Search

Aims: This report aims to present a concise overview and synthesis of current research findings regarding paternal depression in the perinatal period.Methods: A literature search was conducted, primarily via PubMed and PsychNET, for English-language research studies and meta-analyses using combinations of the terms 'perinatal', 'pregnancy', 'postpartum', 'depression' AND 'fathers' OR 'paternal'. Peer-reviewed articles were considered, and a representative sample of literature, with an emphasis on recent publications from a broad range of populations was summarized for each of the following sub-sections: prevalence, risk factors, impact on the infant/child, and healthcare costs.Results: Reported prevalence has ranged from 2.3% to 8.4%, with a significant degree of heterogeneity in rates, due to differences in multiple aspects of the methodology (timing, instruments, etc.). Nevertheless, rates of maternal depression remain higher than paternal depression, and higher rates of one are associated with higher rates of the other. The primary risk factors for paternal depression are maternal depression and the father's history of severe depression, or symptoms of depression or anxiety prenatally. Biological mechanisms may underlie paternal depression, with changes reported in testosterone, cortisol and prolactin levels during this period. Paternal depression has been related to children's behavioral, emotional and social function at 36 months and psychiatric disorders at 7 years, adjusting for maternal depression. Healthcare costs may also be impacted by paternal postpartum depression, with higher father-child dyad costs found after controlling for potential confounders.Conclusions: Focusing on fathers' emotional well-being in the perinatal period is important in itself, as well as for their wives and children. Programs recommending screening for maternal perinatal mood and anxiety disorders should include inquiry regarding the father's emotional state, and if his distress is reported it should be clarified and followed-up by support and intervention as necessary. [ABSTRACT FROM AUTHOR]

Intravascular imaging provides new insights into the condition of vessel walls. This is crucial for cerebrovascular diseases including stroke and cerebral aneurysms, where it may present an important factor for indication of therapy. In this work, we provide new information of cerebral artery walls by combining ex vivo optical coherence tomography (OCT) imaging with histology data sets. To overcome the obstacles of deflated and collapsed vessels due to the missing blood pressure, the lack of co-alignment as well as the geometrical shape deformations due to catheter probing, we developed the new image processing method virtual inflation. We locally sample the vessel wall thickness based on the (deflated) vessel lumen border instead of the vessel's centerline. Our method is embedded in a multi-view framework where correspondences between OCT and histology can be highlighted via brushing and linking yielding OCT signal characteristics of the cerebral artery wall and its pathologies. Finally, we enrich the data views with a hierarchical clustering representation which is linked via virtual inflation and further supports the deduction of vessel wall pathologies. [ABSTRACT FROM AUTHOR]

This multicenter, randomized, double-blind, parallel group, placebo lead-in, placebo-controlled study compared the antianginal and anti-ischemic effects of once-daily bedtime dosing of controlled-onset extended-release (COER-24) verapamil to a once-daily morning dosing of amlodipine +/- atenolol in patients with chronic stable angina. A total of 551 patients with exercise-induced myocardial ischemia and evidence of coronary artery disease were randomized to a 4-week, forced-dose titration treatment period with (1) COER-24 verapamil 240 mg titrated to 480 mg at bedtime (n = 173), (2) amlodipine 5 mg titrated to 10 mg/day (n = 149), (3) amlodipine 5 mg (titrated to 10 mg) plus atenolol 50 mg/day in the A.M. (n = 154), or (4) placebo (n = 75). Treadmill exercise tolerance testing (standard Bruce protocol), and 48-hour ambulatory electrocardiographic (Holter) monitoring were performed at the end of placebo lead-in and double-blind treatment. Each active treatment significantly improved symptom-limited exercise duration and time to moderate angina (p < or = 0.01 vs placebo). For patients with baseline ischemia, amlodipine resulted in a statistically significant increase in total duration of ischemic episodes compared with placebo, whereas COER-24 verapamil and amlodipine plus atenolol resulted in statistically significant decreases compared with placebo and amlodipine. Heart rate at onset of ischemic episodes and ST product were also significantly increased with amlodipine (p < 0.05) compared with either COER-24 or amlodipine plus atenolol. COER-24 and amlodipine alone or in combination with atenolol improved exercise capacity in patients with angina pectoris. COER-24 verapamil monotherapy or amlodipine plus atenolol combination therapy were more effective than amlodipine monotherapy in decreasing ambulatory myocardial ischemia, especially during the hours of 6 A.M. to 12 noon. [ABSTRACT FROM AUTHOR]