Characteristics of frequency content of atrial signal-averaged electrocardiograms during sinus rhythm in patients with paroxysmal atrial fibrillation

To clarify the characteristics of the frequency content of atrial signal-averaged electrocardiograms (ECGs) during sinus rhythm in patients with paroxysmal atrial fibrillation, P wave-triggered signal-averaged ECGs were recorded in 28 patients with and 34 control patients without paroxysmal atrial fibrillation. Fast Fourier transform analysis was performed on the 100-ms segment starting 75 ms before the end of the P wave. An area ratio (AR50) was calculated by dividing the area under the spectrum curve between 20 and 50 Hz, multiplied by 100, by the area between 0 and 20 Hz. Magnitude ratios (MR20, MR30, MR40and MR50) were calculated by dividing the magnitude at 20, 30, 40 and 50 Hz, respectively, multiplied by 100, by the maximal magnitude of the entire signal.AR50was significantly greater in patients with than without paroxysmal atrial fibrillation (62.3 ± 34.2 vs. 42.4 ± 18.4). MRM and MR30were also significantly greater in patients with than without paroxysmal atrial fibrillation (MR2076.1 ± 15.2 vs. 60 ± 20.2; MR3041 ± 18.8 vs. 26.6 ± 14.4), although no significant differences in MR40or MR50were observed between the two patient groups. The difference in MR30between groups remained significant even after taking into account the presence of organic heart disease.It is concluded that, irrespective of the presence of organic heart disease, the terminal portion of the P wave contained significantly more components in the 20- to 50-Hz range, especially around 30 Hz, in patients with than in patients without paroxysmal atrial fibrillation. These results suggest that frequency analysis could characterize atrial signal-averaged ECGs of patients at risk for paroxysmal atrial fibrillation

α-Selective glycosidation of d-tagatofuranose with a 3,4-O-isopropylidene protection

An α-selective glycosidation reaction of D-tagatofuranose was successfully achieved using 3,4-O-isopropylidene-protected D-tagatofuranose as a glycosyl donor. A variety of glycosyl acceptors, including primary, secondary, and β-amino alcohols, and carbohydrates, can be used for this D-tagatofuranosidation reaction with complete α-selectivities and good yields (57-83%). The stereochemistries at the anomeric positions were determined by nuclear Overhauser effect spectroscopic correlations, as well as comparison of the chemical shifts in the 13C NMR spectra

Pravastatin restored the infarct size-limiting effect of ischemic preconditioning blunted by hypercholesterolemia in the rabbit model of myocardial infarction

AbstractOBJECTIVESWe tested to find out whether pravastatin restores the infarct size (IS)-limiting effect of ischemic preconditioning (IP) and if it has any effect on the IP-induced activation of adenosine producing enzyme ecto-5′-nucleotidase which plays a key role in the IP-induced cardioprotection.BACKGROUNDThe IS-limiting effect of IP is blunted by hypercholesterolemia. Recently, HMG-CoA reductase inhibitors are shown to have direct cytoprotective effects.METHODSRabbits were fed with a normal or cholesterol (1%) added diet with or without pravastatin (5 mg/kg/day) treatment. Infarct size was measured after 30 min occlusion and 3 h reperfusion of circumflex coronary artery with or without the IP procedure (5 min occlusion and 10 min reperfusion). Additionally, ecto-5′-nucleotidase activities of ischemic and nonischemic myocardium were measured immediately after IP procedure.RESULTSThis dose of pravastatin did not normalize the increased level of serum cholesterol. The IS-limiting effect of preceding IP (IS reduced from 36.7% to 9.6%, p < 0.001) was abolished by hypercholesterolemia (from 46.1% to 31.3%, p = NS) and restored by pravastatin treatment (from 35.2% to 9.4%, p < 0.001). Pravastatin treatment did not affect IS or the effect of IP under normocholesterolemia. The activation of ecto-5′-nucleotidase presented as the activity ratio of ischemic to nonischemic myocardium (3.1-fold in normocholesterolemia) was blunted by hypercholesterolemia (1.8-fold, p < 0.05) and restored by pravastatin treatment (2.9-fold).CONCLUSIONSPravastatin, at the dose serum cholesterol was not normalized, restored the IS-limiting effect of IP and IP-induced ecto-5′-nucleotidase activation, which were both blunted by hypercholesterolemia. The activation of ecto-5′-nucleotidase may be worth further investigation as a possible mechanism for the hypercholesterolemia-induced retardation and pravastatin-mediated restoration of the cardioprotective effect of IP

The impact of dietary fat type on lipid profiles in lean mass hyper‐responder phenotype

Key Clinical Message Although the lean mass hyper‐responder (LMHR) phenotype is well known, its diagnosis is impeded by the influence of fat type and intake on the lipid profile. Accordingly, a detailed assessment is warranted if LMHR is suspected. Abstract A 47‐year‐old man with suspected familial hypercholesterolemia presented with elevated triglyceride and low‐density lipoprotein cholesterol levels. He had adhered to a ketogenic diet and was suspected of a lean mass hyper‐responder phenotype; however, his lipid profile did not meet the definition. His lipid profile improved through dietary management without medication

Phenotypic homozygous familial hypercholesterolemia successfully treated with proprotein convertase subtilisin/kexin type 9 inhibitors

Key Clinical Message Recent data reveal phenotypic HoFH patients may be responsive to PCSK9 inhibitors, challenging prior assumptions. Genetic testing advancements now more accurately forecast patient responses to these therapies, improving treatment strategies