Search

Pulmonary vascular resistance (PVR) is a marker of pulmonary vascular remodeling. A non-invasive model assessed by cardiovascular magnetic resonance (CMR) has been proposed to estimate PVR. However, its accuracy has not yet been evaluated in patients with heart failure. We prospectively included 108 patients admitted with acute heart failure (AHF), in whom a right heart catheterization (RHC) and CMR were performed at the same day. PVR was estimated by CMR applying the model: PVR = 19.38 − [4.62 × Ln pulmonary artery average velocity (in cm/s)] − [0.08 × right ventricle ejection fraction (in %)], and by RHC using standard formulae. The median age of the cohort was 67 years (interquartile range 58–73), and 34% were females. The median of PVR assessed by RHC and CMR were 2.2 WU (1.5–4) and 5 WU (3.4–7), respectively. We found a weak correlation between invasive PVR and PVR assessed by CMR (Spearman r = 0.21, p = 0.02). The area under the ROC curve for PVR assessed by CMR to detect PVR ≥ 3 WU was 0.57, 95% confidence interval (CI): 0.47–0.68. In patients with AHF, the non-invasive estimation of PVR using CMR shows poor accuracy, as well as a limited capacity to discriminate increased PVR values.

BACKGROUND Optimal management strategy for patients with ST-segment elevation myocardial infarction (STEMI) and multivessel disease (MVD) still remains unclear, especially in the elderly population. The aim of this study was to assess long-term outcomes and predictors of morbi-mortality according to age in patients with a STEMI and MVD. METHODS We prospectively included 381 consecutive patients with a STEMI who underwent primary angioplasty and showed MVD in the angiogram. 111 (29.1%) patients were older than 75 (≥75) years and 270 (70.9%) were younger than 75 (

Objectives This study sought to evaluate the prognostic effect of carbohydrate antigen-125 (CA125)–guided therapy (CA125 strategy) versus standard of care (SOC) after a hospitalization for acute heart failure (AHF). Background CA125 has emerged as a surrogate of fluid overload and inflammatory status in AHF. After an episode of AHF admission, elevated values of this marker at baseline as well as its longitudinal profile relate to adverse outcomes, making it a potential tool for treatment guiding. Methods In a prospective multicenter randomized trial, 380 patients discharged for AHF and high CA125 were randomly assigned to the CA125 strategy (n = 187) or SOC (n = 193). The aim in the CA125 strategy was to reduce CA125 to ≤35 U/ml by up or down diuretic dose, enforcing the use of statins, and tightening patient monitoring. The primary endpoint was 1-year composite of death or AHF readmission. Treatment strategies were compared as a time to first event and longitudinally. Results Patients allocated to the CA125 strategy were more frequently visited, and treated with ambulatory intravenous loop diuretics and statins. Likewise, doses of oral loop diuretics and aldosterone receptor blockers were more frequently modified. The CA125 strategy resulted in a significant reduction of the primary endpoint, whether evaluated as time to first event (66 events vs. 84 events; p = 0.017) or as recurrent events (85 events vs. 165 events; incidence rate ratio: 0.49; 95% confidence interval: 0.28 to 0.82; p = 0.008). The effect was driven by significantly reducing rehospitalizations but not mortality. Conclusions The CA125 strategy was superior to the SOC in terms of reducing the risk of the composite of 1-year death or AHF readmission. This effect was mainly driven by significantly reducing the rate of rehospitalizations. (Carbohydrate Antigen-125-guided Therapy in Heart Failure [CHANCE-HF]; NCT02008110)

Objective: The aim of this case report is to highlight the importance of excluding aortic coarctation in a patient with a bicuspid aortic valve. Clinical Presentation and Intervention: A 56-year-old woman with hypertension was admitted complaining of progressive dyspnea. Transthoracic echocardiography showed a calcified, bicuspid aortic valve with severe stenosis. Aortography revealed the presence of severe narrowing of the aorta between the carotid and subclavian arteries. The patient was referred for cardiovascular surgery in which successful aortic valve replacement and aortic correction were performed. Conclusion: This case report shows an uncommon finding of infantile aortic coarctation in an adult patient admitted with heart failure.

Introduction and objectives: There is current controversy regarding the benefits of percutaneous recanalization (PCI) of chronic total coronary occlusions (CTO). Our aim was to determine acute and follow-up outcomes in our setting. Methods: Two-year prospective registry of consecutive patients undergoing PCI of CTO in 24 centers. Results: A total of 1000 PCIs of CTO were performed in 952 patients. Most were symptomatic (81.5%), with chronic ischemic heart disease (59.2%). Previous recanalization attempts had been made in 15%. The mean SYNTAX score was 19.5 +/- 10.6 and J-score was > 2 in 17.3%. A retrograde procedure was performed in 92 patients (9.2%). The success rate was 74.9% and was higher in patients without previous attempts (82.2% vs 75.2%; P = .001), those with a J-score 20 mm, and blunt proximal cap were independent predictors of failed recanalization. The rate of procedural complications was 7.1%, including perforation (3%), myocardial infarction (1.3%), and death (0.5%). At 1-year of follow-up, 88.2% of successfully revascularized patients showed clinical improvement (vs 34.8%, P < .001), which was associated with lower mortality. At 1-year of follow-up, the mortality rate was 1.5%. Conclusions: Compared with other national registries, patients in the Iberian registry undergoing PCI of a CTO showed similar complexity, success rate, and complications. Successful recanalization was strongly associated with functional improvement, which was related to lower mortality. (C) 2018 Published by Elsevier Espana, S.L.U. on behalf of Sociedad Espanola de Cardiologia.

Background Percutaneous coronary intervention (PCI) of chronic total occlusions (CTO) usually involves multiple overlapping stents implantation to cover long coronary segments. A higher rate of restenosis has been described with stent overlapping. Recently, new long tapered stents emerged as a potential tool for treating long coronary lesions. Feasibility of using these new devices for the CTO PCI has not been described. The aim of this work was to describe our initial experience with 50 and 60 mm-long tapered sirolimus-eluting stents (SES) in CTO PCI. Methods We included 54 consecutive patients who underwent a CTO PCI and in whom an attempt to implant a 50 or 60 mm-long tapered SES was performed. Baseline clinical, angiographic, and procedural characteristics were recorded. Results The median (IQR) age was 64 (58–73) years, and 45 (83.3%) patients were male. The tapered SES 50 and 60 mm-long was successfully implanted in 51 (94.4%) patients. In three patients, a 60 mm-long stent could not be implanted, and two or three overlapped shorter drug-eluting stents were deployed instead. An average of 1.4 ± 0.6 stents per patient was implanted. A single stent was deployed in 32 (59.3%) patients. During a median follow-up of 330 (149–551) days, repeat PCI in the target vessel was performed in two patients. Conclusions The use of the new BioMime Morph™ tapered SES for the treatment of CTO appears to be feasible in a high proportion of procedures. Further studies confirming the feasibility of this approach and its potential clinical advantages are needed.

Objective: The aim of this case report was to highlight the importance of ruling out pheochromocytoma in a patient with Von Hippel-Lindau disease (VHL) and cardiovascular manifestations. Clinical Presentation and Intervention: A 22-year-old woman with type IIb VHL presented with signs and symptoms of acute decompensated heart failure. Transthoracic echocardiography showed a dilated left ventricle with severely depressed ejection fraction, confirmed by MRI. Urinary catecholamine and metanephrine tests had elevated levels and an abdominal MRI showed the presence of two cystic masses at the left hypochondrium. Surgical resection of both masses was performed, confirming the diagnosis of pheochromocytoma and clear cell renal carcinoma on histology. Six-month echocardiography showed a left ventricle with normal diameters and preserved ejection fraction. Genetic analysis revealed a germline mutation (exon 3 deletion of VHL). As there was no family history of VHL, it was determined to be a de novo mutation. Conclusion: This case report showed an atypical manifestation in a patient with VHL and underlines the importance of screening for pheochromocytoma in such patients.

Early stratification of patients according to the risk for developing microvascular obstruction (MVO) after ST-segment elevation myocardial infarction (STEMI) is desirable. We aimed to identify predictors of cardiovascular magnetic resonance (CMR)-derived MVO from clinical+ECG, laboratory and angiographic parameters available on admission.Characteristics available on admission were documented in 97 STEMI patients referred for primary angioplasty. MVO was determined using contrast-enhanced CMR.MVO was present in 44 patients (45%). The C-statistic for predicting MVO was: clinical+ECG (.832), laboratory (.743), and angiographic parameters (.669). Adding laboratory to clinical+ECG information did not improve the C-statistic (.873 vs. .832, p=.2). Further addition of angiographic data (.904) improved the C-statistic of clinical+ECG (p=.04) but not of clinical+ECG and laboratory (p=.2). Independent predictors of MVO using clinical and ECG parameters were: Killip class1 (OR 15.97 95%CI [1.37-186.76], p=.03), diabetes (OR 6.15 95%CI [1.49-25.39], p=.01), age55years (OR 4.70 95%CI [1.56-14.17], p=.006), sum of ST-segment elevation10mm (OR 4.5 95%CI [1.58-12.69], p=.005) and delayed presentation3h (OR 3.80 95%CI [1.19-12.1], p=.02). A score was constructed assigning Killip class1 2 points and the remaining indexes 1 point. The incidence of MVO increased with the score: 0 point: 8.7%; 1 point: 28.1%; 2 points: 71.4%; and 3+ points: 93% (p.0001).MVO can be predicted using parameters already available on patient admission. We developed a clinical-ECG score allowing for early and reliable classification of STEMI patients according to the risk of MVO.

Several works have endorsed a significant role of the immune system and inflammation in the pathogenesis of heart failure. As indirect evidence, an association between a low relative lymphocyte count (RLC%) and worse outcomes found in this population has been suggested. Nevertheless, the role of RLC% for risk stratification in a large and nonselected population of patients with acute heart failure (AHF) has not yet been determined. Thus, the aim of this study was to determine the association between low RLC% and 1-year mortality in patients with AHF and consequently to define whether it has any role for early risk stratification. A total of 1,192 consecutive patients admitted for AHF were analyzed. Total white blood cell and differential counts were measured on admission. RLC% (calculated as absolute lymphocyte count/total white blood cell count) was categorized in quintiles and its association with all-cause mortality at 1 year assessed using Cox regression. At 1 year, 286 deaths (24%) were identified. A negative trend was observed between 1-year mortality rates and quintiles of RLC%: 31.5%, 27.2%, 23.1%, 23%, and 15.5% in quintiles 1 to 5, respectively (p for trend0.001). After thorough covariate adjustment, only patients in the lowest quintile (9.7%) showed an increased risk for mortality (hazard ratio 1.76, 95% confidence interval 1.17 to 2.65, p = 0.006). When RLC% was modeled with restricted cubic splines, a stepped increase in risk was observed patients in quintile 1: those with RLC% values7.5% and5% showed 1.95- and 2.66-fold increased risk for death compared to those in the top quintile. In conclusion, in patients with AHF, RLC% is a simple, widely available, and inexpensive biomarker, with potential for identifying patients at increased risk for 1-year mortality.

To compare a quantitative assessment of contrast cardiovascular magnetic resonance (CMR) after ST-segment elevation myocardial infarction (STEMI) with visual analysis for predicting depressed ejection fraction (dEF) and major adverse cardiac events (MACE). 192 patients underwent CMR at 1 week and 6 months after STEMI. Three quantitative (initial slope, maximal signal intensity and contrast delay in first-pass imaging) and 2 visual perfusion indexes (hypoenhancement in first-pass and microvascular obstruction in late enhancement imaging (LE)) were determined. Quantification of infarct mass and visual assessment of the extent of transmural necrosis (ETN) were also performed. At 6 months, 69 patients displayed dEF. During follow-up (mean 655 days) 20 MACE (death, re-infarction, re-admission for heart failure) occurred. Perfusion quantification took longer (P < 0.001) and, in ROC curve analyses and the C-statistic, was not superior to visual perfusion analysis for predicting late EF or MACE (P = ns). Similarly, infarct size quantification was not superior to visual assessment of ETN (P = ns). In multivariate analyses, only visual assessment of ETN (per segment) predicted dEF (OR 1.30 95%CI [1.04-1.61], P = 0.02) and MACE (HR 1.38 95%CI [1.19-1.60], P < 0.001). Visual analysis of CMR after STEMI is not time consuming and predicts dEF and MACE comparable to quantification. ETN was the strongest parameter.

Introduction and objectives The usefulness of ST-segment elevation resolution (STR) for predicting epicardial reperfusion is well established. However, it is still not clear how ST-segment changes are related to microvascular obstruction (MVO) observed by cardiovascular magnetic resonance (CMR) after primary percutaneous coronary intervention (pPCI) for ST-segment elevation myocardial infarction (STEMI). Methods The study involved 85 consecutive patients admitted for a first STEMI and treated by pPCI who had a patent infarct-related artery. An ECG was recorded on admission and 90 min and 6, 24, 48 and 96 h after pPCI. Thereafter, STR and the sum of ST-segment elevation (sumSTE) in all leads were determined. Results Overall, CMR revealed MVO in 37 patients. In infarcts with MVO, sumSTE was greater both before and after revascularization than in infarcts without MVO ( P ≤.001 at all times). In contrast, there was no significant difference in the magnitude of STR between infarcts with and without MVO 90 min after revascularization ( P =.1), though there was after 6 h ( P P 3 mm 90 min after pPCI was an independent predictor of MVO on CMR, while an STR ≥70% was not (odds ratio=3.1; 95% confidence interval, 1.2–8.4; P =.02). Conclusions MVO was associated with a significantly increased sumSTE at all times after revascularization. The difference in the magnitude of STR between infarcts with and without MVO was significant only >6 h after revascularization. The best predictor of MVO was a sumSTE >3 mm 90 min after pPCI.

Background Low lymphocyte count (LLC), a surrogate for inflammation, has emerged as a potential risk factor for cardiovascular outcomes, especially new ischemic events. To identify patients with non-ST segment elevation acute coronary syndromes (NSTEACS) who benefit from an invasive revascularization strategy remains a challenge. We sought to determine if patients with high-risk NSTEACS who exhibited LLC have a greater reduction in long-term post-discharge myocardial infarction (MI) when managed under a revascularization invasive strategy (RIS) as compared with conservative strategy (CS). Methods Nine hundred seventy two consecutive patients with high-risk NSTEACS were treated under two revascularization strategies (RS): 1) CS, from January 2001 to October 2002 (345 patients; 35.5%) and 2) RIS, from November 2002 to May 2005 (627 patients; 64.5%). LLC was defined as lymphocytes count ≤ 1200 cells/ml (1 vs. 2–4 quartiles). The association between the type of RS and MI was stratified by lymphocyte count status and assessed by Cox regression adapted for competing events. Results At 3-year follow-up, 145 deaths (14.9%), 135 MI (13.9%) and 76 revascularization procedures (7.8%) were registered. In a multivariable setting, LLC patients exhibited a greater MI risk reduction when managed under RIS (HR: 0.40; 95% CI = 0.22–0.72, p = 0.003). Conversely, when LLC was not present, no difference in the rate of MI was detected between the two RS. Conclusions LLC identifies a subgroup of patients with greater reduction in the risk of postdischarge MI when a RIS is applied.

Introduction The association of the temporal evolution of cardiac necrosis marker release with cardiovascular magnetic resonance-derived microvascular perfusion after ST-elevation myocardial infarction is unknown. Methods We analyzed 163 patients with a first ST-elevation myocardial infarction and a patent infarct-related artery treated with thrombolysis (67%) or primary angioplasty (33%). Using first-pass perfusion CMR, abnormal perfusion was defined as a lack of contrast arrival into the infarct area in > 1 segment. Troponin I, creatine kinase MB and myoglobin were measured upon arrival and at 6, 12, 24, 48 and 96 hours after reperfusion. Results Abnormal perfusion was detected in 75 patients (46%) and was associated with a larger release of all 3 necrosis markers after reperfusion and higher peak values. This association was observed in the whole group and separately in patients treated with thrombolysis and primary angioplasty. Out of the 3 markers, troponin levels at 6 hours after reperfusion yielded the largest area under the receiver operating characteristic curve for prediction of abnormal perfusion (troponin: 0.69, creatine kinase MB: 0.65 and myoglobin: 0.58). In a comprehensive multivariate analysis, adjusted for clinical, angiographic, cardiovascular magnetic resonance parameters and all necrosis markers, high troponin levels at 6 hours after reperfusion (>median) independently predicted abnormal microvascular perfusion (OR 2.6 95%CI [1.2 - 5.5], p = .012). Conclusions In ST-elevation myocardial infarction, a larger release of cardiac necrosis markers soon after reperfusion therapy relates to abnormal perfusion. Troponin appears as the most reliable necrosis marker for an early detection of cardiovascular magnetic resonance-derived abnormal microvascular reperfusion.

The presence of microvascular obstruction after ST-segment elevation acute myocardial infarction is associated with a poor outcome. The pathophysiology of this process has not been fully defined. The aim of this study was to investigate the relationship between post-reperfusion lymphopenia and microvascular obstruction.This prospective study involved 212 patients with a first ST-segment elevation acute myocardial infarction who underwent reperfusion with thrombolytic agents or primary angioplasty and who had an open infarct-related artery. Serial measurements of lymphocyte, neutrophil and monocyte counts were taken. Cardiac magnetic resonance was used to detect microvascular obstruction during the first week after the infarction. Imaging was repeated 6 months after infarction.Microvascular obstruction was observed in 67 patients (32%). A post-reperfusion lymphocyte count1800 cells/ml was associated with a higher risk of microvascular obstruction (44% versus 20%; P.001) as well as with a low left ventricular ejection fraction and large left ventricular volumes (P.05). After adjustment for baseline characteristics, ECG findings, necrosis marker levels and angiographic variables, multivariate analysis showed that a post-reperfusion lymphocyte count1800 cells/ml was independently associated with an increased risk of microvascular obstruction (odds ratio=3.2; 95% confidence interval 1.6-6.3; P.001).In ST-segment elevation myocardial infarction, post-reperfusion lymphopenia is an early and powerful predictor of the presence of microvascular obstruction. The pathophysiological and therapeutic implications of this association require further study.

Introduction and objectives. The aims of the study were to characterize myocardial edema after ST-elevation acute myocardial infarction using cardiac magnetic resonance imaging and to investigate its impact on ventricular function and its subsequent evolution. Methods. In total, 134 patients admitted to hospital for a first ST-elevation myocardial infarction who had a patent infarct-related artery underwent cardiac magnetic resonance imaging. Cine images (at rest and with low-dose dobutamine) and edema, perfusion and viability images were acquired. Imaging was repeated after 6 months. Results. In the first week after infarction, edema was detected in at least one segment in 96.6% of patients (4±2.1 segments per patient). Extensive edema (≥4 segments) was associated with large ventricular enddiastolic and end-systolic volumes (P

ObjectivesTo evaluate the prognostic value of a comprehensive cardiac magnetic resonance (CMR) assessment soon after a first ST-segment elevation myocardial infarction (STEMI).BackgroundCMR allows for a simultaneous assessment of wall motion abnormalities (WMA), WMA with low-dose dobutamine (WMA-dobutamine), microvascular obstruction, and transmural necrosis. This approach has been proven to be useful to predict late systolic recovery soon after STEMI. Its prognostic value and the relative prognostic weight of these indexes are not well-defined.MethodsWe studied 214 consecutive patients with a first STEMI treated with thrombolytic therapy or primary angioplasty discharged from hospital. In the first week (7 ± 1 day after infarction), with CMR we determined the extent (number of segments) of WMA, WMA-dobutamine, microvascular obstruction, and transmural necrosis.ResultsDuring a median follow-up of 553 days, 21 major adverse cardiac events (MACE) including 4 cardiac deaths, 6 nonfatal myocardial infarctions, and 11 readmissions for heart failure were documented. The MACE was associated with a larger extent of WMA (8 ± 4 segments vs. 5 ± 3 segments, p < 0.001), WMA-dobutamine (6 ± 4 segments vs. 4 ± 3 segments, p = 0.004), microvascular obstruction (3 ± 3 segments vs. 1 ± 2 segments p

To determine the prognostic and therapeutic implications of stress perfusion cardiovascular magnetic resonance (CMR) on the basis of the ischaemic cascade.Single centre study in a teaching hospital in Spain.Dipyridamole stress CMR was performed on 601 patients with ischaemic chest pain and known or suspected coronary artery disease. On the basis of the ischaemic cascade, patients were categorised in C1 (no evidence of ischaemia, n = 354), C2 (isolated perfusion deficit at stress first-pass perfusion imaging, n = 181) and C3 (simultaneous perfusion deficit and inducible wall motion abnormalities, n = 66). CMR-related revascularisation (n = 102, 17%) was defined as the procedure prompted by the CMR results and carried out within the next three months.During a median follow-up of 553 days, 69 major adverse cardiac events (MACE), including 21 cardiac deaths, 14 non-fatal myocardial infarctions and 34 admissions for unstable angina with documented abnormal angiography were detected. In non-revascularised patients (n = 499), the MACE rate was 4% (14/340) in C1, 20% (26/128) in C2 and 39% (12/31) in C3 (adjusted p value = 0.004 vs C2 and0.001 vs C1). CMR-related revascularisation had neutral effects in C2 (20% vs 19%, 1.1 (0.5 to 2.4), p = 0.7) but independently reduced the risk of MACE in C3 (39% vs 11%, 0.2 (0.1 to 0.7), p = 0.01).Dypiridamole stress CMR is able to stratify risk on the basis of the ischaemic cascade. A small group of patients with severe ischaemia-simultaneous perfusion deficit and inducible wall motion abnormalities-are at the highest risk and benefit most from MACE reduction due to revascularisation.

Neutrophil gelatinase-associated lipocalin (NGAL) has emerged as a renal tubular marker for early renal dysfunction [1]. Recent studies highlighted its role in predicting acute kidney injury (AKI) and clinical outcomes in a wide range of cardiovascular diseases [2], [3], [4] and [5]. However, in heart failure (HF), conflicting results have been reported [4], [5], [6] and [7] and some ambiguities still prevail about the prognostic utility of NGAL beyond standard prognosticators and traditional renal biomarkers. We aimed to evaluate the independent ability of serum NGAL for predicting long-term mortality in patients admitted for acute HF (AHF). We prospectively enrolled 206 patients consecutively admitted for AHF in the Cardiology Department of a third level centre from April 30th 2010 to March 1st 2011. We excluded patients with a diagnosis of pneumonia, sepsis, acute coronary syndrome or end-stage renal failure on dialysis or imminent need of dialysis. Demographic data, medical history, vital signs, 12-lead electrocardiogram, and laboratory data were determined on admission. Left ventricular ejection fraction (LVEF) was assessed by echocardiography during index hospitalization. Treatment was individualized following established guidelines [8].

Purpose: To evaluate dipyridamole cardiac magnetic resonance (MR) imaging in the prediction of major events (MEs) in patients with ischemic chest pain in a large multicenter registry. Materials and Methods: Institutional ethics committee approval and written informed consent were obtained. A total of 1722 patients who were undergoing cardiac MR imaging for chest pain were included. Wall motion abnormalities (WMAs) at rest, hyperemia perfusion defect (PD), late gadolinium enhancement (LGE), and inducible WMA were analyzed (abnormal if more than one abnormal segment was seen) with the 17-segment model. A cardiac MR categorization was created: category 1, no PD, LGE, or inducible WMA; category 2, PD without LGE and inducible WMA; category 3, LGE without inducible WMA; and category 4, inducible WMA. The association with ME was analyzed by using Cox proportional hazard regression multivariate models. Results: During a median follow-up period of 308 days, 61 MEs (4%) occurred (36 cardiac deaths, 25 nonfatal myocardial infarctions). MEs were associated with a greater extent of WMA, PD, LGE, and inducible WMA (P ¿ .001 for all analyses). In multivariable analyses, PD (P = .002) and inducible WMA (P = .0001) were the only cardiac MR predictors. ME rate in categories 1, 2, 3, and 4 was 2% (14 of 901 patients), 3% (six of 219 patients), 4% (15 of 409 patients), and 14% (26 of 193 patients), respectively (category 4 vs category 1, adjusted P < .001). Cardiac MR¿directed revascularization was performed in 242 patients (14%) and reduced the risk of ME in only category 4 (7% [six of 92 patients] vs 26% [26 of 101 patients], P = .0004). Conclusion: Dipyridamole cardiac MR imaging can be used to predict MEs in patients with ischemic chest pain. Patients with inducible WMA are at the highest risk for MEs and benefit the most from revascularization.

[EN] Introduction and objectives: Pharmacoinvasive strategy represents an attractive alternative to primary angioplasty. Using cardiovascular magnetic resonance imaging we compared the left ventricular outcome of the pharmacoinvasive strategy and primary angioplasty for the reperfusion of ST-segment elevation myocardial infarction. Methods: Cardiovascular magnetic resonance was performed 1 week and 6 months after infarction in two consecutive cohorts of patients included in a prospective university hospital ST-segment elevation myocardial infarction registry. During the period 2004-2006, 151 patients were treated with pharmacoinvasive strategy (thrombolysis followed by routine non-immediate angioplasty). During the period 2007-2008, 93 patients were treated with primary angioplasty. A propensity score matched population was also evaluated. Results: At 1-week cardiovascular magnetic resonance, pharmacoinvasive strategy and primary angioplasty patients showed a similar extent of area at risk (29 ± 15 vs. 29 ± 17%, P = .9). Non-significant differences were detected by cardiovascular magnetic resonance at 1 week and at 6 months in infarct size, salvaged myocardium, microvascular obstruction, ejection fraction, end-diastolic volume index and end-systolic volume index (P > .2 in all cases). The same trend was observed in 1-to-1 propensity score matched patients. The rate of major adverse cardiac events (death and/or re-infarction) at 1 year was 6% in pharmacoinvasive strategy and 7% in primary angioplasty patients (P = .7). Conclusions: A pharmacoinvasive strategy including thrombolysis and routine non-immediate angioplasty represents a widely available and logistically attractive approach that yields identical short-term and long-term cardiovascular magnetic resonance-derived left ventricular outcome compared to primary angioplasty. © 2010 Sociedad Española de Cardiología., The present study was supported by the "Instituto de Salud Carlos III'' (PI080128 and Heracles grants).

Little is known about how prognosis is influenced by readmission for acute heart failure (AHF) following non-ST-segment elevation acute coronary syndrome (NSTEACS). The aim of this study was to determine the prognostic effect of a first admission for AHF on the risk of acute myocardial infarction (AMI) or death in patients who survived an episode of high-risk NSTEACS.The study involved 972 consecutive patients with high-risk NSTEACS who survived after hospital admission. Readmission for AHF was selected as the main exposure variable, and its association with subsequent AMI or all-cause death was assessed using Cox proportional hazards models for time-dependent covariates that also included adjustment for competing risks.After a median follow-up period of 30 [interquartile range, 12-48] months, 82 patients (8.4%) were admitted for AHF, 146 (15%) had an AMI, and 202 (20.8%) died. The median time to readmission for AHF was 203 [56-336] days after NSTEACS. Patients readmitted for AHF had an increased risk of subsequent death (hazard ratio [HR]=1.67; 95% confidence interval [CI], 1.13-2.45; P=.009) or AMI (HR=2.15; 95% CI, 1.41-3.27; P.001), which was independent of baseline prognostic and time-dependent variables.Readmission for AHF after high-risk NSTEACS was associated with an increased risk of subsequent death or AMI.

Introduction and objectives. Few data are available on the use of invasive treatment in patients with non-STsegment elevation acute coronary syndrome (NSTEACS) and systolic dysfunction. The aim of this study was to determine the effect of invasive treatment on the prognosis of patients with NSTEACS, with or without systolic dysfunction. Methods. The study included 972 consecutive patients admitted for NSTEACS (i.e. ST-segment depression or an elevated troponin-I level). Systolic dysfunction was defined as an ejection fraction

Dipyridamole stress perfusion cardiovascular magnetic resonance (CMR) is used to detect coronary artery disease (CAD). However, few data are available on the diagnostic value of the systolic dysfunction induced by dipyridamole. This study investigated whether the induction of systolic dysfunction supplements the diagnostic information provided by perfusion imaging in the detection of CAD.Overall, 166 patients underwent dipyridamole CMR and quantitative coronary angiography, with CAD being defined as a stenosisor =70%. Systolic dysfunction at rest, systolic dysfunction with dipyridamole, induced systolic dysfunction, and stress first-pass perfussion deficit (PD) and delayed enhancement were quantified.In the multivariate analysis, PD (hazard ratio [HR]=1.6; 95% confidence interval [CI], 1.33-1.91;P.0001) and induced systolic dysfunction (OR=1.8; 95% CI, 1.18-2.28; P.007) were independently associated with CAD and had a sensitivity and specificity of 92% and 62% and 43% and 96%, respectively. Patients were categorized as having no ischemia (Group 1), PD but no induced systolic dysfunction (Group 2), or induced systolic dysfunction irrespective of PD (Group 3). In Group 3, the prevalence of CAD was higher than in Group 1 or 2 (96% vs. 22% and 79%, respectively; P=.001) and the risk of CAD was two-fold higher than in Group 2 (OR=2.34; 95% CI, 1.07-5.13; P=.034). Compared with Group 2, more hypoperfused segments were observed in Group 3 (6.2+/-2.6 vs. 7.4+/-3.4; P=.044), and more diseased vessels (1.4+/-1.0 vs. 1.8+/-0.9; P=.036). Adding induced systolic dysfunction to perfusion and clinical data improved the multivariate model's C-statistic for predicting CAD (0.81 vs. 0.87; P=.02).Combining induced systolic dysfunction with perfusion imaging increases the diagnostic accuracy of detecting CAD and enables patients with severe ischemia and a high probability of CAD to be identified.

To investigate the safety of discharge of patients deemed at low risk of cardiac events after evaluation in a chest pain unit and to determine the prognostic effect of revascularization of patients deemed at high risk.The study population consisted of 1088 patients presenting at the emergency department from January 15, 2001, to September 1, 2006, with chest pain but without ischemia on electrocardiography or troponin elevation. Patients were managed by a chest pain unit protocol that included early exercise testing. Three groups of patients were distinguished: (1) those discharged after exercise testing (424 [39%]); (2) those in whom unstable angina was ruled out after in-hospital evaluation (208 [19%]); and (3) those in whom unstable angina was confirmed or not ruled out (456 [42%]). Of the 456 patients in group 3, 183 (40%) were revascularized at the index episode. The primary end point was the occurrence of myocardial infarction or death within 1 year. Adjustments were made for patient characteristics and a propensity score for revascularization (c statistic [0.83]).Groups 1 and 2 showed lower rates of the primary end point than group 3 (group 1: 7 [1.7%]; group 2: 1 [0.5%]; group 3: 62 [13.6%]; P=.001). In group 3, revascularization at the index episode did not reduce the primary end point in the univariate (22 [12%] vs 29 [11%]; P=.80) and multivariate (hazard ratio, 1.4; 95% confidence interval, 0.7-2.5; P=.40) analyses. In-hospital revascularization decreased the need for postdischarge revascularization (hazard ratio, 0.3; 95% confidence interval, 0.1-0.7; P=.01).Chest pain unit protocols are associated with safe patient discharge. Although early revascularizations may decrease the need for postdischarge revascularizations, they may not improve 1-year outcomes by reducing the number of myocardial infarctions or deaths.

Neutrophil to lymphocyte ratio (N/L) has been associated with poor outcomes in patients who underwent cardiac angiography. Nevertheless, its role for risk stratification in acute coronary syndromes, specifically in patients with ST-segment elevation myocardial infarction (STEMI), has not been elucidated. We sought to determine the association of N/L maximum value (N/L max) with mortality in the setting of STEMI and to compare its predictive ability with total white blood cell maximum count (WBC max). We analyzed 515 consecutive patients admitted with STEMI to a single university center. White blood cells (WBC) and differential count were measured at admission and daily for the first 96 hours afterward. Patients with cancer, inflammatory diseases, or premature death were excluded, and 470 patients were included in the final analysis. The association between N/L max and WBC max with mortality was assessed by Cox regression analysis. During follow-up, we registered 106 deaths (22.6%). A positive trend between mortality and N/L max quintiles was observed; 6.4%, 12.4%, 11.7%, 34%, and 47.9% of deaths occurred from quintiles 1 to 5 (p0.001), respectively. In a multivariable setting, after adjusting for standard risk factors, patients in the fourth (Q4 vs Q1) and fifth quintile (Q5 vs Q1) showed the highest mortality risk (hazard ratio 2.58, 95% confidence interal 1.06 to 6.32, p = 0.038 and hazard ratio 4.20, 95% confidence interal 1.73 to 10.21, p = 0.001, respectively). When WBC max and cells subtypes were entered together, N/L max remained as the only WBC parameter; furthermore, the model with N/L max showed the most discriminative ability. In conclusion, N/L max is a useful marker to predict subsequent mortality in patients admitted for STEMI, with a superior discriminative ability than total WBC max.