Changes in peak expiratory flow rates using two head-tilt/chin-lift maneuver angles in young healthy conscious volunteers.

BACKGROUND: The head-tilt/chin-lift (HT/CL) maneuver is simple and routinely used to open a closed upper airway. OBJECTIVES: It has yet to be determined whether increasing the HT/CL angle further would be beneficial. METHODS: We enrolled 60 (30 males) 20-year-old conscious participants. Pre-HT/CL, post-HT/CL #1, and post-HT/CL #2 positions were defined as positions in which the angle between the ear-eye line and the horizontal line was 80°, 65°, and 50°, respectively. Peak exploratory flow rates (PEFRs) pre-HT/CL, post-HT/CL #1, and post-HT/CL #2 positions were recorded continuously at 1-minute intervals (one set). Five sets of measurements were performed (total, 15 measurements for each participant). RESULTS: We analysed 900 measurements (180 sets). The mean PEFRs pre-HT/CL, post-HT/CL #1, and post-HT/CL #2 positions were 348.4 ± 96.9, 366.4 ± 104.9, and 378.8 ± 111.2 L/min (percentage change compared to pre-HT/CL, 5.2% and 8.7%), respectively. Significant differences were observed among pre-HT/CL, post-HT/CL #1, and post-HT/CL #2 positions in all participants, as well as in subgroup classified according to sex, and medians of height, body weight, and body mass index. CONCLUSION: Our findings suggest that a greater HT/CL angle would be beneficial, as the PEFR increased gradually. The decreasing manner in the PEFR increase with the HT/CL angle implies the existence of an angle threshold beyond which there were no further benefits in airflow, indicating a minimum in airway resistance. A HT/CL maneuver may be appropriate until locking the atlanto-occipital and cervical spine joints in extension occurs and the chest (sternal notch) begins to rise.

Rosuvastatin Reduces Blood Viscosity in Patients with Acute Coronary Syndrome.

BACKGROUND AND OBJECTIVES: Wall shear stress contributes to atherosclerosis progression and plaque rupture. There are limited studies for statin as a major contributing factor on whole blood viscosity (WBV) in patients with acute coronary syndrome (ACS). This study investigates the effect of statin on WBV in ACS patients. SUBJECTS AND METHODS: We prospectively enrolled 189 consecutive patients (mean age, 61.3±10.9 years; 132 males; ST-segment elevation myocardial infarction, n=52; non-ST-segment elevation myocardial infarction, n=84; unstable angina n=53). Patients were divided into two groups (group I: previous use of statins for at least 3 months, n=51; group II: statin-naïve patients, n=138). Blood viscosities at shear rates of 1 s-1 (diastolic blood viscosity; DBV) and 300 s-1 (systolic blood viscosity; SBV) were measured at baseline and one month after statin treatment. Rosuvastatin was administered to patients after enrollment (mean daily dose, 16.2±4.9 mg). RESULTS: Baseline WBV was significantly higher in group II ([SBV: group I vs group II, 40.8±5.9 mP vs. 44.2±7.4 mP, p=0.003], [DBV: 262.2±67.8 mP vs. 296.9±76.0 mP, p=0.002]). WBV in group II was significantly lower one month after statin treatment ([SBV: 42.0±4.7 mP, p=0.012, DBV: 281.4±52.6 mP, p=0.044]). However, low-density lipoprotein cholesterol level was not associated with WBV in both baseline (SBV: R2=0.074, p=0.326; DBV: R2=0.073, p=0.337) and after one month follow up (SBV: R2=0.104, p=0.265; DBV: R2=0.112, p=0.232). CONCLUSION: Previous statin medication is an important determinant in lowering WBV in patients with ACS. However, one month of rosuvastatin decreased WBV in statin-naïve ACS patients.

Pharmacodynamic effects of cilostazol versus clopidogrel in stented patients under proton pump inhibitor co-administration: the ACCEL-PARAZOL study.

AIM: Proton pump inhibitor (PPI) therapy has been shown to attenuate the antiplatelet effects of clopidogrel. The aim of this study was to compare the antiplatelet effects of cilostazol versus clopidogrel in patients co-administered a PPI. METHODS: We enrolled PPI-naïve stented patients treated with standard clopidogrel and aspirin therapy for at least six months (n=100). The patients were randomly assigned to receive either cilostazol at a dose of 100mg twice daily (CILO group) or clopidogrel at a dose of 75mg daily (CLPD group) in addition to lansoprazole (30mg daily). The platelet aggregation (PA) determined using light transmittance aggregometry and the platelet reactivity index (PRI) obtained using a vasodilator-stimulated phosphoprotein phosphorylation assay were measured before randomization and at the 14-day follow-up visit. The primary endpoint was the PRI value at follow-up. RESULTS: At follow-up, the CLPD group showed similar values of PRI as the CILO group (66.9±14.0% vs. 63.1±14.1%; mean difference: 3.9%; 95% confidence interval of difference: -1.7% to 9.4%; p=0.174). However, the 6µg/mL collagen- and 0.5mg/mL arachidonic acid-induced PA values in the CLPD group were higher than those observed in the CILO group (mean differences: 9.8% to 11.1%; all p values ＜0.001). CYP2C19 loss-of-function allele carriage was the major contributing factor associated with the PRI level in the absence of lansoprazole treatment (with a gene-dose effect); this association was not observed in the subjects receiving lansoprazole co-administration in the CLPD group. CONCLUSIONS: During lansoprazole co-administration, cilostazol treatment achieves a more favorable platelet function profile than clopidogrel therapy. The use of combination treatment with cilostazol and aspirin deserves further attention with respect to the management of stable stented patients requiring PPI co-administration.

Elevated coronary whole blood viscosity in acute coronary syndrome patients.

OBJECTIVES: As most clinical studies measure whole blood viscosity (WBV) from peripheral samples, potential differences in WBV obtained from the coronary arteries are often ignored. This study investigated differences in WBV measured from coronary artery specimens in patients with and without acute coronary syndrome (ACS). METHODS AND RESULTS: Consecutive patients with chest pain who underwent diagnostic coronary angiography were divided into two groups [non-ACS (n = 16), ACS (n = 22)]. The ACS group consisted of unstable angina (n = 13) and acute myocardial infarction (n = 9) patients. Two blood samples were obtained from each patient at the both coronary artery ostia prior to coronary angiography. Low-shear and high-shear blood viscosities (BVs) were measured at shear rates of 1 and 300 s-1, respectively, by a scanning capillary tube viscometer (Bio-Visco Inc., South Korea). Both low-shear and high-shear BVs obtained from peripheral, left and right coronary arteries were not different in both groups. Mean coronary low-shear WBV values obtained in ACS group were 29.2% higher than those in non-ACS group (295.3 ± 87.2 mP vs. 228.5 ± 69.2 mP, p = 0.016). Mean coronary high-shear WBV values obtained in ACS group were 15.6% higher than those in non-ACS group (42.9 ± 10.0 mP vs. 37.1 ± 4.6 mP, p = 0.036). CONCLUSIONS: Direct measurement of WBV from the coronary artery showed no differences with peripheral samples. Future larger studies are needed to clarify our results.

Changes in whole blood viscosity at low shear rates correlate with intravascular volume changes during hemodialysis.

BACKGROUND: Elevated blood viscosity has been shown to be independently correlated with cardiovascular risk factors and associated with increased risk of major cardiovascular events, including death and acute myocardial infarction. The aim of the present study was to investigate changes in whole blood viscosity (WBV) at shear rates of 1, 5, and 300 s-1 before and after hemodialysis in patients with end-stage renal disease (ESRD). We also examined the relationship between the changes of WBV and intravascular blood volume. METHODS: 43 patients with ESRD receiving maintenance hemodialysis were enrolled. WBV was measured using a scanning capillary tube viscometer pre- and post-dialysis to quantify dialytic viscosity surges. Body weight, blood pressure, and hematocrit were also measured before and after hemodialysis, as was the fluid removed during the session. RESULTS: Hemodialysis had a 3 times greater impact on the low-shear WBV at a shear rate of 1 s-1 (i.e., 44.1% change) than on the high-shear WBV at a shear rate of 300 s-1 (i.e., 15.9% change). Changes in the low-shear WBV obtained at shear rates of 1 and 5 s-1 during hemodialysis were significantly correlated with changes in hematocrit. The intravascular blood volume reduction during hemodialysis was positively correlated with the changes in both high-shear and low-shear WBVs. CONCLUSIONS: These results suggest that the WBV parameter may hold additional information beyond hemoconcentration. Further research is needed to evaluate the relationship between low-shear WBV surges and increased morbidity in the patient population with ESRD.