Background: The current study aims at assessment of heart rate variability among children and adolescents with childhood anxiety disorder, using the case-control design. Materials and Methods: The study was carried out at a tertiary care multispecialty hospital. It included 34 children and adolescents with diagnosis of childhood anxiety disorder, in the age range of eight to eighteen years, and 30 age- and sex-matched healthy controls. Heart-rate variability was studied using the standard protocol. Results: Significantly reduced variability of the heart rate was observed in both the time as well as frequency domains in the disorder group as compared to the control group. These findings indicate decreases in the sympathetic and parasympathetic activity in the disorder group, thus representing diminished physiological variability at rest. Conclusions: The notion of autonomic inflexibility, as seen in the current study, has important implications for stability in biological systems. The loss of variability in the physiological systems in general, and in the cardiovascular system in particular, has an association with a number of diseases and dysfunctions.

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Diabetic retinopathy (DR) is one of the most common complications of diabetes and is a leading cause of blindness in people of the working age in Western countries. A major pathology of DR is microvascular complications such as non-perfused vessels, microaneurysms, dot/blot hemorrhages, cotton-wool spots, venous beading, vascular loops, vascular leakage and neovascularization. Multiple mechanisms are involved in these alternations. This review will focus on the role of inflammation in diabetic retinal microvascular complications and discuss the potential therapies by targeting inflammation.

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Background: To investigate the contribution of right ventricular (RV) pacing sites to the cardiac function, this study compares plasma B-type natriuretic peptide (BNP) levels during RV septal and apical pacing in patients implanted with a pacemaker. Materials and Methods and Results: Seventy-four consecutive patients with indication for permanent pacing were included. To provide for the possibility of appropriate subgroup analyses, patients were stratified according to their pacing mode into two groups: Those with dual chamber DDD(R)/VDD pacemakers (41 patients, mean age 54.1±18.4 years), and those with single chamber VVI pacemakers (33 patients, mean age 60.6±18.4 years). A prospective single-blinded randomized design was used. Randomization (1:1 way) was between lead placement on the RV septum or RV apex and occurred during the implant in both groups. Compared to baseline, a significant decrease in BNP (429.8±103 pg/ml and 291.7±138 pg/ml, respectively) levels was observed during DDD(R) /VDD pacing after two months. In contrast, during VVI (R) pacing, a significant increase in BNP levels was observed (657.5±104 pg/ml and 889.5±139 pg/ml, respectively). To determine the impact of pacing sites on cardiac function, we assessed the changes in BNP levels in each group separately. Despite the significant difference in the pattern of changes between the two groups (P < 0.02), no significant changes were observed within groups regarding the acute effect of the pacing site (RV apex vs. RV septal) on BNP levels (P=NS). Conclusions: Our main result showed no significant differences between pacing sites and concluded that hemodynamic improvement could be substantially influenced by pacing mode, more than by pacing site.

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Chronic short sleep duration has been linked to endothelial dysfunction and increased risk of cardiovascular disease. Circulating endothelial progenitor cells (EPCs) are vital to endogenous vascular repair processes and cardiovascular health. We tested the hypothesis that habitual short sleep duration is associated with impairment in EPC number and function. Cells with phenotypic EPC characteristics were isolated from 37 healthy, sedentary adults: 20 with normal sleep duration (13M/7F; age: 59±1 years; sleep duration: 7.7±0.1 h/night) and 17 with short sleep duration (9M/8F; 56±2 years; 6.0±0.2 h/night). EPC number was assessed by flow cytometric analysis of the percentage of peripheral blood mononuclear cells negative for CD45 and positive for CD34, VEGFR-2, and CD133 antigens. EPC colony-forming capacity was determined by colony-forming unit (CFU) assay; migration by Boyden chamber; and intracellular caspase-3 concentrations by immunoassay. There were no significant differences between groups in EPC number (0.001±0.0004 vs. 0.001±0.0003 %), colony-forming capacity (6.1±1.5 vs. 5.4±1.7 CFUs), or migration to VEGF (1410.1±151.2 vs. 1334.3±111.1 AU). Furthermore, there were no group differences in basal and staurosporine-stimulated intracellular concentrations of active caspase-3 (0.3±0.03 vs. 0.5±0.1 ng/mL; and 2.9±0.4 vs. 2.7±0.3 ng/mL), a marker of apoptotic susceptibility. Taken together, these data indicate that short sleep duration is not associated with EPC dysfunction in healthy adults. Numerical and functional impairment in circulating EPCs may not contribute to the increased cardiovascular risk with habitual short sleep duration.

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Background: Healthcare system in most parts of the world functions on a three-tier system, involving primary, secondary, and tertiary care centers. The appropriate and efficient referral system plays crucial role in maximally efficient healthcare delivery. Materials and Methods: In all, 46 referrals made to the medicine department of the hospital over a period of 1 month with chief complaint of chest pain and presumptive diagnosis of myocardial ischemia/infarct by outside physicians were selected randomly. Analysis was done both for extent and clarity of useful information provided. Results: Out of 46 referrals, exact indication for referral was mentioned in 4 (8.7%), time of referral in 2 (4.3%), blood pressure in 38 (17.4%), pulse rate in 29 (63.04%), respiratory rate in 1 (2.17%), electrocardiograph diagnosis was not mentioned in 12 (26.08%), and the contact number/details of referring physician were mentioned in 2 (4.34%). Correct dose of aspirin was given to 27 (58.69%), clopidogrel to 19 (41.30%), statins to 9 (19.45%), angiotensin-converting enzyme inhibitors to 6 (13.04%), beta-blockers to 8 (17.39%), low-molecular weight heparin in 6 (13.04%), and 22 (47.82%) patients warranted thrombolysis, but was given in 12 (54.54%). Conclusions: There is a serious lack of quality and clarity of important information provided while making referrals.

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Marfan syndrome is a systematic genetic disease of the connective tissue. The cardiac affection would predict the prognosis and ischemic stroke might complicate it. The purpose of this work is to discuss the mechanisms of the ischemic stroke in Marfan syndrome which have to be considered in all young patients of ischemic strokes. We report the case of a 17-year-old male patient who presented with right hemiparesis with brachio-facial dominance, hemihypoesthesia and Broca's aphasia; these symptoms were followed by partial right somato-motor epileptic seizure. The cerebral computed tomographic (CT) scan demonstrated early signs of ischemic stroke in the left Sylvian artery. Cardiovascular examination revealed a systolic murmur in the mitral site. Marfan syndrome with infectious endocarditis complicated by ischemic stroke was diagnosed. However, the family pathological history was negative. The Marfan syndrome diagnosis was approved considering the following criteria: Ligamentous hyperlaxity, crystalline ectopia and mitral valve prolapsus with mitral insufficiency. The patient benefited of antibiotherapy for 4 weeks. The patient underwent sessions of motor physical therapy and orthophonic rehabilitation. Then, cardiac surgery was carried out and valvuloplasty was performed. The surgical treatment confirmed the presence of mitral insufficiency and prolapsus of the big mitral valve and multiple friable anterior-posterior vegetations with broken cordage of the small mitral valve. Replacement of the mitral valve was achieved, and the post-surgery follow-ups were simple. The diagnosis of Marfan syndrome was based on well-defined criteria. The evolution of the patient was marked by a complete improvement of the cardiac and motor deficits, and disappearance of the Broca's aphasia. A fibroelastic disease such Marfan syndrome has to be considered in unexplained ischemic stroke in all young patients. Hence, the diagnosis of Marfan syndrome involves an anticipation of the neurovascular complications by early cardiovascular care.

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Coronary artery anomalous course is rare, reported incidence is approximately 0.3-1.3% of patients undergoing coronary angiography and approximately 1% of routine autopsy examinations. A single coronary artery is an unusual congenital anomaly where only one coronary artery arises from the aortic trunk from a single coronary ostium, supplying the entire heart. We describe here a rare case with an unusual dominant left circumflex artery and absent right coronary artery.

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A 62-year-old male patient with previous history of myocardial infarction, akinetic myocardial segments, and an ejection fraction of 31% with the NYHA class III category was selected for the autologous bone marrow (ABM)-derived mononuclear cell fraction injection during CABG surgery. Nitrate augmented myocardial tracer uptake was imaged by ECG gated SPECT pre- and 1 year post-ABM therapy, using radiotracer Tc99m Sestamibi. The baseline gated SPECT demonstrated full thickness infarct in 40% area of LAD territory. Bone marrow aspirate of 20.0 ml from sternum yielding a mono nuclear cell fraction of 4.5 × 10 ⁷ cells/ml was suspended in 2.0 ml of sterile normal saline to be injected at eight sites of the injured myocardium. There were no apparent side effects due to the procedure, i.e., life threatening events, major bleeds, reaction, or shock. The case was followed at the end of 1, 3, 6 months by ECG and Holter monitor and ECG gated SPECT at the end of 12 months. The gated SPECT images demonstrated mild but definitely improved tracer uptake within part of the infarcted segments along with improvement in ejection fraction to 45%, and a clinical change in the NYHA Class to II. Cell-based therapy may offer benefits of induction of normal tissue microenvironment.

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The aryl hydrocarbon receptor (AHR) is an orphan nuclear receptor with a primary function of mediating xenobiotic metabolism through transcriptional activation of Phase I and Phase II drug-metabolizing enzymes. Although no high-affinity physiological activators of AHR have been discovered, the endogenous signaling of the AHR pathway is believed to play an important role in the development and function of the cardiovascular system, based on the observations on ahr gene-deficient mice. The AHR knockout mice develop cardiac hypertrophy, abnormal vascular structure in multiple organs and altered blood pressure depending on their host environment. In this review, the endogenous role of AHR in cardiovascular physiology, including heart function, vascular development and blood pressure regulation has been summarized and discussed.

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