Diffuse plexus-like coronary artery-left ventricular fistulae leading to coronary steal syndrome: a pattern of anomalous coronary microvascularization.

Coronary artery fistulae that drain into the left ventricle are extremely rare, and even fewer cases of fistulae involving all three of the coronary arteries have so far been reported. We herein report a 64-year-old woman with a unique pattern of coronary artery-left ventricular fistulae that involved all three of the coronary arteries. The multiple fistulae presented in a diffuse plexus-like arrangement. The fistulae resulted in a diastolic volume overload of the left ventricle (left-to-left shunt), as well as "coronary steal" with the shunting of blood away from the myocardium since the fistulae represented the path of least resistance.

Nitric Oxide Synthase 1 Adaptor Protein, an Emerging New Genetic Marker for QT Prolongation and Sudden Cardiac Death.

UNLABELLED: Sudden cardiac death (SCD) is defined as sudden unexplained death due to cardiac causes with an acute change in cardiovascular status within 1 hour of onset of symptoms. Alternatively, in unwitnessed cases, SCD can also be defined as a person last seen functionally normal 24 hours before being found dead. Despite significant advances in understanding the pathophysiology of cardiovascular diseases and the resultant improvement in resuscitation science, SCD remains a major healthcare challenge worldwide. Although the most pronounced risk factor for SCD is the presence of coronary artery disease in the setting of a depressed left ventricular function, most deaths occur in the larger, lower-risk subgroups where genetic variations and other conditions may be the precipitating factors in triggering SCD. Recently, a common genetic variation in a neuronal nitric oxide synthase regulator, nitric oxide synthase 1 adaptor protein (NOS1AP) also known as carboxyl-terminal PDZ ligand of neuronal nitric oxide synthase protein (CAPON) gene, has been identified as a new genetic marker in modulating QT interval prolongation and SCD in general populations. Animal study revealed that NOS1AP is expressed in the heart and interacts with NOS1-NO pathways to modulate cardiac repolarization via suppressing the sarcolemmal L-type calcium current and enhancing the IKr current. This important genetic implication was soon replicated in other racial/ethnic populations and extended to a variety of clinical settings including diabetes mellitus, coronary artery disease, myocardial infarction, and congenital or drug-induced long QT syndrome. The purpose of this review aims to provide up-to-date information about the emerging new genetic marker, NOS1AP, in relation to QT prolongation and SCD. KEY WORDS: NOS1AP; QT interval; Sudden cardiac death.

Usefulness of pre-procedure cavotricuspid isthmus imaging by modified transthoracic echocardiography for predicting outcome of isthmus-dependent atrial flutter ablation.

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 < .001). 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.

Safety and effectiveness of primary prevention cardioverter defibrillators in octogenarians.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) reduce the rate of sudden cardiac death (SCD) in patients with cardiomyopathy and reduced left ventricular systolic function. It is unclear if this benefit extends to the very elderly patient population. METHODS: Patients who underwent initial ICD implantation at age 80 or older between January 1995 and April 2010 for primary SCD prevention were identified. Clinical data were collected from the medical record, including periprocedural complications, device type, and therapies delivered. RESULTS: Three-hundred eighty patients were identified; 84 patients met eligibility criteria. The mean age was 82.68 years; mean follow-up was 34 months. Mean left ventricular ejection fraction was 28.1%. Mortality during follow-up was 17.9%. One- and 5-year survival estimates were 100% and 60%, respectively. Periprocedural complications occurred in 9.4% of patients; serious complications occurred in 4.8% with no periprocedural deaths. Device therapies occurred in 11.9% (n = 10) of patients (9.5% appropriate, n = 8; 2.4% inappropriate, n = 2). Cardiac resynchronization therapy-defibrillator (CRT-D) implantation was associated with prolonged median survival and decreased risk of death (hazard ratio 0.212; 95% confidence interval 0.048-.942, P = 0.042) compared to ICD alone. CONCLUSIONS: Implantation of primary prevention ICDs in patients 80 years of age or older was associated with a low risk of serious complications and a 5-year survival estimate of 60%. Inappropriate therapies after implantation were uncommon. CRT-D implantation was associated with a decreased risk of death compared to ICD alone. These data suggest that, in selected patients in this age group, ICD implantation is safe and effective.

Transient ST-segment elevation during transseptal catheterization for atrial fibrillation ablation.

For the treatment of refractory left atrial tachyarrhythmias, including atrial fibrillation, transseptal catheterization is often performed in order to achieve pulmonary vein isolation and left atrial substrate ablation. Herein, we report an unexpected ST-segment elevation in a 71-year-old man during a Brockenbrough transseptal catheterization procedure for atrial fibrillation ablation. The results of immediate coronary angiography were normal. The few reports of similar observations have not yielded a definite conclusion about the underlying pathophysiology of this electrocardiographic phenomenon. We reviewed the medical literature and hypothesize that manipulation of the intraseptal and left atrial ganglion plexuses by the transseptal needle and sheath causes an imbalance in autonomic innervation, which leads to coronary artery spasm and ST-segment elevation. Nonetheless, coronary artery air embolism during the transseptal approach should also be considered in the differential diagnosis. If the elevation is transient and there is no evidence of acute myocardial infarction, we believe that careful monitoring and evaluation are more appropriate than immediate termination of the ablation procedure.

Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases in rapid atrial pacing-induced atrial fibrillation.

Remodeling of atrial extracellular matrix (ECM) in atrial fibrillation (AF) involves changes in the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs). The contributions of MMPs and TIMPs to the pathogenesis of AF development have not been clearly defined. This study evaluated the in situ activity and expression of gelatinases (MMP-2 and MMP-9) and their relationship with TIMP-1 or TIMP-3 in atria undergoing rapid atrial pacing for the induction of AF (4 weeks' pacing followed by 2 weeks of maintained AF) in pigs. In AF atria, in situ gelatinase activity was mainly localized in the interstitium of atrial myocardium, and was significantly larger than that of sinus rhythm control (i.e., sham control). The significant increase of MMP-9 in its pro-form and mRNA level, but not MMP-2, was shown to be responsible for the increased gelatinase activity in atria with AF. The inhibitory activities of glycosylated TIMP-1 and TIMP-3, but not TIMP-2, in AF tissues were markedly elevated and also localized in the atrial interstitium. TIMP-1 was found to be mostly colocalized with gelatinase activity over the AF tissues, implying the coexistence of gelatinase activity and TIMP-1, but TIMP-3 appeared only partially colocalized and discontinued the gelatinase activity surrounding the cardiomyocytes. TIMP-1 and TIMP-3 may play differential roles in the inhibition of gelatinase activity in vivo. Together with the survey of several MMPs transcripts and the level of transforming growth factor-beta1 (TGF-beta1), we proposed that the increased activity of gelatinase (i.e., MMP-9), TIMP-1 and TIMP-3 and their interaction may contribute to atrial ECM remodeling of AF.

Usefulness of interatrial conduction time to distinguish between focal atrial tachyarrhythmias originating from the superior vena cava and the right superior pulmonary vein.

OBJECTIVE: Differentiation of the tachycardia originating from the superior vena cava (SVC) or the right superior pulmonary vein (RSPV) is limited by the similar surface P-wave morphology and intraatrial activation pattern during tachycardia. We sought to find a simple method to distinguish between the two tachycardias by analyzing the interatrial conduction time. METHODS: Sixteen consecutive patients consisting of 8 with SVC tachycardia and the other 8 with RSPV tachycardia were studied. The interatrial conduction time from the high right atrium (HRA) to the distal coronary sinus (DCS) and the intraatrial conduction time from the HRA to the atrial electrogram at the His bundle region (HIS) were measured during the sinus beat (SR) and during the tachycardia-triggering ectopic atrial premature beat (APB). The differences of interatrial (Delta[HRA-DCS](SR-APB)) and intraatrial (Delta[HRA-HIS](SR-APB)) conduction time between SR and APB were then obtained. RESULTS: The mean Delta[HRA-DCS](SR-APB) was 1.0 +/- 5.2 ms (95% confident interval [CI]-3.3-5.3 ms) in SVC tachycardia and 38.5 +/- 8.8 ms (95% CI 31.1-45.9 ms) in RSPV tachycardia. The mean Delta[HRA-HIS](SR-APB) was 1.5 +/- 5.3 ms (95% CI -2.9-5.9 ms) in SVC tachycardia and 19.9 +/- 12.0 ms (95% CI 9.9-29.9 ms) in RSPV tachycardia. The difference of Delta[HRA-DCS](SR-APB) between SVC and RSPV tachycardias was wider than that of Delta[HRA-HIS](SR-APB) (37.5 +/- 9.3 ms vs. 18.4 +/- 15.4 ms, P < 0.01). CONCLUSIONS: The wide difference of the interatrial conduction time Delta[HRA-DCS](SR-APB) between SVC and RSPV tachycardias is a useful parameter to distinguish the two tachycardias and may avoid unnecessary atrial transseptal puncture.

Increased expression of extracellular matrix proteins in rapid atrial pacing-induced atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is characterized by structural remodeling of the extracellular matrix (ECM) in cardiac atrium. OBJECTIVE: The purpose of this study was to gain further insight into atrial ECM remodeling at the molecular level and to test whether altered expression of ECM proteins was associated with the disease. METHODS: Sustained AF was induced in nine adult pigs after 3-4 weeks of continuous rapid atrial pacing at a rate of 600 bpm. Histologic studies and immunohistochemical stain were performed to identify the potential pathologic substrate underlying abnormalities in atrial tissues with sustained AF. RESULTS: In the pathologic findings, the fraction of myocardial ECM (ECM%) was measured, with a significantly greater ECM% found in the AF group compared with the sham operated group (n = 6; i.e., pigs with normal sinus rhythm [SR]). A set of 9,182 genes was screened with cDNA microarray analysis. In AF animals, expression of 121 genes increased and 24 genes decreased by > or =1.75-fold compared with SR animals. Significant up-regulation of fibronectin-1 (4.9-fold), fibrillin-1 (3.1-fold), and fibromodulin (1.9-fold) in the fibrillating atria was confirmed by quantitative real-time reverse transcriptase-polymerase chain reaction. Western blot analysis revealed significantly increased atrial fibronectin-1, fibrillin-1, and fibromodulin in the AF group compared with the SR group (1.5-, 2.7-, and 2.1-fold, respectively). Immunohistochemical staining of AF tissue displayed increased accumulation of fibronectin-1 and fibrillin-1 in the atrial interstitial space. CONCLUSION: Increased expression of ECM proteins in fibrillating atria supports the hypothesis that ECM metabolism contributes to the development of AF.

Altered expression of FHL1, CARP, TSC-22 and P311 provide insights into complex transcriptional regulation in pacing-induced atrial fibrillation.

Atrial fibrillation (AF) is the most common progressive disease in patients with cardiac arrhythmia. AF is accompanied by complex atrial remodeling and changes in gene expression, but only a limited number of transcriptional regulators have been identified. Using a low-density cDNA array, we identified 31 genes involved in transcriptional regulation, signal transduction or structural components, which were either significantly upregulated or downregulated in porcine atria with fibrillation (induced by rapid atrial pacing at a rate of 400-600 bpm for 4 weeks that was then maintained without pacing for 2 weeks). The genes for four and a half LIM domains protein-1 (FHL1), transforming growth factor-beta (TGF-beta)-stimulated clone 22 (TSC-22), and cardiac ankyrin repeat protein (CARP) were significantly upregulated, and chromosome 5 open reading frame gene 13 (P311) was downregulated in the fibrillating atria. FHL1 and CARP play important regulatory roles in cardiac remodeling by transcriptional regulation and myofilament assembly. Induced mRNA expression of both FHL1 and CARP was also observed when cardiac H9c2 cells were treated with an adrenergic agonist. Increasing TSC-22 and marked P311 deficiency could enhance the activity of TGF-beta signaling and the upregulated TGF-beta1 and -beta2 expressions were identified in the fibrillating atria. These results implicate that observed alterations of underlying molecular events were involved in the rapid-pacing induced AF, possibly via activation of the beta-adrenergic and TGF-beta signaling.

Erratum to: Denaturing high-performance liquid chromatography screening of the long QT syndrome-related cardiac sodium and potassium channel genes and identification of novel mutations and single nucleotide polymorphisms.

The name Fon-Jou Hsieh was inadvertently omitted from the list of authors. The name should be added as the third author of the article.

Left atrial dysfunction in patients with atrial fibrillation after successful rhythm control for > 3 months.

BACKGROUND: Large-scale clinical trials have demonstrated that patients with atrial fibrillation (AF), when treated with a rhythm-control strategy, are still at risk for embolic events. We hypothesized that left atrial (LA) dysfunction persisted even after successful maintenance of sinus rhythm for > 3 months. METHODS: A total of 93 patients with AF and satisfactory rhythm control for > 3 months were included. Satisfactory rhythm control was defined as being free of AF based on patient-reported symptoms, monthly ECG follow-up, and ambulatory Holter ECG if needed. Among the 93 patients, 25 patients had sustained AF that was terminated by electrical or pharmacologic cardioversion, while 68 patients had paroxysmal AF under good medical control. Clinical data were obtained, and transthoracic and transesophageal echocardiography were performed after satisfactory rhythm control for > 3 months. RESULTS: Among the 93 patients, 34 patients (37%) had LA dysfunction, defined as LA appendage (LAA) peak emptying velocity < 40 cm/s or spontaneous echo contrast and/or thrombus in the LA or LAA. When compared to the other 59 patients without LA dysfunction, they had larger LA dimension (40 +/- 6 mm vs 36 +/- 8 mm [+/- SD], p = 0.018) but did not differ significantly regarding the left ventricular (LV) chamber size, LV ejection fraction, mitral or tricuspid inflow, and ratio of the amplitude of the waves created by early diastolic filling and atrial contraction. We also analyzed the relationship between LA function and clinical risk factors for stroke, including hypertension, diabetes mellitus, coronary artery disease, age > 65 years, and prior cerebral vascular accident. LA dysfunction was found in 10 of 17 patients (59%) with three or more risk factors. The odds ratio for having LA dysfunction was 3.1 (p = 0.04; 95% confidence interval, 1.1 to 9.1) when compared with patients with less than three risk factors. CONCLUSIONS: LA dysfunction was present in more than one third of AF patients after satisfactory rhythm control for > 3 months. Patients with higher burden (three or more) of clinical risk factors were more likely to have impaired LA function.

Denaturing high-performance liquid chromatography screening of the long QT syndrome-related cardiac sodium and potassium channel genes and identification of novel mutations and single nucleotide polymorphisms.

Mutations in cardiac potassium and sodium channel genes are responsible for several hereditary cardiac arrhythmia syndromes. We established a denaturing high-performance liquid chromatography (DHPLC) protocol for rapid mutation screening of these genes, and reported mutations and variations identified by this method. We included 28 patients with Brugada syndrome, 4 with congenital long QT syndrome (LQTS), 11 with drug-induced LQTS, 4 with idiopathic ventricular fibrillation, and 50 normal volunteers. Polymerase chain reactions were performed to amplify the entire coding region of these genes. DHPLC was used to screen for heteroduplexes then DNA sequencing was performed. With this method, we identified the mutation(s) in all four patients with congenital LQTS (KCNQ1 A341V, KCNH2 N633D, KCNH2 2768Cdel and KCNE1 K70 N Y81C double mutations). We also identified the SCN5A A551T mutation in 1 of the 28 patients with Brugada syndrome. All the above-mentioned mutations were novel except KCNQ1 A341V. No mutations were identified in patients with drug-induced LQTS or idiopathic ventricular fibrillation. In total, 25 single nucleotide polymorphisms were identified, 10 of which were novel. In conclusion, DHPLC is a sensitive and rapid method for detection of cardiac sodium and potassium channel gene mutations.

Activation of the calcineurin-nuclear factor of activated T-cell signal transduction pathway in atrial fibrillation.

STUDY OBJECTIVES: The calcineurin-nuclear factor of activated T-cell (NFAT) signal transduction pathway regulates the expression of a plethora of genes in the myocardium. Cytosolic calcium overloading occurs in atrial fibrillation (AF), and this fulfills the condition needed for activation of this pathway. We therefore investigated the NFAT pathway in atrial tissue in a porcine model of AF. METHODS AND RESULTS: AF was induced in eight adult pigs by rapid atrial pacing. Investigations on the calcineurin and NFAT pathway were performed on transmural left atrial tissue obtained 6 weeks after implantation of the pacemaker (pacing for 4 weeks, and AF without pacing for 2 weeks). In the AF group, the left atrial dimension increased significantly (26 +/- 4 mm vs 31 +/- 4 mm, respectively, p < 0.05 [mean +/- SD]). Calcineurin enzyme activity increased significantly in pigs with AF (n = 8) when compared to control pigs (n = 6) [0.143 +/- 0.034 vs 0.038 +/- 0.063 mmol PO(4)(-) released, p < 0.01]. We found that both NFAT-c3 and NFAT-c4, the downstream effectors of calcineurin, increased significantly in the nuclei in AF tissue using immunoblotting. Translocation of NFAT-c3 and NFAT-c4 into the nuclei was also demonstrated in AF tissue microsections using immunohistochemistry. The electrophoresis mobility shift assay further demonstrated that nuclear extracts from AF tissue had a significantly larger binding capacity for NFAT-specific oligonucleotide probes. CONCLUSIONS: Our results demonstrate that calcineurin activity was increased in AF with subsequent NFAT-c3 and NFAT-c4 translocation into the nucleus. Activation of this signal transduction pathway may play an important role in the pathogenesis of AF.

Usefulness of single-bolus adenosine test for confirming sinus node dysfunction and correlation with atrial overdrive suppression test.

We prospectively studied 42 consecutive patients who had symptomatic sinus node dysfunction and 17 age-matched controls by measuring maximal and corrected maximal sinus node recovery times with an atrial overdrive suppression test and single-bolus adenosine administration (0.15 mg/kg). We found a positive correlation between the 2 methods, with reasonably good sensitivity, specificity, and predictive accuracy.

Use of double-potential barrier to identify functional isthmus at the cavotricuspid isthmus for facilitating catheter ablation of isthmus-dependent atrial flutter.

INTRODUCTION: The aim of the study was to identify an alternative target for more effective radiofrequency catheter ablation (RFCA) of isthmus-dependent atrial flutter (AFL). METHODS AND RESULTS: We hypothesized that a functional isthmus formed by preexisting double potential barrier at the cavotricuspid isthmus (CTI) could serve as a new target site for facilitating RFCA of AFL. Forty-three consecutive patients with recurrent isthmus-dependent AFL were studied using three-dimensional navigated magnetic mapping and ablation technique. Twenty patients (47%, group A) were shown to have a narrower functional channel at the CTI (functional isthmus). The remaining 23 patients did not have this feature (53%, group B). In group A, double potentials were clustered near the border of the inferior vena cava (IVC) of the CTI and served as a functional channel along the tricuspid annulus (TA). The interspike interval of double potentials was 87 +/- 26 ms near the IVC border and 45 +/- 17 ms (P < 0.0001) near the TA border of CTI. RFCA targeting at the functional isthmus in group A resulted in interruption of bidirectional transisthmus conduction with fewer radiofrequency pulses (6.7 +/- 4.7 in group A vs 21.1 +/- 17.1 pulses in group B, P < 0.001), shorter ablation line (11.6 +/- 4.0 mm vs 37.8 +/- 7.2 mm, P < 0.0001) with no arrhythmia recurrence. These functional isthmuses were found to be located at the lateral third of CTI in 12 patients, middle third in 7, and medial third in 1. This finding is different from that obtained by the conventional method in group B (lateral in 5, middle in 16, medial in 2, P < 0.038). CONCLUSION: In our study, a functional, rather than anatomic, isthmus formed by preexisting double-potential barrier at the CTI was identified in 47% of patients with isthmus-dependent AFL. It is a useful guide to facilitate RFCA of isthmus-dependent AFL.

Functional genomic study on atrial fibrillation using cDNA microarray and two-dimensional protein electrophoresis techniques and identification of the myosin regulatory light chain isoform reprogramming in atrial fibrillation.

INTRODUCTION: Functional and structural changes of atrial tissue occur during the natural course of atrial fibrillation (AF), and these changes may contribute to further AF. We investigated the changes in AF tissue using cDNA microarray and two-dimensional protein electrophoresis techniques. METHODS AND RESULTS: We established a porcine model of AF by rapid right atrial appendage pacing at a rate of 600/min. Atrial tissue was obtained after rapid atrial depolarization for 6 weeks. Microarrays containing 6,035 cDNA clones were used to evaluate the alterations of mRNA. Two-dimensional protein electrophoresis was performed to compare protein patterns. In cDNA microarray studies, we identified 387 genes with significant change in the left atrium and 81 genes in the right atrium. Among the genes, the ventricular isoform of the myosin regulatory light chain (MLC-2V) showed the greatest fold of change (9.4 and 7.3 in the left and right atrium, respectively). In protein electrophoresis, the expression levels of three protein spots spanning from 18 to 20 kDa in the acidic region (PI 4.5-5.0) were specifically elevated in the AF group. Interestingly, through tandem mass spectrometric analysis, these three spots were identified as MLC-2V. Thus, MLC-2V expression at the mRNA and protein levels corresponded well, and both indicated a significant increase in AF. CONCLUSION: Both cDNA microarray and two-dimensional polyacrylamide protein electrophoresis studies revealed characteristic changes in AF tissue. We demonstrated the reprogramming of myosin regulatory light chain isoform composition, with a significant increase of its ventricular isoform (MLC-2V).

Brugada syndrome--an under-recognized electrical disease in patients with sudden cardiac death.

In 1992, Brugada and Brugada described 8 patients with a history of aborted sudden death and a distinct ECG pattern of right bundle-branch block with ST segment elevation in leads V1-V3 and normal QT interval in the absence of any structural heart disease. It is called Brugada syndrome now and is believed to be responsible for 4-12% of all sudden deaths and around 20% of deaths in patients with structurally normal hearts. Although this syndrome is observed worldwide and the exact prevalence is unknown, it is more common in the Southeast Asian countries. Repeated syncope, ventricular fibrillation, and sudden cardiac death have been reported in patients with Brugada syndrome. The clinical presentation of Brugada syndrome is distinguished by a male predominance and the appearance of arrhythmic events at an average age of 40 years. The Brugada syndrome is inherited in an autosomal dominant manner with incomplete penetrance and an incidence ranging between 5 and 66 per 10,000. The surface ECG manifestations of the syndrome can transiently disappear, but can be unmasked by potent sodium channel blockers in some cases. Mutations of the cardiac sodium channel SCN5A have been detectable in <20% of patients with Brugada syndrome. Recent genetic studies have confirmed the genetic heterogeneity of the disorder. Antiarrhythmic drugs appear to be of little use in prolonging survival and in preventing recurrences of ventricular arrhythmias. To date, implantable cardioverter defibrillator remains the best therapy to prevent sudden death in these patients.

Review of catheter thrombectomy devices.

Acute massive pulmonary embolism (PE) is a frequently fatal event that causes significant compromise of hemodynamic stability. Unfortunately, mortality rates for PE have remained relatively constant despite advances in prophylactic and treatment measures. In addition to embolus size, symptom recognition for diagnosis and emergent treatment are two distinct factors that dictate survival. Treatment generally includes thrombolytic agents; however, not all patients are candidates for aggressive thrombolytic management. Development of catheter thrombectomy devices provides an alternative treatment modality for severe cases when thrombolytics are contraindicated. Catheter thrombectomy devices have undergone major advances over the last decade, but literature support of their success is limited.