Impact of Leadless Pacemaker Therapy on Cardiac and Atrioventricular Valve Function Through 12 Months of Follow-Up.

BACKGROUND: Endocardial pacemaker leads and right ventricular (RV) pacing are well-known causes of tricuspid valve, mitral valve, and cardiac dysfunction. Lead-related adverse consequences can potentially be mitigated by leadless pacemaker (LP) therapy by eliminating the presence of a transvalvular lead. This study assessed the impact of LP placement on cardiac and valvular structure and function. METHODS: Echocardiographic studies before and 12±1 months after LP implantation were performed between January 2013 and May 2018 at our center and compared with age- and sex-matched controls of dual-chamber transvenous pacemaker recipients. RESULTS: A total of 53 patients receiving an LP were included, of whom 28 were implanted with a Nanostim and 25 with a Micra LP device. Tricuspid valve regurgitation was graded as being more severe in 23 (43%) patients at 12±1 months compared with baseline ( P<0.001). Compared with an apical position, an RV septal position of the LP was associated with increased tricuspid valve incompetence (odds ratio, 5.20; P=0.03). An increase in mitral valve regurgitation was observed in 38% of patients ( P=0.006). LP implantation resulted in a reduction of RV function, according to a lower tricuspid annular plane systolic excursion ( P=0.003) and RV tricuspid lateral annular systolic velocity ( P=0.02), and a higher RV Tei index ( P=0.04). LP implantation was further associated with a reduction of left ventricular ejection fraction ( P=0.03) and elevated left ventricular Tei index ( P=0.003). The changes in tricuspid valve regurgitation in the LP group were similar to the changes in the dual-chamber transvenous pacemaker control group (43% versus 38%, respectively; P=0.39). CONCLUSIONS: LP therapy is associated with an increase in tricuspid valve dysfunction through 12 months of follow-up; yet it was comparable to dual-chamber transvenous pacemaker systems. Furthermore, LP therapy seems to adversely impact mitral valve and biventricular function.

Leadless pacemaker implantation after explantation of infected conventional pacemaker systems: A viable solution?

BACKGROUND: Conventional cardiac device infections are increasing in incidence, causing significant morbidity and mortality. Leadless pacemaker (LP) therapy may provide new opportunities for the management of pacemaker (PM) infections as it does not require implantation of transvenous leads and a pectoral pocket. OBJECTIVE: We sought to evaluate the effect of early and late LP implantation in patients diagnosed with device infection. METHODS: Patients receiving an LP at our center after conventional PM lead extraction due to infection between December 1, 2013 and November 30, 2017 were included. RESULTS: A total of 17 patients (mean age 77.4 ± 7.77 years) underwent LP implantation (ie, 11 with Nanostim leadless cardiac pacemaker [Abbott, Chicago, IL] and 6 with Micra transcatheter pacing system [Medtronic, Minneapolis, MN]) after successful PM system explantation. In 9 PM-dependent patients, a temporary transvenous pacing system was placed as a bridge to permanent LP implantation. Early LP implantation was performed in 6 patients (<1 week), and in the remaining patients, the LP was placed at a later stage (>1 week). All patients experienced no LP infection during a mean follow-up of 16 ± 12 months, including 7 patients with a history of recurrent device infections with a mean follow-up of 20 ± 14 months. CONCLUSION: Early and late LP placement after infected conventional pacing system explantation was a viable option in our case series. This therapy may provide an alternative strategy in the management of device infection, if confirmed by subsequent prospective randomized trials, particularly for patients who are PM dependent or have a history of recurrent device infections.

Bursts of reperfusion arrhythmias occur independently of area at risk size and are the first marker of reperfusion injury.

BACKGROUND: The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ. METHODS: 68 STEMI patients from the MAST study with 24-hour, continuous, 12­lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data. RESULTS: VA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteristics, comorbidities, infarct location, number of diseased coronary vessels, or duration of ischemia between groups with and without VA burst. IS was significantly smaller in the group without VA bursts (median 9.3% vs 17.0%; p = 0.025). Infarct ESA did not significantly differ between the population with and without VA burst; median 24.3% vs 20.0%; p = 0.15. CONCLUSION: VA bursts are a marker for larger IS independent of AAR, assessed by surrogate markers. These findings support the hypothesis that VA bursts are a marker of reperfusion damage occurring downstream at myocellular level.

Reperfusion ventricular arrhythmia bursts identify larger infarct size in spite of optimal epicardial and microvascular reperfusion using cardiac magnetic resonance imaging.

AIMS: Ventricular arrhythmia (VA) bursts following recanalisation in acute ST-elevation myocardial infarction (STEMI) are related to larger infarct size (IS). Inadequate microvascular reperfusion, as determined by microvascular obstruction (MVO) using cardiac magnetic resonance imaging (CMR), is also known to be associated with larger IS. This study aimed to test the hypothesis that VA bursts identify larger infarct size in spite of optimal microvascular reperfusion. METHODS: All 65 STEMI patients from the Maastricht ST elevation (MAST) study with brisk epicardial flow (TIMI 3), complete ST recovery post-percutaneous coronary intervention and early CMR were included. Using 24-hour Holter registrations from the time of admission, VA bursts were identified against subject-specific Holter background VA rates using a statistical outlier method. MVO and final IS were determined using delayed enhancement CMR. RESULTS: MVO was present in 37/65 (57%) of patients. IS was significantly smaller in the group without MVO (median 9.4% vs. 20.5%; p < 0.001). IS in the group with MVO did not differ depending on VA burst ( n = 28/37; median 20.8% vs. 19.7%; p = 0.64). However, in the group without MVO, VA burst was associated with significantly larger IS ( n = 17/28; median 10.5% vs. 4.1%; p = 0.037). In multivariable analyses, VA burst as well as anterior infarct location remained independent predictors of larger infarct size. CONCLUSION: In the presence of suboptimal reperfusion with MVO by CMR, VA burst does not further define MI size. However, with optimal TIMI 3 reperfusion and optimal microvascular perfusion (i.e. no MVO), VA burst is associated with larger IS, indicating that VA burst is a marker of additional cell death.

What is the best ST-segment recovery parameter to predict clinical outcome and myocardial infarct size? Amplitude, speed, and completeness of ST-segment recovery after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction.

AIMS: ST-segment recovery (STR) is a strong mechanistic correlate of infarct size (IS) and outcome in ST-segment elevation myocardial infarction (STEMI). Characterizing measures of speed, amplitude, and completeness of STR may extend the use of this noninvasive biomarker. METHODS AND RESULTS: Core laboratory continuous 24-h 12-lead Holter ECG monitoring, IS by single-photon emission computed tomography (SPECT), and 30-day mortality of 2 clinical trials of primary percutaneous coronary intervention in STEMI were combined. Multiple ST measures (STR at last contrast injection (LC) measured from peak value; 30, 60, 90, 120, and 240min, residual deviation; time to steady ST recovery; and the 3-h area under the time trend curve [ST-AUC] from LC) were univariably correlated with IS and predictive of mortality. After multivariable adjustment for ST-parameters and GRACE risk factors, STR at 240min remained an additive predictor of mortality. Early STR, residual deviation, and ST-AUC remained associated with IS. CONCLUSIONS: Multiple parameters that quantify the speed, amplitude, and completeness of STR predict mortality and correlate with IS.

Ventricular arrhythmia burst is an independent indicator of larger infarct size even in optimal reperfusion in STEMI.

OBJECTIVE: We hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of larger infarct size despite optimal epicardial and microvascular perfusion. METHODS: 126 STEMI patients were studied with 24h continuous, 12-lead Holter monitoring. Myocardial blush grade (MBG) was determined and VA bursts were identified against subject-specific background VA rates in core laboratories. Delayed-enhancement cardiovascular magnetic resonance imaging was used to determine infarct size. RESULTS: In the group with MBG 3 no significant differences were found for baseline characteristics between burst versus no burst (102 vs. 24). In those with optimal epicardial and microvascular reperfusion (TIMI 3, stable ST-recovery, and MBG 3), VA burst was associated with larger infarct size (N=102/126; median 11.0 vs. 5.1%; p=0.004). CONCLUSION: In the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.

Prospective evaluation of where reperfusion ventricular arrhythmia "bursts" fit into optimal reperfusion in STEMI.

BACKGROUND: Early reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infarction. VA (ventricular arrhythmia) bursts after recanalization of the culprit vessel have been found to be related to larger infarct size (IS), using SPECT. OBJECTIVE: The hypothesis was tested that this finding could be confirmed in an independent cohort using a more accurate technique, i.e. delayed-enhancement cardiovascular magnetic resonance imaging (DE-CMR). METHODS: All 196 patients from the PREPARE and MAST studies who had 24-hour, continuous, 12-lead Holter, started before primary percutaneous coronary intervention resulting in brisk TIMI (thrombolysis in myocardial infarction) 3 flow and stable ST-recovery were included. VA bursts were identified against subject-specific background VA rates using a previously published statistical outlier method. IS was assessed using DE-CMR. Angiography, Holter and DE-CMR results were assessed in core laboratories, blinded to all other data. RESULTS: VA bursts were present in 154/196 (79%) of patients. Baseline characteristics between the groups with and without bursts were similar. VA burst was associated with significantly larger infarct size in the population as a whole (median 11.3% vs 5.3%; p=0.001) and also when divided in non-anterior (median 9.9% vs 4.9%; p=0.003) and anterior myocardial infarction (median 21.4% vs 12.0%; p=0.48), the latter not reaching statistical significance due to the small subset of patients. CONCLUSION: Beyond the classical markers of "optimal" reperfusion such as TIMI 3 flow and stable ST-segment recovery, VA bursts occurring during the reperfusion phase are an early electrobiomarker of larger IS. CLINICAL TRIAL REGISTRATION: PREPARE: ISRCTN71104460 http://www.controlled-trials.com/ISRCTN71104460.

Pressure-controlled intermittent coronary sinus occlusion (PICSO) in acute ST-segment elevation myocardial infarction: results of the Prepare RAMSES safety and feasibility study.

AIMS: Pressure-controlled intermittent coronary sinus occlusion (PICSO) may improve myocardial perfusion after pPCI. We evaluated the safety and feasibility of PICSO after pPCI for STEMI, and explored its effects on infarct size and myocardial function. METHODS AND RESULTS: Thirty patients were enrolled following successful pPCI of a left anterior descending coronary artery culprit lesion for anterior STEMI, in whom PICSO for 90 minutes was attempted. Infarct size and myocardial function were assessed by cardiovascular magnetic resonance (CMR) at two to five days and four months post pPCI. An independent core laboratory selected matched historical control patients with CMR data for comparison. PICSO was initiated in 19 patients (63%), and could be maintained for 90 (±2) minutes in 12 patients (40%). Major adverse safety events occurred in one patient (3%). Comparing all PICSO-treated patients to matched controls demonstrated no significant differences in infarct size or myocardial recovery. However, infarct size reduction from two to five days to four months was greater for patients successfully treated with PICSO compared with matched controls (41.6±8.2% vs. 27.7±9.9%, respectively; p=0.04). CONCLUSIONS: PICSO is safe in the setting of STEMI, although feasibility was limited. Administration of sufficient PICSO therapy may be associated with enhanced myocardial recovery during follow-up, warranting further evaluation of this novel therapy.

Admission lipoprotein-associated phospholipase A2 activity is not associated with long-term clinical outcomes after ST-segment elevation myocardial infarction.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity is a biomarker predicting cardiovascular diseases in a real-world. However, the prognostic value in patients undergoing primary percutaneous coronary intervention (pPCI) for ST-segment elevation myocardial infarction (STEMI) on long-term clinical outcomes is unknown. METHODS: Lp-PLA2 activity was measured in samples obtained prior to pPCI from consecutive STEMI patients in a high-volume intervention center from 2005 until 2007. Five years all-cause mortality was estimated with the Kaplan-Meier method and compared among tertiles of Lp-PLA2 activity during complete follow-up and with a landmark at 30 days. In a subpopulation clinical endpoints were assessed at three years. The prognostic value of Lp-PLA2, in addition to the Thrombolysis In Myocardial Infarction or multimarker risk score, was assessed in multivariable Cox regression. RESULTS: The cohort (n = 987) was divided into tertiles (low <144, intermediate 144-179, and high >179 nmol/min/mL). Among the tertiles differences in baseline characteristics associated with long-term mortality were observed. However, no significant differences in five years mortality in association with Lp-PLA2 activity levels were found; intermediate versus low Lp-PLA2 (HR 0.97; CI 95% 0.68-1.40; p = 0.88) or high versus low Lp-PLA2 (HR 0.75; CI 95% 0.51-1.11; p = 0.15). Both in a landmark analysis and after adjustments for the established risk scores and selection of cases with biomarkers obtained, non-significant differences among the tertiles were observed. In the subpopulation no significant differences in clinical endpoints were observed among the tertiles. CONCLUSION: Lp-PLA2 activity levels at admission prior to pPCI in STEMI patients are not associated with the incidence of short and/or long-term clinical endpoints. Lp-PLA2 as an independent and clinically useful biomarker in the risk stratification of STEMI patients still remains to be proven.

Percutaneous coronary intervention for acute coronary syndrome due to graft failure: use of bare-metal and drug-eluting stents and subsequent long-term clinical outcome.

OBJECTIVES: To describe clinical outcome after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) due to graft failure. BACKGROUND: Limited data are available on outcome after PCI for graft failure-induced ACS in the drug-eluting stent (DES) era. METHODS: Patients were identified who underwent PCI either with DES or BMS for ACS due to graft failure between January 2003 and December 2008. Follow-up was performed at 1 year and April 2011. The primary endpoint was the composite of death, myocardial infarction (MI), or target vessel revascularization (TVR). Kaplan-Meier estimates were calculated at 1 and 5-year follow-up. Predictors were identified by backward selection in Cox proportional hazards models. RESULTS: A total of 92 patients underwent PCI, of which 77 were treated with bare metal stents (BMS) and 15 with DES. Patient and procedural characteristics were similar in both groups. Mean follow-up was 3.2 years. Five-year composite event rate was 65.9% after BMS vs. 43.4% after DES implantation (P = 0.17). Individual endpoints were comparable in both groups. Recurrence of angina, hospitalization, and repeat interventions were similar. After multivariable adjustment, the use of DES was not associated with a significant reduction in the primary endpoint (HR = 0.44, 0.18-1.04, p = 0.06). CONCLUSION: In patients presenting with ACS due to acute graft failure, long-term outcomes remain poor. In a nonrandomized comparison with BMS, DES use was not associated with significant improved long-term clinical outcomes.

Clinical outcome after surgical or percutaneous revascularization in coronary bypass graft failure.

AIMS: To describe long-term outcome following surgical and percutaneous revascularization in graft failure. METHODS: We analyzed consecutive patients with graft failure after heart-team assignment to percutaneous coronary intervention (PCI) or redo coronary artery bypass grafting (CABG) between 2003 and 2008. The primary endpoint was the composite of death, myocardial infarction (MI) or target vessel revascularization (TVR). Kaplan-Meier event rate estimates were calculated up to a 5-year follow-up. Independent predictors for outcomes were identified by backward selection in a multivariable Cox proportional hazard model. RESULTS: We identified 287 patients treated for graft failure: 243 with PCI and 44 with redo CABG. Patients undergoing PCI more frequently presented with ST-elevated myocardial infarction (STEMI) (P < 0.001), multivessel disease (P < 0.001), vein graft failure (P = 0.04), a history of MI (P < 0.001) and shorter time-to-graft failure (P = 0.001). Bare-metal stents (BMS) were used in 81.3% of the PCI-treated lesions and drug-eluting stents (DES) in 18.7%. The median follow-up was 3.9 years. Five-year rate of composite all-cause death, MI or TVR was 57.6% after PCI and 51% after CABG (P = 0.51). Repeat revascularization [TVR and target lesion revascularization (TLR)] was 30.7 and 21.3% after PCI, and 8.0 and 3.2% following CABG (P = 0.009; P = 0.008). In the PCI group, BMS was associated with higher rates of TVR (35.1 vs. 12.6%; P = 0.04) and TLR (24.8 vs. 7.6%; P = 0.04), but similar rate of death or MI compared with DES. Independent predictors for the primary outcome were creatinine [hazard ratio 1.008 per µmol/l, 95% confidence interval (CI) 1.005-1.011, P < 0.001] and peak creatine kinase MB (hazard ratio 1.001 per U/l, 95% CI 1.000-1.002, P = 0.027). CONCLUSION: Clinical outcomes are similarly poor after heart-team triage for surgical or percutaneous intervention in patients with graft failure. Repeat revascularization occurred more frequent after PCI, particularly following BMS implantation.

Short- and long-term prognostic value of the TIMI risk score after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction.

OBJECTIVES: We investigated the short- and long-term predictive value of the TIMI risk score regarding mortality for patients treated with primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction (STEMI). BACKGROUND: Data on the long-term predictive value of the TIMI risk score is sparse. METHODS: We used data from 3,609 STEMI patients undergoing PPCI in a high-volume PCI center in The Netherlands. Cumulative event rates according to TIMI score variables were estimated with the Kaplan-Meier method and compared with the log-rank test. The original TIMI risk score was modified based on the availability of the data in the single center registry. RESULTS: Higher TIMI scores were associated with significantly higher mortality at short- and long-term follow-up (P < 0.001 for both). Age and Killip Class IV at presentation were significant predictors for both short- and long-term mortality. Patients with an anterior MI, heart frequence >100 beats per minute, or systolic blood pressure <100 mmHG had a worse short-term prognosis compared to those who had not. However, long-term mortality was nonsignificantly different. The presence of a history of diabetes/hypertension and weight had only long-term prognostic value. Time to PPCI did not have any prognostic value. CONCLUSIONS: Our current report shows that the TIMI risk score has both short- and long-term discriminative value. The different variables contained in the TIMI risk score predict short-term prognosis, others predominantly long-term mortality, whereas some are predictive for both.

Multiple biomarkers for the prediction of short and long-term mortality after ST-segment elevation myocardial infarction: the Amsterdam Groningen collaboration.

Multiple biomarkers improve prognostication for long-term mortality in ST-segment elevation myocardial infarction (STEMI). However, one-third of mortality after STEMI occurs within initial discharge. Our objective was to determine whether multiple biomarkers (glucose, N-terminal pro-brain natriuretic peptide (NT-proBNP), and estimated glomerular filtration rate (eGFR)) predict both short-term as long-term mortality in STEMI. We used a patient-pooled dataset of consecutive STEMI patients, with complete biomarkers, who underwent primary percutaneous coronary intervention (PCI) in two single centers (Amsterdam and Groningen). With a previously developed multimarker risk score, based on three biomarkers, patients were indicated as low-, intermediate- or high risk. Cumulative 4-year mortality was estimated with the Kaplan-Meier method and compared with a log-rank test. We compared short-term and long-term mortality with a landmark set at 30 days because previous studies have shown that mortality largely occurs within 30 days. A total of 2,355 STEMI-patients were treated with primary PCI. The mortality rates in the low- (n = 1,531), intermediate- (n = 403) and high-risk (n = 421) groups were 4.8, 16.1, and 43.9 %, respectively. The differences were observed at a follow-up up to 30 days (log-rank p < 0.001) as well as after 30 days (log-rank p < 0.001). A multimarker risk score, based on admission levels of glucose, NT-proBNP, and eGFR identifies STEMI patients at low-, intermediate-, and high-risk for short-term and long-term mortality.

Multiple biomarkers at admission are associated with angiographic, electrocardiographic, and imaging cardiovascular mechanistic markers of outcomes in patients undergoing primary percutaneous coronary intervention for acute ST-elevation myocardial infarction.

BACKGROUND: The multimarker risk score, based on estimated glomerular filtration rate, glucose, and N-terminal probrain natriuretic peptide (NT-proBNP), has been shown to predict mortality in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). In this study, we investigated the relation between the multimarker risk score and cardiovascular mechanistic markers of outcomes in STEMI patients undergoing PPCI. METHODS: Complete biomarkers were available in 197 patients with STEMI. Angiographic Thrombolysis In Myocardial Infarction flow grade and myocardial blush grade at the end of the PPCI, electrocardiographic ST-segment resolution (STR) at the time of last contrast injection and 240 minutes after last contrast, and cardiac magnetic resonance (CMR) left ventricular ejection fraction (LVEF) and infarct size at 4 to 6 months after the index event were available. RESULTS: In linear regression models, higher multimarker scores were associated with worse angiographic (P < .01 for both outcomes), electrocardiographic (P < .001 for the association with STR at last contrast, and P < .01 for STR at 240 minutes), and CMR outcomes (P < .01 for both). CONCLUSIONS: The multimarker risk score is associated with angiographic, electrocardiographic, and CMR mechanistic markers of outcomes. These data support the ability of the multimarker risk score to identify patients at high risk for suboptimal reperfusion and CMR outcomes and may aid in the early triage of patients who stand to benefit most of adjuvant treatments in STEMI.

Gender difference in the prognostic value of estimated glomerular filtration rate at admission in ST-segment elevation myocardial infarction: a prospective cohort study.

OBJECTIVE: To evaluate gender differences in the prognostic value of renal function for mortality in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). DESIGN: Prospective single-center cohort. SETTING: Single tertiary referral center in Amsterdam, The Netherlands. Patients consecutive STEMI patients undergoing PPCI (1412 men and 558 women). MAIN OUTCOME MEASURE: The authors calculated adjusted HRs for 3-year all-cause mortality according to the presence of a reduced renal function (estimated glomerular filtration rate <60 ml/min) using Cox proportional hazards models. In order to investigate a possible gender difference in the prognostic value of a reduced renal function, a comparison was made between the HRs of male and female patients and an interaction term was added to the model and tested for significance. Adjustments were made for age, body mass index, history of diabetes or hypertension, systolic blood pressure and heart rate, anterior myocardial infarction and time to treatment. RESULTS: In male patients, a reduced renal function was associated with increased 3-year mortality (adjusted HR 6.31, 95% CI 3.74 to 10.63, p<0.001). A reduced renal function was associated with a twofold increase in the mortality hazard in female patients (adjusted HR 2.22, 95% CI 1.25 to 3.94, p=0.006). CONCLUSIONS: In this large single-centre registry of STEMI patients undergoing PPCI, renal dysfunction as assessed by estimated glomerular filtration rate had prognostic significance for mortality in both male and female patients.

P2Y12 platelet inhibition in clinical practice.

Platelet adhesion, activation and aggregation play a pivotal role in atherothrombosis. Intracoronary atherothrombosis is the most common cause of the development of acute coronary syndrome (ACS), and plays a central role in complications occurring around percutaneous coronary intervention (PCI) including recurrent ACS, procedure-related myocardial infarction or stent thrombosis. Inhibition of platelet aggregation by medical treatment impairs formation and progression of thrombotic processes and is therefore of great importance in the prevention of complications after an ACS or around PCI. An essential part in the platelet activation process is the interaction of adenosine diphosphate (ADP) with the platelet P2Y12 receptor. The P2Y12 receptor is the predominant receptor involved in the ADP-stimulated activation of the glycoprotein IIb/IIIa receptor. Activation of the glycoprotein IIb/IIIa receptor results in enhanced platelet degranulation and thromboxane production, and prolonged platelet aggregation. The objectives of this review are to discuss the pharmacological limitations of the P2Y12 inhibitor clopidogrel, and describe the novel alternative P2Y12 inhibitors prasugrel and ticagrelor and the clinical implications of the introduction of these new medicines.

Impact of early, late, and no ST-segment resolution measured by continuous ST Holter monitoring on left ventricular ejection fraction and infarct size as determined by cardiovascular magnetic resonance imaging.

BACKGROUND: The goal of this study is to determine the predictive value of ST-segment resolution (STR) early after percutaneous coronary intervention (PCI), late STR, and no STR for left ventricular ejection fraction (LVEF) and infarct size (IS) by cardiovascular magnetic resonance (CMR) at follow-up in patients with ST-segment elevation myocardial infarction. METHODS: The analysis included 199 patients who were enrolled in the PRoximal Embolic Protection in Acute myocardial infarction and Resolution of ST-Elevation trial and in whom both continuous ST Holter and CMR at follow-up were available. Patients were stratified into 3 groups: (1) early complete (≥70%) STR measured immediately after last contrast injection (n = 113); (2) late complete STR (n = 52), defined as complete STR from 30 to 240 minutes after PCI; and (3) no complete STR after 240 minutes (n = 34). RESULTS: Patients with early STR had more preserved LVEF and smaller IS compared to patients with late STR or no STR (LVEF: early STR, 54% ± 8%; late STR, 46% ± 13%; no STR, 43% ± 11%; and IS: 3.9 ± 3.3 g/m(2); 8.0 ± 6.9 g/m(2); 12.0 ± 6.0 g/m(2); respectively; all P < .0001). Early STR was independently predictive for LVEF (ß = 8.5; P = .0005) and IS (ß = -7.0; P < .0001). Late STR was not predictive for LVEF (ß = 1.6; P = .51) but predictive for IS (ß = -3.5; P = .003). CONCLUSIONS: Patients with early complete STR after primary PCI have better preserved LVEF and smaller IS. Patients with late complete STR do not have better preserved LVEF but do have smaller IS. ST-segment resolution is a strong, independent predictor of LVEF and IS as assessed by CMR.

Multiple biomarkers at admission significantly improve the prediction of mortality in patients undergoing primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction.

OBJECTIVES: We investigated whether multiple biomarkers improve prognostication in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention. BACKGROUND: Few data exist on the prognostic value of combined biomarkers. METHODS: We used data from 1,034 STEMI patients undergoing primary percutaneous coronary intervention in a high-volume percutaneous coronary intervention center in the Netherlands and investigated whether combining N-terminal pro-brain natriuretic peptide, glucose, C-reactive protein, estimated glomerular filtration rate, and cardiac troponin T improved the prediction of mortality. A risk score was developed based on the strongest predicting biomarkers in multivariate Cox regression. The additional prognostic value of the strongest predicting biomarkers to the established prognostic factors (age, body weight, diabetes, hypertension, systolic blood pressure, heart rate, anterior myocardial infarction, and time to treatment) was assessed in multivariable Cox regression. RESULTS: During follow-up (median, 901 days), 120 of the 1,034 patients died. In Cox regression, glucose, estimated glomerular filtration rate, and N-terminal pro-brain natriuretic peptide were the strongest predictors for mortality (p < 0.05, for all). A risk score incorporating these biomarkers identified a high-risk STEMI subgroup with a significantly higher mortality when compared with an intermediate- or low-risk subgroup (p < 0.001). Addition of the 3 biomarkers to established prognostic factors significantly improved prediction for mortality, as shown by the net reclassification improvement (0.481, p < 0.001) [corrected] and integrated discrimination improvement (0.0226, p = 0.03) [corrected]. CONCLUSIONS: Our data suggest that addition of a multimarker to a model including established risk factors improves the prediction of mortality in STEMI patients undergoing primary percutaneous coronary intervention. Furthermore, the use of a simple risk score based on these biomarkers identifies a high-risk subgroup.