Background: MacIver and Townsend's hypothesis predicts, based on a mathematical model

The intra + interDC + TC predicts clinical response after CRT more accurately than TC alone, due to greater TA in the NICD subgroup.

The role of oxidative stress (OXS) due to myocardial nitric oxide synthase (NOS) uncoupling related to oxidative depletion of its cofactor tetrahydrobiopterin (BH 4 ) emerged in the pathogenesis of heart failure with preserved ejection fraction (HFPEF).We determined the prevalence of 6 single nucleotide polymorphisms (SNPs) of genes encoding enzymes related to OXS, BH 4 metabolism and NOS function in >60-year-old 94 patients with hypertension and 18 age-matched controls with normal EF. Using echocardiography 56/94(60%) patients with hypertension had left ventricular (LV) diastolic dysfunction (HTDD+ group), 38/94(40%) patients had normal LV diastolic function (HTDDgroup). Four SNPs (rs841, rs3783641, rs10483639, rs807267) of guanosine triphosphate cyclohydrolase-1, the rate limiting enzyme in BH 4 synthesis, 1 (rs4880) of manganese superoxide dismutase, and 1 (rs1799983) of endothelial NOS genes were genotyped using real time PCR method and Taqman probes. Protein carbonylation (PC), BH 4 and total biopterin levels were measured from plasma samples. No between-groups difference in minor allele frequency (MAF) of SNPs was found. We calculated a genetic score indicating risk for OXS based on the MAFs of the SNPs. A high genetic risk for OXS was significantly associated with HTDD+ even after adjustment for confounding variables [OR(95%CI):4.79(1.12-20.54); p=0.035]. In both patient groups PC (p<0.05 for both), plasma BH 4 (p<0.01 for both) and in the HTDD+ group total biopterin (p<0.05) increased vs. controls. In conclusion, in patients with hypertension and normal EF, a potential precursor of HFPEF, a partly genetically determined increased OXS seems to be associated with the presence of LV diastolic dysfunction.key words: hypertension, heart failure with preserved ejection fraction, oxidative stress 3

Objectives: The diagnostic values of the aVR lead or "Vereckei algorithm," and the lead II R-wave peak time (RWPT) criterion, recently devised for the differential diagnosis of wide QRS complex tachycardias (WCTs), were compared.Methods: A total of 212 WCTs (142 ventricular tachycardias [VTs], 62 supraventricular tachycardias [SVT], and eight preexcitation SVTs) from 145 patients with proven electrophysiologic diagnoses were retrospectively analyzed by seven examiners blinded to the electrophysiologic diagnoses. Results:The overall test accuracy of the Vereckei algorithm was superior to that of the RWPT criterion (84.3% vs. 79.6%; p = 0.0003). The sensitivity of the Vereckei algorithm for VT diagnosis was greater than that of RWPT criterion (92.4% vs. 79.1%; p < 0.0001). The negative predictive value (NPV) for the Vereckei algorithm was also greater (77.8%; 95% confidence interval [CI] = 73.6% to 82.1%) than that of the RWPT criterion (61.6%; 95% CI = 57.6% to 65.6%). The specificity of the Vereckei algorithm was lower than that of the RWPT criterion (64.7% vs. 80.9%; p < 0.0001). The positive predictive value (PPV) was also lower for the Vereckei algorithm (86.4%; 95% CI = 84.4% to 88.4%) than for the RWPT criterion (90.9%; 95% CI = 89.1% to 92.8%). Incorrect diagnoses made by the Vereckei algorithm were mainly due to misdiagnosis of SVT as VT (65.7% of cases), and those made by the RWPT criterion were due to the more dangerous misdiagnosis of VT as SVT (72.5% of cases). Conclusions:The Vereckei algorithm was superior in overall test accuracy, sensitivity, and NPV for VT diagnosis and inferior in specificity and PPV to the RWPT criterion. All of these parameters were lower in "real life" than those reported by the original authors for each of the particular electrocardiographic methods.ACADEMIC EMERGENCY MEDICINE 2013; 20:1121-1130 © 2013 by the Society for Academic Emergency Medicine E lucidation of the mechanism of sustained, monomorphic wide QRS complex tachycardia (WCT) is a common diagnostic dilemma for the emergency physician. When confronted with the 12-lead WCT electrocardiogram (ECG), a correct diagnosis is vital not only for acute dysrhythmia treatment, but for further prognosis and subsequent work-up, as well as management. Because ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrant intraventricular conduction account for the vast majority of WCTs (80 and 15% to 20%, respectively), the clinically relevant problem is the distinction of VT from SVT with aberrant intraventricular conduction (SVT-A) in the differential diagnosis of WCTs. Other rare causes of WCT, such as SVT with anterograde conduction over an accessory pathway (preexcitation SVT), drug toxicity, electrolyte disorders (hyperkalemia), ventricular paced rhythm, or ECG artifact, account for only a small