Challenges of Anticoagulant Therapy in Atrial Fibrillation-Focus on Gastrointestinal Bleeding.

The rising prevalence and the complexity of atrial fibrillation (AF) pose major clinical challenges. Stroke prevention is accompanied by non-negligible risks, making anticoagulant treatment an ongoing challenge for the clinician. Current guidelines recommend direct oral anticoagulants (DOACs) over warfarin for stroke prevention in most AF patients, mainly due to the ease of their use. However, assessing the bleeding risk in patients receiving oral anticoagulants remains-particularly in the case of DOACs-highly challenging. Using dose-adjusted warfarin increases threefold the risk of gastrointestinal bleeding (GIB). Although the overall bleeding risk appears to be lower, the use of DOACs has been associated with an increased risk of GIB compared to warfarin. Accurate bleeding (including GIB-specific) risk scores specific for DOACs remain to be developed. Until then, the assessment of bleeding risk factors remains the only available tool, although the extent to which each of these factors contributes to the risk of bleeding is unknown. In this paper, we aim to provide a comprehensive review of the bleeding risk associated with oral anticoagulant therapy in AF patients, with a highlight on the latest insights into GIB associated with oral anticoagulation; we emphasize questions that remain to be answered; and we identify hotspots for future research.

Platelets and Their Role in Hemostasis and Thrombosis-From Physiology to Pathophysiology and Therapeutic Implications.

Hemostasis is a physiological process critical for survival. Meanwhile, thrombosis is amongst the leading causes of death worldwide, making antithrombotic therapy one of the most crucial aspects of modern medicine. Although antithrombotic therapy has progressed tremendously over the years, it remains far from ideal, and this is mainly due to the incomplete understanding of the exceptionally complex structural and functional properties of platelets. However, advances in biochemistry, molecular biology, and the advent of 'omics' continue to provide crucial information for our understanding of the complex structure and function of platelets, their interactions with the coagulation system, and their role in hemostasis and thrombosis. In this review, we provide a comprehensive view of the complex role that platelets play in hemostasis and thrombosis, and we discuss the major clinical implications of these fundamental blood components, with a focus on hemostatic platelet-related disorders and existing and emerging antithrombotic therapies. We also emphasize a number of questions that remain to be answered, and we identify hotspots for future research.

Prognostic significance of a low T/R ratio in Brugada syndrome.

OBJECTIVES: To determine the prognostic value of a low T/R ratio, defined as the amplitude ratio between the T waves and the R waves, in patients (pts) with a spontaneous type-1 Brugada pattern (SBT1). BACKGROUND: Abnormalities of myocardial repolarization may play a key role in the initiation of ventricular fibrillation (VF) in Brugada syndrome (BrS). Recent studies have shown that the height of the T waves and the T/R ratio are inversely proportional to sudden cardiac arrest (SCA) risk in early repolarization syndrome and hypertrophic cardiomyopathy. METHODS: In an international retrospective study, we reviewed 115 pts. (105 males, 91.3%). 45 had VF and/or SCA (38.7 ±â€¯11.5 years old, all males), while 70 (49.3 ±â€¯12.0 years, 10 women) remained free of ventricular arrhythmia. 6 ECG markers plus the T/R ratio in leads V5 & II were studied. RESULTS: The T/R ratio among leads II & V5 was significantly lower in the VF/SCA group (0.24 [0.14; 0.38]vs. 0.34 [0.24; 0.45]; p = 0.006). 44.4% of pts. in the VF/SCA group had a lowest T/R ratio among leads II & V5 ≤ 0.17 compared to 11.4% in the non-VF/SCA group (p < 0.001). In multivariate analysis, a lowest T/R ratio among leads II & V5 ≤ 0.17 was independently associated with VF/SCA (OR 6.10, 95% CI 1.92-19.40; p = 0.002). Type 1 Brugada pattern in the peripheral leads (OR 10.78) and early repolarization (OR 3.60) were other independent markers of VF/SCA. CONCLUSION: A low T/R ratio among leads II & V5 is an independent marker for VF/SCA risk in patients with type-1 Brugada pattern.

Prediction of ventricular arrhythmias in patients with a spontaneous Brugada type 1 pattern: the key is in the electrocardiogram.

AIMS: There is currently no reliable tool to quantify the risks of ventricular fibrillation or sudden cardiac arrest (VF/SCA) in patients with spontaneous Brugada type 1 pattern (BrT1). Previous studies showed that electrocardiographic (ECG) markers of depolarization or repolarization disorders might indicate elevated risk. We aimed to design a VF/SCA risk prediction model based on ECG analyses for adult patients with spontaneous BrT1. METHODS AND RESULTS: This retrospective multicentre international study analysed ECG data from 115 patients (mean age 45.1 ± 12.8 years, 105 males) with spontaneous BrT1. Of these, 45 patients had experienced VF/SCA and 70 patients did not experience VF/SCA. Among 10 ECG markers, a univariate analysis showed significant associations between VF/SCA and maximum corrected Tpeak-Tend intervals ≥100 ms in precordial leads (LMaxTpec) (P < 0.001), BrT1 in a peripheral lead (pT1) (P = 0.004), early repolarization in inferolateral leads (ER) (P < 0.001), and QRS duration ≥120 ms in lead V2 (P = 0.002). The Cox multivariate analysis revealed four predictors of VF/SCA: the LMaxTpec [hazard ratio (HR) 8.3, 95% confidence interval (CI) 2.4-28.5; P < 0.001], LMaxTpec + ER (HR 14.9, 95% CI 4.2-53.1; P < 0.001), LMaxTpec + pT1 (HR 17.2, 95% CI 4.1-72; P < 0.001), and LMaxTpec + pT1 + ER (HR 23.5, 95% CI 6-93; P < 0.001). Our multidimensional penalized spline model predicted the 1-year risk of VF/SCA, based on age and these markers. CONCLUSION: LMaxTpec and its association with pT1 and/or ER indicated elevated VF/SCA risk in adult patients with spontaneous BrT1. We successfully developed a simple risk prediction model based on age and these ECG markers.

Atrial electrical remodeling induced by chronic ischemia and inflammation in patients with stable coronary artery disease.

The pathophysiology of coronary artery disease (CAD) includes low-grade chronic inflammation. At its turn, inflammation is known to promote myocardial structural remodeling and to increase vulnerability to atrial arrhythmias. Meanwhile, the impact of chronic inflammation on the electrophysiological properties of the atria remains unknown. We aimed to evaluate the impact of low-grade chronic inflammation on atrial electrophysiology in patients with stable CAD undergoing elective coronary artery bypass grafting (CABG). Circulating levels of several inflammatory, angiogenesis, and endothelial dysfunction markers were determined 1 day before CABG in 30 consecutive CAD patients. Right atrial appendage samples were collected during the CABG procedure; action potential recordings were performed in six study patients using the microelectrode technique. Interleukin (IL)-1b (r = 1.00, P = 0.01), IL-6 (r = 0.98, P < 0.01), vascular endothelial growth factor (VEGF) (r = 0.98, P < 0.01), and hemoglobin (r = 0.98, P < 0.01) levels significantly positively correlated with the duration of atrial depolarization. Consequently, IL-6, VEGF, and hemoglobin (r = -0.86, P = 0.03 for all) levels significantly negatively correlated with the velocity of atrial depolarization. There was no significant correlation between any of the studied markers levels and any of the other parameters of the action potential (all P > 0.05). The present study is the first to demonstrate that in patients with stable CAD, chronic inflammation and ischemia are associated with pro-arrhythmic atrial electrical remodeling. These changes may contribute to the increased propensity to postoperative atrial arrhythmias seen in some of the patients undergoing CABG.

Laboratory Monitoring: A Turning Point in the Use of New Oral Anticoagulants.

Large clinical trials have demonstrated that new oral anticoagulants (NOACs) are at least as efficient as vitamin K antagonists (VKAs) in preventing thromboembolic events, while providing a better safety profile. The relatively stable pharmacokinetics and pharmacodynamics, the reduced reports on food and drug interactions, and the wide therapeutic windows of NOACs appear to provide a more predictable anticoagulant effect than that observed with VKAs, enabling the use of fixed doses without the need for monitoring. However, the safe implementation of NOACs may require additional judgment, and one should not have the erroneous impression that NOACs are free from interactions or that inter- and intra-individual variability is absent with NOACs. In fact, a consensus seems to have been reached concerning the usefulness of "circumstantial" testing in certain clinical scenarios. Recent data also suggest that factors such as intercurrent diseases, drug interactions, and inexplicable variability may occasionally alter the anticoagulant effect of NOACs. Furthermore, the issue of nonadherence, already high in VKA-treated patients, may represent an even greater clinical concern with NOACs, given their short half-lives. This review aims to underline the main arguments that support the need for NOAC monitoring, at least in selected categories of patients. Additionally, an overview of classic coagulation assays and novel laboratory techniques that may provide a tool for NOAC monitoring is also provided.

Inflammation, a link between obesity and atrial fibrillation.

Despite the long belief that the role of the adipose tissue was restricted to that of a passive store of triglycerides and a rich source of fatty acids, accumulating data demonstrates that the adipose tissue acts as an endocrine organ, capable of producing a large number of cytokines incriminated in generating a systemic inflammatory status. At its turn, this adiposity-related pro-inflammatory status appears to promote a large range of cardiovascular disorders, including atrial fibrillation (AF). Recent studies suggest that, in addition to systemic adiposity, the volume of the pericardial fat of the entire heart, and particularly of that overlying the atria, may represent an even more important risk factor for AF. This review focuses on the most relevant clinical and experimental data that bridge adiposity-induced inflammation and AF, and provides, through a multidisciplinary approach, a discussion that integrates both the current knowledge regarding the prolific activity of systemic and pericardial adipose tissue as sources of inflammatory mediators and the main effects of adiposity-induced inflammation on the most relevant electrophysiological, structural, and autonomic mechanisms responsible for AF.

Long-standing arterial hypertension is associated with Pitx2 down-regulation in a rat model of spontaneous atrial tachyarrhythmias.

AIMS: The timecourse of left atrial Pitx2 down-regulation in the setting of atrial tachyarrhythmias remains unknown. Accordingly, we aimed to assess the age dependency of left atrial Pitx2 expression in an experimental model of spontaneous atrial tachyarrhythmias in rats. METHODS AND RESULTS: Atrial sampling was performed in three groups (n = 4 each) of young (14-week-old), adult (24-week-old), and ageing (48-week-old) spontaneously hypertensive rats (SHRs), in which we previously demonstrated the age dependency of spontaneous atrial tachyarrhythmias, and three groups (n = 4 each) of age-matched normotensive Wistar-Kyoto (WKY) rats. mRNA expression of Pitx2 was studied using real-time polymerase chain reaction. Ageing SHRs presented significantly lower left atrial Pitx2 expressions compared with age-matched WKY rats (P = 0.02), while no significant difference was observed between young or adult SHRs and age-matched WKY rats (both P > 0.05). Among SHRs, Pitx2 expressions showed a progressive, age-dependent decrease (34.9 ± 6.7 in young SHRs, 17.1 ± 3.6 in adult SHRs, and 10.7 ± 1.7 in ageing SHRs, P = 0.04) and were significantly negatively correlated with both age (Spearman r = -0.86, P < 0.01) and heart weight (Spearman r = -0.76, P < 0.01). CONCLUSION: The present study suggests the presence of age-dependent left atrial Pitx2 down-regulation in SHRs. The strong negative correlation between left atrial Pitx2 expression and heart weight among SHRs may indicate a link between long-standing arterial hypertension and Pitx2-related atrial arrhythmogenicity.

Pyridostigmine enhances atrial tachyarrhythmias in aging spontaneously hypertensive rats.

This study examined whether chronic administration of pyridostigmine, a reversible cholinesterase inhibitor, would exacerbate episodes of spontaneous atrial tachyarrhythmia (AT) in conscious, aging, spontaneously hypertensive rats (SHRs). Telemetric recordings of electrocardiogram (ECG, n = 5) and ECG/arterial pressure (n = 3) were performed in male 49-week old SHRs. After a 1-week period of continuous recording under baseline conditions, rats were implanted with osmotic minipumps that delivered pyridostigmine (15 mg/kg/day subcutaneously) for either 1 (n = 8) or 3 (n = 5) weeks. In the latter case, sympathovagal balance was assessed during the last infusion week by measuring heart rate (HR) changes in response to administration of cardiac autonomic blockers. An additional 1-week recording was performed after explantation of minipumps. Significant (P = 0.02) reductions in HR with no consistent changes in arterial pressure were observed. Frequency and duration of AT episodes were increased by pyridostigmine (0.01 ≤ P ≤ 0.07). This increase was sustained across the 3-week treatment period and reversible after cessation of treatment. Autonomic blockade revealed that intrinsic HR was above (P = 0.04) resting HR, pointing to a shift of sympathovagal balance towards vagal predominance. However, the respiratory-related component of HR variability (high-frequency power of RR interval) was lowered (P = 0.01) by pyridostigmine treatment, indicating reduced vagal modulation of HR. The results are consistent with a pathogenic role of the parasympathetic nervous system in the aging SHR model, and raise the possibility that sustained vagal activation may facilitate atrial arrhythmias.

Oxidative Stress, Inflammation, and Mitochondrial Dysfunction: A Link between Obesity and Atrial Fibrillation.

The adipose tissue has long been thought to represent a passive source of triglycerides and fatty acids. However, extensive data have demonstrated that the adipose tissue is also a major endocrine organ that directly or indirectly affects the physiological functions of almost all cell types. Obesity is recognized as a risk factor for multiple systemic conditions, including metabolic syndrome, type 2 diabetes mellitus, sleep apnea, cardiovascular disorders, and many others. Obesity-related changes in the adipose tissue induce functional and structural changes in cardiac myocytes, promoting a wide range of cardiovascular disorders, including atrial fibrillation (AF). Due to the wealth of epidemiologic data linking AF to obesity, the mechanisms underlying AF occurrence in obese patients are an area of rich ongoing investigation. However, progress has been somewhat slowed by the complex phenotypes of both obesity and AF. The triad inflammation, oxidative stress, and mitochondrial dysfunction are critical for AF pathogenesis in the setting of obesity via multiple structural and functional proarrhythmic changes at the level of the atria. The aim of this paper is to provide a comprehensive view of the close relationship between obesity-induced oxidative stress, inflammation, and mitochondrial dysfunction and the pathogenesis of AF. The clinical implications of these mechanistic insights are also discussed.

Progressive endothelial damage revealed by multilevel von Willebrand factor plasma concentrations in atrial fibrillation patients.

AIMS: Abnormal plasma concentrations of von Willebrand factor (vWF), a marker of prothrombotic risk, have been found in atrial fibrillation (AF) patients, but the extent of this variation is not clear. This study aimed to investigate the effect of different clinical forms of AF on plasma concentrations of vWF at different levels of the circulatory tree, both intracardiac and extracardiac. METHODS AND RESULTS: Peripheral (Pf), left atrial (LA), and coronary sinus (CS) blood samples were obtained during cardiac catheterization from 52 patients with paroxysmal AF (PAF), 36 with persistent AF (PsAF), and 17 control subjects (Ct) with left-sided accessory pathway Wolff-Parkinson-White syndrome. Plasma concentrations of vWF were determined by immunoturbidimetry. Compared with Ct, patients with PAF had higher LA plasma levels of vWF (P = 0.004), but similar Pf and CS levels (both P > 0.30). In contrast, patients with PsAF had higher plasma concentrations of vWF in Pf (P = 0.04), LA (P < 0.001), and CS (P = 0.04) samples compared with Ct. Left atrial plasma concentrations of vWF in patients with PsAF were also higher than in the PAF group (P = 0.04). CONCLUSION: Regardless of the clinical form of the arrhythmia, AF patients presented significantly higher plasma concentrations of vWF compared with sinus rhythm controls. Multilevel vWF plasma concentration assessment suggests an association between the clinical evolution of AF and the progression of endothelial dysfunction. Further studies will have to establish the exact mechanisms that link endothelial dysfunction and stroke in the context of AF.

In-hospital heart rate turbulence and microvolt T-wave alternans abnormalities for prediction of early life-threatening ventricular arrhythmia after acute myocardial infarction.

BACKGROUND: In the setting of primary prevention, most implantable cardiac defibrillators (ICD) are implanted more than 6 months after acute myocardial infarction (AMI). Abnormal heart rate turbulence (HRT) and T-wave alternans (TWA) are predictors of long-term sudden cardiac death (SCD). We intended to assess the predictive value of HRT and TWA for early post-AMI SCD and life-threatening ventricular arrhythmias (VA). METHODS: One hundred ninety-nine consecutive patients with AMI were prospectively included (age 61.7 years, LV ejection fraction 45%). One hundred eighty-three patients (92%) underwent percutaneous coronary intervention. We assessed HRT using turbulence slope (TS), turbulence onset (TO), and TWA on channels 1 and 2 (TWA1 and TWA2) using the modified moving average method. Predictive performance for SCD/VA was assessed by area under the receiver operating curve characteristic (ROC-AUC). RESULTS: Within 6 months after AMI, 2 patients (1%) developed life-threatening VA and 3 (1.5%) experienced SCD. TO and TWA1 had poor ROC-AUC (both 0.64) whereas TS and TWA2 failed to show any predictive performance (ROC-AUC 0.48 and 0.57, respectively). When combining TO and TWA1, ROC-AUC increased to 0.80. Importantly, when considering the subset of patients with a LV ejection fraction ≤40%, the combined variable of TO and TWA1 remained strongly predictive of a short-term event (ROC-AUC 0.86). CONCLUSIONS: Combined assessment of HRT and TWA showed a high predictive performance for SCD or life-threatening VA within 6 months after AMI. This combined Holter ECG index could be useful to identify high-risk patients who might benefit from early ICD implantation.

Prevention of contrast-associated acute kidney injury in an era of increasingly complex interventional procedures.

Radiological and interventional cardiology procedures are in continuous expansion, leading to an important increase in the incidence of contrast-associated acute kidney injury (CA-AKI). Although numerous methods of CA-AKI prevention have been studied, at present, there is no consensus on the definition of this entity or on its prevention. In this paper, we aim to provide a critical analysis of the existing data on the epidemiology, pathophysiology, and clinical significance of CA-AKI. Existing and emergent approaches for CA-AKI prevention are also discussed, with a focus on parenteral fluid administration and on the most recent clinical and experimental data. We also emphasize a number of questions that remain to be answered, and we identify hotspots for future research.

Unprovoked atrial tachyarrhythmias in aging spontaneously hypertensive rats: the role of the autonomic nervous system.

Experimental models of unprovoked atrial tachyarrhythmias (AT) in conscious, ambulatory animals are lacking. We hypothesized that the aging, spontaneously hypertensive rat (SHR) may provide such a model. Baseline ECG recordings were acquired with radiotelemetry in eight young (14-wk-old) and eight aging (55-wk-old) SHRs and in two groups of four age-matched Wistar-Kyoto (WKY) rats. Quantification of AT and heart rate variability (HRV) analysis were performed based on 24-h ECG recordings in unrestrained rats. All animals were submitted to an emotional stress protocol (air-jet). In SHRs, carbamylcholine injections were also performed. Spontaneous AT episodes were observed in all eight aging SHRs (median, 91.5; range, 4-444 episodes/24 h), but not in young SHRs or WKY rats. HRV analysis demonstrated significantly decreased low frequency components in aging SHRs compared with age-matched WKY rats (P < 0.01) and decreased low/high frequency ratios in both young (P < 0.01) and aging (P = 0.01) SHRs compared with normotensive controls. In aging SHRs, emotional stress significantly reduced the number of arrhythmic events, whereas carbamylcholine triggered AT and significantly increased atrial electrical instability. This study reports the occurrence of unprovoked episodes of atrial arrhythmia in hypertensive rats, and their increased incidence with aging. Our results suggest that autonomic imbalance with relative vagal hyperactivity may be responsible for the increased atrial arrhythmogenicity observed in this model. We also provide evidence that, in this model, the sympatho-vagal imbalance preceded the occurrence of arrhythmia. These results indicate that aging SHRs may provide valuable insight into the understanding of atrial arrhythmias.

Increased intracardiac vascular endothelial growth factor levels in patients with paroxysmal, but not persistent atrial fibrillation.

AIMS: Although inflammation appears to play a pivotal role in the pathophysiology of atrial fibrillation (AF), the source of inflammation is unknown. We hypothesized that multilevel measurement of several inflammatory proteins in AF patients would help assess the extent and the source of inflammation. METHODS AND RESULTS: Thirty-nine patients with paroxysmal AF, 33 with persistent AF, and 9 control patients with Wolff-Parkinson-White syndrome were enrolled. Peripheral, left atrial, coronary sinus, and pulmonary vein blood samples were obtained during catheterization. Serum levels of vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), soluble intercellular adhesion molecule 1 (sICAM-1), and transforming growth factor-ß1 (TGF-ß1) were measured at the four sampled sites. Interleukin-8, sICAM-1, and TGF-ß1 levels did not differ among groups at any of the sampled sites. Peripheral VEGF levels were higher in both paroxysmal and persistent AF patients than in controls (P ≤ 0.03). Left atrial VEGF levels were higher in paroxysmal AF (P = 0.05), but not in persistent AF (P = 0.32), compared with controls. Coronary sinus and pulmonary vein VEGF levels did not differ significantly among groups. CONCLUSIONS: Low levels of several inflammatory markers in both paroxysmal and persistent AF patients suggest that the inflammatory process is of low grade, if present. In the context of normal pulmonary vein VEGF levels, the heart itself is the most likely source of high left atrial VEGF levels in paroxysmal AF patients; however, this disorder appears to be a transient event in the natural history of AF.

Autonomic imbalance and atrial ectopic activity-a pathophysiological and clinical view.

The heart is one of the most richly innervated organs and the impact of the complex cardiac autonomic network on atrial electrophysiology and arrhythmogenesis, including on atrial ectopy, is widely recognized. The aim of this review is to discuss the main mechanisms involved in atrial ectopic activity. An overview of the anatomic and physiological aspects of the cardiac autonomic nervous system is provided as well as a discussion of the main pathophysiological pathways linking autonomic imbalance and atrial ectopic activity. The most relevant data on cardiac neuromodulation strategies are emphasized. Unanswered questions and hotspots for future research are also identified.

Targeting Myocardial Fibrosis-A Magic Pill in Cardiovascular Medicine?

Fibrosis, characterized by an excessive accumulation of extracellular matrix, has long been seen as an adaptive process that contributes to tissue healing and regeneration. More recently, however, cardiac fibrosis has been shown to be a central element in many cardiovascular diseases (CVDs), contributing to the alteration of cardiac electrical and mechanical functions in a wide range of clinical settings. This paper aims to provide a comprehensive review of cardiac fibrosis, with a focus on the main pathophysiological pathways involved in its onset and progression, its role in various cardiovascular conditions, and on the potential of currently available and emerging therapeutic strategies to counteract the development and/or progression of fibrosis in CVDs. We also emphasize a number of questions that remain to be answered, and we identify hotspots for future research.

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats.

Animal studies have brought important insights into our understanding regarding atrial fibrillation (AF) pathophysiology and therapeutic management. Reentry, one of the main mechanisms involved in AF pathogenesis, requires a certain mass of myocardial tissue in order to occur. Due to the small size of the atria, rodents have long been considered 'resistant' to AF. Although spontaneous AF has been shown to occur in rats, long-term follow-up (up to 50 weeks) is required for the arrhythmia to occur in those models. The present work describes an experimental protocol of transesophageal atrial burst pacing for rapid and efficient induction of AF in rats. The protocol can be successfully used in rats with healthy or remodeled hearts, in the presence of a wide variety of risk factors, allowing the study of AF pathophysiology, identification of novel therapeutic targets, and evaluation of novel prophylactic and/or therapeutic strategies.

Neutrophil gelatinase-associated lipocalin monitoring reveals persistent subclinical kidney injury following intraarterial administration of iodinated contrast agents.

Clinically overt contrast-induced nephropathy (CIN) is one of the most feared complications in patients exposed to iodinated contrast media and has been extensively studied over the years. Meanwhile, the incidence and evolution of subclinical contrast-induced kidney injury remain elusive. With the continuous increase in the number of patients that are repeatedly exposed to contrast media, elucidating these issues is of critical importance. Accordingly, we aimed to evaluate the incidence and the evolution of clinical and subclinical kidney injury in patients exposed to contrast media. A total of 178 patients who underwent elective percutaneous angioplasty procedures were evaluated prospectively. Serum creatinine and neutrophil gelatinase-associated lipocalin (NGAL) levels were evaluated pre-procedurally, 48 h and 1 month after administration of contrast media. The evolution of creatinine and NGAL levels was analyzed at the three time points, and the potential predictors of contrast-induced clinical and subclinical renal injury were evaluated. Clinically overt CIN occurred in 10 (5.6%) patients. Baseline serum creatinine and the volume of contrast media were the only independent predictors of CIN and in all 10 patients creatinine levels returned to baseline by 1 month (p = 0.32). Subclinical contrast-induced kidney injury was much more common, affecting 32 (17.9%) patients, was only predicted by the baseline serum creatinine, and persisted in 53.1% of patients after 1 month. This study showed that whereas clinically overt CIN is rather rare and regressive, subclinical contrast-induced kidney injury is considerably more frequent, affecting almost 18% of patients that receive intraarterial contrast media. More importantly, subclinical kidney injury persisted after 1 month in more than 50% of the initially affected patients, who may thus be at increased risk for further renal impairment, particularly if exposed to nephrotoxic agents or repeated administration of contrast media.

The CHA2DS2-VASc Score Predicts New-Onset Atrial Fibrillation and Hemodynamic Complications in Patients with ST-Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention.

Arrhythmic and hemodynamic complications related to ST-segment elevation myocardial infarction (STEMI) represent a major clinical challenge. Several scores have been developed to predict mortality in STEMI. However, those scores almost exclusively include factors related to the acute phase of STEMI, and no score has been evaluated to date for its ability to specifically predict arrhythmic and hemodynamic complications. We, thus, aimed to assess the ability of chronic risk factors burden, as expressed by the CHA2DS2-VASc score, to predict STEMI-related arrhythmic and hemodynamic complications. Data were collected from 839 consecutive STEMI patients treated by primary percutaneous coronary interventions (pPCI). CHA2DS2-VASc and GRACE scores were calculated for all patients, and their ability to predict STEMI-related arrhythmic (i.e., new-onset atrial fibrillation (AF), ventricular tachycardia/fibrillation) and hemodynamic (i.e., cardiogenic shock, asystole) complications was assessed in univariate and multiple regression analysis. Arrhythmic and hemodynamic complications occurred in 14.8% and 10.2% of patients, respectively. Although the GRACE score outweighed the CHA2DS2-VASc score in the ability to predict STEMI-related hemodynamic complications (p < 0.0001), both scores had a similar predictive value for STEMI-related new-onset AF (p = 0.20), and both remained independent predictors of new-onset AF and of hemodynamic complications in the multiple regression analyses. A CHA2DS2-VASc score > 2 points independently predicted new-onset AF (p < 0.01) and hemodynamic complications (p = 0.04). Alongside the GRACE score, the CHA2DS2-VASc score independently predicted new-onset AF and hemodynamic complications in STEMI patients treated by pPCI. These data suggest that a combination of acute and chronic risk factors could provide additional benefit in identifying patients at risk of STEMI-related complications, who could benefit from closer follow-up and more intensive prophylactic and therapeutic strategies.