incidence, temporal trends, and prognostic impact of heart failure complicating acute myocardial infarction. The SWEDEHEART Registry (Swedish Web-System for Enhancement and Development of EvidenceBased Care in Heart Disease Evaluated According to Recommended Therapies): a study of 199,851 patients admitted with index acute myocardial infarctions, 1996 to 2008, JACC Heart Fail. 3 (3) (2015) 234–242. [4] M.F. Minicucci, P.S. Azevedo, B.F. Polegato, S.A. Paiva, L.A. Zornoff, Heart failure after myocardial infarction: clinical implications and treatment, Clin. Cardiol. 34 (7) (2011) 410–414. [5] M.A. Pfeffer, E. Braunwald, Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications, Circulation 81 (4) (1990) 1161–1172. [6] T. Killip 3rd, J.T. Kimball, Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients, Am. J. Cardiol. 20 (4) (1967) 457–464.