Diagnostic approach to cardiac amyloidosis: A case report. / Amiloidose cardíaca - abordagem diagnóstica, a propósito de um caso clínico.

The authors present a case of systemic amyloidosis with cardiac involvement. We discuss the need for a high level of suspicion to establish a diagnosis, diagnostic techniques and treatment options. Our patient was a 78-year-old man with chronic renal disease and atrial fibrillation admitted with acute decompensated heart failure of unknown cause. The transthoracic echocardiogram revealed severely impaired left ventricular function with phenotypic overlap between hypertrophic and restrictive cardiomyopathy. After an extensive diagnostic workup, which included an abdominal fat pad biopsy, the final diagnosis was amyloidosis.

Estimating glomerular filtration rate in acute coronary syndromes: Different equations, different mortality risk prediction.

AIMS: Renal dysfunction is a powerful predictor of adverse outcomes in patients hospitalized for acute coronary syndrome. Three new glomerular filtration rate (GFR) estimating equations recently emerged, based on serum creatinine (CKD-EPIcreat), serum cystatin C (CKD-EPIcyst) or a combination of both (CKD-EPIcreat/cyst), and they are currently recommended to confirm the presence of renal dysfunction. Our aim was to analyse the predictive value of these new estimated GFR (eGFR) equations regarding mid-term mortality in patients with acute coronary syndrome, and compare them with the traditional Modification of Diet in Renal Disease (MDRD-4) formula. METHODS AND RESULTS: 801 patients admitted for acute coronary syndrome (age 67.3±13.3 years, 68.5% male) and followed for 23.6±9.8 months were included. For each equation, patient risk stratification was performed based on eGFR values: high-risk group (eGFR<60ml/min per 1.73m(2)) and low-risk group (eGFR⩾60ml/min per 1.73m(2)). The predictive performances of these equations were compared using area under each receiver operating characteristic curves (AUCs). Overall risk stratification improvement was assessed by the net reclassification improvement index. The incidence of the primary endpoint was 18.1%. The CKD-EPIcyst equation had the highest overall discriminate performance regarding mid-term mortality (AUC 0.782±0.20) and outperformed all other equations (ρ<0.001 in all comparisons). When compared with the MDRD-4 formula, the CKD-EPIcyst equation accurately reclassified a significant percentage of patients into more appropriate risk categories (net reclassification improvement index of 11.9% (p=0.003)). The CKD-EPIcyst equation added prognostic power to the Global Registry of Acute Coronary Events (GRACE) score in the prediction of mid-term mortality. CONCLUSION: The CKD-EPIcyst equation provides a novel and improved method for assessing the mid-term mortality risk in patients admitted for acute coronary syndrome, outperforming the most widely used formula (MDRD-4), and improving the predictive value of the GRACE score. These results reinforce the added value of cystatin C as a risk marker in these patients.

Rotational atherectomy: Technical update.

Percutaneous coronary intervention is currently the most common form of revascularization for symptomatic coronary artery disease. In elderly, diabetic and renal patients, there is an increased prevalence of calcified coronary disease. Rotational atherectomy (RA) can be useful in the treatment of these lesions. Plaque removal was initially proposed as an alternative to balloon angioplasty, hence RA required high-velocity protocols with large-sized burrs (over 2.0 mm). With a high incidence of acute complications and disappointing restenosis rates, the use of RA dwindled. However, the advent of drug-eluting stents, which significantly decreased the rate of restenosis, led to the repositioning of RA as an adjunctive technique in the preparation of densely calcified lesions, improving stent delivery and expansion. In recent years, a better understanding of the mechanism of action of RA has changed it from a plaque debulking to a compliance modifying technique. As a result, RA has become less aggressive, using smaller size burrs and lower rotational speeds. This conservative approach has improved immediate results, with increased safety and better long-term outcomes. In this review paper, the technique of RA is explained in the light of current knowledge.

Fever-induced type 1 Brugada pattern.

Brugada syndrome, first described over 20 years ago, is characterized by a typical electrocardiographic pattern with coved-type ST-segment elevation in the right precordial leads and a high risk of sudden death in otherwise healthy young adults. The electrocardiographic pattern is sometimes intermittent, and fever is a possible trigger. The authors present the case of a 68-year-old woman who came to the emergency department with fever and syncope. A diagnosis of community-acquired pneumonia was made. The electrocardiogram performed when the patient had fever revealed a type 1 Brugada pattern, which disappeared after the fever subsided. After other causes of Brugada-like pattern were excluded, Brugada syndrome was diagnosed and a cardioverter-defibrillator was implanted. This case demonstrates that this entity can be diagnosed at more advanced ages and highlights the usefulness of electrocardiography in a febrile state.

Continuous infusion or bolus injection of loop diuretics for patients admitted for severe acute heart failure: is one strategy better than the other?

INTRODUCTION AND OBJECTIVES: Intravenous loop diuretics are an essential part of acute heart failure management; however, data to guide their use is sparse. Our aim was to compare continuous intravenous infusion of loop diuretics with intravenous bolus administration in terms of efficacy and adverse events in patients admitted with severe acute heart failure. METHODS: Over a period of three years, 110 patients were admitted to our cardiac intensive care unit with acute heart failure. Clinical, laboratory and prognostic parameters were compared according to the diuretic strategy used and mortality and readmission for acute heart failure during follow-up were analyzed. RESULTS: Previous medical history was similar in the two groups. At admission, the continuous infusion group met criteria for worse prognosis: lower systolic blood pressure (p=0.011), more severe renal injury (p=0.008), lower left ventricular ejection fraction (p=0.016) and higher incidence of restrictive pattern of diastolic dysfunction (p=0.032). They were more often treated with vasopressors (p=0.003), inotropes (p=0.010), renal support therapy (p=0.003) and non-invasive ventilation (p<0.001). They had longer hospitalizations (p=0.014) and a higher incidence of cardiorenal syndrome (p=0.009); however, at discharge, there were no differences in renal function between the groups. In-hospital mortality was similar, and during follow-up there were no differences in mortality or readmission for acute heart failure. CONCLUSIONS: Continuous infusion was preferred in patients presenting with worse clinical status, in whom renal dysfunction was transiently worse. However, in-hospital mortality and creatinine at discharge were similar. Continuous infusion thus appears to counteract the initial dire prognosis of more unstable patients.

When what appears to be mitral stenosis is not: diagnostic and therapeutic implications.

The authors report the case of a 53-year-old man, with a long-standing history of mild mitral stenosis, admitted for worsening fatigue. Transthoracic echocardiography (limited by poor image quality) showed mitral annular calcification, leaflets that were difficult to visualize and an estimated mitral valve area of 1.8 cm(2) by the pressure half-time method. However, elevated mean transmitral and right ventricle/right atrium gradients were identified (39 and 117 mmHg, respectively). This puzzling discrepancy in the echocardiographic findings prompted investigation by transesophageal echocardiography, which revealed an echogenic structure adjacent to the mitral annulus, causing severe obstruction (effective orifice area 0.7 cm(2)). The suspicion of supravalvular mitral ring was confirmed during surgery. Following ring resection and mitral valve replacement there was significant improvement in the patient's clinical condition and normalization of the left atrium/left ventricle gradient. Supravalvular mitral ring is an unusual cause of congenital mitral stenosis, characterized by an abnormal ridge of connective tissue on the atrial side of the mitral valve, which often obstructs mitral valve inflow. Few cases have been reported, most of them in children with concomitant congenital abnormalities. Diagnosis of a supravalvular mitral ring is challenging, since it is very difficult to visualize in most diagnostic tests. It was the combination of clinical and various echocardiographic findings that led us to suspect this very rare condition, enabling appropriate treatment, with excellent long-term results.

Phenotypic expression in hypertrophic cardiomyopathy and late gadolinium enhancement on cardiac magnetic resonance.

INTRODUCTION AND AIM: The prognostic value of late gadolinium enhancement (LGE) for risk stratification of hypertrophic cardiomyopathy (HCM) patients is the subject of disagreement. We set out to examine the association between clinical and morphological variables, risk factors for sudden cardiac death and LGE in HCM patients. METHODS: From a population of 78 patients with HCM, we studied 53 who underwent cardiac magnetic resonance. They were divided into two groups according to the presence or absence of LGE. Ventricular arrhythmias and morbidity and mortality during follow-up were analyzed. RESULTS: Patients with LGE were younger at the time of diagnosis (p=0.046) and more often had a family history of sudden death (p=0.008) and known coronary artery disease (p=0.086). On echocardiography they had greater maximum wall thickness (p=0.007) and left atrial area (p=0.037) and volume (p=0.035), and more often presented a restrictive pattern of diastolic dysfunction (p=0.011) with a higher E/É ratio (p=0.003) and left ventricular systolic dysfunction (p=0.038). Cardiac magnetic resonance supported the association between LGE and previous echocardiographic findings: greater left atrial area (p=0.029) and maximum wall thickness (p<0.001) and lower left ventricular ejection fraction (p=0.056). Patients with LGE more often had an implantable cardioverter-defibrillator (ICD) (p=0.015). At follow-up, no differences were found in the frequency of ventricular arrhythmias, appropriate ICD therapies or mortality. CONCLUSIONS: The presence of LGE emerges as a risk marker, associated with the classical predictors of sudden cardiac death in this population. However, larger studies are required to confirm its independent association with clinical events.

Fabry disease presenting as apical left ventricular hypertrophy in a patient carrying the missense mutation R118C.

Anderson-Fabry disease is an X-linked lysosomal storage disorder caused by abnormalities of the GLA gene, which encodes the enzyme α-galactosidase A. A deficiency of this enzyme leads to the lysosomal accumulation of glycosphingolipids, which may cause left ventricular hypertrophy that is typically concentric and symmetric. We present the case of a 60-year-old woman with symptoms of dyspnea, atypical chest pain and palpitations, in whom a transthoracic echocardiogram revealed an apical variant of hypertrophic cardiomyopathy. Analysis of specific sarcomeric genetic mutations was negative. The patient underwent a screening protocol for Anderson-Fabry disease, using a dried blood spot test, which was standard at our institution for patients with left ventricular hypertrophy. The enzymatic activity assay revealed reduced α-galactosidase A enzymatic activity. Molecular analysis identified a missense point mutation in the GLA gene (p.R118C). This case report shows that Anderson-Fabry disease may cause an apical form of left ventricular hypertrophy. The diagnosis was only achieved because of systematic screening, which highlights the importance of screening for Anderson-Fabry disease in patients with unexplained left ventricular hypertrophy, including those presenting with more unusual patterns, such as apical variants of left ventricular hypertrophy. This case also supports the idea that the missense mutation R118C is indeed a true pathogenic mutation of Anderson-Fabry disease.

Cardiorenal syndrome in acute heart failure: a vicious cycle?

INTRODUCTION AND OBJECTIVE: Worsening renal function has an unquestionably negative impact on prognosis in patients with acute heart failure (HF). In Portugal there is little information about the importance of this entity in HF patients admitted to hospital. The objective of this work was to assess the prevalence of cardiorenal syndrome and to identify its key predictors and consequences in patients admitted for acute HF. METHODS: This was a retrospective study of 155 patients admitted for acute HF. Cardiorenal syndrome was defined as an increase in serum creatinine of ≥26.5 µmol/l. Clinical, laboratory and echocardiographic parameters were analyzed and compared. Mortality was assessed at 30 and 90 days. RESULTS: Cardiorenal syndrome occurred in 46 patients (29.7%), 5.4 ± 4.4 days after admission; 66.7% (n=24) did not recover baseline creatinine levels. The factors associated with cardiorenal syndrome were older age, chronic renal failure, moderate to severe mitral regurgitation, higher admission blood urea nitrogen, creatinine and troponin I, and lower glomerular filtration rate. Patients who developed cardiorenal syndrome had longer hospital stay, were treated with higher daily doses of intravenous furosemide, and more often required inotropic support and renal replacement therapy. They had higher in-hospital and 30-day mortality, and multivariate analysis identified cardiorenal syndrome as an independent predictor of in-hospital mortality. CONCLUSIONS: Renal dysfunction is common in acute HF patients, with a negative impact on prognosis, which highlights the importance of preventing kidney damage through the use of new therapeutic strategies and identification of novel biomarkers.

Cardiac involvement in antiphospholipid syndrome associated with Sneddon syndrome: a challenging diagnosis.

Sneddon syndrome is a rare clinical entity characterized by the association of ischemic cerebrovascular disease and livedo reticularis. The authors report a case of stroke and myocardial infarction in a 39-year-old man with Sneddon syndrome and antiphospholipid syndrome who subsequently met some criteria for systemic lupus erythematosus, highlighting the complexity of cardiovascular involvement in systemic diseases.

Can cardiac computed tomography predict cardiovascular events in asymptomatic type-2 diabetics?: results of a long term follow-up.

BACKGROUND: Doubts remain about atherosclerotic disease and risk stratification of asymptomatic type-2 diabetic patients (T2DP). This study aims to evaluate the usefulness of calcium score (CS) and coronary computed tomography (CT) angiography (CTA) to predict fatal and non fatal cardiovascular events (CVEV) in T2DP. METHODS: Eighty-five consecutive T2DP undergoing CT (Phillips Brilliance, 16-slice) with CS and CTA were prospectively enrolled in a transversal case-control study. Patients were followed for 48 months (range 18 - 68) to assess CVEV: cardiovascular death, acute coronary syndrome, revascularisation and stroke. Potential predictors of CVEV were identified. Predictive models based on clinical features, CTA and CS were created and compared. RESULTS: Performing CT impacted T2DP treatment. Cardiovascular risk was lowered during follow-up but metabolic control remained suboptimal. CVEV occurred in 11.8% T2DP (3.1%/year). CS ≥86.6 was predictor of CVEV over time, with a high negative predictive value, an 80% sensitivity and 74.7% specificity. Although its prognostic value was not independent of the presence/absence of obstructive CAD, adding CS and CTA data to clinical parameters improved the prediction of CVEV: the combined model had the highest AUC (0.888, 95%CI 0.789-0.987, p < 0.001) for the prediction of the study endpoints. CONCLUSIONS: CS showed great value in T2DP risk stratification and its prognostic value was further enhanced by CTA data. Information provided by CT may help predict CVEV in T2DP and potentially improve their outcome.

Atrial fibrillation in acute pulmonary embolism: prognostic considerations.

AIMS: Although it is accepted that atrial fibrillation (AF) may be both the contributing factor and the consequence of pulmonary embolism (PE), data on the prognostic role of AF in patients with acute venous thromboembolism are scarce. Our aim was to study whether AF had a prognostic role in patients with acute PE. METHODS: Retrospective cohort study involving 270 patients admitted for acute PE. Collected data: past medical history, analytic/gasometric parameters, admission ECG and echocardiogram, thoracic CT angiography. Patients followed for 6 months. An analysis was performed in order to clarify whether history of AF, irrespective of its timing, helps predict intrahospital, 1-month and 6-month all-cause mortality. RESULTS: Patients with history of AF, irrespective of its timing (n=57, 21.4%), had higher intrahospital (22.8% vs 13.1%, p=0.052, OR 2.07, 95% CI 0.98 to 4.35), 1-month (35.1% vs 16.9%, p=0.001, OR 3.16, 95% CI 1.61 to 6.21) and 6-month (45.6% vs 17.4%, p<0.001, OR 4.67, 95% CI 2.37 to 9.21) death rates. The prognostic power of AF was independent of age, NT-proBNP values, renal function and admission blood pressure and heart rate and additive to mortality prediction ability of simplified PESI (AF: p=0.021, OR 2.31, CI 95% 1.13 to 4.69; simplified PESI: p=0.002, OR 1.47, CI 95% 1.15 to 1.89). The presence of AF at admission added prognostic value to previous history of AF in terms of 1-month and 6-month all-cause mortality prediction, although it did not increase risk for intrahospital mortality. CONCLUSIONS: The presence of AF, irrespective of its timing, may independently predict mortality in patients with acute PE. These data should be tested and validated in prospective studies using larger cohorts.

Stroke prediction with an adjusted R-CHA2DS2VASc score in a cohort of patients with a Myocardial Infarction.

INTRODUCTION: A new risk stratification scheme incorporating the original CHADS2 score and renal function, entitled R(2)CHADS(2), was validated in the ROCKET-AF and ATRIA study cohorts. AIMS: Adjusting and validating a modified R-CHA2DS2VASc score as a predictor of ischaemic stroke and all-cause mortality in patients discharged following admission for a Myocardial Infarction (MI). MATERIALS AND METHODS: Observational retrospective single-centre cohort study including 1711 patients admitted with MI and discharged alive. We tested the prognostic performance of R-CHA2DS2VASc, based on the original CHA2DS2VASc score with few modifications (addition of renal function parameters [glomerular filtration rate and urea], performance of a revascularization procedure and history of atrial fibrillation). R-CHA2DS2VASc was evaluated for its discriminative performance and calibration in the prediction of ischaemic stroke (primary endpoint), all-cause mortality and a composite endpoint of ischemic stroke plus all-cause mortality (secondary outcomes) during follow-up. RESULTS: R-CHA2DS2VASc score's areas under the curve (AUC) for the occurrence of primary and secondary outcomes were: Ischaemic stroke: AUC 0.717 ± 0.031, p<0.001 (vs. 0.681 ± 0.043 for CHA2DS2VASc, p=0.290); all-cause mortality during follow-up: AUC 0.811 ± 0.014, p<0.001 (vs. 0.782 ± 0.019 for GRACE, p=0.245); composite endpoint: AUC 0.803 ± 0.014, p<0.001. The integrated discrimination improvement index (IDI) and relative IDI for the primary endpoint were 0.015 and 28.2%, respectively, while the IDI and relative IDI for all-cause mortality were 0.13 and 72.1%, suggesting a large improvement in risk stratification. An R-CHA2DS2VASc score below 3 had a negative predictive value of 98.6% for the occurrence of ischaemic stroke. CONCLUSIONS: The modified R-CHA2DS2VASc score has shown good calibration and high discriminative performance in the prediction of post-discharge ischaemic stroke and all-cause mortality. The inclusion of renal function in thromboembolic risk predicting schemes seems warranted.

[Severe aortic stenosis and cardiogenic shock: a therapeutic challenge]. / Estenose aórtica grave e choque cardiogénico: um desafio terapêutico.

Acute heart failure in patients with severe aortic stenosis and left ventricular systolic dysfunction is well known for its dire prognosis and limited therapeutic options. The authors describe the case of a man admitted for non-ST-elevation myocardial infarction. Diagnostic exams revealed severe aortic stenosis, with good left ventricular systolic function, and two-vessel coronary artery disease. The development of cardiogenic shock with left ventricular systolic dysfunction on day four led to changes in the therapeutic strategy. Percutaneous aortic balloon valvuloplasty coupled with complete myocardial revascularization was performed with a view to future surgical intervention. After discharge, the patient was readmitted with acute pulmonary edema, cardiogenic shock and cardiopulmonary arrest. Ventilator weaning was not possible due to acute heart failure and so it was decided to administer levosimendan, which resulted in substantial clinical and echocardiographic improvement. The patient subsequently underwent successful aortic valve replacement. This case highlights the challenge that characterizes the management of patients with concomitant coronary artery disease, left ventricular systolic dysfunction and severe aortic stenosis. Percutaneous aortic balloon valvuloplasty and levosimendan were safe and effective in the treatment of acute heart failure, acting as a bridge to surgery.

Mean corpuscular volume and red cell distribution width as predictors of left atrial stasis in patients with non-valvular atrial fibrillation.

BACKGROUND: The role of erythrocyte indexes for the prediction of left atrial stasis, assessed by transesophageal echocardiography in patients with non-valvular atrial fibrillation, has not been previously clarified. METHODS: Single center cross-sectional study comprising 247 consecutive patients admitted to the emergency department due to symptomatic atrial fibrillation and undergoing transesophageal echocardiogram evaluation for exclusion of left atrial appendage thrombus (LAAT) before cardioversion. All patients had a complete blood count performed up to 12 hours prior to the transesophageal echocardiogram. Markers of left atrial stasis were sought: LAAT, dense spontaneous echocardiographic contrast (DSEC) and low flow velocities (LFV) in the left atrial appendage. Erythrocyte indexes' accuracy for detecting transesophageal echocardiogram changes was evaluated through receiver operating curve analysis. Binary logistic multivariate analysis, using solely erythrocyte indexes and in combination with other variables (i.e. CHADS2, CHA2DS2VASc classifications and left ventricle ejection fraction), was used for transesophageal echocardiogram endpoints prediction. RESULTS: LAAT was found in 8.5%, DSEC in 26.1% and LFV in 12.1%. Mean corpuscular volume and red cell distribution width were independent predictors of LAAT and DSEC. Despite adding incremental predictive value to each other, when clinical risk factors from CHADS2 and CHA2DS2VASc classifications and left ventricle ejection fraction were added to the models, only mean corpuscular volume remained an independent predictor of LAAT and DSEC. CONCLUSIONS: These findings suggest that mean corpuscular volume and red cell distribution width may be linked to left atrial stasis markers.

Mean platelet volume is associated with the presence of left atrial stasis in patients with non-valvular atrial fibrillation.

BACKGROUND: Mean platelet volume has been associated with stroke in patients with atrial fibrillation. However, its role as a predictor of left atrial stasis, assessed by transesophageal echocardiography, in patients with non-valvular atrial fibrillation has not yet been clarified. METHODS: Single center cross-sectional study comprising 427 patients admitted to the emergency department due to symptomatic atrial fibrillation and undergoing transesophageal echocardiogram evaluation for exclusion of left atrial appendage thrombus before cardioversion. All patients had a complete blood count performed in the 12 hours prior to transesophageal echocardiogram. Markers of left atrial stasis were sought: left atrial appendage thrombus, dense spontaneous echocardiographic contrast and low flow velocities in the left atrial appendage. The presence of at least one of the former markers of left atrial stasis was designated left atrial abnormality. Binary logistic multivariate analysis was used for obtaining models for the prediction of transesophageal echocardiogram endpoints. RESULTS: Left atrial appendage thrombus was found in 12.2%, dense spontaneous echocardiographic contrast in 29.7%, low flow velocities in 15.3% and left atrial abnormality in 34.2%. Mean platelet volume (exp ß = 3.41 p = 0.048) alongside with previous stroke or transient ischemic attack (exp ß = 5.35 p = 0.005) and troponin I (exp ß = 5.07 p = 0.041) were independent predictors of left atrial appendage thrombus. Mean platelet volume was also incorporated in the predictive models of dense spontaneous echocardiographic contrast, low flow velocities and left atrial abnormality, adding predictive value to clinical, echocardiographic and laboratory variables. CONCLUSIONS: These findings suggest that mean platelet volume may be associated with the presence of markers of left atrial stasis, reinforcing a likely cardioembolic mechanism for its association with stroke in patients with non-valvular atrial fibrillation.

BLEED-Myocardial Infarction Score: Predicting mid-term post-discharge bleeding events.

AIM: To derive and validate a score for the prediction of mid-term bleeding events following discharge for myocardial infarction (MI). METHODS: One thousand and fifty patients admitted for MI and followed for 19.9 ± 6.7 mo were assigned to a derivation cohort. A new risk model, called BLEED-MI, was developed for predicting clinically significant bleeding events during follow-up (primary endpoint) and a composite endpoint of significant hemorrhage plus all-cause mortality (secondary endpoint), incorporating the following variables: age, diabetes mellitus, arterial hypertension, smoking habits, blood urea nitrogen, glomerular filtration rate and hemoglobin at admission, history of stroke, bleeding during hospitalization or previous major bleeding, heart failure during hospitalization and anti-thrombotic therapies prescribed at discharge. The BLEED-MI model was tested for calibration, accuracy and discrimination in the derivation sample and in a new, independent, validation cohort comprising 852 patients admitted at a later date. RESULTS: The BLEED-MI score showed good calibration in both derivation and validation samples (Hosmer-Lemeshow test P value 0.371 and 0.444, respectively) and high accuracy within each individual patient (Brier score 0.061 and 0.067, respectively). Its discriminative performance in predicting the primary outcome was relatively high (c-statistic of 0.753 ± 0.032 in the derivation cohort and 0.718 ± 0.033 in the validation sample). Incidence of primary/secondary endpoints increased progressively with increasing BLEED-MI scores. In the validation sample, a BLEED-MI score below 2 had a negative predictive value of 98.7% (152/154) for the occurrence of a clinically significant hemorrhagic episode during follow-up and for the composite endpoint of post-discharge hemorrhage plus all-cause mortality. An accurate prediction of bleeding events was shown independently of mortality, as BLEED-MI predicted bleeding with similar efficacy in patients who did not die during follow-up: Area Under the Curve 0.703, Hosmer-Lemeshow test P value 0.547, Brier score 0.060; low-risk (BLEED-MI score 0-3) event rate: 1.2%; intermediate risk (score 4-6) event rate: 5.6%; high risk (score ≥ 7) event rate: 12.5%. CONCLUSION: A new bedside prediction-scoring model for post-discharge mid-term bleeding has been derived and preliminarily validated. This is the first score designed to predict mid- term hemorrhagic risk in patients discharged following admission for acute MI. This model should be externally validated in larger cohorts of patients before its potential implementation.