A prospective study on the prevalence of neurally mediated hypotension in systemic lupus erythematosus

<p class="abstract"><strong>Background:</strong> Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease which affects skin and organ systems. Cardiovascular manifestations are one of the important cause for mortality and morbidity in SLE. Neurally mediated hypotension (NMH) caused by autonomic neuropathy is found to be associated with fibromyalgia responsible for chronic fatigue syndrome in SLE. Our study aims to find the prevalence of NMH in SLE.</p><p class="abstract"><strong>Methods:</strong> This is a prospective study conducted in the Department of Dermatology, Chengalpattu Medical College from May 2017 to December 2018. All SLE patients who attended the Dermatology OPD were included in the study. The diagnosis of SLE was made based on the ARA criteria. After obtaining informed consent, baseline blood pressure of all patients included in the study were recorded. In patients with low blood pressure other causes of hypotension were ruled out. Patients with no discernible cause of hypotension were subjected to the two stage tilt table test. A drop in systolic BP of &gt;20 mm of Hg or diastolic BP of &gt;10 mm of Hg is considered to be positive.<strong></strong></p><p class="abstract"><strong>Results:</strong> A total of 20 patients were included in the study, of which 19 were female and one male. The mean age was 31.7 years. 70% of the SLE patients included in our study were found to have NMH.</p><p><strong>Conclusions:</strong> Neurally Mediated Hypotension was found to be highly prevalent in SLE.</p>

Failure of propranolol to prevent tilt-evoked systemic vasodilatation, adrenaline release and neurocardiogenic syncope

In patients with neurocardiogenic syncope, head-up tilt often evokes acute loss of consciousness accompanied by vasodilatation, increased plasma adrenaline and systemic hypotension. Since hypotension increases adrenaline levels and adrenaline can produce skeletal muscle vasodilatation by activating β2 receptors, adrenaline might induce a positive feedback loop precipitating circulatory collapse. We hypothesized that propranolol, a non-selective β-blocker, would prevent adrenaline-induced vasodilatation and thereby prevent syncope. Eight subjects with recurrent neurocardiogenic syncope and previously documented tilt-induced syncope with elevated plasma adrenaline levels participated in the present study. Subjects underwent tilt table testing after receiving oral propranolol or placebo in a double-blind randomized crossover fashion. Haemodynamic and neurochemical variables were measured using intra-arterial monitoring, impedance cardiography, arterial blood sampling and tracer kinetics of simultaneously infused [3H]noradrenaline and [3H]adrenaline. The occurrence of tilt-induced neurally mediated hypotension and syncope, duration of tilt tolerance, extent of the decrease in SVRI (systemic vascular resistance index) and magnitude of plasma adrenaline increases did not differ between the propranolol and placebo treatment phases. SVRI was inversely associated with fractional increase in plasma adrenaline during both phases. One subject did not faint when on propranolol; this subject's response is discussed in the context of central effects of propranolol. In this small, but tightly controlled, study, propranolol did not prevent tilt-induced vasodilatation, syncope or elevated plasma adrenaline.