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Summary Background: Stroke is a major complication of nonvalvular atrial fibrillation (AF). Despite its proven efficacy in stroke prevention, oral anticoagulation (OAC) is associated to a significant increase in bleeding complications. New techniques such as percutaneous left atrial appendage (LAA) closure were developed. Aim: To evaluate immediate, mid- and long-term outcomes after percutaneous LAA closure in Tunisian patients presenting with nonvalvular AF. Methods and Results: Nineteen patients with nonvalvular AF were prospectively enrolled for percutaneous LAA closure between February 2013 and June 2014. The Watchman device was used in all LAA closure procedures. Clinical and echocardiographic follow-up were carried-out at 1, 6, 12 months and six years in all patients. Mean age was 68.4 ± 7.5 years. Thirteen patients were female, 16 had hypertension, 12 had diabetes mellitus and seven had a history of stroke or transient ischemic attack (TIA). Average CHA2DS2VASc (Congestive Heart Failure/Left Ventricular Dysfunction, Hypertension, Age≥75, Diabetes mellitus, Stroke/Transient Ischemic Attack/Thromboembolic event, Vascular disease,Age≥65, Sex category) score was 4.2 ± 1.5 and HAS-BLED (Hypertension, Abnormal renal/liver function, Stroke, Bleeding tendency, Labile INR, Age≥65, Drugs) score was 3.5 ± 1. Ten patients had a history of severe bleeding. Procedural success was achieved in all patients. Pericardial effusion with tamponade was reported in one case. No post-procedural death was reported. Regular follow-up at 1, 6 and12 months then every year up to 6 years reported no stroke, no thromboembolic event, no Watchman device thrombosis and three cases of death caused by a respiratory problem and cancers. Conclusion According to this study, LAA closure with Watchman device was safe and effective in preventing stroke in patients with nonvalvular AF and contra indication to OAC.

BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV 2) may cause damage of the cardiovascular system during the acute phase of infection. However, Recent studies described a mid and long-term subtle cardiac injuries after recovery from acute Coronavirus disease 19 (COVID-19).The aim of this study was to determine the relationship between the severity of chest computed tomography (CT) lesions and the persistence of subtle myocardial injuries at mid-term follow-up of patients recovered from COVID-19 infection.MethodsAll COVID-19 patients were enrolled prospectively in this study. Sensitive troponin T (hsTnT) and chest CT scan was performed in all patients at the acute phase of Covid-19 infection. At the mid-term follow up, conventional transthoracic echocardiograph and global longitudinal strain (GLS) of left and right ventricles (LV and RV) were determined and compared between patients with chest CT scan lesions less than 50% (Group 1) and those with severe chest CT scan greater or equal to 50% (Group 2).ResultsThe mean age was 55 more or less than 14 years. Both LV GLS and RV GLS were significantly decreased in the group 2 (p=0.013 and p=0.011, respectively). LV GLS value more than -18% was noted in 43% of all the patients and RV GLS value more than -20% was observed in 48% of them. The group with severe chest CT scan lesions included more patients with reduced LV GLS and reduced RV GLS than the group with mild chest CT scan lesions (G1:29% vs. G2:57%, p=0.002) and (G1:36% vs. G2:60 %, p=0.009) respectively).ConclusionPatients with severe chest CT scan lesions are more likely to develop subclinical myocardial damage. TTE could be recommended in patients recovering from COVID-19 to detect subtle LV and RV lesions.Trial registrationThe cohort of patients is a part of the research protocol (IORG 00093738 N°102/OMB 0990-0279) approved by the Hospital Ethics Committee.

Coronary artery disease is the leading cause of death in emerging countries. Contemporary data about clinical profile and prognosis in Tunisian patients presenting for non ST-elevation acute coronary syndrome (NSTE-ACS) are lacking.We sought to study the risk profile and 3-year mortality predictors in Tunisian patients presenting for NSTE-ACS in the contemporary setting.In this single center study, data about all consecutive patients presenting to our center for NSTE-ACS from April 2014 to July 2016 were extracted and outcomes exhaustively updated. 3-year mortality predictors were determined by multivariable survival analysis.A total of 340 patients were included, of which 204 (61.8%) were male. Mean age was 63.6 ± 10.3 years. Prevalence of diabetes mellitus, hypertension and smoking was 57.3%, 62.4%, and 45.3%, respectively. In-hospital, 6, 12 and 36-month mortality rate was 2.3%, 3.2%, 7.1% and 15.2%, respectively. In multivariable survival analysis, independent predictors of death were age75 (HR=5.45, 95% CI: 2.9-10.03, p0.001), ST-segment deviation (HR=1.86, 95% CI: 1.04-3.33, p=0.036), anemia (HR=2.56, 95% CI: 1.41-4.67, p=0.002), left ventricular ejection fraction (LVEF)40% (HR=3.5, 95% CI: 1.84-6.67, p0.001) and a Global Registry of Acute Coronary Events (GRACE) score ≥140 (HR=2.38, 95% CI: 1.02-5.57, p=0.044).In Tunisian patients presenting for NSTE-ACS, long-term mortality was high. Advanced age, ST-segment deviation, anemia, LVEF40% and a GRACE score ≥140 were independent long-term predictors of death.

Background.Cardiomyopathy mediated by iron disposition in cardiomyocytes is a dreadful cause of morbidity and mortality in patients with beta thalassemia major (BTM). Conventional transthoracic echocardiography (TTE) parameters are preserved at late stages of cardiomyopathy induced by iron overload. Therefore, cardiac imaging modalities based on myocardial deformation such as strain imaging are used for early detection of cardiac iron overload.Aim.To demonstrate the contribution of longitudinal strain (LS) in early detection of cardiac iron overload in children with BTM.Methods.Sixty children (30 children with BTM and 30 healthy controls) were enrolled in this study. Conventional TTE study was performed in both patient and control groups. LV regional longitudinal strain (RLS) were determined and compared between the two study groups.Results.Mean age was 10.4 ± 5years in BTM group compared to 10.2 ± 5 years in control group (p=0.876). Compared to control group, there was no significant difference in conventional TTE parameters except for indexed left atrium (LA) area and volume. LA was significantly larger in BTM children (27.59 ±13.1ml/m² vs. 18.23 ± 4.33 ml/m², p=0.001). RLS was lower in anterior, septal and inferior walls in basal and middle segments of LV in BTM group while there was no significant difference in RLS in apical segment between the two groups (-27.30 ± 5.1 vs. -28.83 ± 4.33, p=0.22).Conclusion.In asymptomatic BMT children with normal conventional TTE parameters, LS could be used for the detection of subclinical myocardial dysfunction.

Background Coronary artery diseases remain the leading cause of death in the world. The management of this condition has improved remarkably in the recent years owing to the development of new technical tools and multicentric registries. Objective The aim of this study is to investigate the in-hospital and 1-year clinical outcomes of patients treated with percutaneous coronary intervention (PCI) in Tunisia. Methods We will conduct a prospective multicentric observational study with patients older than 18 years who underwent PCI between January 31, 2020 and June 30, 2020. The primary end point is the occurrence of a major adverse cardiovascular event, defined as cardiovascular death, myocardial infarction, cerebrovascular accident, or target vessel revascularization with either repeat PCI or coronary artery bypass grafting (CABG). The secondary end points are procedural success rate, stent thrombosis, and the rate of redo PCI/CABG for in-stent restenosis. Results In this study, the demographic profile and the general risk profile of Tunisian patients who underwent PCI and their end points will be analyzed. The complexity level of the procedures and the left main occlusion, bifurcation occlusion, and chronic total occlusion PCI will be analyzed, and immediate as well as long-term results will be determined. The National Tunisian Registry of PCI (NATURE-PCI) will be the first national multicentric registry of angioplasty in Africa. For this study, the institutional ethical committee approval was obtained (0223/2020). This trial consists of 97 cardiologists and 2498 patients who have undergone PCI with a 1-year follow-up period. Twenty-eight catheterization laboratories from both public (15 laboratories) and private (13 laboratories) sectors will enroll patients after receiving informed consent. Of the 2498 patients, 1897 (75.9%) are managed in the public sector and 601 (24.1%) are managed in the private sector. The COVID-19 pandemic started in Tunisia in March 2020; 719 patients (31.9%) were included before the COVID-19 pandemic and 1779 (60.1%) during the pandemic. The inclusion of patients has been finished, and we expect to publish the results by the end of 2022. Conclusions This study would add data and provide a valuable opportunity for real-world clinical epidemiology and practice in the field of interventional cardiology in Tunisia with insights into the uptake of PCI in this limited-income region. Trial Registration Clinicaltrials.gov NCT04219761; https://clinicaltrials.gov/ct2/show/NCT04219761 International Registered Report Identifier (IRRID) RR1-10.2196/24595

BACKGROUND Coronary diseases remain the first cause of death in the world; the management of this condition has improved, thanks to new technical tools and multicentric registries. Recently in Tunisia, the number of intervention procedures has markedly increased, giving the explosion of cardiovascular risk factors among Tunisian people. OBJECTIVE The aim of the study was to investigate the in-hospital and one-year clinical outcome of patients treated with percutaneous coronary intervention (PCI) in Tunisia. METHODS We will conduct a prospective, multicentric, observational study including patients > 18 year-old who underwent a PCI between 31January and 30 June 2020. The primary end point are the occurrence of a major adverse cardiovascular event , defined as cardiovascular death, myocardial infarction, cerebrovascular accident, and target vessel revascularization with either repeat PCI or coronary artery bypass surgery (CABG). Secondary end-points consist in procedural success rate, stent thrombosis, and the rate of redo-PCI/CABG for in-stent restenosis. RESULTS Results will be available at the end of the study as well as the demographic profile and general risk profile of Tunisian patients undergoing PCI. The complexity level of procedures, as left main, bifurcation, chronic occlusion PCI will be analyzed and immediate as well as long term results will be determined. NATURE-PCI will be the first national multicentric registry of angioplasty in Africa. CONCLUSIONS This study would add data and provide a valuable opportunity for real-world clinical epidemiology and practice in the field of interventional cardiology in Tunisia with insights into the uptake of contemporary coronary artery disease in this developing region. CLINICALTRIAL clinicaltrials.gov

Clopidogrel non-responsiveness is multifactorial; several genetic and non-genetic factors may contribute to impaired platelet inhibition. The goal of this study is to determine the effect of the cytochrome P450 CYP2C19*2 polymorphism on the platelet response to clopidogrel in patients with and without diabetes mellitus (DM). We conducted an observational study in patients with coronary artery disease and consequent exposure to clopidogrel therapy (75 mg/day for at least 7 consecutive days). We have analyzed two groups of patients: group I (DM patients) and group II (non-diabetes mellitus patients). Platelet reactivity was assessed by the VerifyNow P2Y12 assay and high on clopidogrel platelet reactivity (HPR) was defined as P2Y12 reaction units (PRU) ≥ 208. Genotyping for CYP2C19*2 polymorphism was performed by PCR-RFLP. We have included 150 subjects (76 DM and 74 non-diabetes mellitus patients). The carriage of CYP2C19*2 allele, in DM patients, was significantly associated to HPR (odds ratio (OR) 4.437, 95% confidence interval (CI) 1.134 to 17.359; p = 0.032). Furthermore, 8.4% of the variability in percent inhibition by clopidogrel could be attributed to CYP2C19*2 carrier status. However, in non-diabetes mellitus patients, there was no significant difference in platelet response to clopidogrel according to the presence or absence of CYP2C19*2 allele carriage (OR 1.260, 95% CI 0.288 to 5.522; p = 0.759). Our study suggests that the carriage of CYP2C19*2 polymorphism, in DM patients, might be a potential predictor of persisting HPR in these high-risk individuals. Clinical Trials.gov NCT03373552 (Registered 13 December 2017)

Background: Hyperglycemia on-admission is a powerful predictor of adverse events in patients presenting for ST-elevation myocardial infarction (STEMI). Aim: In this study, we sought to determine the prognostic value of hyperglycemia on-admission in Tunisian patients presenting with STEMI according to their diabetic status. Methods: Patients presenting to our center between January 1998 and September 2014 were enrolled. Hyperglycemia was defined as a glucose level ≥11 mmol/L. In-hospital prognosis was studied in diabetic and non-diabetic patients. The predictive value for mortality of glycemia level on-admission was assessed by mean of the area under receiver operating characteristic (ROC) curve calculation. Results: A total of 1289 patients were included. Mean age was 60.39 ± 12.8 years and 977 (77.3%) patients were male. Prevalence of diabetes mellitus was 70.2% and 15.2% in patients presenting with and without hyperglycemia, respectively (p

Background: Brugada syndrome (BrS) is a rare inherited cardiac arrhythmia associated with a high risk of sudden cardiac death (SCD) due to ventricular fibrillation (VF). BrS is characterized by coved-type ST-segment elevation in the right precordial leads (V1-V3). Mutations in SCN5A gene coding for the α-subunit of the NaV1.5 cardiac sodium channel are identified in 15–30% of BrS cases. Genetic testing of BrS patients generally involves sequencing of the protein-coding portions and flanking intronic regions of SCN5A. This excludes the 5′UTR and 3′UTR from the routine genetic testing. Methods: We here screened the coding sequence, the flanking intronic regions as well as the 5′ and 3′UTR regions of SCN5A gene and further five candidate genes (GPD1L, SCN1B, KCNE3, SCN4B, and MOG1) in a Tunisian family diagnosed with BrS. Results: A new SCN5A-Q1000K mutation was identified along with two common polymorphisms (H558R and D1819). Multiple genetic variants were identified on the SCN5A 3′UTR, one of which is predicted to create additional microRNA binding site for miR-1270. Additionally, we identified the hsa-miR-219a-rs107822. No relevant coding sequence variant was identified in the remaining studied candidate genes. Conclusions: The absence of genotype-phenotype concordance within all the identified genetic variants in this family gives extra evidences about the complexity of the disease and suggests that the occurrence and prognosis of BrS is most likely controlled by a combination of multiple genetic factors, rather than a single variant. Most SCN5A variants were localized in non-coding regions hypothesizing an impact on the miRNA-target complementarities. Keywords: SCN5A, Brugada syndrome, 3′UTR, microRNAs, Genotype-phenotype correlation

Brugada syndrome is an inherited arrhythmia characterized by a particular ECG pattern typically distinguished by a coved-type ST segment elevation in the right precordial leads, conferring a high risk of sudden cardiac death in young adults and less frequently in infants and children. The ST segment elevation in the Brugada syndrome can be very dynamic and modified by several factors such as fever, diet, and raised plasma insulin concentration, autonomic activity, alcohol and cocaine toxicity, and medication. Approximately 20%–25% of BrS patients are genetically diagnosed with pathogenic variations in SCN5A gene encoding for the cardiac sodium channel. However, known BrS-susceptibility genes can only explain 30%–35% of clinically diagnosed cases, indicating that 65%–70% of BrS patients remain genetically unsolved. The incomplete penetrance of BrS mutations and the dynamic ECG manifestations confer difficulties in establishing a clear genotype-phenotype correlation. Brugada syndrome patients are particularly recommended to follow a lifestyle where the ECG triggering factors should be avoided in order to minimize the risk of Brugada-associated arrhythmia and sudden death.

Brugada syndrome (BrS) is a rare inherited cardiac arrhythmia associated with a high risk of sudden cardiac death (SCD) due to ventricular fibrillation (VF). BrS is characterized by coved-type ST-segment elevation in the right precordial leads (V1-V3) in the absence of structural heart disease. This pattern is spontaneous, or is unmasked by intravenous administration of Class I antiarrhythmic drugs. The SCN5A-encoded α-subunit of the NaV1.5 cardiac sodium channel has been linked to BrS, and mutations in SCN5A are identified in 15–30% of BrS cases. Genetic testing of BrS patients generally involves sequencing of protein-coding portions and flanking intronic regions of SCN5A, according to recent international guidelines. This excludes the regulatory untranslated regions (5’UTR and 3’UTR) from the routine genetic testing of BrS patients. We here screened the coding sequence, the flanking intronic regions as well as the 5’ and 3’UTR regions of SCN5A gene and further five candidate genes (GPD1L, SCN1B, KCNE3, SCN4B, and MOG1) in a Tunisian family diagnosed with Brugada syndrome.A new Q1000K mutation was identified on the SCN5A gene along with two common polymorphisms (H558R and D1819). Furthermore, multiple genetic variants were identified on the SCN5A 3’UTR, one of which is predicted to create additional microRNA (miRNAs) binding site for miR-1270. Additionally, we identified the hsa-miR-219a rs107822. No relevant coding sequence variant was identified in the remaining studied candidate genes. Although Q1000K is localized in the conserved binding site of MOG1 which predicts a functional consequence, this new mutation along with the additional variants were differentially distributed among the family members without any clear genotype-phenotype concordance. This gives extra evidences about the complexity of the disease and suggests that the occurrence and prognosis of BrS is most likely controlled by a combination of multiple genetic factors and exposures, rather than a single polymorphism/mutation. Most SCN5A polymorphisms were localized in non-coding regions hypothesizing an impact on the miRNA-target complementarities. In this regard, over-expression of miR-1270 led to a significant decrease of luciferase activity suggesting a direct role regulating SCN5A. Therefore, genetic variants that disrupt its binding affinity to SCN5A 3’UTR and/or its expression might cause loss of normal repression control and be associated to BrS.

International audience; The c.61\₆3dupCTG (L10) allele of rs72555377 polymorphism in PCSK9 has been reported to be associated with low-density lipoprotein-cholesterol (LDL-C) levels and with a decreased risk of coronary artery disease (CAD). We investigated the effect of two known alleles for rs72555377, L10 and L11, on the risk of CAD in a Tunisian cohort (218 patients diagnosed by angiography and 125 control subjects). Two subgroups of patients were defined by their level of stenosis: >= 50% for CAD and = 50% in two or three major coronary arteries (0.210 vs 0.125, p = 0.028). Multiple regression analysis showed that the L10 allele was significantly associated with a reduced risk of CAD (p = 0.049, OR = 0.51[0.26-1.00]), and with its reduced severity (p = 0.045, OR = 0.44[0.20-0.98]). The L10 allele is associated with a reduced risk and severity of CAD, seemingly independently of its LDL-lowering effect, suggesting a direct effect of PCSK9 on atherogenesis.

Matrix metalloproteinases (MMPs) play an important role in early atherosclerosis, extracellular matrix remodeling, plaque rupture and myocardial infarction. MMP gene polymorphisms contribute to the risk of developing cardiovascular diseases. In this study, we investigated, for the first time, the association between MMP-1-16071G/2G, MMP-12 -82A/G and MMP-12 1082A/G genotypes and haplotypes and the risk of ischemic stroke (IS) among patients with type 2 diabetes mellitus (T2DM). To examine whether these genetic polymorphisms are associated with susceptibility to IS, 196 patients with IS and 192 controls were examined by PCR-based RFLP. When the analyses were adjusted for multiple risk factors, no interaction between T2DM and MMP-1-1607 1G/2G polymorphism on the risk of ischemic stroke was found (p=0.074). However, MMP-12 polymorphisms genotypes were associated with the higher risk of IS in diabetic patients compared with total patients. The -82G-1082G haplotype of MMP-12 polymorphisms was associated with higher risk of ischemic stroke in diabetic patients [AOR=2.33; 95% CI (1.25-3.62), P=0.032]. These findings showed that there was an important joint effect of the MMP-12 polymorphisms and T2DM on the risk of IS and therefore it can be considered as a potential marker of cerebrovascular disorders in diabetic patients.

Summary Background Infective endocarditis (IE) is a rare condition in the paediatric setting. No data on the epidemiology and prognosis of IE in children are available from North African countries. Aim To investigate the epidemiological profile and prognosis of IE in children in Tunisia. Methods All patients aged ≤ 18 years presenting with IE in three Tunisian tertiary care centres between January 1997 and September 2013 were included. Clinical features and 30-day and 6-month mortality rates were studied. Factors predictive of death at 6-month follow-up were determined. Results A total of 73 patients were included in the present study. The mean age was 12 ± 4.8 years; 35 (50.7%) patients were male. Rheumatic heart disease (RHD) was the underlying heart disease in 17 (23.3%) cases and IE occurred in a structurally normal heart in 36 (49.3%) cases. Staphylococcus species were isolated in 17 (23.3%) cases. Regarding IE localization, the mitral valve was involved in 28 (38.4%) cases and the aortic valve in 14 (19.2%) cases. Recourse to surgery was reported in 37 (50.7%) cases. Thirty-day and 6-month mortality rates were 13.6% and 19.2%, respectively. Heart failure on admission or during the hospital course, acute renal failure and neurological complications were significantly associated with death at 6-month follow-up in the univariate analysis and after adjustment for age and sex. Conclusions In the Tunisian context, IE in children is still characterized by the high prevalence of RHD as an underlying heart disease. Short- and long-term mortality rates remain high. Heart failure, acute renal failure and neurological complications are significantly associated with death at 6-month follow-up.

Prehospital thrombolysis (pHT) is recommended by the European Society of Cardiology (ESC) as a surrogate to primary percutaneous coronary intervention (pPCI) in acute ST-elevation myocardial infarction(STEMI) when transfer delays are long. We sought to study early outcomes in patients presenting for

Diabetic patients presenting for acute ST-elevation myocardial infarction (STEMI) are at high risk of adverse events during hospital course. On the other hand, renal failure on admission is common in this population. We sought to determine the early prognosis of diabetic patients presenting for

Acute coronary syndromes are a leading cause of death worldwide and in developing countries. In Tunisia, patients presenting for ST-elevation myocardial infarction (STEMI) have a particular risk profile. Thus, we sought to determine prognostic features and predictors of adverse outcomes in Tunisian

In the setting of ST-elevation myocardial infarction (STEMI), early reperfusion either by prehospital thrombolysis (pHT) or primary percutaneous coronary intervention (pPCI) is associated with better in-hospital and long-term outcomes. We sought to evaluate the impact on early outcomes of

In patients managed by primary percutaneous coronary intervention (pPCI) for ST-elevation myocardial infarction (STEMI), the no-reflow phenomenon is assessed in different ways, according to studies. Nevertheless, it is well-established as a powerful predictor of poor prognosis. We sought to

Serum cystatin C concentration was recently reported as a marker of cardiovascular disease (CVD). In the present study, we evaluated the association between the increase of serum cystatin C levels and the risk of CVD in type 2 diabetes. 42 patients with type 2 diabetes were included in the present study; 27 of them have CVD. The control group consisted of 30 healthy adults. Cystatin C, creatinine, microalbuminuria and CRP were measured on Cobas 6000(TM). Cystatine C level was significantly higher in patients with CVD. A significant difference in serum cystatin C was found in patients with and without CVD among albuminuria. No difference in serum cystatin C levels was found according to number of affected vessels. A cystatin C level above 1.10 mg/L was associated with increase of risk of CVD with significant difference (OR = 42.52; IC 95% 1.455 to 1242.827 and p = 0.029). Our results suggested that the increase of serum cystatin C concentrations is a potential marker for CVD in diabetes.

Anemia is regarded as a powerful predictor of in-hospital major events in patients presenting for acute coronary syndrome. We sought to determine clinical and prognostic correlates of anemia in patients presenting for acute ST-elevation myocardial infarction (STEMI) in our region. A total of 1498

Background Autosomal dominant hypercholesterolemia (ADH) is commonly caused by mutations in the low-density lipoprotein (LDL) receptor gene ( LDLR ), in the apolipoprotein B-100 gene ( APOB ), or in the proprotein convertase subtilisin kexine 9 gene ( PCSK9 ). ADH subjects carrying a mutation in LDLR present highly variable plasma LDL-cholesterol (LDL-C). This variability might be due to environmental factors or the effect of some modifying genes such as PCSK9 and APOE . Aims We investigated the molecular basis of thirteen Tunisian ADH families and attempted to determine the impact of PCSK9 and APOE gene variations on LDL-cholesterol levels and on the variable phenotypic expression of the disease. Methods and results Fifty six subjects were screened for mutations in the LDLR gene through direct sequencing. The causative mutation was found to segregate with the disease in each family and a new frameshift mutation, p.Met767CysfsX21, was identified in one family. The distribution of total- and LDL-cholesterol levels, adjusted for age and gender, among homozygous and heterozygous ADH patients varied widely. Within seven families, nine subjects presented low LDL-cholesterol levels despite carrying a mutation in the LDLR gene. To identify the molecular actors underlying this phenotypic variability, the PCSK9 gene was screened using direct sequencing and/or enzymatic restriction analysis, and the apo E genotypes were determined. A new missense variation (p.Pro174Ser) in the PCSK9 gene was identified and characterized as a new putative loss-of-function mutation. Conclusion Genetic variations in PCSK9 and APOE genes could explain only part of the variability observed in the phenotypic expression in Tunisian ADH patients carrying mutations in the LDLR gene. Other genetic variants and environmental factors very probably act to fully explain this phenotypic variability.

Hyperglycemia on-admission has been identified as a powerful predictor of adverse outcomes in patients presenting with acute ST-elevation myocardial infarction (STEMI). Nevertheless, the prognostic value of hyperglycemia is still to be investigated in diabetic versus non-diabetic patients. In the

Renal artery stenosis (RAS) is a strong independent predictor of mortality in patients with coronary artery disease (CAD). The study aimed to determine the prevalence of RAS in patients with significant CAD in order to develop and validate a score predicting RAS. Three hundred consecutive patients (50 females) with significant CAD underwent abdominal aortography following coronary angiography to screen for significant RAS defined as luminal narrowing of 50% or more. Univariate and multivariate analyses were performed comparing patients with and without RAS. Significant factors associated with RAS were included in constructing a score that predicts RAS. The score was internally validated in patients randomly selected from the entire study group (validation group; n = 103), using ROC curves and the Hosmer–Lemeshow goodness-of-fit test. Twenty-seven patients (9%) had a significant RAS. Multivariate analysis showed that age over 65 years (OR = 4.1%, 95% CI = 1.6-10.3, p = 0.003) and hypertension (OR = 3.1, 95% CI = 1.2–7.7, p = 0.015) were independent predictors of RAS. The predictive score including these two variables and three others (female gender, renal and insufficiency, and more than 2- or 3-vessel disease) ranged from 0 to 7. Internal validation showed a good performance (ROC curve = 0.79 and χ2 Lemeshow = 3.45). For a score of less than 2, the negative predictive value is 98%. The rate of significant RAS in patients with significant CAD was 9%. The performance of our predictive score was good, and significant reduction in the need to perform systematic abdominal aortography could be expected with the use of this score.