ABSTRACT
OBJECTIVE: Radial artery occlusion (RAO) is a common complication during transradial coronary intervention. Its incidence is variably reported in literature and its predictors are not completely understood. In this study, we aimed to define the incidence and factors influencing RAO in patients undergoing transradial coronary intervention. METHODS: This was a single-center prospective study (October 2018 to September 2019) that enrolled 1,754 patients who were evaluated for RAO 24 hours after transradial coronary intervention. Univariate as well as multivariate analyses were done to identify patient and procedure related factors predicting the occurrence of RAO. RESULTS: A total of 1,374 patients (78.3%) underwent angioplasty, whereas 380 (21.7%) underwent angiography alone. RAO was diagnosed in 11.97% patients. Lower glomerular filtration rate, multiple puncture attempts for radial artery access, larger sheath size, complex nature of interventional procedure, longer homeostasis time, and forearm hematoma formation were independent predictors for RAO. CONCLUSION: RAO was not an uncommon complication in transradial coronary interventions, especially in the Indian population; and the knowledge of predictors may be helpful in its prevention.
Subject(s)
Arterial Occlusive Diseases , Radial Artery , Arterial Occlusive Diseases/diagnostic imaging , Arterial Occlusive Diseases/epidemiology , Arterial Occlusive Diseases/etiology , Cardiac Catheterization/methods , Coronary Angiography/adverse effects , Heart , Humans , Incidence , Prospective Studies , Radial Artery/diagnostic imagingABSTRACT
BACKGROUND: Forearm hematomas are not uncommon after transradial coronary interventions. The present study describes the incidence and predictors of forearm hematoma formation after transradial coronary interventions. METHODS: This was a prospective study in 1754 patients undergoing angiography/angioplasty through transradial access. Each procedure was performed using optimum levels of anticoagulation, hydrophilic sheaths, and post-procedural patent hemostasis protocols. Patients were evaluated for forearm hematoma immediately after the procedure, after radial band removal, and on the next day of the procedure. Severity of hematomas was graded according to the Early Discharge after Transradial Stenting of Coronary Arteries Study scale. Univariate and multivariate logistic regression analyses were done to determine the predictors of hematoma formation. RESULTS: Mean age of the patients was 56.31 years and 82.2% were males. A total of 1374 (78.3%) patients underwent angioplasty while 380 (21.7%) underwent angiography. Forearm hematoma developed in 187 (10.7%) patients. Grade I hematoma was most common (3.53%) followed by Grade II (3.08%), Grade III (2.83%) and Grade IV (1.25%) hematoma. None of the patients required vascular or surgical interventions for this complication. Female gender, multiple puncture attempts, intensive antiplatelet therapy, complex procedure and longer hemostasis time were significant predictors of forearm hematoma formation post transradial coronary interventions. CONCLUSIONS: Forearm hematoma developed in substantial proportion of patients undergoing transradial coronary interventions and interventional variables were predominantly associated with hematoma formation. Pre-emptive knowledge of modifiable interventional risk factors can help in reducing the burden of this complication.
Subject(s)
Kearns-Sayre Syndrome/diagnosis , Adult , Diagnosis, Differential , Electrocardiography , Humans , MaleABSTRACT
Although temporary transvenous pacing is life-saving in patients with myocardial infarction who develop bradyarrhythmias, the electrical complications resulting from it can be fatal and are rarely reported. We report here a patient with acute inferior wall myocardial infarction who required temporary transvenous pacing due to second-degree atrioventricular block accompanied with hypotension. Following coronary angiography and successful revascularisation, the patient developed multiple episodes of monomorphic and polymorphic ventricular tachycardia as well as ventricular fibrillation which on careful inspection were found to be initiated by fusion of the intrinsic and paced complexes. The problem of malignant ventricular tachycardia was solved by simple removal of the pacing lead. To the best of our knowledge, malignant ventricular tachycardia of both monomorphic and polymorphic types initiated by fusion complexes in a paced patient has not been reported in literature.
