Thyroid hormone treatment in the management of treatment-resistant unipolar depression: a systematic review and meta-analysis.

BACKGROUND: Treatment with thyroid hormones is occasionally used in the management of treatment-resistant depression. However, the evidence supporting this treatment is not fully established. The aim of this study was to systematically review the literature on the effect of adjunctive thyroid hormone in the management of treatment-resistant unipolar depression and to provide a pooled estimate of its efficacy. METHODS: The study is registered with PROSPERO (reg. no. CRD42018108088) and followed the PRISMA guidelines. Searches were carried out on June 24, 2019, in PubMed, EMBASE, and PsycINFO. Each record was screened independently by at least two reviewers. In instances of discrepancies, consensus was reached upon discussion. Pooled efficacy estimates were calculated based on response rates (decrease of ≥50% on the primary outcome measure) using random effect statistics. RESULTS: The search yielded 1355 records. Based on the screening of these records, we identified 10 studies that met the inclusion criteria (total number of patients = 663). The comparison of response to thyroid hormones vs. placebo resulted in an odds ratio of 1.56 (95% CI: 0.50-4.84). Similarly, the comparison of response to thyroid hormones vs. lithium resulted in an odds ratio of 1.91 (95% CI: 0.85-4.26). Thus, adjunctive therapy with thyroid hormones was not superior to placebo or lithium in the management of treatment-resistant unipolar depression. CONCLUSION: According to this review and meta-analysis, there is not sufficient evidence to support the use of adjunctive thyroid hormones for treatment-resistant unipolar depression.

Peripheral flow response to transient arterial forearm occlusion does not reflect myocardial perfusion reserve.

BACKGROUND: Ultrasonographic evaluation of systemic arterial function is widely available, and a close relation of endothelial function in the coronary and brachial arteries has been documented. It is unknown, however, whether a similar correlation exists for their 2 microcirculatory territories and thus whether assessment of the systemic microcirculation can be used similarly as a surrogate marker of myocardial perfusion. METHODS AND RESULTS: Twenty-three patients with documented coronary artery disease (CAD; 66+/-9 years old, 18 men), 16 patients with syndrome X (SX; 56+/-5 years old, 13 women), and 45 healthy control subjects (C; 34+/-9 years old, 22 men) were studied. Myocardial perfusion was measured at rest and after dipyridamole (0.56 mg. kg(-1). min(-1) over 4 minutes) by PET, and brachial artery blood flow was measured at rest and after transient forearm ischemia by standard Doppler ultrasound techniques. Dipyridamole increased myocardial perfusion in all groups (mL. g(-1). min(-1): CAD, 0.89+/-0.27 versus 1.62+/-0.67, P:<0.001; SX, 0.82+/-0.16 versus 1.67+/-0.49, P:<0.001; and C, 0.82+/-0.15 versus 2.32+/-0.64, P:<0.001). Postocclusion forearm flow increased similarly in all groups (CAD, 52+/-18 versus 174+/-77 mL/min, P:<0.001; SX, 49+/-29 versus 202+/-82 mL/min, P:<0.001; and C, 61+/-34 versus 229+/-108 mL/min, P:<0.001). No significant correlations were found between peripheral and myocardial microcirculatory beds for either resting flow, hyperemic flow, or flow reserve in any of the groups (r(2)<0.1, P:=NS). CONCLUSIONS: The peripheral perfusion responses to transient forearm ischemia do not correlate with dipyridamole-induced myocardial hyperemia. The lack of correlation indicates different mechanisms of microvascular activation or regulation and confirms that extrapolations between findings in the 2 vascular beds are not suitable.

Altered regulation of the myocardial microcirculation in young smokers.

Smoking is known to affect microcirculatory function in a middle-aged population. However, the effects of smoking on myocardial perfusion in young smokers have not been studied. Myocardial perfusion was measured in 15 smokers (24 +/- 2 years) and 15 nonsmokers (24 +/- 3 years) using positron emission tomography. Myocardial perfusion was measured at rest, during cold stress and during dipyridamole. Resting myocardial blood flow was similar in the two groups. The well-described correlation between rate-pressure product and myocardial blood flow was present only in the nonsmokers (r(2) = 0.61, p < 0.001). Myocardial blood flow corrected for the rate-pressure product declined during cold by 20% in the smokers [1.11 +/- 0.28 vs. 0.92 +/- 0.20 ml x g(-1) x min(-1) (p = 0.012)], but remained unchanged in nonsmokers [1.11 +/- 0.25 vs. 1.09 +/- 0.30 ml x g(-1) x min(-1) (p = NS)]. Dipyridamole-induced hyperemia was similar in the two groups [2.23 +/- 0.78 vs. 2.42 +/- 0.65 ml x g(-1) x min(-1) (p = NS)]. In conclusion, smoking induces abnormalities in myocardial microcirculatory regulation in young otherwise healthy smokers. The coronary flow reserve, however, is not significantly altered.

Evaluation of regional myocardial perfusion in patients with severe left ventricular dysfunction: comparison of 13N-ammonia PET and 99mTc sestamibi SPECT.

OBJECTIVE: Positron emission tomography (PET) scanning with 13N-ammonia and 18FDG is well established for the detection of myocardial viability. Due to the limited availability of PET facilities, recent studies have combined technetium 99m sestamibi single photon emission computed tomography (SPECT) with 18FDG PET or 18FDG SPECT. This approach enables simultaneous assessment of regional myocardial blood flow and metabolism and substantially increases the capacity for viability detection. To validate whether 99mTc-Sestamibi SPECT can replace 13N-ammonia PET, we compared these two modalities in patients with severe left ventricular dysfunction due to coronary artery disease. MATERIALS AND METHODS: Thirty-one patients (mean age 57+/-8 years; mean ejection fraction 27%+/-8%) with angiographically verified coronary artery disease were included. In random order, ammonia-PET and sestamibi-SPECT scans were performed. In a 20-segment model of the left ventricle, two blinded observers scored a total of 610 segments on a five-point scale. In a subset of 20 patients, 400 segments were scored twice to evaluate the observer variations of the two techniques. Segmental score differences were used to compare the imaging modalities. The impact on viability detection was assessed by combining the two flow tracers with FDG PET. RESULTS: Segmental comparison of the PET and SPECT studies yielded similar (difference < or = 1) results in 74% of segments, reflecting regional concordance values in the lateral, apical, anterior, septal, and inferior myocardial walls of 86%, 82%, 71%, 66%, and 63%, respectively. The differences in the septal and inferior walls were primarily due to overestimation of perfusion defects by sestamibi SPECT, which yielded a higher proportion of mismatch patterns in those regions. The overall observer variations of the PET and SPECT studies were 7.5% and 5.8%. CONCLUSION: Myocardial perfusion imaging with 13N-ammonia PET and 99mTc-sestamibi SPECT yielded similar results in patients with severe left ventricular dysfunction, except for the septal and inferior regions. In these regions, SPECT tended to overestimate perfusion defects. Hence, attenuation correction should be considered when combining FDG PET and sestamibi SPECT for diagnosing myocardial viability to avoid overestimation of mismatch patterns in those regions.

Studies of multilayers and thin-foil x-ray mirrors using a soft x-ray diffractometer.

A versatile x-ray diffractometer is described in detail. Two applications to the study of x-ray optical elements are presented. The first is a Bragg reflection study of state-of-the-art multilayers deposited both on conventional Si-wafer substrates and on superpolished substrates such as fused quartz and electroless nickel. These data are compared to data previously obtained at FeKα. The second study is a reflectivity and scattering study of various thin-foil x-ray reflectors proposed for up-coming x-ray satellite missions. All the data have been obtained at MgKα = 1.2536 keV.