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Vol. 68. Issue 3.
Pages 234-241 (March 2015)
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Vol. 68. Issue 3.
Pages 234-241 (March 2015)
Special article
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Update on Ischemic Heart Disease and Intensive Cardiac Care
Actualización en cardiopatía isquémica y cuidados críticos cardiológicos
Alessandro Sionisa,
Corresponding author

Corresponding author: Hospital Universitario de la Santa Creu i Sant Pau, Instituto de Investigación Biomédica Sant Pau (IIB Sant Pau), Sant Antoni M. Claret 167, 08025 Barcelona, Spain.
, Juan Miguel Ruiz-Nodarb, Antonio Fernández-Ortizc, Francisco Marínd, Emad Abu-Assie, Oscar Díaz-Castrof, Ivan J. Nuñez-Gilc, Rosa-Maria Lidóng
a Servicio de Cardiología, Hospital Universitario de la Santa Creu i Sant Pau, Barcelona, Spain
b Servicio de Cardiología, Hospital General Universitario de Alicante, Alicante, Spain
c Servicio de Cardiología, Hospital Clínico San Carlos, Universidad Complutense de Madrid, Madrid, Spain
d Servicio de Cardiología, Hospital Clínico Universitario Virgen de la Arrixaca, El Palmar, Murcia, Spain
e Servicio de Cardiología, Hospital Clínico Universitario, Santiago de Compostela, A Coruña, Spain
f Servicio de Cardiología, Complejo Hospitalario Universitario de Pontevedra, Pontevedra, Spain
g Servicio de Cardiología, Hospital Universitario Valld’Hebron, Barcelona, Spain
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Table. Relevant Molecular Biomarkers in Studies Published in Recent Months

This article summarizes the main developments reported in 2014 on ischemic heart disease, together with the most important innovations in intensive cardiac care.

Acute coronary syndrome
Myocardial infarction
Acute cardiac care

Se revisan los principales avances publicados en el año 2014 sobre cardiopatía isquémica, junto con las novedades más relevantes acerca de cuidados críticos cardiológicos.

Palabras clave:
Síndrome coronario agudo
Infarto de miocardio
Cuidados críticos cardiológicos
Full Text

According to data from the RECALCAR registry,1 31.2% of the total number of deaths in 2010 in Spain were due to cardiovascular diseases. Nevertheless, Spain has one of the lowest mortality rates for coronary artery disease (CAD) in Europe for both sexes. Recent data indicate that Spanish mortality rates for cardiovascular diseases have dropped 36% in men and 40% in women since the mid-1970s.

This year, results from the DIOCLES2 study have been published for the management and prognosis of acute coronary syndrome (ACS) in Spain. This is part of an ongoing project by the Coronary Artery Disease and Acute Cardiac Care Group to promote periodical ACS registries. These registries provide valuable information about the prognosis and management of ACS over time in our country.3–5 The DIOCLES study included 2557 patients who were hospitalized between January and June, 2012, with suspected ACS in 44 randomly-selected Spanish hospitals. Hospital mortality was 4.1%, which is significantly lower than the rate reported in the latest MASCARA6 registry (5.7%), as seen in the Table.7–28 Among the 1602 patients with non—ST-segment elevation ACS (NSTEACS) included in the registry (62.7% of the total), the use of p2y12 inhibitors increased (from 42%- 91%), the use of glycoprotein IIb/IIIa inhibitors decreased (from 21% to 4%, respectively), and the use of angiography during hospitalization increased (from 63% to 81%) as did percutaneous coronary intervention (PCI) rates (from 34% to 53%). These data confirm the gradual incorporation of clinical practice guideline recommendations in Spain; at the same time, ACS-related in-hospital mortality had significantly decreased.


Relevant Molecular Biomarkers in Studies Published in Recent Months

Molecule  Use/association  Reference 
Proinflammatory cytokine/nuclear protein HMGB1  Levels proportional to coronary atherosclerosis  Haghjooy-Javanmard, et al7 
Serum choline plasmalogens (phospholipids)  Markers of coronary atherosclerosis  Nishimukai et al8 
GDF 15  Association with ischemic heart disease severity; better than ischemia-modified albumin and PAPP-A  Fan et al9 
HBA1c in nondiabetic patients  Independent predictor of coronary artery disease and its severity  Garg et al10 
Serum tryptase  Prognostic relationship between tryptase levels and the SYNTAX score in acute coronary syndrome  Pastorello et al11 
Adiponectin and derivatives  Development of coronary disease  Wang et al12 
    Kawagoe et al13 
Circulating adipokines  Ischemia confirmed with SPECT  Hung et al14 
Apelin  Plasma levels correlated inversely with severity and directly with plaque stability in patients with acute coronary syndrome  Zhou et al15 
Serum adropin  Low levels related with infarction in coronary patients  Yu et al16 
FGF23  Cardiovascular prognosis and influence in response to treatment with ACE inhibitors  Udell et al17 
Circulating osteoglycin and NGAL/MMP9  Predictors of 1-year events after angiography; expressed in vulnerable plaques  Cheng et al18 
S100A9 (platelet protein)  Elevated in patients with infarction; involved in the pathway of thrombosis  Wang et al19 
Serum TGF-β1 and SMAD3  Associated with coronary disease; useful for risk stratification and diagnosis  Chen et al20 
sST2 soluble  Predictor of long-term mortality in stable coronary disease, complementary to NT-proBNP and TnT  Dieplinger et al21 
Levels of HDL-C  Prognostic after acute coronary syndrome (Spanish cohort) and in stable patients (COURAGE substudy)  Fácila et al22 
    Acharjee et al23 
PSA and fPSA  Related with extension and prognosis in acute coronary syndrome  Durmaz et al24 
BNP/NT-proBNP  Detection of ischemia after exercise; prognostic over the long term in stable coronary heart disease (meta-analysis)  Lee et al25 
    Wei et al26 
Monocyte chemoattractant protein-1, galectin-3  Associated with cardiovascular events  Tuñón et al27 
Copeptin (carboxyl-terminus of the vasopressin prohormone secreted stoichiometrically with arginine-vasopressin from the neurohypophysis)  As a dual marker strategy, combining myocardial damage (cTn) and endogenous stress (copeptin); early diagnostic accuracy for AMI  Rubini Gimenez et al28 

ACE, angiotensin-converting enzyme; AMI, acute myocardial infarction; BNP, brain natriuretic peptide; cTn: cardiac troponin; FGF23, fibroblast growth factor 23; fPSA, free prostate-specific antigen; GDF 15, growth differentiation factor 15; HBA1c, glycated hemoglobin; HDL-C, high-density lipoprotein cholesterol; HMGB1, high-mobility group protein B1; MMP-9, matrix metallopeptidase 9; NGAL, neutrophil gelatinase-associated lipocalin; NT-proBNP, N-terminal pro-brain natriuretic peptide; PAPP-A, pregnancy-associated plasma protein A; PSA, prostate-specific antigen; SMAD3, decapentaplegic homolog 3; SPECT, single-photon emission computed tomography; sST2, soluble suppression of tumorigenicity 2; TGF-β1, transforming growth factor β1; TnT, troponin T.

Interesting data have also been provided by the EURHOBOP registry,29 which shows important differences among European countries in ACS management. The study included 12 231 consecutive ACS patients who had been admitted to hospital from 2008 to 2010 in 7 European countries (Germany, Spain, Finland, France, Greece, Italy, and Portugal). There was a higher prevalence of smokers in Greece, France and Spain, and there were more diabetic patients in Spain and Portugal. In patients with NSTEACS (67.2% of the total), the most notable difference was fewer angiographies and coronary revascularizations in southern European countries: 66.1% in France, 57.4% in Germany, 44.1% in Finland, 37.3% in Spain, 33.4% in Portugal, and 19.6% in Greece. It should be remembered that these data are from 2010 and, as shown by the DIOCLES study data from 2012, these differences have been decreasing in recent years in Spain.

The differences in CAD prognosis according to sex are still controversial. In the recently published RESCATE II study,30 mortality was similar in women and in men 28 days after an initial ACS (5.57% and 4.46%, respectively; P = .39), but 7-year mortality was higher in men (hazard ratio [HR] = 1.93; 95% confidence interval [95%CI], 1.46-2.56; P < .001).


There is a growing interest in understanding which underlying mechanisms lead to atherosclerotic plaque destabilization and the subsequent appearance of ACS. Local and systemic inflammation play a fundamental role in the pathophysiology of ACS. A related review by Libby et al31 merits attention as it offers a global perspective of the mechanisms by which inflammation can lead to the appearance of ACS. These observations have important potential therapeutic implications for the prevention of ACS and its recurrence.


The RECALCAR registry1 has demonstrated a high prevalence of classic cardiovascular risk factors in Spain, which is disproportionate with the low incidence of cardiovascular diseases compared with other European countries. A possible explanation for this contrast is that the negative impact on health of some of these risk factors, such as the increasing rates of obesity and diabetes as well as smoking in women, still has not had sufficient time to increase the incidence of cardiovascular diseases.

In the EUROASPIRE (European Action on Secondary Prevention through Intervention to Reduce Events) IV study,32 most patients did not meet the established therapeutic objectives for their risk factors, even though a high percentage of patients with CAD received proper treatment. According to a recent meta-analysis, approximately 9% of cardiovascular events in Europe could be attributed to a low degree of adherence to treatment with statins and antihypertensive medications as there is an inverse association between the degree of adherence and the risk of events.33

The latest data from clinical drug trials have focused on antidiabetic and hypolipidemic agents. Two dipeptidyl peptidase-4 inhibitors, saxagliptin and alogliptin, were tested in the SAVOR-TIMI 5334,35 and EXAMINE36 studies, respectively. Both inhibitors were not inferior to placebo for the appearance of adverse cardiovascular events. Saxagliptin, however, was associated with an increase in hospitalizations due to heart failure (HR = 1.27; 95%CI, 1.07-1.51), especially in patients with elevated levels of natriuretic peptides, a history of heart failure, or chronic kidney failure. Therefore, its use is not recommended in patients with cardiovascular disease.35

Although low high-density lipoprotein cholesterol levels are a powerful independent predictor for cardiovascular risk, recent data suggest that this may not be applicable to high-risk patients treated with statins. When low high-density lipoprotein cholesterol levels were evaluated in patients treated with different statin doses low high-density lipoprotein cholesterol levels were only related to increased cardiovascular risk in those not taking statins or only taking low statin doses, but not in those taking high doses.37 In a recent meta-analysis, high-density lipoprotein cholesterol-targeted drug treatments with niacin, fibrates, and cholesteryl ester transfer protein inhibitors (combined with statins) did not reduce the number of cardiovascular events.38

An important innovation is the publication of the results obtained with PCSK9 inhibitors. These drugs had already been shown to be effective at significantly reducing low-density lipoprotein cholesterol in phase II studies. The reduction was maintained with a 1-year treatment, showing good tolerance to the drug, in the recent OSLER study.39 The results of the LAPLACE-2 study40 have also shown that the combination of evolucumab and a statin significantly reduced low-density lipoprotein cholesterol when compared with a statin plus ezetimibe or a statin alone.

The GAUSS-241 and MENDEL-242 studies evaluated the efficacy of evolucumab in hypercholesterolemic patients with intolerance to statins. In both studies, significant reductions were obtained in low-density lipoprotein cholesterol compared to ezetimibe and placebo, with no increase in adverse effects. Despite promising results, PCSK9 inhibitors will have to demonstrate their superiority over statins in the prevention of cardiovascular events. Lastly, we should not forget that the greatest efforts for prevention should target lifestyle changes.


The field of biomarkers continues to be dominated by troponins, as seen in the TRAPID-AMI study,43 which was presented at the most recent congress of the European Society of Cardiology. It involved a prospective validation of an algorithm that predicted the determination of ultrasensitive troponin T both at admission and 1 h afterward in a cohort of 1282 individuals who were treated for chest pain in the emergency department. The algorithm was able to rule out ACS in 63.4% of the patients, with a negative predictive value for infarction of 99.1%. The mortality rate in this group of patients was 0.1%, which confirms that this algorithm is safe and effective when used in conjunction with the patient medical history, physical examination, and electrocardiogram.

We have also seen the presentation of new and interesting diagnostic/prognostic point scales that combine clinical variables and biomarkers, such as the BIO-VILCAD44 in chronic CAD and INTERHEART-cholesterol,45 which analyzed a Spanish cohort with chest pain.

Data about the value of membrane microvesicles (particles that are generally derived from platelets) in infarction46 or microRNA in several contexts have expanded the scope of both diagnostic and prognostic studies.47–49 New data have also been published about B-type natriuretic peptide24,26 and copeptin.27 The current state of nontroponin biomarkers is summarized in the Figure and is discussed in extensive detail by Millard and Tranter50 in their excellent review.


Hospital mortality (A) and 6-month mortality (B) stratified by type of acute coronary syndrome in the DIOCLES and MASCARA registries; ACS, acute coronary syndrome; DIOCLES: Descripción de la Cardiopatía Isquémica en el Territorio Español; MASCARA: Manejo del Síndrome Coronario Agudo. Registro Actualizado; NSTEACS, non—ST-segment elevation myocardial infarction.


As for physiological or imaging techniques, it is important to highlight the publication of consensus documents: one about the definitions of ischemia with various diagnostic methods,51 and another about the criteria for the appropriate use of the different multimodal diagnostic techniques in chronic CAD.52

A prospective study of 3656 patients evaluated the usefulness of additional diagnostic tests after diagnostic ergometry. The diagnostic performance of ergometry was lower in patients with a negative test and those who showed rapid recovery of electrical changes. Meanwhile, it was higher in those who had a clinically positive test (typical angina), even in the absence of electrocardiographic changes, or in patients with positive clinical and electric ergometry.53 Using speckle tracking on stress echocardiography, Peteiro et al54 observed that basal rotation at peak exercise is deteriorated in patients with an ischemic response to exercise. In contrast, apical rotation and torsion are similar to those of patients with normal tests.

In noninvasive angiography by multidetector computed tomography (CT), a new analysis of the ROMICAT-II (Rule Out Myocardial Infarction/Ischemia Using Computer-Assisted Tomography II) study showed that, in patients with chest pain and initially normal electrocardiogram and troponins, the detection of high-risk plaque on multidetector CT was an independent prognostic factor of significant coronary disease, and it was shown to be useful for clinical staging.55 Furthermore, several articles have validated the long-term prognostic value of multidetector CT in patients with suspected CAD.55–57

In nuclear medicine, the combination of single-photon emission CT/CT to determine fractional flow reserve also improved the detection of coronary disease.58 In addition, the SPARC study59 analyzed the 2-year treatment costs in 1703 patients with suspected coronary disease, which were less for single-photon emission CT compared with multidetector CT and positron emission tomography, with no differences in mortality rate. Researchers of the BASKET LATE IMAGING study60 showed the prognostic value of single-photon emission CT for detecting ischemia 5 years after percutaneous revascularization. They indicated that abnormal findings are frequent, regardless of symptoms, and are usually located in regions that had not been treated.

Inducible ischemia, detected with stress cardiac magnetic resonance, was the most powerful predictor for major events in 391 patients with ventricular dysfunction.61 Last of all, the CE-MARC study62 showed higher sensitivity of cardiovascular magnetic resonance compared with single-photon emission CT in 235 women and 393 men with suspected angina; no differences were detected between sexes.


The results of the SIGNIFY63 clinical trial were presented at the most recent congress of the European Society of Cardiology. The study randomly assigned 19 102 patients with stable CAD, without heart failure, and with a heart rate of ≥ 70 beats per minute to receive either ivabradine or a placebo with optimal medical treatment. The primary outcome was a composite of cardiovascular mortality and nonfatal myocardial infarction. The incidence of bradycardia was significantly greater in the ivabradine group (18.0% vs 2.3%; P < .001), and was the main reason for suspending the drug. After a follow-up of 27.8 months, no significant differences were observed in the primary objective between the ivabradine and placebo groups (6.8% vs 6.4%, respectively; HR = 1.08; 95%CI, 0.96-1.20; P = .20). Likewise, no significant differences were found between the ivabradine and placebo groups for the secondary endpoints of cardiovascular death and nonfatal myocardial infarction. In the patients with angina, ivabradine significantly reduced the number of angina episodes (P = .01). However, in patients with Canadian Cardiovascular Society functional class ≥ II, ivabradine significantly increased the incidence of the primary objective (7.6% vs 6.5%; P = .02) while the absolute risk for cardiovascular death and nonfatal myocardial infarction increased by 1.1%. Given these results, it is expected that the indications for ivabradine in stable CAD will be revised.

At the same congress, the 2-year follow-up results were presented from the FAME 2 study.64 In 1220 patients with stable CAD, the fractional flow reserve (FFR) was measured of the stenoses that were visible on angiography. The 888 patients with at least 1 stenosis with an FFR ≤ 0.80 were randomized to either FFR-guided PCI and treatment with medication or medication alone. The primary outcome was a combination of all-cause death, nonfatal myocardial infarction and urgent revascularization. The incidence of the primary endpoint was significantly lower in the PCI group (8.1% vs 19.5%; HR = 0.39; 95%CI, 0.26-0.57; P < .001), basically due to less urgent revascularization in the PCI group, and no significant differences were observed in mortality or nonfatal myocardial infarction. Therefore, in patients with stable CAD, FFR-guided PCI improves results compared with medication alone. Furthermore, in this study, patients with angiographic stenosis and FFR > 0.80 showed good results with drug therapy alone.


Results have been published from an interesting subanalysis of the PLATO study centered around 5366 patients (48.4% of all NSTEACS) managed without revascularization for the first 10 days after randomization.65 Researchers observed a reduction in the risk for ischemic events that was similar to the PCI treatment groups, with no increased risk of hemorrhages.

As for the optimal duration of treatment with dual antiplatelet therapy after ACS, data continue to appear that corroborate the importance of following the recommendation of clinical guidelines and maintaining dual antiplatelet therapy for at least 12 months. The data of a prospective cohort of 56 440 patients with ACS out of the SWEDEHEART (Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies) registry66 clearly show an increase in risk of death, stroke and reinfarction (HR = 0.84; 95%CI, 0.75-0.95) in patients who stop dual antiplatelet therapy within 3 months after ACS, compared with those who continued this therapy for more than 3 months. Although the risk for major hemorrhages was higher in patients with longer dual antiplatelet therapy (HR = 1.56; 95%CI, 1.18-2.07), the number of bleeding events in absolute terms was small.

The FAMOUS-NSTEMI study67 randomly assigned 350 patients with NSTEACS to either an FFR-guided revascularization strategy or angiography-guided standard care. The 12-month revascularization rate was higher in the group without FFR, but no differences were seen in quality of life or other events. Fractional flow reserve measurement was associated with a change in treatment for 21.6% of the patients.

With regards to pharmacological innovation, this year there has been a report of the failure of Lp-PLA2 inhibitors (lipoprotein-associated phospholipase A2) to prevent ischemic events after ACS. The VISTA-16 study68 randomized 5145 patients to receive either varespladib (500mg/day) or placebo; treatment was initiated within the first 96h following an ACS and lasted for a duration of 16 weeks. This study was prematurely interrupted due to the lack of effectiveness in the main outcome of cardiovascular death, infarction, stroke or unstable angina, and due to a greater risk of infarction in patients treated with varespladib (3.4%) compared with placebo (2.2%) (HR = 1.66; 95%CI, 1.16-2.39). Results have also been published from the SOLID-TIMI 52 study,69 which compared darapladib (160mg/day) with placebo in 13 026 patients after ACS. Treatment with darapladib did not reduce the incidence of recurrent coronary events (death, infarction, or urgent need for revascularization) compared with placebo: 16.3% and 15.6% at 3 years, respectively (HR = 1.00; 95%CI, 0.91-1.09).


Among the new studies presented within the last year, 2 clinical trials merit comment as they reexamine an old argument: should all the arteries be revascularized during primary PCI or only the culprit artery? The PRAMI study70 attempted to answer this question by randomly assigning 465 patients in 5 hospitals in the United Kingdom to either a complete, preventive revascularization strategy or to revascularization of only the culprit artery. The complete revascularization strategy significantly reduced the primary outcome of death from cardiac causes, nonfatal myocardial infarction, or refractory angina at 2 years, with no differences observed in cardiac death. This strategy was most recently evaluated in another British randomized trial, the CvLPRIT study,71 with only 296 patients. The results were similar in the significant reduction of the primary endpoint (which in this instance also included hospitalizations due to heart failure) with revascularization of all the lesions, although mortality was similar and the benefits obtained were in the reduction of repeat PCI or rehospitalizations.

The new guidelines on myocardial revascularization72 maintain the recommendation of revascularizing only the culprit artery during primary PCI and opting for revascularization that is as complete as possible in patients with shock or persistent ischemia after opening the hypothetical culprit artery (class II indication, level of evidence A). A “staged” revascularization strategy that takes place over several days or weeks continues to be the recommendation for the revascularization of nonculprit lesions in patients with symptoms or inducible ischemia (class II indication, level of evidence A).

Another aspect that is still being analyzed is thrombus aspiration during primary PCI. The 1-year follow-up has been published from the TASTE (Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia) study,73 which randomly assigned 7244 patients to routine thrombus aspiration or conventional PCI. Routine aspiration did not reduce mortality, the combined primary endpoint, or thrombosis of the stent the first year. The new guidelines for coronary revascularization reduce the indication of thrombus aspiration during primary PCI, which is currently class II, level of evidence B (may be considered in selected patients).72

The ATLANTIC study74 is a double-blind trial that studied the effectiveness and safety of prehospital treatment with ticagrelor in conjunction with acetylsalicylic acid compared with in-hospital administration. It analyzed coronary flow restoration in the blocked artery, resolution of the ST segment, as well as pretreatment safety. The objective of effectiveness, however, was not met. The pretreatment strategy was safe, with a hemorrhage rate that was low and identical to that in the patients with in-hospital ticagrelor treatment. There was a significant reduction in stent thrombosis in the prehospital strategy group. Furthermore, there was a benefit of pretreatment in the patient subgroup not receiving morphine. The most important limitation of this study is undoubtedly the short time interval between drug administration and reperfusion (48min between randomization and angiography; 31min between the 2 loading doses).

This year, 2 Spanish groups have published their results in the field of reperfusion injury. The METOCARD study75 showed a reduction in infarct size with metoprolol treatment before primary PCI in patients with Killip class I or II infarction. A large-scale clinical trial will analyze the impact of this strategy in terms of the reduction of clinical events. Furthermore, the Ischemic Postconditioning on Microvascular Obstruction in Reperfused Myocardial Infarction clinical assay76 studied the role of postconditioning with balloon inflations after the opening of the artery in patients treated with primary PCI. There was no significant difference between the treatment groups in microvascular obstruction or other parameters for myocardial injury measured by cardiovascular magnetic resonance on the fourth day. Interest in this strategy seems to be waning due to the lack of consistent results and objective benefits.


Elderly patients have higher baseline risk, comorbidities and frailty, which makes them more susceptible to iatrogenesis, which can restrict the use of certain therapies. This year, Revista Española de Cardiología has published an excellent review about the management of these patients.77 It shows that, despite the lack of representation of this age group in many studies, older patients generally benefit from the same therapeutic measures as younger adult populations. Along this same idea, data from a Swedish series have shown that senior patients with ACS are treated conservatively and have fewer angiographies than younger patients, even in advanced healthcare systems in this day and age.78 A meta-analysis of more than 9100 clinical trial patients with NSTEACS has demonstrated that elderly patients experience greater benefits from an invasive approach with early angiography than younger patients, while mortality and recurrence of infarctions are lower.79

Undoubtedly, frailty assessment should be considered part of the systematic medical workup of hospitalized senior patients. In this regard, data should be highlighted from the Swedish SCAAR registry80 about 4876 primary PCI in octogenarian patients (mean age 83 years) who had had NSTEACS in the previous 10 years. The data showed a small reduction in mortality in the first year (26% vs 23%) but no significant reduction in the rates of reinfarction, heart failure, stroke, or bleeding.


Regarding women with ACS, a recent review underlines the well-known disparities in greater diagnostic delay, less use of the invasive approach and other measures with demonstrated effectiveness, higher risk of hemorrhage, and poorer short-term prognosis than in men of the same age.81 The greatest gap was observed among younger adults and patients with ST-segment elevation myocardial infarction, which persisted after controlling for other risk factors. These differences could be explained not only by biological and hormonal factors, but also by others that make men and women different, such as their distinct social roles.

The impact of cardiovascular risk factors is not the same in both sexes. In a recent meta-analysis with more than 850 000 patients and more than 28 000 events, the presence of diabetes mellitus had a much greater impact in women than in men, which resulted in the women having a 40% higher risk for developing CAD.82

It is also clear that women have a greater prevalence of nonatherosclerotic coronary disease, especially before menopause. A recent article studied 366 women under the age of 55 with ACS from the GENESIS PRAXY study,83 all of whom had undergone angiography. In 10% of patients, the lesions were spontaneous coronary dissection, which in many cases had angiographic findings that were compatible with fibromuscular dysplasia. Despite having a lower lesion load and fewer risk factors on hospital admission, the prognosis after hospital discharge of these patients was poor, with a 1-year mortality rate of 7% and a rehospitalization rate of 17%.


Firstly, we highly recommend the excellent series of review articles about different topics related to critical care that has been published since August 2013 in the New England Journal of Medicine.84

General critical care

It is important to highlight a new contribution to one of the classic debates in medicine: should patients with hypovolemic shock be resuscitated with colloids or crystalloids? The multicenter CRISTAL study85 compared treatment with either colloids or crystalloids in more than 2800 patients with hypovolemic shock. There was no difference in the primary outcome of 28-day mortality, but at 90 days there were fewer deaths in colloid-treated patients (relative risk = 0.92; 95%CI, 0.86-0.99; P = .03), who also needed less vasopressor treatment and mechanical ventilation (secondary outcome). Unlike previous reports, no differences were detected in renal failure or the need for renal replacement therapy between the 2 groups.

Another controversial topic refers to the theoretical renal protective effect and increased diuresis of low-dose dopamine treatment in patients with acute heart failure. The multicenter, double-blind, randomized ROSE trial86 compared the effect of additional treatment with dopamine at a dose of 2μg/kg/min with nesiritide at a dose of 0.005μg/kg/min in more than 200 patients with acute heart failure and renal dysfunction (estimated glomerular filtration rate, 15-60mL/min/1.73 m2) treated with diuretics. No differences were observed in the primary endpoints of 72h cumulative urine volume and change in serum cystatin C concentrations. The authors conclude that neither of the 2 drugs had a favorable impact on diuresis or renal function.86

Healthcare personnel attire is an aspect of the medical profession that is rooted in culture and tradition. Nonetheless, information about its role in the cross-transmission of infectious diseases is limited. In an interesting consensus article, Bearman et al87 analyzed the available evidence in order to develop attire recommendations. In short, the recommendations for in-hospital apparel include: “bare below the elbow strategy”, meaning a short-sleeve shirt or scrubs with no wristwatch or jewelry; limited use of white coats and, whenever possible, removal of the white coat before coming into contact with the patients; if a necktie is worn, it should not come into contact with the patient; the hospital should provide frequent laundering (daily would be ideal) of white coats and hospital scrubs; and, stethoscopes should be cleaned between patient visits.

Cardiac arrest

In the last year, the results from a new and controversial international randomized trial have once again discussed the indication of therapeutic hypothermia in unconscious patients after resuscitation from cardiac arrest. In the TTM trial,88 a total of 939 unconscious patients were randomly assigned after resuscitation from cardiac arrest to receive treatment with therapeutic hypothermia with a target temperature of either 33°C or 36°C (control group). Surprisingly, there were no differences in the primary outcome of all-cause mortality between the 2 treatment groups (50% in patients from the 33°C group and 48% in the 36°C group). After 180 days, there was also no significant difference observe in the secondary composite endpoint: poor neurological function or death evaluated with the Cerebral Performance Category scale and the modified Rankin scale. The results from the analyses adjusted for known prognostic factors were similar. As mentioned in the accompanying editorial article,89 perhaps the most important message that can be extracted from this trial is that the care that these patients received, including temperature control, is effective and improves survival after cardiopulmonary resuscitation. Few medical procedures have achieved an absolute improvement of this magnitude in the same period.

Another aspect that has been debated is the optimal moment to begin therapeutic hypothermia. In a recent randomized trial, Kim et al90 assigned 1359 patients with prehospital cardiac arrest who had been resuscitated by paramedics to a strategy of rapid prehospital cooling with 4°C saline compared with standard care. Although the prehospital cooling group reached the target temperature of 34°C more quickly, there were no differences in the primary outcomes of survival or neurological status between the 2 groups. Due to the above reasons, future studies will be necessary to clarify which temperature control strategy is best in patients who have been resuscitated after cardiac arrest and to define the optimal moment for the application of this strategy.

Finally, in an interesting analysis of more than 18 000 patients who had been resuscitated after cardiac arrest, significant differences were found in survival according to the season of the year and time of day of the cardiac arrest. Nighttime and winter cardiac arrests were associated with lower survival. These differences continued to be significant in the multivariate analysis after adjusting for several recognized prognostic factors.91


None declared.

Sociedad Española de Cardiología. Registro RECALCAR. La atención al paciente con cardiopatía en el Sistema Nacional de Salud. Recursos, actividad y calidad asistencial. Informe 2013. 2013. Available at:
J.A. Barrabés, A. Bardají, J. Jiménez-Candil, F. Del Nogal Sáez, V. Bodí, N. Basterra, et al.
Pronóstico y manejo del síndrome coronario agudo en España en 2012: estudio DIOCLES.
Rev Esp Cardiol., (2014),
A. Cabadés, L. López-Bescós, F. Arós, A. Loma-Osorio, X. Bosch, P. Pabón, et al.
Variabilidad en el manejo y pronóstico a corto y medio plazo del infarto de miocardio en España: el estudio PRIAMHO.
Rev Esp Cardiol., 52 (1999), pp. 767-775
F. Arós, J. Cuñat, A. Loma-Osorio, E. Torrado, X. Bosch, J.J. Rodríguez, et al.
Tratamiento del infarto agudo de miocardio en España en el año 2000. El estudio PRIAMHO II.
Rev Esp Cardiol., 56 (2003), pp. 1165-1173
H. Bueno, A. Bardají, A. Fernández-Ortiz, J. Marrugat, H. Martí, M. Heras.
Manejo del síndrome coronario agudo sin elevación del segmento ST en España. Estudio DESCARTES (Descripción del Estado de los Síndromes Coronarios Agudos en un Registro Temporal Español).
Rev Esp Cardiol., 58 (2005), pp. 244-252
I. Ferreira-González, G. Permanyer-Miralda, J. Marrugat, M. Heras, J. Cuñat, E. Civeira, et al.
Estudio MASCARA (Manejo del Síndrome Coronario Agudo. Registro Actualizado). Resultados globales.
Rev Esp Cardiol., 61 (2008), pp. 803-816
S. Haghjooy-Javanmard, M. Sadeghi, S. Safavi, M. Gheraati, N. Dana.
Prognostic value of the high-mobility group box-1 in young patients with chest pain.
ARYA Atheroscler., 10 (2014), pp. 154-158
M. Nishimukai, R. Maeba, A. Ikuta, N. Asakawa, K. Kamiya, S. Yamada, et al.
Serum choline plasmalogens-those with oleic acid in sn-2-are biomarkers for coronary artery disease.
Clin Chim Acta., 437 (2014), pp. 147-154
R. Fan, X.L. Zhao, H. Wang, H.Y. He, Z.P. Peng, B. Yang, et al.
Abnormal methylation of the sex-determining region Y-box 17 (SOX17) promoter predicts poor prognosis in myelodysplastic syndrome.
Clin Lab., 60 (2014), pp. 1465-1474
N. Garg, N. Moorthy, A. Kapoor, S. Tewari, S. Kumar, A. Sinha, et al.
Hemoglobin A(1c) in nondiabetic patients: an independent predictor of coronary artery disease and its severity.
Mayo Clin Proc., 89 (2014), pp. 908-916
E.A. Pastorello, N. Morici, L. Farioli, M. Di Biase, L.M. Losappio, M. Nichelatti, et al.
Serum tryptase: a new biomarker in patients with acute coronary syndrome?.
Int Arch Allergy Immunol., 164 (2014), pp. 97-105
Y. Wang, A. Zheng, Y. Yan, F. Song, Q. Kong, S. Qin, et al.
Association between HMW adiponectin, HMW-total adiponectin ratio and early-onset coronary artery disease in Chinese population.
Atherosclerosis., 235 (2014), pp. 392-397
J. Kawagoe, T. Ishikawa, H. Iwakiri, H. Date, T. Imamura, K. Kitamura.
Association between adiponectin production in coronary circulation and future cardiovascular events in patients with coronary artery disease.
Int Heart J., 55 (2014), pp. 239-243
T.T. Hung, V.C. Chiang, A. Dawson, R.L. Lee.
Understanding of factors that enable health promoters in implementing health-promoting schools: a systematic review and narrative synthesis of qualitative evidence.
PLoS One., 9 (2014), pp. e108284
Y. Zhou, Y. Wang, S. Qiao.
Apelin: a potential marker of coronary artery stenosis and atherosclerotic plaque stability in ACS patients.
Int Heart J., 55 (2014), pp. 204-212
H.Y. Yu, P. Zhao, M.C. Wu, J. Liu, W. Yin.
Serum adropin levels are decreased in patients with acute myocardial infarction.
Regul Pept., 190-191 (2014), pp. 46-49
J.A. Udell, D.A. Morrow, P. Jarolim, S. Sloan, E.B. Hoffman, T.F. O’Donnell, et al.
Fibroblast growth factor-23, cardiovascular prognosis, and benefit of angiotensin-converting enzyme inhibition in stable ischemic heart disease.
J Am Coll Cardiol., 63 (2014), pp. 2421-2428
J.M. Cheng, K.M. Akkerhuis, O. Meilhac, R.M. Oemrawsingh, H.M. García-García, R.J. Van Geuns, et al.
Circulating osteoglycin and NGAL/MMP9 complex concentrations predict 1-year major adverse cardiovascular events after coronary angiography.
Arterioscler Thromb Vasc Biol., 34 (2014), pp. 1078-1084
Y. Wang, C. Fang, H. Gao, M.L. Bilodeau, Z. Zhang, K. Croce, et al.
Platelet-derived S100 family member myeloid-related protein-14 regulates thrombosis.
J Clin Invest., 124 (2014), pp. 2160-2171
C. Chen, W. Lei, W. Chen, J. Zhong, X. Gao, B. Li, et al.
Serum TGF-β1 and SMAD3 levels are closely associated with coronary artery disease.
BMC Cardiovasc Disord., 14 (2014), pp. 18
B. Dieplinger, M. Egger, M. Haltmayer, M.E. Kleber, H. Scharnagl, G. Silbernagel, et al.
Increased soluble ST2 predicts long-term mortality in patients with stable coronary artery disease: results from the Ludwigshafen risk and cardiovascular health study.
Clin Chem., 60 (2014), pp. 530-540
L. Fácila, J. Núñez, J. Sanchis, A. Cordero, O. Fabregat-Andrés, S. Morell.
Lipoproteínas de alta densidad tras un síndrome coronario agudo, evaluando el riesgo residual.
Rev Esp Cardiol., 66 (2013), pp. 65-66
S. Acharjee, W.E. Boden, P.M. Hartigan, K.K. Teo, D.J. Maron, S.P. Sedlis, et al.
Low levels of high-density lipoprotein cholesterol and increased risk of cardiovascular events in stable ischemic heart disease patients: A post-hoc analysis from the COURAGE Trial (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation).
J Am Coll Cardiol., 62 (2013), pp. 1826-1833
T. Durmaz, H. Ayhan, T. Keleş, E. Bilen, M. Akçay, N. Akar Bayram, et al.
Is there a relationship between acute coronary syndrome and prostate specific antigen level?.
Urol J., 11 (2014), pp. 1278-1286
G. Lee, S.M. Sou, R. Twerenbold, T. Reichlin, S. Oshima, T. Hochgruber, et al.
B-type natriuretic peptide and clinical judgment in the detection of exercise-induced myocardial ischemia.
Am J Med., 127 (2014), pp. 427-435
G. Wei, R. Yaqi, W. Ningfu, H. Xuwei.
N-terminal prohormone B-type natriuretic peptide and cardiovascular risk in stable coronary artery disease: a meta-analysis of nine prospective studies.
Rev Cardiovasc Med., 14 (2013), pp. e92-e98
J. Tuñón, L. Blanco-Colio, C. Cristóbal, N. Tarín, J. Higueras, A. Huelmos, et al.
Usefulness of a combination of monocyte chemoattractant protein-1, galectin-3, and N-terminal probrain natriuretic peptide to predict cardiovascular events in patients with coronary artery disease.
Am J Cardiol., 113 (2014), pp. 434-440
M. Rubini Gimenez, K. Wildi, C. Mueller.
¿Qué deben saber los cardiólogos sobre la copeptina?.
Rev Esp Cardiol., 67 (2014), pp. 519-521
R. André, V. Bongard, R. Elosua, I. Kirchberger, D. Farmakis, U. Häkkinen, et al.
International differences in acute coronary syndrome patients’ baseline characteristics, clinical management and outcomes in Western Europe: the EURHOBOP study.
Heart., 100 (2014), pp. 1201-1207
C. García-García, L. Molina, I. Subirana, J. Sala, J. Bruguera, F. Arós, et al.
Diferencias en función del sexo en las características clínicas, tratamiento y mortalidad a 28 días y 7 años de un primer infarto agudo de miocardio. Estudio RESCATE II.
Rev Esp Cardiol., 67 (2014), pp. 28-35
P. Libby, I. Tabas, G. Fredman, E.A. Fisher.
Inflammation and its resolution as determinants of acute coronary syndromes.
Circ Res., 114 (2014), pp. 1867-1879
S. Gielen, U. Landmesser.
The Year in Cardiology 2013: cardiovascular disease prevention.
Eur Heart J., 35 (2014), pp. 307-312
R. Chowdhury, H. Khan, E. Heydon, A. Shroufi, S. Fahimi, C. Moore, et al.
Adherence to cardiovascular therapy: a meta-analysis of prevalence and clinical consequences.
Eur Heart J., 34 (2013), pp. 2940-2948
B.M. Scirica, D.L. Bhatt, E. Braunwald, P.G. Steg, J. Davidson, B. Hirshberg, SAVOR-TIMI 53 Steering Committee and Investigators, et al.
Saxagliptin and cardiovascular outcomes in patients with type 2 diabetes mellitus.
N Engl J Med., 369 (2013), pp. 1317-1326
B.M. Scirica, E. Braunwald, I. Raz, M.A. Cavender, D.A. Morrow, P. Jarolim, SAVOR-TIMI 53 Steering Committee and Investigators, et al.
Heart failure, saxagliptin and diabetes mellitus: observations from the SAVOR-TIMI 53 Randomized Trial.
W.B. White, C.P. Cannon, S.R. Heller, S.E. Nissen, R.M. Bergenstal, G.L. Bakris, EXAMINE investigators, et al.
Alogliptin after acute coronary syndrome in patients with type 2 diabetes.
N Engl J Med., 369 (2013), pp. 1327-1335
A.P. Van de Woestijne, Y. Van der Graaf, A.-H. Liem, M.J.M. Cramer, J. Westerink, F.L.J. Visseren.
Low high-density lipoprotein cholesterol is not a risk factor for recurrent vascular events in patients with vascular disease on intensive lipid-lowering medication.
J Am Coll Cardiol., 62 (2013), pp. 1834-1841
D. Keene, C. Price, M.J. Shun-Shin, D.P. Francis.
Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients.
BMJ., 349 (2014), pp. g4379
M.J. Koren, R.P. Giugliano, F.J. Raal, D. Sullivan, M. Bolognese, G. Langslet, et al.
Efficacy and safety of longer-term administration of evolocumab (AMG 145) in patients with hypercholesterolemia: 52-week results from the Open-Label Study of Long-Term Evaluation Against LDL-C (OSLER) randomized trial.
Circulation., 129 (2014), pp. 234-243
J.G. Robinson, B.S. Nedergaard, W.J. Rogers, J. Fialkow, J.M. Neutel, D. Ramstad, et al.
Effect of evolocumab or ezetimibe added to moderate- or high-intensity statin therapy on LDL-C lowering in patients with hypercholesterolemia: the LAPLACE-2 randomized clinical trial.
JAMA., 311 (2014), pp. 1870-1882
E. Stroes, D. Colquhoun, D. Sullivan, F. Civeira, R.S. Rosenson, G.F. Watts, et al.
Anti-PCSK9 antibody effectively lowers cholesterol in patients with statin intolerance: the GAUSS-2 randomized, placebo-controlled phase 3 clinical trial of evolocumab.
J Am Coll Cardiol., 63 (2014), pp. 2541-2548
M.J. Koren, P. Lundqvist, M. Bolognese, J.M. Neutel, M.L. Monsalvo, J. Yang, et al.
Anti-PCSK9 monotherapy for hypercholesterolemia: the MENDEL-2 randomized, controlled phase III clinical trial of evolocumab.
J Am Coll Cardiol., 63 (2014), pp. 2531-2540
Mueller C. High-Sensitivity Cardiac Troponin T Assay for Rapid Rule Out of Acute Myocardial Infarction (TRAPID-AMI). Available at:
M.E. Kleber, G. Goliasch, T.B. Grammer, S. Pilz, A. Tomaschitz, G. Silbernagel, et al.
Evolving biomarkers improve prediction of long-term mortality in patients with stable coronary artery disease: the BIO-VILCAD score.
J Intern Med., 276 (2014), pp. 184-194
A. Cordero, R. López-Palop, P. Carrillo, B. Miralles, M.D. Masiá, V. Bertomeu-Martínez.
Valor pronóstico de la escala INTERHEART-colesterol para pacientes que ingresan por dolor torácico.
Rev Esp Cardiol., 67 (2014), pp. 578-580
P. Vélez, A.F. Parguiña, R. Ocaranza-Sánchez, L. Grigorian-Shamagian, I. Rosa, S. Alonso-Orgaz, et al.
Identification of a circulating microvesicle protein network involved in ST-elevation myocardial infarction.
Thromb Haemost., 112 (2014), pp. 716-726
J.F. O'Sullivan, A. Neylon, C. McGorrian, G.J. Blake.
MicroRNA Expression in Coronary Artery Disease.
MicroRNA., 2 (2014), pp. 205-211
H.W. Wang, T.S. Huang, H.H. Lo, P.H. Huang, C.C. Lin, S.J. Chang, et al.
Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease.
Arterioscler Thromb Vasc Biol., 34 (2014), pp. 857-869
H.W. Wang, H.H. Lo, Y.L. Chiu, S.J. Chang, P.H. Huang, K.H. Liao, et al.
Dysregulated miR-361-5p/VEGF axis in the plasma and endothelial progenitor cells of patients with coronary artery disease.
R.W. Millard, M. Tranter.
Biomarcadores no troponínicos, complementarios, alternativos y presuntos, para el síndrome coronario agudo: nuevos recursos para los futuros instrumentos de cálculo del riesgo.
Rev Esp Cardiol., 67 (2014), pp. 312-320
L.J. Shaw, D.S. Berman, M.H. Picard, M.G. Friedrich, R.Y. Kwong, G.W. Stone, et al.
Comparative definitions for moderate-severe ischemia in stress nuclear, echocardiography, and magnetic resonance imaging.
JACC Cardiovasc Imaging., 7 (2014), pp. 593-604
M.J. Wolk, S.R. Bailey, J.U. Doherty, P.S. Douglas, R.C. Hendel, C.M. Kramer, et al.
ACCF/AHA/ASE/ASNC/HFSA/HRS/SCAI/SCCT/SCMR/STS 2013 multimodality appropriate use criteria for the detection and risk assessment of stable ischemic heart disease: a report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, and Society of Thoracic Surgeons.
J Am Coll Cardiol., 63 (2014), pp. 380-406
M.P. Christman, M.S. Bittencourt, E. Hulten, E. Saksena, J. Hainer, H. Skali, et al.
Yield of downstream tests after exercise treadmill testing: a prospective cohort study.
J Am Coll Cardiol., 63 (2014), pp. 1264-1274
J. Peteiro, A. Bouzas-Mosquera, G. Barge-Caballero, D. Martinez, J.C. Yañez, M. Lopez-Perez, et al.
Torsión ventricular izquierda durante el ejercicio en pacientes con y sin respuesta isquémica a la ecocardiografía de ejercicio.
Rev Esp Cardiol., 67 (2014), pp. 706-716
S.B. Puchner, T. Liu, T. Mayrhofer, Q.A. Truong, H. Lee, J.L. Fleg, et al.
High-risk plaque detected on coronary CT angiography predicts acute coronary syndromes independent of significant stenosis in acute chest pain: results from the ROMICAT-II trial.
J Am Coll Cardiol., 64 (2014), pp. 684-692
S. Dougoud, T.A. Fuchs, J. Stehli, O.F. Clerc, R.R. Buechel, B.A. Herzog, et al.
Prognostic value of coronary CT angiography on long-term follow-up of 6.9 years.
Int J Cardiovasc Imaging., 30 (2014), pp. 969-976
M. Hadamitzky, S. Täubert, S. Deseive, R.A. Byrne, S. Martinoff, A. Schömig, et al.
Prognostic value of coronary computed tomography angiography during 5 years of follow-up in patients with suspected coronary artery disease.
Eur Heart J., 34 (2013), pp. 3277-3285
B. Hsu, F.C. Chen, T.C. Wu, W.S. Huang, P.N. Hou, C.C. Chen, et al.
Quantitation of myocardial blood flow and myocardial flow reserve with (99m)Tc-sestamibi dynamic SPECT/CT to enhance detection of coronary artery disease.
Eur J Nucl Med Mol Imaging., 41 (2014), pp. 2294-2306
M.A. Hlatky, D. Shilane, R. Hachamovitch, M.F. Dicarli.
Economic outcomes in the Study of Myocardial Perfusion and Coronary Anatomy Imaging Roles in Coronary Artery Disease registry: the SPARC Study.
J Am Coll Cardiol., 63 (2014), pp. 1002-1008
M.J. Zellweger, G. Fahrni, M. Ritter, R.V. Jeger, D. Wild, P. Buser, BASKET Investigators, et al.
Prognostic value of “routine” cardiac stress imaging 5 years after percutaneous coronary intervention: the prospective long-term observational BASKET (Basel Stent Kosteneffektivitäts Trial) LATE IMAGING study.
JACC Cardiovasc Interv, 7 (2014), pp. 615-621
O. Husser, J.V. Monmeneu, C. Bonanad, M.P. Lopez-Lereu, J. Nuñez, M.J. Bosch, et al.
Valor pronóstico de la isquemia miocárdica y la necrosis en pacientes con la función ventricular izquierda deprimida: un registro multicéntrico con resonancia magnética cardiaca de estrés.
Rev Esp Cardiol., 67 (2014), pp. 693-700
J.P. Greenwood, M. Motwani, N. Maredia, J.M. Brown, C.C. Everett, J. Nixon, et al.
Comparison of cardiovascular magnetic resonance and single-photon emission computed tomography in women with suspected coronary artery disease from the Clinical Evaluation of Magnetic Resonance Imaging in Coronary Heart Disease (CE-MARC) Trial.
Circulation., 129 (2014), pp. 1129-1138
K. Fox, I. Ford, P.G. Steg, J.C. Tardif, M. Tendera, R. Ferrari, SIGNIFY Investigators.
Ivabradine in stable coronary artery disease without clinical heart failure.
N Engl J Med., 37 (2014), pp. 1091-1099
B. De Bruyne, W.F. Fearon, N.H. Pijls, E. Barbato, P. Tonino, Z. Piroth, FAME 2 Trial Investigators, et al.
Fractional flow reserve-guided PCI for stable coronary artery disease.
N Engl J Med., 371 (2014), pp. 1208-1217
D. Lindholm, C. Varenhorst, C.P. Cannon, R.A. Harrington, A. Himmelmann, J. Maya, et al.
Ticagrelor vs. clopidogrel in patients with non-ST-elevation acute coronary syndrome with or without revascularization: results from the PLATO trial.
Eur Heart J., 35 (2014), pp. 2083-2093
C. Varenhorst, K. Jensevik, T. Jernberg, A. Sundström, P. Hasvold, C. Held, et al.
Duration of dual antiplatelet treatment with clopidogrel and aspirin in patients with acute coronary syndrome.
Eur Heart J., 35 (2014), pp. 969-978
J. Layland, K.G. Oldroyd, N. Curzen, A. Sood, K. Balachandran, R. Das, et al.
Fractional flow reserve vs. angiography in guiding management to optimize outcomes in non-ST-segment elevation myocardial infarction: the British Heart Foundation FAMOUS-NSTEMI randomized trial.
S.J. Nicholls, J.J.P. Kastelein, G.G. Schwartz, D. Bash, R.S. Rosenson, M.A. Cavender, et al.
Varespladib and cardiovascular events in patients with an acute coronary syndrome: the VISTA-16 randomized clinical trial.
JAMA., 311 (2014), pp. 252-262
M.L. O’Donoghue, E. Braunwald, H.D. White, D.P. Steen, M.A. Lukas, E. Tarka, et al.
Effect of darapladib on major coronary events after an acute coronary syndrome: the SOLID-TIMI 52 randomized clinical trial.
JAMA., 312 (2014), pp. 1006-1015
D.S. Wald, J.K. Morris, N.J. Wald, A.J. Chase, R.J. Edwards, L.O. Hughes, PRAMI Investigators, et al.
Randomized trial of preventive angioplasty in myocardial infarction.
N Engl J Med., 369 (2013), pp. 1115-1123
A.H. Gershlick.
Complete versus Lesion only PRimary-PCI Trial (CvLPRIT): treat the infarct related artery only or all lesions.
European Society of Cardiology, (2014),
S. Windecker, P. Kolh, F. Alfonso, J.P. Collet, J. Cremer, V. Falk, et al.
2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS).
Eur Heart J., 35 (2014), pp. 2541-2619
B. Lagerqvist, O. Fröbert, G.K. Olivecrona, T. Gudnason, M. Maeng, P. Alström, et al.
Outcomes 1 year after thrombus aspiration for myocardial infarction.
N Engl J Med., 371 (2014), pp. 1111-1120
G. Montalescot, A.W. Van’t Hof, F. Lapostolle, J. Silvain, J.F. Lassen, L. Bolognese, ATLANTIC Investigators, et al.
Prehospital ticagrelor in ST-segment elevation myocardial infarction.
N Engl J Med, 371 (2014), pp. 1016-1027
B. Ibanez, C. Macaya, V. Sánchez-Brunete, G. Pizarro, L. Fernández-Friera, A. Mateos, et al.
Effect of early metoprolol on infarct size in ST-segment-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention: the Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction (METOCARD-CNIC) trial.
Circulation., 128 (2013), pp. 1495-1503
V. Bodi, J.M. Ruiz-Nodar, E. Feliu, G. Minana, J. Nunez, O. Husser, et al.
Effect of ischemic postconditioning on microvascular obstruction in reperfused myocardial infarction. Results of a randomized study in patients and of an experimental model in swine.
Int J Cardiol., 175 (2014), pp. 138-146
S. Savonitto, N. Morici, S. De Servi.
El tratamiento de síndromes coronarios agudos de ancianos y pacientes con comorbilidades.
Rev Esp Cardiol., 67 (2014), pp. 564-573
B. Libungan, T. Karlsson, G. Hirlekar, P. Albertsson, J. Herlitz, A. Ravn-Fischer.
Delay and inequality in treatment of the elderly with suspected acute coronary syndrome.
Int J Cardiol., 176 (2014), pp. 946-950
F. Angeli, P. Verdecchia, S. Savonitto, N. Morici, S. De Servi, C. Cavallini.
Early invasive versus selectively invasive strategy in patients with non-ST-segment elevation acute coronary syndrome: impact of age.
Catheter Cardiovasc Interv., 83 (2014), pp. 686-701
M.A. Velders, S.K. James, B. Libungan, G. Sarno, O. Fröbert, J. Carlsson, et al.
Prognosis of elderly patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention in 2001 to 2011: A report from the Swedish Coronary Angiography and Angioplasty Registry (SCAAR) registry.
Am Heart J., 167 (2014), pp. 666-673
M. Izadnegahdar, C. Norris, P. Kaul, L. Pilote, K.H. Humphries.
Basis for sex-dependent outcomes in acute coronary syndrome.
Can J Cardiol., 30 (2014), pp. 713-720
S.A. Peters, R.R. Huxley, M. Woodward.
Diabetes as risk factor for incident coronary heart disease in women compared with men: a systematic review and meta-analysis of 64 cohorts including 858,507 individuals and 28,203 coronary events.
Diabetologia., 57 (2014), pp. 1542-1551
A.N. Cheema, H.A. Lawati, A. Bagai, M. Eisenberg, A. Shimony, D. So, et al.
Spontaneous coronary artery dissection in young women presenting with acute coronary syndrome: angiographic findings from the GENESIS PRAXY Study.
J Am Coll Cardiol., 63 (2014), pp. A3
S. Finfer, J.L. Vincent.
Critical care—an all-encompassing specialty.
N Engl J Med., 369 (2013), pp. 669-670
D. Annane, S. Siami, S. Jaber, C. Martin, S. Elatrous, A.D. Declère, et al.
Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: the CRISTAL randomized trial.
JAMA., 310 (2013), pp. 1809-1817
H.H. Chen, K.J. Anstrom, M.M. Givertz, L.W. Stevenson, M.J. Semigran, S.R. Goldsmith, et al.
Low-dose dopamine or low-dose nesiritide in acute heart failure with renal dysfunction: the ROSE acute heart failure randomized trial.
JAMA., 310 (2013), pp. 2533-2543
G. Bearman, K. Bryant, S. Leekha, J. Mayer, L.S. Munoz-Price, R. Murthy, et al.
Healthcare personnel attire in non-operating-room settings.
Infect Control Hosp Epidemiol., 35 (2014), pp. 107-121
N. Nielsen, J. Wetterslev, T. Cronberg, D. Erlinge, Y. Gasche, C. Hassager, TTM Trial Investigators, et al.
Targeted temperature management at 33°C versus 36°C after cardiac arrest.
N Engl J Med., 369 (2013), pp. 2197-2206
J.C. Rittenberger, C.W. Callaway.
Temperature management and modern post-cardiac arrest care.
N Engl J Med., 369 (2013), pp. 2262-2263
F. Kim, G. Nichol, C. Maynard, A. Hallstrom, P.J. Kudenchuk, T. Rea, et al.
Effect of prehospital induction of mild hypothermia on survival and neurological status among adults with cardiac arrest: a randomized clinical trial.
L.I.M. Karlsson, M. Wissenberg, E.L. Fosbøl, C.M. Hansen, F.K. Lippert, A. Bagai, et al.
Diurnal variations in incidence and outcome of out-of-hospital cardiac arrest including prior comorbidity and pharmacotherapy: a nationwide study in Denmark.
Resuscitation., 85 (2014), pp. 1161-1168
Copyright © 2014. Sociedad Española de Cardiología
Revista Española de Cardiología (English Edition)

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