All is not lost, when lead goes in the wrong direction

Left sided superior vena cava (SVC) is an uncommon anomaly noted in the general population. It adds complexity to the procedure, when attempting to place pacing or defibrillator devices into the heart. Here we report a case where the leads were placed through the left sided SVC into the right sided chambers giving an interesting X-ray appearance

Ventricular Arrhythmia Discriminator Programming and the Impact on the Incidence of Inappropriate Therapy in Patients with Implantable Cardiac Defibrillators

Background: The incidence of inappropriate therapy from implantable cardioverter defibrillators (ICDs) has been reduced by programming ventricular arrhythmia discriminators (VAD) on at the time of implant. Objective: To determine which VAD is most effective in preventing inappropriate therapy.Methods and Results: Dual chamber ICD (n=48) or cardiac resynchronization therapy defibrillator (CRT-D) (n=55) implantation was performed in 103 patients (M=94, F=9). Patients were followed prospectively for therapy events (shock or anti-tachycardia pacing) for a mean 362±289 days. Events were correlated with clinical characteristics and VAD programming. Of the 103 pts followed, 11 received inappropriate therapy (IT), 15 received appropriate therapy (AT), and 77 received no therapy (NT). In the AT and IT groups, a total of 207 events (ATP=171, shock=36) were observed. A total of sixty-four electrograms (EGMs) were analyzed. Programming VADs "ON" versus "OFF" reduced the incidence of IT events compared to those receiving AT or NT events (p<.01), with a trend in fewer patients receiving IT (31.3% "ON" vs 55.6% "OFF", p = 0.131). Programming atrial fibrillation (AF) detection ON resulted in fewer patients receiving IT compared to those receiving AT or NT (3.6% vs 19%, p<.05). Furthermore, programming AF or AFL algorithms "ON", resulted in overall fewer episodes of IT therapy (p<.01). Conclusions: AF or AFL discriminators significantly reduced the incidence of IT, and were predominantly responsible for the benefits from VAD programming observed in this study. Activating these features as part of routine ICD or CRT-D programming may provide a simple and effective alternative to the use of more complex and multiple VAD strategies

Sarcoidosis And Atrial Fibrillation: A Rare Association And Interlink With Inflammation

We report a case of sarcoidosis presenting initially as atrial fibrillation(AF). His response to anti-arrhythmic treatment strategy was suboptimal. On initiation of immunosuppressive therapy, AF was better controlled. This interesting case highlights a likely link between inflammation and pathogenesis of atrial fibrillation

Cardiovascular Problems in the Fragile X Premutation.

There is a dearth of information about cardiovascular problems in fragile X premutation carriers who have 55-200 CGG repeats in fragile X mental retardation 1 (FMR1) gene. The FMR1 expansion in the premutation range leads to toxic RNA gain-of-function resulting in cellular dysregulation. The mechanism of RNA toxicity underlies all of the premutation disorders including fragile X-associated tremor/ataxia syndrome, fragile X-associated primary ovarian insufficiency, and fragile X-associated neuropsychiatric disorder. Cardiovascular problems particularly autonomic dysfunction, hypertension, and cardiac arrhythmias are not uncommon in premutation carriers. Some arterial problems and valvular heart diseases have also been reported. This article reviews cardiovascular problems in premutation carriers and discusses possible contributing mechanisms including RNA toxicity and mild fragile X mental retardation protein deficiency. Further research studies are needed in order to prove a direct association of the cardiovascular problems in fragile X premutation carriers because such knowledge will lead to better preventative treatment

Cardiovascular Problems in the Fragile X Premutation.

There is a dearth of information about cardiovascular problems in fragile X premutation carriers who have 55-200 CGG repeats in fragile X mental retardation 1 (FMR1) gene. The FMR1 expansion in the premutation range leads to toxic RNA gain-of-function resulting in cellular dysregulation. The mechanism of RNA toxicity underlies all of the premutation disorders including fragile X-associated tremor/ataxia syndrome, fragile X-associated primary ovarian insufficiency, and fragile X-associated neuropsychiatric disorder. Cardiovascular problems particularly autonomic dysfunction, hypertension, and cardiac arrhythmias are not uncommon in premutation carriers. Some arterial problems and valvular heart diseases have also been reported. This article reviews cardiovascular problems in premutation carriers and discusses possible contributing mechanisms including RNA toxicity and mild fragile X mental retardation protein deficiency. Further research studies are needed in order to prove a direct association of the cardiovascular problems in fragile X premutation carriers because such knowledge will lead to better preventative treatment