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Objective Implantable cardiac defibrillators (ICDs) for primary prevention (PP) of sudden cardiac arrest (SCA) are well-established but underutilized globally. The Improve SCA study has identified a cohort of patients called 1.5 primary prevention (1.5PP) based on PP patients with the presence of certain risk factors. We evaluated the cost-effectiveness of ICD therapy compared to no ICD among the PP population and the subset of 1.5PP patients in Taiwan. Methods A Markov model was run over a lifetime time horizon from the Taiwan payer perspective. Mortality and utility estimates were obtained from the literature (PP) and the IMPROVE SCA trial (1.5PP). Cost inputs were obtained from the Taiwan National Health Insurance Administration (NHIA), Ministry of Health and Welfare. We used a willingness-to-pay (WTP) threshold of NT$2,100,000, as established through standard WTP research methods and in alignment with World Health Organization recommendations. Results The total discounted costs for ICD therapy and no ICD therapy were NT$1,664,259 and NT$646,396 respectively for PP, while they were NT$2,410,603 and NT$905,881 respectively for 1.5PP. Total discounted QALYs for ICD therapy and no ICD therapy were 6.48 and 4.98 respectively for PP, while they were 10.78 and 7.71 respectively for 1.5PP. The incremental cost effectiveness ratio was NT$708,711 for PP and NT$441,153 for 1.5PP, therefore ICD therapy should be considered cost effective for PP and highly cost effective for 1.5PP. Conclusions ICD therapy compared to no ICD therapy is cost-effective in the whole PP population and highly cost-effective in the subset 1.5PP population in Taiwan.

Impaired left atrial appendage ejection fraction (LAA-EF) and peak LAA flow velocity (LAA-FV) are associated with high thromboembolic risks in patients with atrial fibrillation (AF). Herein, we examined LAA function among patients with atrial flutter (AFL) stratified by the CHA2DS2-VASc score using transesophageal echocardiography (TEE). Of 231 consecutive patients with typical AFL, 84 who fulfilled the inclusion criteria were enrolled. Among them, 57 had ongoing AFL and were divided into the isolated AFL (n = 38) and AFL with paroxysmal AF (PAF) (n = 19) groups, depending on whether they had sporadic AF before TEE. The remaining 27 patients with spontaneous sinus rhythm during TEE were designated as controls. Both the LAA-FV (31.9 cm/s vs. 51.5 cm/s, P = 0.004) and LAA-EF (28.4% vs. 36.5%, P = 0.024) measured during AFL were significantly lower in the AFL + PAF group than in the isolated AFL group. Significant inverse correlations between the CHA2DS2-VASc score and LAA-EF were identified in the AFL (P = 0.008) and AFL + PAF (P = 0.032) groups. We observed progressive LAA dysfunction in patients with AFL + PAF compared with that in patients with isolated AFL, and the LAA-EF was inversely correlated with the CHA2DS2-VASc score in these patients. Our findings may have implications on the application of thromboprophylactic therapy in patients with AFL.

QRS duration has been associated with the response to cardiac resynchronization therapy (CRT). However, the methods for defining QRS duration to predict the outcome of CRT have discrepancies in previous reports. The aim of this study was to determine an optimal measurement of QRS duration to predict the response to CRT.Sixty-one patients who received CRT were analyzed. All patients had class III-IV heart failure, left ventricular ejection fraction not more than 35%, and complete left bundle branch block. The shortest, longest, and average QRS durations from the 12 leads of each electrocardiogram (ECG) were measured. The responses to CRT were determined using the changes in echocardiography after 6 months. Thirty-five (57.4%) patients were responders and 26 (42.6%) patients were non-responders. The pre-procedure shortest, average, and longest QRS durations and the QRS shortening (ΔQRS) of the shortest QRS duration were significantly associated with the response to CRT in a univariate logistic regression analysis (P = 0.002, P = 0.03, P = 0.04 and P = 0.04, respectively). Based on the measurement of the area under curve of the receiver operating characteristic curve, only the pre-procedure shortest QRS duration and the ΔQRS of the shortest QRS duration showed significant discrimination for the response to CRT (P = 0.002 and P = 0.038, respectively). Multivariable logistic regression showed the pre-procedure shortest QRS duration is an independent predictor for the response to CRT.The shortest QRS duration from the 12 leads of the electrocardiogram might be an optimal measurement to predict the response to CRT.

BACKGROUND Studies investigating the risk of cardiac dysrhythmia warranting permanent pacemaker therapy for end-stage renal disease (ESRD) patients are limited. This study investigated the incidence rate of permanent cardiac pacing in dialysis patients. METHODS Using the Taiwan National Health Insurance Database, we identified 28 471 newly diagnosed ESRD patients in 2000-2010 [9700 on peritoneal dialysis (PD) and 18 771 on hemodialysis (HD)] and 113 769 randomly selected controls without kidney disease, frequency-matched by sex, age and diagnosis date. We also established propensity score-matched HD and PD cohorts with 9700 patients each. Incidence rates and hazard ratios (HRs) of implantation were evaluated by the end of 2011. Complications were also evaluated among patients with implantation. RESULTS The incidence rates of permanent pacemaker implantation were 5.93- and 3.50-fold greater in HD and PD patients than in controls (1.44 and 0.85 versus 0.24 per 1000 person-years, respectively). The adjusted HRs (aHRs) of implantation were 3.26 [95% confidence interval (CI) = 2.41-4.42] and 2.36 (95% CI = 1.56-3.58) for HD and PD patients, respectively, compared with controls. The pacemaker implantation rate was 0.33 per 1000 person-years greater in the propensity score-matched HD cohort than in the PD cohort, with an aHR of 1.30 (95% CI = 0.82-2.05) for the HD cohort compared with the PD cohort. CONCLUSIONS Dialysis patients are at an increased risk of dysrhythmia requiring pacemaker implantation compared with the general population. The risks are not significantly different between HD and PD patients.

Idiopathic ventricular fibrillation (IVF) is a cause of sudden cardiac death (SCD). The frequency of mutations in disease-causing genes ranges, on average, between 16 and 48% in SCD cases. This study aimed to identify novel mutations in IVF patients withoutGenomic DNA extracted from peripheral blood samples obtained from five patients with IVF and WES was used to identify mutations associated with IVF. Candidate variants were validated by Sanger sequencing.Four patients harbored suspected mutations in 100 inherited cardiomyopathy-and channelopathy-associated genes (e.g.,This study revealed the effectiveness of WES for IVF patients without

Background Familial sick sinus syndrome is associated with gene mutations and dysfunction of ion channels. In contrast, degenerative fibrosis of the sinus node tissue plays an important role in the pathogenesis of acquired sick sinus syndrome. There is a close relationship between transforming growth factor-β1 mediated cardiac fibrosis and acquired arrhythmia. It is of interest to examine whether transforming growth factor-β1 is involved in the pathogenesis of acquired sick sinus syndrome. Methods Overall, 110 patients with acquired SSS and 137 age/gender-matched controls were screened for transforming growth factor-β1 and cardiac sodium channel gene polymorphisms using gene sequencing or restriction fragment length polymorphism methods. An enzyme-linked immunosorbent assay was used to determine the serum level of transforming growth factor-β1. Results Two transforming growth factor-β1 gene polymorphisms (C-509T and T+869C) and one cardiac sodium channel gene polymorphism (H588R) have been identified. The C-dominant CC/CT genotype frequency of T869C was significantly higher in acquired sick sinus syndrome patients than in controls (OR 2.09, 95% CI 1.16–3.75, P = 0.01). Consistently, the level of serum transforming growth factor-β1 was also significantly greater in acquired sick sinus syndrome group than in controls (5.3±3.4 ng/ml vs. 3.7±2.4 ng/ml, P = 0.01). In addition, the CC/CT genotypes showed a higher transforming growth factor-β1 serum level than the TT genotype (4.25 ± 2.50 ng/ml vs. 2.71± 1.76 ng/ml, P = 0.028) in controls. Conclusion Transforming growth factor-β1 T869C polymorphism, correlated with high serum transforming growth factor-β1 levels, is associated with susceptibility to acquired sick sinus syndrome.

Long QT syndrome (LQTS) is a genetic cardiac disease. Gene mutation affects the structure or function of ion channels that are associated with a high risk of sudden death. The goal of this study was to determine the frequency of KCNQ1, KCNH2, and SCN5A mutations in LQTS in a Taiwanese population. Genomic DNA was extracted from peripheral blood samples obtained from 5 patients with LQTS and the family members of 3 LQTS patients. High resolution melting (HRM) analysis and direct DNA sequencing were used to characterize the KCNQ1, KCNH2, and SCN5A genetic variations. HRM analysis was successfully optimized for 14 of the 16 exons of the KCNQ1, 5 of the 15 exons of the KCNH2, and 23 of the 27 exons of the SCN5A. HRM and direct DNA sequencing was applied to the cohort of 5 cases and some of their family. The genetic testing revealed two pathogenic mutations (p.T309I in KCNQ1 and p.R744fs in KCNH2) and all of the mutational frequencies in KCNQ1 and KCNH2 were 20%. In the two patients who carry the pathogenic mutation presenting with recurrent syncope due to ventricular fibrillation, an implantable cardioverter defibrillator was implanted. We also discovered 11 polymorphisms in KCNQ1, 3 in KCNH2, and 5 in SCN5A. Two-fifths of cases (40%) presented with one of the three major LQTS-causing gene mutations.

We encountered a 40-year-old man with recurrent symptomatic palpitations manifested as monomorphic ventricular tachycardia (VT) of a right bundle branch block (RBBB) pattern with an inferior frontal axis. Physical examination, chest roentgenogram, and echocardiogram were unremarkable. The VT could be provoked by treadmill exercise testing. Electrophysiologic study revealed that the VT could be reproducibly initiated with either atrial or ventricular pacing at cycle lengths between 500 and 400 ms. With overdrive ventricular pacing, the VT could be terminated. Of note was the observation that intravenous adenosine was not effective, but intravenous verapamil could interrupt the VT. The VT was pace mapped to be arising from a site at the left ventricular outlet tract (LVOT). Notably, during pace mapping, the pacing spike was immediately followed by the beginning of the paced QRS complex, and during VT, there was no time delay between the earliest local activation and the onset of QRS complex. Furthermore, there was no mid-diastolic activity or Purkinje potential that could be recorded during sinus rhythm and VT. Subsequently, the VT was successfully ablated with radiofrequency energy as guided by pace mapping. In summary, an idiopathic VT arising from the LVOT was found to be cycle lengths- and catecholamine-dependent, adenosine-insensitive but verapamil responsive. These unusual features suggest that either microreentry or triggered activity could be the underlying mechanism.

This article describes the additional use of incremental atrial burst pacing (A1A1) and double atrial extrastimulation with a predefined fast pathway conducted A2 (A1A2A3), rather than single atrial extrastimulation (A1A2) only, to characterize typical atrioventricular nodal reentrant tachycardia (AVNRT). The authors noted an additional 32% of patients had multiple anterograde AV nodal physiology demonstrated when A1A1 or A1A2A3 protocols were deployed compared to more conventional A1A2 protocols. The A2H2max (449 +/- 147 vs 339 +/- 94 ms) and A3H3max (481 +/- 120 vs 389 +/- 85 ms) were higher in 31 patients where multiple jumps in the AV nodal conduction curve were obtained (group 1) compared to 192 patients where only single jump was obtained (group 2) (both P0.01). Postablation, the degree of reduction of A2H2max (49%) and A3H3max (50%) in group 1 was greater than in group 2 (38% and 42%, respectively, P0.05). In seven of group 1 patients in whom A1A2A3 stimulation was required to reveal multiple jumps, the A2H2max remained unchanged after ablation (237 +/- 89 vs 214 +/- 59, P0.05). A3H3max was the only parameter that shortened significantly after ablation. Generally, successful ablation resulted in loss of multiple discontinuities in A1A1/A1H1 or A2A3/A3H3 curves. In conclusion, a combination of A1A2, A1A1, and A1A2A3 are required to fully elucidate AVNRT. Significant shortening of AHmax or loss of multiple jumps after ablation indicates successful elimination of AVNRT in these patients.

Idiopathic left ventricular tachycardia (ILVT) is a distinct entity that arises in the left ventricle, may have reentrant mechanism and is verapamil-sensitive. Pleomorphism as defined by multiple ventricular tachycardia morphologies is usually associated with either coronary artery disease or cardiomyopathy but very rare in cases of ILVT. In this case report, we describe an unusual case of ILVT with two ECG morphologies of the opposite axis that were successfully eliminated with radiofrequency ablation. The successful ablation sites were closely located to each other in the left lower ventricular septum.

Left ventricular systolic function was studied in 40 patients with atrial fibrillation using a matrix-array transducer, which enables 2 simultaneous orthogonal views to be obtained in a biplane mode. Bland-Altman analysis showed excellent correlation and agreement between the systolic parameters of a single beat with identical RR1 and RR2 intervals and the measured average value over all cardiac cycles.

Purposes Reciprocal changes are frequent in patients with acute ST-segment elevation myocardial infarction (STEMI). However, their prognostic significance is not clear in patients undergoing immediate invasive intervention. Basic Procedure We retrospectively examined 165 consecutive patients with STEMI receiving immediate invasive intervention. The first electrocardiography taken in the emergency department was analyzed. Patients were assigned to 2 groups: with a reciprocal change (group I, n = 100) and without a reciprocal change (group II, n = 65). Main Findings Electrocardiographs revealed that more anterolateral and inferior STEMI occurred in group I and more anterior STEMI occurred in group II. In the emergency department, group I had lower systolic and diastolic blood pressures, higher ventricular tachycardia and fibrillation rates, and higher cardiopulmonary resuscitation rates than did group II. Upon admission, peak troponin I levels were significantly higher in group I, and more group I patients required intra-aortic balloon pumping support. This unstable hemodynamic condition in group I patients was reflected by their higher in-hospital mortality rate. Multivariate analysis showed that age (odds ratio [OR], 1.103; 95% confidence interval [CI], 1.022-1.190; P = .012), Killip class (OR, 2.785; 95% CI, 1.049-7.400; P = .040), and reciprocal change (OR, 9.553; 95% CI, 1.146-79.608; P = .037) remained as independent predictors of in-hospital mortality. Actuarial freedom from all-cause mortality was worse in group I ( P = .046). Principal Conclusions The data suggest that patients with STEMI with reciprocal electrocardiographic changes have unstable hemodynamic status and poorer outcomes. Further prospective studies using a larger patient population are needed.

Background It is well known that familial sick sinus syndrome (SSS) is caused by functional alterations of ion channels and gap junction. Limited information is available on the mechanism of age-related non-familial SSS. Although evidence shows a close link between arrhythmia and the renin-angiotensin system (RAS), it remains to be determined whether the RAS is involved in the pathogenesis of non-familial SSS. Methods In this study, 113 patients with documented non-familial SSS and 125 controls were screened for angiotensinogen (AGT) and gap junction protein-connexin 40 (Cx40) promoter polymorphisms by gene sequencing, followed by an association study. A luciferase assay was used to determine the transcriptional activity of the promoter polymorphism. The interaction between nuclear factors and the promoter polymorphism was characterized by an electrophoretic mobility shift assay (EMSA). Results Association study showed the Cx40 -44/+71 polymorphisms are not associated with non-familial SSS; however, it indicated that four polymorphic sites at positions -6, -20, -152, and -217 in the AGT promoter are linked to non-familial SSS. Compared to controls, SSS patients had a lower frequency of the G-6A AA genotype (OR 2.88, 95% CI 1.58–5.22, P = 0.001) and a higher frequency of the G allele at -6 position (OR 2.65, 95% CI 1.54–4.57, P = 0.0003). EMSA and luciferase assays confirmed that nucleotide G at position -6 modulates the binding affinity with nuclear factors and yields a lower transcriptional activity than nucleotide A (P

Background Anatomic characteristics of the cavotricuspid isthmus (CTI) have been reported to be related to the outcome of atrial flutter ablation therapy. However, preprocedural evaluation of CTI anatomy using modified transthoracic echocardiography to guide atrial flutter ablation has not been well described. Methods Transthoracic echocardiography was prospectively performed before atrial flutter ablation in 42 patients with typical CTI-dependent atrial flutter. A modified apical long-axis view was designed to visualize and evaluate anatomic characteristics of the CTI and Eustachian ridge (ER). A prominent ER, extending from the inferior vena cava to the interatrial septum, is defined as an extensive ER. Results Twenty-eight patients had straightforward ablation procedures, and 14 patients had difficult ablation procedures. Two patients with difficult procedures had unsuccessful ablation. Multivariate analysis (using CTI length, the presence of a pouch or recess, ER morphology, and significant tricuspid regurgitation as variables) showed that the presence of extensive ER was the only independent predictor of a difficult ablation procedure. The ablation time in patients with extensive ER ( n = 13) was significantly longer than in those patients with nonextensive ER ( n = 29) (1,638.4 ± 1,548.3 vs 413.8 ± 195.5 sec, P = .015). The incidence of difficulty in achieving bidirectional isthmus block was also higher in patients with extensive ER (10 of 13 vs four of 29, P Conclusion Preprocedural transthoracic echocardiography using a modified apical long-axis view is useful to characterize the morphology of the CTI and the ER. An extensive ER is a strong predictor for difficult ablation of CTI-dependent atrial flutter.

Atrial fibrillation (AF), the most common sustained arrhythmia requiring treatment worldwide, is one of the major causes of ischemic stroke. Although amiodarone is commonly used for rhythm control in AF, its relationship with stroke has rarely been addressed. We evaluated 16,091 patients who were diagnosed with AF (Classification of Diseases, 9th Revision, Clinical Modification [ICD-9-CM] 427.31 and 427.32) between 1998 and 2011; the date of AF diagnosis was set as the index date. Patients with a history of stroke (ICD-9-CM 430–438) who received amiodarone before the index date or during the following 30 days, or who experienced stroke within 30 days of receiving amiodarone were excluded. Finally, 7548 patients with AF were included in this study and divided into 2 groups according to whether they received amiodarone (Anatomical Therapeutic Chemical code C01BD01) during the study period. The risk of ischemic stroke in AF patients receiving amiodarone was 1.81-fold (95% confidence interval [CI] 1.52–2.16), 1.79-fold (95% CI 1.50–2.14), and 1.78-fold (95% CI 1.49–2.13) higher than in those who did not receive amiodarone, according to crude, Model 1, and Model 2 Cox proportional hazard regression models, respectively. In a demographically stratified analysis, the risk of ischemic stroke was significantly higher in patients aged

Background: The cephalic vein approach is a preferred route for endocardial lead implantation; however, it is associated with a significant failure rate. Anatomic abnormalities likely play an important role, but specific features have not been well characterized. Methods: Color Doppler ultrasonography was performed in 82 consecutive patients prior to endocardial lead implantation. Venous diameter, depth, flow velocity, and morphology were evaluated and comparisons made between the successful and failed implantations at various stages of the procedure. Results: Endocardial lead implantation was unsuccessful in 14 patients (17%), with eight patients of venous isolation failure, 4 patients of cannulation failure, and 2 patients of guidewire crossing failure. Venous diameter was found to be the only independent predictor for isolation and implantation failure. The best cutoff value of cephalic venous diameter to predict unsuccessful cephalic venous approach was ≤2.2 mm. In total, there were 10 patients with extensive cephalic vein tortuosity. In seven of these 10 patients, the incidence of standard guidewire crossing failure was significantly higher than that without a tortuous cephalic vein (7/10 vs 6/60, P < 0.001). After switching to a hydrophilic guidewire, crossing and navigation were successful in five of the seven patients. Conclusions: Color Doppler imaging is useful to identify cephalic vein characteristics. A small venous diameter is the ultrasonographic predictor for failure of cephalic vein approach. A tortuous venous morphology is associated with a high incidence of guidewire crossing failure, which can be mostly overcome by using a hydrophilic guidewire.

Single-beat determination of left ventricular systolic function at a beat with equal subsequent cardiac cycles has been proposed as an accurate method in atrial fibrillation. However, there has still been substantial variability between the values calculated from beats with equal subsequent cycles. Therefore, some refinement on the single-beat method is needed. In 100 patients with atrial fibrillation, Doppler aortic flow time-velocity integral was determined for at least 20 consecutive cardiac cycles. The values at beats with equal subsequent cardiac cycles were chosen and compared with the average values over all cardiac cycles. The values at beats with cycle lengths shorter than 500 milliseconds were usually far below the average values over all cardiac cycles. Bland-Altman agreement analysis revealed improved accuracy by gradually narrowing the range of the limits of agreement when 2 or 3 beats with equal subsequent cycles and cycle lengths longer than 500 milliseconds were used for evaluation.

Electrophysiological characteristics of an accessory pathway (AP) with a long ventriculoatrial (VA) interval (arbitrarily defined as > or = 50 ms and absence of continuous electrical activity) and no retrograde decremental property are described in this study. Fifteen patients (group 1) were compared with 171 patients with normal VA conduction (group 2). Mean VA conduction time was 77 +/- 24 versus 34 +/- 12 ms in group 1 versus group 2, respectively. Group 1 patients were older (55 +/- 14 vs 40 +/- 14 years), the male to female ratio was higher (2.8 vs 1.6), and APs were more prevalent on the right (60%) but manifest APs were lower (20% vs 54%) compared to group 2 patients (P < 0.05 in all cases). QRS morphology during induced atrioventricular reciprocating tachycardia was identical in both groups but the tachycardia cycle length was longer in group 1 (373 +/- 29 vs 344 +/- 50 ms, P < 0.05). Retrograde AP block cycle length and effective refractory period were greater in group 1 (362 +/- 59 vs 293 +/- 57 ms; 330 +/- 58 vs 273 +/- 55 ms, both P < 0.05). Adenosine (up to 18 mg) and verapamil (5-10 mg) failed to block the VA conduction via AP during ventricular pacing. In group 1 the number of radiofrequency lesions for a successful ablation were significantly less (3 +/- 2 vs 6 +/- 5, P < 0.05). In conclusion, APs with a long VA interval and no decremental retrograde conduction have electrophysiological characteristics that are different from those with a short VA interval. Role of aging deserves further exploration.

Venous thrombosis induced by a transvenous permanent pacemaker is a common complication. However, superior vena cava (SVC) syndrome caused by pacemaker leads is only occasionally seen and its prevalence has been estimated to be less than 1 in 1000 pacemaker patients. Herein, we report a Taiwanese patient of high grade AV block, who presented with SVC syndrome 2 years after transvenous permanent pacemaker implantation. This case features fibrotic stenosis of the junction of right brachiocephalic trunk and SVC, and an extensive thrombus formation resulting in complete obliteration of the left brachiocephalic vein. The collateral circulation was so delicate that he still could lead a rather normal life, even if anticoagulant therapy proved to be ineffective from an angiographic point of view.

Background —Characterization of typical atrioventricular nodal reentrant tachycardia (AVNRT) with continuous AVN conduction (A 1 A 2 /A 2 H 2 ) curves by double atrial extrastimulation (A 1 A 2 A 3 ) has never been systematically studied. Methods and Results —This study was composed of 33 patients with typical AVNRT and continuous AVN conduction curves (group 1) and 103 patients with AVNRT and discontinuous AVN conduction curves (group 2). Using A 1 A 2 A 3 with predefined fast pathway–conducted A 2 , we examined the effects of slow pathway ablation on the A 2 A 3 /A 3 H 3 curves in both groups. In group 1, anterograde AVN effective refractory period (272±33 versus 277±47 ms, P >0.05) and AVN Wenckebach block cycle length (320±45 versus 343±59 ms, P >0.05) remained unchanged after ablation. A 2 H 2 max was shorter in group 1 than group 2 (237±89 versus 395±72 ms, P P P >0.05) after ablation. A 1 A 2 A 3 could further disclose discontinuous A 2 A 3 /A 3 H 3 curves in 29 patients of group 1. A 3 H 3 max shortened in both groups (375±81 versus 238±82 ms, P P 2 A 3 /A 3 H 3 curves in the 4 patients of group 1 with continuous A 2 A 3 /A 3 H 3 curves. Conclusions —Use of A 1 A 2 A 3 could expose discontinuous A 2 A 3 /A 3 H 3 curves in most patients with continuous A 1 A 2 /A 2 H 2 curves. Significant shortening of A 3 H 3 max after ablation may be indicative of successful elimination of AVNRT.

The knowledge on allergic shiners is extremely limited. A conceivable tool able to quantify allergic shiners has not been established.We sought to determine the significance and changeability of allergic shiners through our newly developed computerized method.We developed a novel computerized method to measure allergic shiners and enrolled a cohort of children with or without allergic rhinitis. Children with allergic rhinitis were prospectively assessed. A standardized digital photograph was taken during each visit, and a modified Pediatric Rhinoconjunctivitis Quality of Life Questionnaire was completed. Subject global assessment for nose symptoms and subject global assessment for eye symptoms (SGAE) were self-recorded daily.We included 126 children with allergic rhinitis and 123 healthy control subjects. One hundred three (82%) participants with allergic rhinitis completed at least 4 prospective assessments. Shiners were darker (P.001) and larger (P.001) in children with allergic rhinitis. Darkness and sizes of allergic shiners were paradoxically inversely correlated (P = .02). Darkness of allergic shiners positively correlated with the duration of allergic rhinitis, practical problem scores, and SGAE values (P = .02, P = .004, and P = .002, respectively), but sizes of allergic shiners did not. Shiners were found to be darker in children with scores of eye symptoms of greater than 6, scores of practical problems of greater than 5, and SGAE values of greater than 0 (P = .02, P.001, and P = .003, respectively), whereas shiners were larger in children with scores of other symptoms of greater than 9 and activity limitations of greater than 4 (P = .02 and P = .002, respectively).Computer-analyzed allergic shiners correlate with the chronicity and severity of allergic rhinitis.