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Selected AbstractsThe Influence of Left Ventricle Diastolic Function on Natriuretic Peptides Levels in Patients with Atrial FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2009DAWID BAKOWSKI M.D., Ph.D. Background:The diagnosis of the impaired left ventricle (LV) diastolic function during atrial fibrillation (AF) using traditional methods is very difficult. Natriuretic peptides seem to be useful for assessment of diastolic function in patients with AF. Aim:To evaluate the influence of LV diastolic dysfunction on natriuretic peptides concentrations and to assess the diagnostic value of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in patients with AF and impaired LV diastolic function. Methods:The study included 42 patients (23 males, 19 females), aged 58.6 ± 8.2 years with nonvalvular persistent AF with preserved LV systolic function who were converted into sinus rhythm by DC cardioversion (CV) and maintained sinus rhythm for at least 30 days. Echocardiography (ECG), ANP, and BNP level measurements were taken at baseline 24 hours before CV and 24 hours and 30 days after CV. On the 30th day following CV in patients with sinus rhythm, Doppler ECG was performed to assess LV diastolic function. Results:Thirty days after CV, normal LV diastolic function in 15 patients and impaired diastolic function in 27 patients was diagnosed: 20 with impaired LV relaxation and seven with impaired LV compliance. During AF and 24 hours, and 30 days after sinus rhythm restoration, significantly higher ANP and BNP levels were observed in patients with LV diastolic dysfunction as compared to the subgroup with normal LV diastolic function. The average values of ANP during AF in patients with normal and impaired diastolic function were 167.3 ± 70.1 pg/mL and 298.7 ± 83.6 pg/mL, respectively (P < 0.001), and the average values of BNP in the above mentioned subgroups were 49.5 ± 14.7 pg/mL and 145.6 ± 49.6 pg/mL respectively (P < 0.001). While comparing the diagnostic value of both natriuretic peptides it was noted that BNP was a more specific and sensitive marker of impaired LV diastolic function. ANP value >220.7 pg/mL measured during AF identified patients with impaired LV diastolic function with 85% sensitivity and 90% specificity. BNP value >74.7 pg/mL proved 95% sensitive and 100% specific in the diagnosing of such a group. Conclusions:The increase of ANP/BNP concentration in patients with AF results not only from the presence of AF, but also reflects the impaired LV diastolic function. Natriuretic peptides, especially BNP, may be useful in diagnosing LV diastolic dysfunction in patients with AF. [source] Synchronized diapause termination of the peach twig borer Anarsia lineatella (Lepidoptera: Gelechiidae): Brownian motion with drift?PHYSIOLOGICAL ENTOMOLOGY, Issue 1 2010PETROS T. DAMOS The course of diapause development is studied for the first time for Anarsia lineatella (Zeller) (Lepidoptera: Gelechiidae) under field and laboratory conditions for three successive years (2005,2007) in northern Greece. Photoperiod has a significant influence on diapause termination and the mean number of days to pupation decreases progressively throughout the winter season. Cold storage, for at least 30 days at 4°C, results in a synchronized reactivation of the larvae, with the developmental time of larvae chilled for 45 and 60 days at 4°C becoming significantly shorter. A theoretical stochastic description of the effect of chilling on diapause termination is attempted. Larvae have discrete ,physiological stages' with different degrees of diapause intensity, and the insect passes through those stages with a probability distribution S(t) that evolves over time. This pattern of progressive transition is similar to Brownian motion and finally leads to a successfully synchronized diapause break in spring. Hence, A. lineatella overwinters in a weak diapause state and may complete diapause development in late January, although it shows synchronized termination in early February, after the experience of essential chilling. [source] Different angiotensin-converting enzyme inhibitors have similar clinical efficacy after myocardial infarctionBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 2 2008Morten L. Hansen What is already known about this subject ,,Treatment with an angiotensin-converting enzyme (ACE) inhibitor benefits many patients with cardiovascular disease. ,,ACE inhibitors are generally assumed to be equally effective, but this has never been fully verified in clinical trials. What this study adds ,,Studying the association among ACE inhibitors after myocardial infarction demonstrated similarity in clinical outcome and supports a dosage,response relationship. ,,Therefore, for long-term benefits for patients who need treatment with an ACE inhibitor, a focus of treatment at the recommended dosage is most important and not which ACE inhibitor is used. Aim Therapy with angiotensin-converting enzyme (ACE) inhibitors is common after myocardial infarction (MI). Given the lack of randomized trials comparing different ACE inhibitors, the association among ACE inhibitors after MI in risk for mortality and reinfarction was studied. Methods Patients hospitalized with first-time MI (n = 16 068) between 1995 and 2002, who survived at least 30 days after discharge and claimed at least one prescription of ACE inhibitor, were identified using nationwide administrative registries in Denmark. Results Adjusted Cox regression analysis demonstrated no differences in risk for all-cause mortality, but patients using captopril had higher risk of reinfarction (hazard ratio 1.18, 95% confidence interval 1.05, 1.34). However, following adjustment for differences in used dosages, all ACE inhibitors had similar clinical efficacy. Risk of all-cause mortality: trandolapril (reference) 1.00, ramipril 0.97 (0.89, 1.05), enalapril 1.04 (0.95, 1.150), captopril 0.95 (0.83, 1.08), perindopril 0.98 (0.84, 1.15) and other ACE inhibitors or angiotensin II receptor blockers (ARB) 1.06 (0.94, 1.19). Reinfarction: trandolapril (reference) 1.00, ramipril 0.98 (0.89, 1.08), enalapril 1.04 (0.92, 1.17), captopril 1.05 (0.89, 1.25), perindopril 0.96 (0.81, 1.14) and other ACE inhibitors or ARB 0.99 (0.86, 1.14). Furthermore, the association between ARBs and clinical events was similar to ACE inhibitors (trandolapril reference): all-cause mortality 0.99 (0.84, 1.16) and recurrent MI 0.99 (0.83, 1.19). Conclusions Our results suggest a class effect among ACE inhibitors when used in comparable dosages. Focus on treatment at the recommended dosage is therefore most important, and not which ACE inhibitor is used. [source] Usefulness of translesional pressure gradient and pharmacological provocation for the assessment of intermediate renal artery diseaseCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 3 2006Noah J. Jones MD Abstract Objective: We sought to determine the hemodynamic significance of intermediate RAS by measuring translesional systolic pressure gradients (TSPG), using a pressure-sensing guidewire at baseline and after acetylcholine (ACh) induced hyperemia, following selective renal artery angiography. Background: Renal artery stenosis (RAS) is a cause of reversible hypertension and nephropathy. Stenting effectively relieves RAS, however improvement in blood pressure control or renal function is variable and unpredictable. Hemodynamic significance is usually present with RAS when diameter stenosis is >75%, but is less predictable in intermediate (30%,75%) RAS. Methods: Twenty-two patients (26 renal arteries) with uncontrolled hypertension underwent invasive hemodynamic assessment because of intermediate RAS, defined as radiocontrast angiographic diameter stenosis (DS) between 30% and 75% (quantitative DS was measured prospectively). Translesional pressure gradients were measured using a 0.014" pressure-sensing wire. Hyperemia was induced by administration of intrarenal ACh. Results: Visual and measured angiographic lesion severity did not correlate with TSPG either at baseline (visual DS, R2 = 0.091, P = 0.13; measured DS, R2 = 0.124, P = 0.07) or with hyperemia (visual DS, R2 = 0.057, P = 0.24; measured DS, R2 = 0.101, P = 0.12). Baseline and maximal hyperemic gradient did correlate (R2 = 0.567; P < 0.05). Pharmacological provocation produced a significant increase in TSPG (mean; baseline, 18 ± 21 vs. hyperemia, 34 ± 41 mm Hg; P < 0.05). A hemodynamically significant lesion (TSPG > 20 mm Hg) was found in 14/26 (54%) arteries (13 patients); 13 (60%) patients subsequently underwent renal artery stenting for hemodynamically significant RAS. At follow-up (at least 30 days), there was a significant decrease in systolic blood pressure (mean; 167 ± 24 vs. 134 ± 19 mm Hg; P < 0.001). Conclusions: Intrarenal administration of ACh induces hyperemia and can be used to unmask resistive renal artery lesions. Gradient measurement and induced hyperemia may be warranted in the invasive assessment of intermediate renal artery stenoses, rather than relying on stenosis severity alone. Further study is needed to determine whether translesional pressure gradients and pharmacological provocation predict clinical benefit after renal artery stenting. © 2006 Wiley-Liss, Inc. [source] The pharmacodynamic equivalence of levothyroxine and liothyronine: a randomized, double blind, cross-over study in thyroidectomized patientsCLINICAL ENDOCRINOLOGY, Issue 5 2010Francesco S. Celi Summary Context, The substitution of liothyronine (L-T3) for levothyroxine (L-T4) is commonly employed during thyroid hormone (TH) withdrawal in preparation for diagnostic and therapeutic interventions on thyroid cancer patients. Presently, only limited data are available on the L-T3 for L-T4 therapeutic substitution. Objective, To characterize the pharmcodynamic equivalence of L-T3 and L-T4. Design, Randomized, double-blind, cross-over intervention study. Setting, NIH clinical center. Patients, Ten thyroidectomized patients. Interventions, Study participants were treated with L-T3 or L-T4 with a target TSH , 0·5 , 1·5 mU/l for at least 30 days before undergoing inpatient testing. Following testing, subjects crossed-over according to the same scheme. Main outcome measures, Area under the serum concentration,time curve of TSH from 0 to 60 min (AUC0,60) and peak TSH serum concentration (Cmax) following thyrotropin-releasing hormone (TRH) stimulation test, total L-T4 and L-T3 dose (mcg/kg), and L-T4/L-T3 ratio. Results, No difference was observed for time 0 TSH values between L-T3 and L-T4 replacement phases (1·48 ± 0·77 vs. 1·21 ± 0·62 mU/l, P = 0·293) at average daily doses of 40·3 ± 11·3 mcg L-T3 and 115·2 ± 38·5 mcg L-T4, L-T3: L-T4 ratio 0·36 ± 0·06. TRH stimulation test resulted in similar L-T3 vs. L-T4 TSH responses with AUC0,60 of 326·1 (95% CI 232·6,457·1) and 247·1 (95% CI 153·8,397·1) mU* min/l (P = 0·285); and Cmax of 6·83 (95% CI 4·88,9·55) and 5·23 (95% CI 3·31,8·3) mU/l (P = 0·383). Conclusions, This is the first study addressing the equivalency between L-T3 and L-T4 therapy measured by baseline and TRH-stimulated TSH. The therapeutic substitution of L-T3 for L-T4 was achieved at approximately 1:3 ratio. 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