Sudden cardiac death in long-term follow-up in patients treated with primary percutaneous coronary intervention.

Objective. Most studies analyzing predictors of sudden cardiac death (SCD) after acute myocardial infarction included only high-risk patients or index reperfusion had not been performed in all patients. The aim of our study was to analyze the incidence of SCD and determine the predictors of SCD occurrence during 6-year follow-up of unselected patients with ST-elevation myocardial infarction (STEMI), treated with primary percutaneous coronary intervention (pPCI). Method. we analysed 3114 STEMI patients included included in the University Clinical Center of Serbia STEMI Register. Patients presenting with cardiogenic schock were excluded. Echocardiographic examination was performed before hospital discharge. Results. During 6-year follow-up, lethal outcome was registered in 297 (9.5%) patients, of whom 95 (31.9%) had SCD. The highest incidence of SCD was recorded in the first year of follow-up, when SCD was registered in 25 patients, which is 26.3% of the total number of patients who had had SCD, i.e. 0.8% of the patients analyzed. The independent predictors for the occurrence of SCD during 6-year follow-up were EF < 45% (HR 3.07, 95% 1.87-5.02), post-procedural TIMI flow <3 (HR 2.59, 95%CI 1.37-5.14), reduced baseline kidney function (HR 1.87, 95%CI 1.12-2.93) and Killip class >1 at admission (HR 1.69, 95%CI 1.23-2.97). Conclusion. There is a low incidence of SCD in unselected STEMI patients treated with primary PCI. Predictors of SCD occurence during long-term follow-up in analyzed patients are clinical variables that are easily recorded during index hospitalization and include: EF ≤45%, post-procedural flow TIMI < 3, Killip class >1, and reduced baseline kidney function.

Antioxidant Genetic Variants Modify Echocardiography Indices in Long COVID.

Although disturbance of redox homeostasis might be responsible for COVID-19 cardiac complications, this molecular mechanism has not been addressed yet. We have proposed modifying the effects of antioxidant proteins polymorphisms (superoxide dismutase 2 (SOD2), glutathione peroxidase 1 (GPX1), glutathione peroxidase 3 (GPX3) and nuclear factor erythroid 2-related factor 2, (Nrf2)) in individual susceptibility towards the development of cardiac manifestations of long COVID-19. The presence of subclinical cardiac dysfunction was assessed via echocardiography and cardiac magnetic resonance imaging in 174 convalescent COVID-19 patients. SOD2, GPX1, GPX3 and Nrf2 polymorphisms were determined via the appropriate PCR methods. No significant association of the investigated polymorphisms with the risk of arrhythmia development was found. However, the carriers of variant GPX1*T, GPX3*C or Nrf2*A alleles were more than twice less prone for dyspnea development in comparison with the carriers of the referent ones. These findings were even more potentiated in the carriers of any two variant alleles of these genes (OR = 0.273, and p = 0.016). The variant GPX alleles were significantly associated with left atrial and right ventricular echocardiographic parameters, specifically LAVI, RFAC and RV-EF (p = 0.025, p = 0.009, and p = 0.007, respectively). Based on the relation between the variant SOD2*T allele and higher levels of LV echocardiographic parameters, EDD, LVMI and GLS, as well as troponin T (p = 0.038), it can be proposed that recovered COVID-19 patients, who are the carriers of this genetic variant, might have subtle left ventricular systolic dysfunction. No significant association between the investigated polymorphisms and cardiac disfunction was observed when cardiac magnetic resonance imaging was performed. Our results on the association between antioxidant genetic variants and long COVID cardiological manifestations highlight the involvement of genetic propensity in both acute and long COVID clinical manifestations.

The Impact of Kidney Function on the Slow-Flow/No-Reflow Phenomenon in Patients Treated with Primary Percutaneous Coronary Intervention: Registry Analysis.

Objective: The objective of this study is to analyze the impact of declining kidney function on the occurrence of the slow-flow/no-reflow phenomenon in patients with ST-elevation myocardial infarction (STEMI) treated with primary PCI (pPCI), as well as the analysis of the prognostic impact of the slow-flow/no-reflow phenomenon on short- and long-term mortality in these patients. Methods: We analyzed 3,115 consecutive patients. A value of the glomerular filtration rate (eGFR) at the time of admission of eGFR <90 ml/min/m2 was considered a low baseline eGFR. The follow-up period was 8 years. Results: The slow-flow/no-reflow phenomenon through the IRA was registered in 146 (4.7%) patients. Estimated GFR of <90 ml/min/m2 was an independent predictor for the occurrence of the slow-flow/no-reflow phenomenon (OR 2.91, 95% CI 1.25-3.95, p < 0.001), and the risk for the occurrence of the slow-flow/no-reflow phenomenon increased with the decline of the kidney function: eGFR 60-89 ml/min/m2: OR 1.94 (95% CI 1.22-3.07, p = 0.005), eGFR 45-59 ml/min/m2: OR 2.55 (95% CI 1.55-4.94, p < 0.001), eGFR 30-44 ml/min/m2: OR 2.77 (95% CI 1.43-5.25, p < 0.001), eGFR 15-29 ml/min/m2: OR 5.84 (95% CI 2.84-8.01, p < 0.001). The slow-flow/no-reflow phenomenon was a strong independent predictor of short- and long-term all-cause mortality: 30-day mortality (HR 2.62, 95% CI 1.78-3.57, p < 0.001) and 8-year mortality (HR 2.09, 95% CI 1.49-2.09, p < 0.001). Conclusion: Reduced baseline kidney function was an independent predictor for the occurrence of the slow-flow/no-reflow phenomenon, and its prognostic impact started with the mildest decrease in eGFR (below 90 ml/min/m2) and increased with its further decline. The slow-flow/no-reflow phenomenon was a strong independent predictor of mortality in the short- and long-term follow-up of the analyzed patients.

Impact of acute hyperglycemia on layer-specific left ventricular strain in asymptomatic diabetic patients: an analysis based on two-dimensional speckle tracking echocardiography.

BACKGROUND: Hyperglycemia has detrimental effect on ischemic myocardium, but the impact of acute hyperglycemia on the myocardium in asymptomatic diabetic patients has not been fully elucidated. Thus, this follow-up study was aimed to investigate the effects and reversibility of acute hyperglycemia on regional contractile function of left ventricle (LV) in diabetic patients without cardiovascular disease. METHODS: The two-dimensional speckle tracking echocardiography (2D-STE), including multilayer strain analysis, was used for evaluation of global and regional LV function in asymptomatic, normotensive patients with uncomplicated diabetes, with acute hyperglycemia ( ≥ 11.1 mmol/l) (Group A, n = 67), or with optimal metabolic control (fasting plasma glucose < 7 mmol/l and HbA1c < 7%) (Group B, n = 20), while 20 healthy individuals served as controls (Group C). In group A, after 72 h of i.v. continuous insulin treatment (at the time euglycemia was achieved) (second examination) and after 3 months following acute hyperglycemia (third examination) 2D-STE was repeated. RESULTS: Global longitudinal strain (GLS) (- 19.6 ± 0.4%) in Group A was significantly lower in comparison to both groups B (- 21.3 ± 0.4%; p < 0.05) and C (- 21.9 ± 0.4%; p < 0.01) at baseline, while we could not detect the differences between groups B and C. Peak systolic longitudinal endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) layer strain were significantly lower in group A at baseline compared to both groups B and C. Deterioration in peak systolic circumferential strain was observed at basal LV level, in all three layers (Endo, Mid and Epi) and in mid-cavity LV level in Epi layer in group A in comparison to group C. Moreover, in group A, after euglycemia was achieved (at second and third examination) GLS, as well as peak longitudinal and circumferential strain remain the same. CONCLUSION: Acute hyperglycemia in asymptomatic diabetic patients has significant negative effects on systolic LV myocardial mechanics primarily by reducing GLS and multilayer peak systolic longitudinal and circumferential strain which was not reversible after three months of good glycemic control.

Using the RISK-PCI Score in the Long-Term Prediction of Major Adverse Cardiovascular Events and Mortality after Primary Percutaneous Coronary Intervention.

BACKGROUND/AIM: The RISK-PCI is a simple score for the prediction of 30-day major adverse cardiovascular events (MACE) and mortality in patients treated with primary PCI (pPCI). The aim of the present study is to evaluate the prognostic performance of the RISK-PCI score in predicting MACE and mortality in the long-term follow-up of STEMI patients treated with pPCI. METHOD: The present study enrolled 2,096 STEMI patients treated with pPCI included in the RISK-PCI trial. Patients presenting with cardiogenic shock were excluded. The composite end-point MACE comprising cardiovascular mortality, nonfatal reinfarction and stroke. Patients were followed up at 6 years after enrollment. RESULTS: One-year and 6-year MACE occurred in 229 (10.9%) and 285 (13.6%) patients, respectively; and 1-year and 6-year mortality occurred in 128 (6.2%) and 151 (7.2%) patients, respectively. The RISK-PCI score was an independent predictor for 1-year MACE (HR 1.24, 95% CI 1, 18-1.31, p < 0.001), 6-year MACE (HR 1.22, 95% CI 1.16-1.28, p < 0.001), 1-year mortality (HR 1.21, 95% CI 1.13-1.29, p < 0.001), and 6-year mortality (HR 1.23, 95% CI 1.15-1.31, p < 0.001). The discrimination of the RISK-PCI score to predict 1-year and 6-year MACE and mortality was good: for 1-year MACE c-statistic 0.78, for 6-year MACE c-statistic 0.75, for 1-year mortality c-statistic 0.87, and for 6-year mortality c-statistic 0.83. The nonsignificant Hosmer-Lemeshow goodness-of-fit estimates for 1-year MACE (p=0.619), 6-year MACE (p=0.319), 1-year mortality (p=0.258), and 6-year mortality (p=0.540) indicated a good calibration of the model. CONCLUSION: The RISK-PCI score demonstrates good characteristics in the assessment of the risk for the occurrence of MACE and mortality during long-term follow-up after pPCI.

Clinical Significance of Laboratory-determined Aspirin Poor Responsiveness After Primary Percutaneous Coronary Intervention.

AIMS: The objective of the present substudy was to examine whether aspirin poor/high responsiveness (APR/AHR) is associated with increased rates of major adverse cardiovascular events (MACE) and serious bleeding after primary percutaneous coronary intervention (PPCI). METHODS: We analyzed 961 consecutive ST-elevation acute myocardial infarction patients who underwent PPCI between February 2008 and June 2011. Multiplate analyser (Dynabite, Munich, Germany) was used for the assessment of platelet reactivity. APR/AHR were defined as the upper/lower quintiles of ASPI values, determined 24 h after aspirin loading. APR patients were tailored using 300 mg maintenance dose for 30 days. The co-primary end points at 30 days were: MACE (death, non-fatal infarction, ischemia-driven target vessel revascularization and ischemic stroke) and serious bleeding according to the BARC classification. RESULTS: One hundred and 90 patients were classified as APR, and 193 patients as AHR. At admission, compared with aspirin sensitive patients (ASP), patients with APR had more frequently diabetes, anterior infarction and heart failure, while AHR patients had reduced values of creatine kinase, leukocytes, heart rate and systolic blood pressure. Compared with ASP, the rates of 30-day primary end points did not differ neither in APR group including tailored patients (MACE, adjusted OR 1.02, 95%CI 0.47-2.17; serious bleeding, adjusted OR 1.92, 95%CI 0.79-4.63), nor in patients with AHR (MACE, adjusted OR 1.58, 95%CI 0.71-5.51; serious bleeding, adjusted OR 0.69, 95%CI 0.22-2.12). CONCLUSIONS: The majority of APR patients were suitable for tailoring. Neither APR including tailored patients nor AHR were associated with adverse 30-day efficacy or safety clinical outcomes.

B-type Natriuretic Peptide and RISK-PCI Score in the Risk Assessment in Patients with STEMI Treated by Primary Percutaneous Coronary Intervention.

BACKGROUND: RISK-PCI score is a novel score for risk stratification of patients with ST elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (pPCI). The aim of this study was to evaluate the role of B-type natriuretic peptide (BNP) and the RISK-PCI score for early risk assessment in patients with STEMI treated by pPCI. METHODS: In 120 patients with STEMI treated by pPCI, BNP was measured on admission before pPCI. The primary end point was 30-day mortality. RESULTS: The ROC curve analysis revealed that the most powerful predictive factors of 30-day mortality were the plasma level of BNP ≥ 206.6 pg/mL with the sensitivity of 75% and specificity of 87.5% and the RISK-PCI score ≥ 5.25 with the sensitivity of 75% and specificity of 85.7%. Thirty-day mortality was 6.7%. After multivariate adjustment, admission BNP (≥ 206.6 pg/mL) (OR 2.952, 95% CI 1.072 - 8.133, p = 0.036) and the RISK-PCI score (≥ 5.25) (OR 2.284, 95% CI 1.140-4.578, p = 0.020) were independent predictors of 30-day mortality. The area under the ROC curve using the RISK-PCI score and BNP to detect mortality was 0.828 (p = 0.002) and 0.903 (p < 0.001), respectively. Addition of BNP to RISK-PCI score increased the area under the ROC to 0.949 (p < 0.001), but this increase measured by the c-statistic was not significant (p = 0.107). Furthermore, the significant improvement in risk reclassification (p < 0.001) and the integrated discrimination index (p = 0.042) were observed with the addition of BNP to RISK-PCI score for 30-day mortality. CONCLUSIONS: BNP on admission and the RISK-PCI score were the independent predictors of 30-day mortality in patients with the STEMI treated by pPCI. BNP in combination with the RISK-PCI score showed the way to more accurate risk assessment in patients with STEMI treated by pPCI.

Cardiac Magnetic Resonance Imaging as a Risk Stratification Tool in COVID-19 Myocarditis.

The aim of this retrospective study was to identify myocardial injury after COVID-19 inflammation and explore whether myocardial damage could be a possible cause of the persistent symptoms following COVID-19 infection in previously healthy individuals. This study included 139 patients who were enrolled between January and June 2021, with a mean age of 46.7 ± 15.2 years, of whom 68 were men and 71 were women without known cardiac or pulmonary diseases. All patients underwent clinical work-up, laboratory analysis, cardiac ultrasound, and CMR on a 1.5 T scanner using a recommended protocol for morphological and functional assessment before and after contrast media application with multi-parametric sequences. In 39% of patients, late gadolinium enhancement (LGE) was found as a sign of myocarditis. Fibrinogen was statistically significantly higher in patients with LGE than in those without LGE (4.3 ± 0.23 vs. 3.2 ± 0.14 g/L, p < 0.05, respectively), as well as D-dimer (1.8 ± 0.3 vs. 0.8 ± 0.1 mg/L FEU). Also, troponin was statistically significantly higher in patients with myocardial LGE (13.1 ± 0.4 ng/L) compared to those with normal myocardium (4.9 ± 0.3 ng/L, p < 0.001). We demonstrated chest pain, fatigue, and elevated troponin to be independent predictors for LGE. Septal LGE was shown to be a predictor for arrhythmias. The use of CMR is a potential risk stratification tool in evaluating outcomes following COVID-19 myocarditis.

Long-Term Prognostic Impact of Stress Hyperglycemia in Non-Diabetic Patients Treated with Successful Primary Percutaneous Coronary Intervention.

BACKGROUND: stress hyperglicemia (SH) is common in patients with ST-elevation myocardial infraction (STEMI). The aims of this study were to analyze the impact of SH on the incidence of all-cause mortality and major adverse cardiovascular events (MACE-cardiovascular death, nonfatal reinfarction, target vessel revascularization, and stroke) in STEMI patients without diabetes mellitus (DM) who have been treated successfully with primary PCI (pPCI). METHOD: we analyzed 2362 STEMI patients treated with successful pPCI (post-procedural flow TIMI = 3) and without DM and cardiogenic shock at admission. Stress hyperglycemia was defined as plasma glucose level above 7.8 mmol/L at admission. The follow-up period was 8 years. RESULTS: incidence of SH was 26.9%. Eight-year all-cause mortality and MACE rates were significantly higher in patients with SH, as compared to patients without SH (9.7% vs. 4.2%, p < 0.001, and 15.7% vs. 9.4%, p < 0.001). SH was an independent predictor of short- and long-term all-cause mortality (HR 2.19, 95%CI 1.16-4.18, and HR 1.99, 95%CI 1.03-3.85) and MACE (HR 1.49, 95%CI 1.03-2.03, and HR 1.35, 95%CI 1.03-1.89). CONCLUSION: despite successful revascularization, SH at admission was an independent predictor of short-term and long-term (up to eight years) all-cause mortality and MACE, but its negative prognostic impact was stronger in short-term follow-up.

Long-Term Prognosis after ST-Elevation Myocardial Infarction in Patients with Premature Coronary Artery Disease.

BACKGROUND: A significant percentage of younger patients with myocardial infarction have premature coronary artery disease (CAD). The aims of this study were to analyze all-cause mortality and major adverse cardiovascular events (MACEs cardiovascular death, non-fatal reinfarction, stroke, target vessel revascularization) during eight-year follow-up in patients with ST-elevation myocardial infarction (STEMI) and premature CAD. METHOD: We analyzed 2560 STEMI patients without previous CAD and without cardiogenic shock at admission who were treated with primary PCI. CAD was classified as premature in men aged <50 years and women <55 years. RESULTS: Premature CAD was found in 630 (24.6%) patients. Patients with premature CAD have fewer comorbidities and better initial angiographic findings compared to patients without premature CAD. The incidence of non-fatal adverse ischemic events was similar to the incidence in older patients. Premature CAD was an independent predictor for lower mortality (HR 0.50 95%CI 0.28-0.91) and MACEs (HR 0.27 95%CI 0.15-0.47). In patients with premature CAD, EF < 40% was the only independent predictor of mortality (HR 5.59 95%CI 2.18-8.52) and MACEs (HR 4.18, 95%CI 1.98-8.13). CONCLUSIONS: Premature CAD was an independent predictor for lower mortality and MACEs. In patients with premature CAD, EF < 40% was an independent predictor of eight-year mortality and MACEs.

Spontaneous coronary artery dissection in women in the generative period: clinical characteristics, treatment, and outcome-a systematic review and meta-analysis.

Introduction: Spontaneous coronary artery dissection (SCAD) is a non-traumatic and non-iatrogenic separation of the coronary arterial wall. Materials and methods: This systematic review and meta-analysis is reported following the PRISMA guidelines and is registered in the PROSPERO database. A literature search was focused on female patients in generative period (16-55 of age) with acute coronary syndrome (ACS) caused by SCAD, and comparison from that database NP-SCAD (spontaneous coronary artery dissection in non pregnant women) and P-SCAD (spontaneous coronary artery dissection in pregnant women). Results: 14 studies with 2,145 females in the generative period with ACS caused by SCAD were analyzed. The median age was 41 years (33.4-52.3 years). The most common risk factor was previous smoking history in 24.9% cases. The most common clinical presentation of ACS was STEMI in 47.4%. Conservative treatment was reported in 41.1%. PCI was performed in 32.7%, and 3.8% of patients had CABG surgery. LAD was the most frequently affected (50.5%). The prevalence of composite clinical outcomes including mortality, non-fatal MI and recurrent SCAD was 3.3% (95% CI: 1.4-5.1), 37.7% (95% CI: 1.9-73.4) and 15.2% (95% CI: 9.1-21.3) of patients. P-SCAD compared to NP-SCAD patients more frequently had STEMI (OR = 3.16; 95% CI: 2.30-4.34; I2 = 64%); with the left main and LAD more frequently affected [(OR = 14.34; 95% CI: 7.71-26.67; I2 = 54%) and (OR = 1.57; 95% CI: 1.06-2.32; I2 = 23%)]; P-SCAD patients more frequently underwent CABG surgery (OR = 6.29; 95% CI: 4.08-9.70; I2 = 0%). NP-SCAD compared to P-SCAD patients were more frequently treated conservatevly (OR = 0.61; 95% CI: 0.37-0.98; I2 = 0%). In P-SCAD compared to NP-SCAD mortality rates (OR = 1.13; 95% CI: 0.06-21.16; I2 = not applicable) and reccurence of coronary artery dissection (OR = 2.54; 95% CI: 0.97-6.61; I2 = 0%) were not more prevalent. Conclusion: The results of this meta-analysis indicated that patients with P-SCAD more frequently had STEMI, and events more frequently involved left main and LAD compared to NP-SCAD patients. Women with NP-SCAD were significantly more often treated conservatively compared to P-SCAD patients. P-SCAD compared to NP-SCAD patients did not have significantly higher mortality rates or recurrent coronary dissection.

The 'peptide for life' initiative in the emergency department study.

AIMS: Natriuretic peptide (NP) uptake varies in Emergency Departments (EDs) across Europe. The 'Peptide for Life' (P4L) initiative, led by Heart Failure Association, aims to enhance NP utilization for early diagnosis of heart failure (HF). We tested the hypothesis that implementing an educational campaign in Western Balkan countries would significantly increase NP adoption rates in the ED. METHODS AND RESULTS: This registry examined NP adoption before and after implementing the P4L-ED study across 10 centres in five countries: Bosnia and Herzegovina, Croatia, Montenegro, North Macedonia, and Serbia. A train-the-trainer programme was implemented to enhance awareness of NP testing in the ED, and centres without access received point-of-care instruments. Differences in NP testing between the pre-P4L-ED and post-P4L-ED phases were evaluated. A total of 2519 patients were enrolled in the study: 1224 (48.6%) in the pre-P4L-ED phase and 1295 (51.4%) in the post-P4L-ED phase. NP testing was performed in the ED on 684 patients (55.9%) during the pre-P4L-ED phase and on 1039 patients (80.3%) during the post-P4L-ED phase, indicating a significant absolute difference of 24.4% (95% CI: 20.8% to 27.9%, P < 0.001). The use of both NPs and echocardiography significantly increased from 37.7% in the pre-P4L-ED phase to 61.3% in the post-P4L-ED phase. There was an increased prescription of diuretics and SGLT2 inhibitors during the post-P4L-ED phase. CONCLUSIONS: By increasing awareness and providing resources, the utilization of NPs increased in the ED, leading to improved diagnostic accuracy and enhanced patient care.

Rationale and design of the on-treatment PLAtelet Reactivity-Guided Therapy Modification FOR ST-Segment Elevation Myocardial Infarction (PLATFORM) randomized trial.

OBJECTIVES: The present trial aims at examining whether antiplatelet regimen modification, guided by assessment of the on-treatment platelet reactivity, might result with clinical benefit in moderate to high-risk patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). BACKGROUND: High platelet reactivity has been associated with an increased rate of ischemic events after PCI. Recent large trials did not show a clinical benefit of platelet reactivity-guided therapy modification in acute coronary syndrome patients treated by PCI. METHODS: PLATFORM is an investigator-initiated, prospective, randomized, parallel-group, controlled clinical trial. Approximately 632 STEMI patients with intermediate to high-risk (RISK-PCI score >3) clinical features undergoing PPCI will be randomly allocated to treatment modification or standard therapy. Low responders to aspirin will receive 200 mg aspirin for 30 days. Low responders to clopidogrel will receive 180 mg ticagrelor for 1 year. The primary end-point is the time to the first composite major adverse cardiovascular events (MACE) including death, nonfatal infarction, stroke, or immediate target vessel revascularization. Key safety end-point is the rate of TIMI major bleeding unrelated to coronary artery bypass graft surgery. Our secondary end-points are individual components of MACE, definite stent thrombosis, total bleeding, and the need for blood transfusions. Patients will be followed-up at 30 days and at 1 year after PPCI. CONCLUSION: PLATFORM will determine whether the platelet reactivity-guided use of ticagrelor in combination with 200 mg aspirin, compared with standard antiplatelet regimen, improves clinical outcome in moderate to high-risk STEMI patients undergoing PPCI. CLINICAL TRIAL REGISTRATION: U.S. National Institutes of Health (NIH) at www.clinicaltrials.gov. ClinicalTrials.gov Identifier: NCT01739556, and Current Controlled Trials at www.controlledtrials.com. International Standard Randomized Controlled Trial Number ISRCTN83081599.

Simple risk algorithm to predict serious bleeding in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention: RISK-PCI bleeding score.

BACKGROUND: Bleeding is a potentially catastrophic complication after primary percutaneous coronary intervention (PPCI). It occurs most frequently within the first 30 days following the intervention. The aim of this study was to generate a simple and accurate risk model for the prediction of bleeding after PPCI. METHODS AND RESULTS: The training set included 2,096 patients enrolled in the RISK-PCI trial. The model was validated using a database of 961 patients enrolled in the ART-PCI trial. Bleeding was defined as type ≥3a bleeding according to the Bleeding Academic Research Consortium definition. Multivariate logistic regression was used to evaluate the predictors of outcome. A sum of weighted points for specific predictors was calculated to determine the final score. The model included 5 independent predictors of 30-day bleeding: gender (female); history of peptic ulcer; creatinine clearance at admission (<60 ml/min); hemoglobin at presentation (<125 g/dl); and Killip class >1 heart failure at admission. The model showed good discrimination and calibration for the prediction of bleeding in the derivation set (C-statistic, 0.79; goodness of fit, P=0.12) and in the validation set (C-statistic, 0.76; goodness of fit, P=0.37). Patients were classified into 3 risk classes and the observed incidence of 30-day bleeding of 1.0%, 3.5% and 10.7% corresponded to the low-, intermediate- and high-risk classes, respectively. CONCLUSIONS: A simple risk model was developed that has a reasonably good capacity for the prediction of 30-day bleeding after PPCI.

Usefulness of the RISK-PCI score to predict stent thrombosis in patients treated with primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: a substudy of the RISK-PCI trial.

Stent thrombosis (ST) is an important cause of death after primary percutaneous coronary intervention (pPCI). This substudy aimed at evaluating the usefulness of the RISK-PCI score, originally developed for the prediction of 30-day major adverse cardiovascular events, to predict the occurrence of ST after pPCI. We analyzed 1972 consecutive patients who underwent pPCI with stent implantation between February 2007 and December 2009. Early ST (EST), late ST (LST), and cumulative 1-year ST (CST) were the predefined end points. Definite, probable, and possible ST were included. Models discrimination and calibration to predict ST was tested using receiver-operating characteristics curves and the goodness-of-fit (GoF) test. Sensitivity analyses and 1000-resample bootstrapping were used to evaluate the model's performance. The rates of EST, LST, and CST were 4.6, 1.4, and 6.0 %, respectively. Compared with controls, the cumulative ST group was associated with much higher rates of adverse clinical outcomes at 30-day follow-up (adjusted odds ratio (OR) for death 6.45, adjusted OR for major bleeding 4.41) and at 12-month follow-up (adjusted OR for death 7.35, adjusted OR for major bleeding 4.56). Internal validation confirmed a reasonably good discrimination and calibration of the RISK-PCI score for the prediction of EST (area under the curve (AUC) 0.71, GoF 0.42), LST (AUC 0.69, GoF 0.36), and CST (AUC 0.70, GoF 0.22) after pPCI. ST after pPCI is associated with adverse 30-day and 1-year clinical outcomes. We conclude that the risk of ST could be accurately assessed using the RISK-PCI score, which might help in deciding upon measures aimed at preventing adverse prognosis.

Prognostic Impact of Non-Cardiac Comorbidities on Long-Term Prognosis in Patients with Reduced and Preserved Ejection Fraction following Acute Myocardial Infarction.

BACKGROUND: We aimed to analyze the prevalence and long-term prognostic impact of non-cardiac comorbidities in patients with reduced and preserved left-ventricular ejection fraction (EF) following ST-elevation myocardial infarction (STEMI). METHOD: A total of 3033 STEMI patients undergoing primary percutaneous coronary intervention (pPCI) were divided in two groups: reduced EF < 50% and preserved EF ≥ 50%. The follow-up period was 8 years. RESULTS: Preserved EF was present in 1726 (55.4%) patients and reduced EF was present in 1389 (44.5%) patients. Non-cardiac comorbidities were more frequent in patients with reduced EF compared with patients with preserved EF (38.9% vs. 27.4%, respectively, p < 0.001). Lethal outcome was registered in 240 (17.2%) patients with reduced EF and in 40 (2.3%) patients with preserved EF, p < 0.001. Diabetes and chronic kidney disease (CKD) were independent predictors for 8-year mortality in patients with preserved EF. In patients with reduced EF, CKD was independently associated with 8-year mortality. CONCLUSION: In patients who had reduced EF, the prevalence of non-cardiac comorbidities was higher than in patients who had preserved EF after STEMI. Only diabetes mellitus and CKD were independently associated with 8-year mortality in analyzed patients.

Chronic or Changeable Infarct Size after Spontaneous Coronary Artery Dissection.

Spontaneous coronary artery dissection (SCAD) could be the cause of acute myocardial infarction (AMI) and sudden cardiac death. Clinical presentations can vary considerably, but the most common is the elevation of cardiac biomarkers associated with chest discomfort. Different pathological etiology in comparison with Type 1 AMI is the underlying infarct size in this population. A 42-year-old previously healthy woman presented with SCAD. Detailed diagnostical processing and treatment which were performed could not prevent myocardial injury. The catheterization laboratory was the initial place for the establishment of a diagnosis and proper management. The management process can be very fast and sometimes additional imaging methods are necessary. Finding predictors of SCAD recurrence is challenging, as well as predictors of the resulting infarct scar size. Patients with recurrent clinical symptoms of chest pain, ST elevation, and complication represent a special group of interest. Therapeutic approaches for SCAD range from the "watch and wait" method to complete revascularization with the implantation of one or more stents or aortocoronary bypass grafting. The infarct size could be balanced through the correct therapeutical approach, and, proper multimodality imaging would be helpful in the assessment of infarct size.

Drugs for spontaneous coronary dissection: a few untrusted options.

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome that is often overlooked, misdiagnosed, and maltreated. Medical treatment poses a significant challenge because of the lack of randomized studies to guide treatment. The initial clinical presentation should guide medical and interventional management. Fibrinolytic agents and anticoagulants should be avoided because they could favor hematoma propagation. In patients with SCAD, antiplatelet therapy should be prescribed especially dual antiplatelet therapy (DAPT) consisting of aspirin and clopidogrel, whereas potent P2Y12 inhibitors, e.g., ticagrelor and prasugrel, should be avoided. If a stent was used, DAPT should be continued for 12 months. Aspirin only can be an option for patients without "high-risk" angiographic features-thrombus burden, critical stenosis, and decreased coronary flow. Beta-blocking (BB) agents should be used to prevent recurrence of SCAD. There is a general agreement that angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, mineralocorticoid antagonists, and loop diuretics should be used in patients with SCAD experiencing the symptoms of heart failure and a decrease in left ventricular ejection fraction below 50%. Although without firm evidence, statins can be used in SCAD due to their pleiotropic properties. The results of a randomized trial on the use of BB and statins are awaited. Aggregation of data from national registries might point out truly beneficial medications for patients with SCAD.

Pathophysiology of spontaneous coronary artery dissection: hematoma, not thrombus.

Spontaneous coronary artery dissection (SCAD) accounts for 1.7%-4% of all acute coronary syndrome presentations, particularly among young women with an emerging awareness of its importance. The demarcation of acute SCAD from coronary atherothrombosis and the proper therapeutic approach still represents a major clinical challenge. Certain arteriopathies and triggers are related to SCAD, with high variability in their prevalence, and often, the cause remains unknown. The objective of this review is to provide contemporary knowledge of the pathophysiology of SCAD and possible therapeutic solutions.

Invasive imaging modalities in a spontaneous coronary artery dissection: when "believing is seeing".

Spontaneous coronary artery dissection (SCAD) is a rare but increasingly recognized cause of acute coronary syndrome (ACS) with recent advancements in cardiac imaging facilitating its identification. However, SCAD is still often misdiagnosed due to the absence of angiographic hallmarks in a significant number of cases, highlighting the importance of meticulous interpretation of angiographic findings and, when necessary, additional usage of intravascular imaging to verify changes in arterial wall integrity and identify specific pathoanatomical features associated with SCAD. Accurate diagnosis of SCAD is crucial, as the optimal management strategies for patients with SCAD differ from those with atherosclerotic coronary disease. Current treatment strategies favor a conservative approach, wherein intervention is reserved for cases with persistent ischemia, patients with high-risk coronary anatomy, or patients with hemodynamic instability. In this paper, we provide a preview of invasive imaging modalities and classical angiographic and intravascular imaging hallmarks that may facilitate proper SCAD diagnosis.