Cervical vagal nerve stimulation activates the stellate ganglion in ambulatory dogs.

BACKGROUND AND OBJECTIVES: Recent studies showed that, in addition to parasympathetic nerves, cervical vagal nerves contained significant sympathetic nerves. We hypothesized that cervical vagal nerve stimulation (VNS) may capture the sympathetic nerves within the vagal nerve and activate the stellate ganglion. MATERIALS AND METHODS: We recorded left stellate ganglion nerve activity (SGNA), left thoracic vagal nerve activity (VNA), and subcutaneous electrocardiogram in seven dogs during left cervical VNS with 30 seconds on-time and 30 seconds off time. We then compared the SGNA between VNS on and off times. RESULTS: Cervical VNS at moderate (0.75 mA) output induced large SGNA, elevated heart rate (HR), and reduced HR variability, suggesting sympathetic activation. Further increase of the VNS output to >1.5 mA increased SGNA but did not significantly increase the HR, suggesting simultaneous sympathetic and parasympathetic activation. The differences of integrated SGNA and integrated VNA between VNS on and off times (ΔSGNA) increased progressively from 5.2 mV-s {95% confidence interval (CI): 1.25-9.06, p=0.018, n=7} at 1.0 mA to 13.7 mV-s (CI: 5.97-21.43, p=0.005, n=7) at 1.5 mA. The difference in HR (ΔHR, bpm) between on and off times was 5.8 bpm (CI: 0.28-11.29, p=0.042, n=7) at 1.0 mA and 5.3 bpm (CI 1.92 to 12.61, p=0.122, n=7) at 1.5 mA. CONCLUSION: Intermittent cervical VNS may selectively capture the sympathetic components of the vagal nerve and excite the stellate ganglion at moderate output. Increasing the output may result in simultaneously sympathetic and parasympathetic capture.

Best clinical trials reported in 2010.

Each year, a number of clinical trials emerge with data sufficient to change clinical practice. Determining which findings will result in practice change and which will provide only incremental benefit can be a dilemma for clinicians. The authors review selected clinical trials reported in 2010 in journals, at society meetings, and at conferences, focusing on those studies that have the potential to change clinical practice. This review offers 3 separate means of analysis: an abbreviated text summary, organized by subject area; a comprehensive table of relevant clinical trials that provides a schematic review of the hypotheses, interventions, methods, primary end points, results, and implications; and a complete bibliography for further reading as warranted. It is hoped that this compilation of relevant clinical trials and their important findings released in 2010 will be of benefit in the everyday practice of cardiovascular medicine.

Causes and management of drug-induced long QT syndrome.

Long QT syndrome (LQTS) is characterized by inherited or acquired prolonged QT interval on the surface electrocardiogram. This can lead to torsade de pointes ventricular tachycardia (TdP VT) and ventricular fibrillation. In the acquired form of the disease, medications from several classes can cause TdP VT or potentiate the electrocardiographic findings. These include class IA and III antiarrhythmics, antibiotics (macrolides and quinolones), antidepressants (tricyclics and selective serotonin reuptake inhibitors), antipsychotics (haloperidol and phenothiazines), and antiemetics (ondansetron and prochlorperazine). We present four cases of drug-induced LQTS resulting in life-threatening cardiac arrhythmias. Antiarrhythmic medications were the cause in two cases, and the other two cases involved noncardiac medications. All four patients had at least one risk factor for LQTS in addition to the offending drug, including female gender, hypokalemia, hypomagnesemia, and bradycardia. In one patient, amiodarone was administered for treatment of VT, although the correct diagnosis was actually TdP VT. In patients with polymorphic VT or ventricular fibrillation without a significant history of cardiovascular disease, drug-induced LQTS should be high in the differential diagnosis. Prompt diagnosis is key, as amiodarone, while often used to suppress VT, is potentially harmful in the setting of LQTS and TdP VT.

Problems of nonadherence in cardiology and proposals to improve outcomes.

At least 1 in 7 cardiology patients now reports nonadherence to prescribed medications, potentially leading to negative outcomes across a broad range of cardiovascular diseases. This nonadherence can begin as early as the time of prescription or any time thereafter and occurs for a variety of reasons, including communication difficulties, polypharmacy, and a variety of objective and perceived side-effects. Among elderly, low-income, and disabled patients, drug costs represent a growing source of medication nonadherence and can be markedly reduced through the use of drug assistance programs and low-cost generic medications without sacrificing evidence-based therapy. Depression also contributes strongly to nonadherence and is widely prevalent in cardiovascular populations. Improvements in depression are mirrored by improvements in adherence. A systematic screening to identify the presence of nonadherence and many of its causes can be accomplished with minimal impact on visit length. In conclusion, once specific concerns are recognized, options frequently exist to help patients and providers address many of the most common difficulties.