Summary Introduction Recent evidence implicates a cholinergic anti-inflammatory pathway. Because vagus nerve activity mediates some heart rate variability (HRV), this qualitative review examines the literature concerning circulating cytokines and HRV in cardiovascular function in humans. This qualitative review examines the literature concerning circulating cytokines and HRV in cardiovascular function in humans. Methods Thirteen studies on HRV, inflammation, and cardiovascular function were located by electronic library search and descriptively reviewed. Results The relationship between HRV and inflammation was studied in healthy controls, patients with acute or stable coronary heart disease (CHD), patients with metabolic syndrome or impaired glucose tolerance and patients with kidney failure. Investigations focused mainly on lnterleukin-6 (IL-6) and C-reactive peptide (CRP). The majority of reviewed studies reported that parasympathetic nervous system tone as inferred from heart rate variability is inversely related to inflammatory markers (r values between −0.2 and −0.4). The relationships with inflammatory markers were similar whether derived from ECG signals as short as 5–30 min or from 24-h ECG readings for HRV analyses. While inflammatory markers appear to be related to HRV, it is a mistake to assume that the traditional “vagal measures” of HRV (such as high frequency heart rate variability) are the driving factors. Indeed, low frequency heart rate variability, a complex measure reflecting both parasympathetic and sympathetic activity, is the more commonly associated measure linked to inflammatory markers. Discussion Heart rate variability is inversely correlated with inflammatory markers in healthy individuals as well as in those with cardiovascular diseases.

The prevalence, clinical presentation, and risk factors for hyperlactatemia among patients receiving antiretroviral therapy was determined during a 1-month period for patients in the Swiss HIV Cohort Study. Overall, 73 (8.3%) of 880 patients presented an increase in serum lactate of >1.1 times the upper normal limit (UNL). For 9 patients (1%), lactate elevation was moderate or severe (>2.2 times the UNL). Patients who presented with hyperlactatemia were more likely to be receiving stavudine with or without didanosine (odds ratio, 2.7; 95% confidence interval, 1.5-4.8), as compared with patients who received zidovudine-based regimens. The risk increased with increasing time receiving stavudine with or without didanosine. The association between hyperlactatemia and stavudine with or without didanosine was not biased by these medications being more recently available and, therefore, being given preferentially to patients who had prolonged use of nucleoside analog reverse-transcriptase inhibitors. Hyperlactatemia was associated with lipoatrophy, hyperlipidemia, and hyperglycemia. Age, sex, or stage of infection with human immunodeficiency virus were not predictive of hyperlactatemia. Determination of lactate levels may prove useful in the screening for mitochondrial toxicity.

We prospectively assessed the 1-month prevalence of abnormal body fat distribution in HIV-infected individuals. Of 1,359 patients treated with antiretroviral drugs, 578 (43%) had signs of abnormal fat distribution. Peripheral fat loss was observed in 382 patients (28%), whereas 412 (30%) had signs of fat accumulation. The presence of lipodystrophy (peripheral fat loss with or without fat accumulation) was found to be independently associated with increasing age (less than 35 years of age as a reference group: 35 to 41 years of age, OR = 1.5 [95% CI, 1.1-2.3]; and older than 41 years of age, OR = 2.4 [95% CI, 1.7-3.5]), current use of stavudine (OR = 2.4 [95% CI, 1.8-3.3]), current use of abacavir (OR = 2.1 [95% CI, 1.3-3.4]), and elevated lactate level (OR = 1.6 [95% CI, 1.1-2.4]). The prevalence of lipodystrophy was higher among patients who had received stavudine for a longer period (no stavudine in the current combination as a reference group: <6 months, OR = 1.1 [95% CI, 0.6-1.8]; 6-24 months, OR = 2.4 [95% CI, 1.7-3.5]; and >24 months, OR = 3.2 [95% CI, 2.4-4.3]). This study confirms the association between the use of stavudine and lipodystrophy.

Obstructive sleep apnea (OSA) is a common disease with significant medical and psychiatric comorbidities. The literature documenting the effects of continuous positive airway pressure (CPAP) treatment on mood in OSA patients is mixed. We previously observed that 1 week of CPAP treatment did not result in improvements in mood beyond those observed in a group treated with placebo-CPAP. This study examined the effect of a 2 week CPAP treatment on mood in a placebo-controlled design in OSA patients. Fifty patients with untreated sleep apnea were evaluated by polysomnography and completed the Profile of Mood States (POMS) pre-/post-treatment. The patients were randomized for 2 weeks to either therapeutic CPAP or placebo-CPAP (at insufficient pressure). Both the therapeutic CPAP and the placebo-CPAP groups showed significant improvements in POMS total score, tension, fatigue, and confusion. No significant time × treatment effect was observed for either group. We could not show a specific beneficial impact of CPAP treatment on mood in OSA patients.