Distribution of abnormal potentials in chronic myocardial infarction using a real time magnetic resonance guided electrophysiology system

Background

Identification of viable slow conduction zones manifested by abnormal local potentials is integral to catheter ablation of ventricular tachycardia (VT) sites. The relationship between contrast patterns in cardiovascular magnetic resonance (CMR) and local electrical mapping is not well characterized. The purpose of this study was to identify regions of isolated, late and fractionated diastolic potentials in sinus rhythm and controlled-paced rhythm in post-infarct animals relative to regions detected by late gadolinium enhancement CMR (LGE-CMR).

Methods

Using a real-time MR-guided electrophysiology system, electrogram (EGM) recordings were used to generate endocardial electroanatomical maps in 6 animals. LGE-CMR was also performed and tissue classification (dense infarct, gray zone and healthy myocardium) was then correlated to locations of abnormal potentials.

Results

For abnormal potentials in sinus rhythm, relative occurrence was equivalent 24%, 27% and 22% in dense scar, gray zone and healthy tissue respectively (p = NS); in paced rhythm, the relative occurrence of abnormal potentials was found to be different with 30%, 42% and 21% in dense scar, gray zone and healthy myocardium respectively (p = 0.001). For location of potentials, in the paced case, the relative frequency of abnormal EGMs was 19.9%, 65.4% and 14.7% in the entry, central pathway and exit respectively (p = 0.05), putative regions being defined by activation times.

Conclusions

Our data suggests that gray zone quantified by LGE-CMR exhibits abnormal potentials more frequently than in healthy tissue or dense infarct when right ventricular apex pacing is used.     

Analysis & commentary: Global prevention and control of type 2 diabetes will require paradigm shifts in policies within and among countries

Continued increases in the prevalence of and disproportionate health spending associated with type 2 diabetes argue for policies focused on preventing that condition and treating it appropriately, even as we strive to improve coordination of care for coexisting chronic diseases. This article argues that four policy paradigm shifts will be necessary to achieve that specific emphasis on type 2 diabetes: conceptually integrating primary and secondary prevention along a clinical continuum; recognizing the central importance of early detection of prediabetes and undiagnosed diabetes in implementing cost-effective prevention and control; integrating community and clinical expertise, and resources, within organized and affordable service delivery systems; and sharing and adopting evidence-based policies at the global level.     

Nutrition Research in India: Underweight,Stunted, or Wasted?

India has experienced dramatic economic growth in the past 2 decades accompanied by a rising burden of noncommunicable diseases, which coexists with the unfinished agenda of undernutrition. Tackling these dual challenges requires strong investment in nutrition research. We compared India's research output with another rapidly developing country (China) and an established developed country (USA). We analyzed trends for each country between the periods 2000 to 2005 and 2006 to 2010, in terms of quantity and quality of the publications. India produced 2,712 articles (1.9% of the global total) in the 2000 to 2005 period and 3,999 articles (2.1%) in the 2006 to 2010 period, and the country impact factor was 191 and 174, respectively. The contributions to the top 10 nutrition journals during 2006 to 2010 was 1%. India must increase investment in and attention towards quality nutrition research and address potential barriers to publish.     

Evidence of Reduced β-Cell Function in Asian Indians With Mild Dysglycemia

OBJECTIVE

To examine β-cell function across a spectrum of glycemia among Asian Indians, a population experiencing type 2 diabetes development at young ages despite low BMI.

RESEARCH DESIGN AND METHODS

One-thousand two-hundred sixty-four individuals without known diabetes in the Diabetes Community Lifestyle Improvement Program in Chennai, India, had a 75-g oral glucose tolerance test, with glucose and insulin measured at 0, 30, and 120 min. Type 2 diabetes, isolated impaired fasting glucose (iIFG), isolated impaired glucose tolerance (iIGT), combined impaired fasting glucose and impaired glucose tolerance, and normal glucose tolerance (NGT) were defined by American Diabetes Association guidelines. Measures included insulin resistance and sensitivity (homeostasis model assessment of insulin resistance [HOMA-IR], modified Matsuda Index, 1/fasting insulin) and β-cell function (oral disposition index = [Δinsulin_0–30/Δglucose_0–30] × [1/fasting insulin]).

RESULTS

Mean age was 44.2 years (SD, 9.3) and BMI 27.4 kg/m² (SD, 3.8); 341 individuals had NGT, 672 had iIFG, IGT, or IFG plus IGT, and 251 had diabetes. Patterns of insulin resistance or sensitivity were similar across glycemic categories. With mild dysglycemia, the absolute differences in age- and sex-adjusted oral disposition index (NGT vs. iIFG, 38%; NGT vs. iIGT, 32%) were greater than the differences in HOMA-IR (NGT vs. iIFG, 25%; NGT vs. iIGT, 23%; each P < 0.0001). Compared with NGT and adjusted for age, sex, BMI, waist circumference, and family history, the odds of mild dysglycemia were more significant per SD of oral disposition index (iIFG: odds ratio [OR], 0.36; 95% CI, 0.23–0.55; iIGT: OR, 0.37; 95% CI, 0.24–0.56) than per SD of HOMA-IR (iIFG: OR, 1.69; 95% CI, 1.23–2.33; iIGT: OR, 1.53; 95% CI, 1.11–2.11).

CONCLUSIONS

Asian Indians with mild dysglycemia have reduced β-cell function, regardless of age, adiposity, insulin sensitivity, or family history. Strategies in diabetes prevention should minimize loss of β-cell function.Type 2 diabetes mellitus is a global problem, with 80% of all cases worldwide occurring in low- and middle-income countries (1). However, despite the increasing prevalence of type 2 diabetes, the etiology of the disease remains incompletely understood. Previously invoked as the driving feature of diabetes, increased insulin resistance can trigger increased insulin production to maintain normoglycemia and, over time, can strain β cells to the point at which insulin production is no longer adequate (2–4), i.e., β-cell “exhaustion.” Characteristics associated with insulin resistance, particularly older age, obesity, and physical inactivity, are strong risk factors for diabetes (5).Yet, poor β-cell function also may have more of a primary role in diabetes development. The inadequate β-cell response to physiologic needs for insulin not only may be an acquired feature (e.g., as a result of insulin resistance) but also, at least in some individuals, may be an inherent feature. β-Cell dysfunction has been detected early in the pathogenesis of the disease (6), with recent cross-sectional and longitudinal studies detecting dysfunction in people with prediabetes or even normoglycemia (7–10). Supported by recent genetic discoveries (11), these studies suggest that some individuals have an underlying susceptibility to poor β-cell function (12) and that β-cell dysfunction may be an early driving metabolic feature of diabetes development.Most studies of diabetes pathogenesis have been conducted in populations of European descent; however, more people have diabetes in other populations worldwide. Asian Indians, in particular, experience high rates of type 2 diabetes (13) at younger ages and lower BMI values (14) compared with other populations. They have high basal insulin levels (15) that are not entirely explained by obesity or adverse fat distribution (16), which are commonly cited factors related to insulin resistance. Considering these characteristics, Asian Indians may be an ideal population to utilize for developing a better understanding of the relative roles of β-cell function and insulin resistance in the pathogenesis of type 2 diabetes. Previous studies that have examined the etiology of diabetes in Asian Indians have produced conflicting findings. Altered β-cell function has been associated with impaired glucose tolerance (IGT) (17), has not been associated with IGT (18,19), and has been associated with impaired fasting glucose (IFG) but not IGT (20). Furthermore, β-cell function has not always been evaluated rigorously in Asian Indians (i.e., expressed relative to the insulin resistance of each individual) (21). We investigated the associations between the pathophysiologic mechanisms of insulin resistance and β-cell function with glycemic status in a large cohort (n = 1,264) of Asian Indians in Chennai, India.     

A blind controlled trial of phase-contrast microscopy by two observers for evaluating the source of haematuria

Two observers, unaware of each other's findings and of the diagnosis, examined red cells in the urine of 109 patients by phase-contrast microscopy. All specimens were examined uncentrifuged by inverted microscopy, and 48 of the 109 were also examined under a light microscope after centrifugation. We were unable to confirm with either method the close correlation between red-cell morphology and diagnosis reported in previous studies, and our 2 observers differed in their interpretation on 38% of occasions. Proteinuria associated with the presence of casts in uncentrifuged urine examined by inverted microscopy was a better indication than red-cell morphology of renal parenchymal disease.