Neural Activity and Ventricular Fibrillation

Bleich, Howard L.; Boro, Emily S.; Lown, Bernard; Verrier, Richard L.

doi:10.1056/nejm197605202942107

Cited by 589 publications

(29 citation statements)

References 21 publications

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“…Reductions in these time-domain HRV measures have been considered to reflect diminished vagal and/or increased sympathetic modulation of sinus node, and this interpretation is well in keeping not only with experimental studies on proarrhythmic effects of sympathetic activation (Lown and Verrier, 1976;Schwartz et al, 1992) but also with the capability of these measures in identifying patients with an increased cardiac mortality (Bigger et al, 1988;La Rovere et al, 2003). The power spectra were computed for the low-frequency band (LF, 0.04-0.15 Hz) as a measure of both sympathetic and parasympathetic function and for the high-frequency band (HF, 0.15-0.4 Hz) as a measure of parasympathetic function.…”

Section: Physiological Outcome Measuresmentioning

confidence: 61%

Altered cardiorespiratory coupling in young male adults with excessive online gaming

Chang

Kim

Jung

et al. 2015

Biological Psychology

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Section: Physiological Outcome Measuresmentioning

confidence: 61%

Altered cardiorespiratory coupling in young male adults with excessive online gaming

Chang

Kim

Jung

et al. 2015

Biological Psychology

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“…52 Normal cardiac mechanical and electrical function results from a balance of sympathetic and parasympathetic tone. In the setting of cardiac disease, this balance may be disrupted; sympathoexcitation can precipitate VT/VF and parasympathetic activation can be protective.…”

Section: Risk Stratification In Left Ventricular Dysfunction and Amentioning

confidence: 99%

Sudden Cardiac Death Risk Stratification

Deyell

Krahn

Goldberger

2015

Circulation Research

106

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Arrhythmic sudden cardiac death (SCD) may be due to ventricular tachycardia/fibrillation (SCD-VT/VF) or pulseless electrical activity/asystole. Effective risk stratification to identify patients at risk of arrhythmic SCD is essential for targeting our health care and research resources to tackle this important public health issue. Although our understanding of SCD due to pulseless electrical activity/asystole is growing, the overwhelming majority of research in risk stratification has focused on SCD-VT/VF. This review focuses on existing and novel risk stratification tools for SCD-VT/VF. For patients with left ventricular dysfunction and/or myocardial infarction, advances in imaging, measures of cardiac autonomic function, and measures of repolarization have shown considerable promise in refining risk. Yet the majority of SCD-VT/VF occurs in patients without known cardiac disease. Biomarkers and novel imaging techniques may provide further risk stratification in the general population beyond traditional risk stratification for coronary artery disease alone. Despite these advances, significant challenges in risk stratification remain that must be overcome before a meaningful impact on SCD can be realized.

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“…It has been shown that diabetic subjects with alterations of cardiac sympathetic innervation, tone, and/or responsiveness exhibit abnormal myocardial blood flow regulation 55-60 , which may increase mortality associated with myocardial ischemia. Regional cardiac sympathetic imbalance may promote malignant arrhythmogenesis and cardiac death, particularly when accompanied by reduced parasympathetic tone and myocardial ischemia 61-63 . Consequently, sudden cardiac death is the ultimate severe clinical consequence of cardiac autonomic neuropathy and is the single greatest cause of mortality in CKD patients on dialysis 9 .…”

Section: Cardiac Autonomic Neuropathymentioning

confidence: 99%

The Management of Diabetic Neuropathy in CKD

Pop‐Busui

Roberts

Pennathur

et al. 2010

American Journal of Kidney Diseases

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Case Presentation A 64-year-old male with a 15-year history of poorly controlled type 2 diabetes and a 10-year history of hypertension and hyperlipidemia had developed multiple diabetes-related complications within the last 5 years. He first developed albuminuria 5 years ago, and over the next several years experienced fairly rapid decline in kidney function, with eGFR of 55 mL/min/1.73m2 noted 2 years ago. He was diagnosed with proliferative retinopathy 5 years ago and underwent laser photocoagulation. Four years ago, he noted symptoms of peripheral neuropathy manifested as shooting pain and numbness with loss of light touch, thermal and vibratory sensation in a stocking distribution. Last year he developed a non-healing ulcer on the plantar aspect of his left foot which was complicated with gangrene and resulted in a below-the-knee amputation of the left leg one year ago. He now reports a new onset of weakness, lightheadedness and dizziness on standing that affects his daily activities. He reports lancinating pain in his right lower extremity, worse in the evening. Medications include: neutral protamine Hagedorn insulin twice daily and regular insulin on a sliding scale, metoprolol 50 mg/d, lisinopril 40 mg/d, atorvastatin 80 mg/d, furosemide 40 mg/d and aspirin 81 mg/d. Blood pressure is 127/69 mm Hg with a pulse rate of 96 bpm while supine and 94/50 mmHg with a pulse rate of 102 bpm while standing. Strength is normal but with a complete loss of all sensory modalities to the knee in his remaining limb and up to the wrists in both upper extremities, and he is areflexic. Today's laboratory evaluations show a serum creatinine of 2.8 mg/dl, an estimated GFR (eGFR) of 24 ml/min/1.73m2, a hemoglobin A1c (HbA1c) of 7.9 % and 2.1 g of urine protein per gram of creatinine. What would be the most appropriate management for this patient?

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Neural Activity and Ventricular Fibrillation

Cited by 589 publications

References 21 publications

Altered cardiorespiratory coupling in young male adults with excessive online gaming

Altered cardiorespiratory coupling in young male adults with excessive online gaming

Sudden Cardiac Death Risk Stratification

The Management of Diabetic Neuropathy in CKD

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