Background: LDL cholesterol can either be calculated or measured directly. Clinical guidelines recommend using calculated LDL to guide therapy, as the evidence base for lipid management is derived almost exclusively from trials using calculated LDL, with direct measurement of LDL being reserved for those not fasting or significant hypertriglyceridemia. Our aim was to determine the clinical equivalence of directly measured LDL and fasting calculated LDL. Design: Eighty-one subjects had at least 1 calculated and direct LDL performed simultaneously; 64 had a repeat lipid assessment after 4 to 6 weeks of therapy, resulting in 145 pairs of calculated and direct LDL. Correlation between direct and calculated LDL was determined using Pearson's correlation coefficient. The relationship between direct and calculated LDL was also evaluated from a clinical perspective. Direct and calculated LDL were considered “clinically concordant” when the difference between calculated and direct LDL fulfilled 3 criteria: 1) < 6% difference (incremental LDL lowering provided by 1 titration of statin dose, e.g. simvastatin 20 to 40 mg), 2) < 10 mg/dL difference, and 3) placement in the same ATP III LDL cut points (e.g. <100, 100-129). Direct and calculated LDL were considered “clinically discordant” when the difference between calculated and direct LDL fulfilled 3 criteria: 1) ≥ 12% difference (incremental LDL lowering provided by 2 statin titration steps, e.g. from simvastatin 20 to 80 mg), 2) ≥ 10 mg/dL difference, and 3) placement in different ATP III LDL cut points. Results: There was significant correlation between direct and calculated LDL(r=0.93). Clinical concordance between calculated and direct LDL was present in 40% of patients. Clinical discordance was noted in 25% of patients. One-third of patients had > 15 mg/dL difference between direct and calculated LDL, while 25% had > 20 mg/dL difference. In 47% of subjects, the difference between direct and calculated LDL at baseline and follow-up changed by a minimum of 10% or 10 mg/dL. Conclusion: Our findings suggest that directly measured LDL is not clinically equivalent to calculated LDL. This puts into question the current recommendation of using direct LDL in situations where calculated LDL would be inaccurate.
The effects of intracoronary verapamil and nitroglycerin on collateral blood flow were compared under conditions where coronary perfusion pressure was held constant with a servopump and the systemic effects of the drugs were minimal. Both drugs were infused into 12 anesthetized dogs after occlusion of the left anterior descending coronary artery (LAD) and regional myocardial blood flow (MBF) was measured using microspheres. Before the LAD occlusion, the myocardium not perfused by the LAD was labeled to permit calculation of the fraction of tissue normally perfused in the LAD samples and corrections for collateral flow. The central ischemic zone contained 2.5 +/- 0.3% normally perfused myocardium and a 4-mm border zone contained 26.8 +/- 4.3% normal myocardium. This border zone contained 10% of the total tissue supplied by the LAD. The MBF in the central ischemic zone increased from 0.101 +/- 0.019 to 0.113 +/- 0.022 ml/min/g after verapamil infusion (NS) and to 0.149 +/- 0.024 ml/min/g after nitroglycerin (p less than 0.01). Uncorrected MBF in the border zone increased significantly after infusion of both verapamil (0.469 +/- 0.085 ml/min/g, p less than 0.01) and nitroglycerin (0.398 +/- 0.056, p less than 0.05). When corrections were made for interdigitating normal tissue in the border zone, only the MBF after nitroglycerin was significantly increased. Thus, nitroglycerin significantly increased the collateral blood flow to ischemic tissue in the central ischemic and border zones, but verapamil did not.
To compare the cerebral vascular and metabolic effect of an isoflurane-nitrous oxide mixture to an equipotent dose of isoflurane at 1.1 minimum alveolar anesthetic concentration (MAC), and to study the interaction between nitrous oxide and isoflurane anesthesia, we measured right middle cerebral artery blood flow velocity (Vmca) and cerebral arteriovenous oxygen content difference (AVDO2) in six healthy patients during normocapnia and normothermia under the following sequence of steady-state anesthetic conditions: Condition A, 0.5 MAC of isoflurane, Condition B, 0.5 MAC of isoflurane + 0.6 MAC of N2O, Condition C, 1.1 MAC of isoflurane + 0.6 MAC of N2O, and Condition D, 1.1 MAC of isoflurane. The study entry sequence was randomized. Vmca and AVDO2 during 1.1 MAC of isoflurane (Condition D) was 48 ± 7 cm/s and 3.9 ± 0.6 vol%, respectively. Substituting 0.6 MAC of isoflurane with an equipotent concentration of N2O (Condition B) resulted in an increase in both Vmca and AVDO2 of approximately 20% (P < 0.05). These findings suggest that the increase in flow was accompanied by an even greater increase in metabolic rate. Adding 0.6 MAC of N2O to 1.1 MAC of isoflurane (Condition C) also increased Vmca (P < 0.05). We conclude that N2O is a more potent cerebral vasodilator than an equipotent dose of isoflurane alone in humans.
'%3e%3cpath fill='%23012169' d='M0 0v30h60V0z'/%3e%3cpath stroke='%23fff' stroke-width='6' d='m0 0 60 30m0-30L0 30'/%3e%3cpath stroke='%23C8102E' stroke-width='4' d='m0 0 60 30m0-30L0 30' clip-path='url(%23b)'/%3e%3cpath stroke='%23fff' stroke-width='10' d='M30 0v30M0 15h60'/%3e%3cpath stroke='%23C8102E' stroke-width='6' d='M30 0v30M0 15h60'/%3e%3c/g%3e%3c/svg%3e)
