Title: Pressure Frequency Characteristics of the Pericardial Space and Thorax During Subxiphoid Access for Epicardial Ventricular Tachycardia Ablation
Topic: Arrhythmias
Date Posted: 5/24/2010
Author(s): Mahapatra S, Tucker-Schwartz J, Wiggins D, et al.
Citation: Heart Rhythm 2010;7:604-609.
Clinical Trial: No
Study Question: Are pressure-frequency measurements helpful for identifying the pericardial space during percutaneous access procedures?
Methods: Pressure was measured for 2 minutes in the pericardial space and in the thorax during sheath withdrawal in 20 patients who underwent subxyphoid percutaneous access of the pericardial space for epicardial ablation of ventricular tachycardia (VT). All patients were intubated and ventilated at 12 breaths/minute. Spectral analysis of the pressure recordings was performed offline by fast Fourier transformation.
Results: The mean pressures in the thorax (7.7 mm Hg) and pericardial space (7.8 mm Hg) did not differ significantly. Spectral analysis demonstrated a single peak at a mean of 0.2 Hz in the thorax pressure recordings and a dominant frequency at a mean of 0.2 Hz plus a second, smaller peak at a mean of 1.16 Hz in the pericardial pressure recordings.
Conclusions: Spectral analysis of pressure recordings reflects the respiratory rate in the thorax and the respiratory rate plus the heart rate in the pericardial space. These pressure-frequency characteristics are useful for identifying the pericardial space during pericardial access procedures.
Perspective: One of the limiting factors for widespread adaptation of epicardial ablation into clinical practice is the risk of right ventricular perforation. Fluoroscopy with contrast injections is helpful but not foolproof. The technique described in this study may facilitate recognition of when the percutaneous needle has passed from the thorax into the pericardial space. However, use of this technique in clinical practice will require the availability of a needle that has a pressure sensor at its tip and the capability for online spectral analysis. Fred Morady, M.D., F.A.C.C.
Title: Impact of Cytochrome P450 2C19 Loss-of-Function Polymorphism and of Major Demographic Characteristics on Residual Platelet Function After Loading and Maintenance Treatment With Clopidogrel in Patients Undergoing Elective Coronary Stent Placement
Topic: Interventional Cardiology
Date Posted: 5/24/2010 5:00:00 PM
Author(s): Hochholzer W, Trenk D, Fromm MF, et al.
Citation: J Am Coll Cardiol 2010;55:2427-2434.
Clinical Trial: No
Related Resources
JACC Article: Impact of Cytochrome P450 2C19 Loss-of-Function Polymorphism and of Major Demographic Characteristics on Residual Platelet Function After Loading and Maintenance Treatment With Clopidogrel in Patients Undergoing Elective Coronary Stent Placement
Study Question: What is the relative impact of demographic and clinical variables versus the cytochrome P450 2C19 (CYP2C19) polymorphism on antiplatelet effects of clopidogrel?
Methods: This analysis enrolled 760 patients undergoing elective coronary stent implantation after loading with 600 mg of clopidogrel. Residual platelet aggregation was determined by optical aggregometry (adenosine diphosphate 5 µmol/L) before discharge. The investigators analyzed the predictive value of the CYP2C19*2 polymorphism and baseline variables for an insufficient antiplatelet response by multivariable regression analysis and classification and regression trees analysis, and determined the proportion responsible for the antiplatelet response of these predictors by multivariable linear regression analysis.
Results: Major independent predictors for an insufficient antiplatelet response to clopidogrel were CYP2C19*2 carrier status (odds ratio [OR], 2.74; 95% confidence interval [CI], 1.93-3.90) together with age (OR, 1.03; 95% CI, 1.01-1.05), diabetes mellitus (OR, 1.75; 95% CI, 1.19-2.56), and body mass index (OR, 1.06; 95% CI, 1.02-1.11). The classification and regression trees analysis demonstrated that CYP2C19*2 carrier status followed by diabetes mellitus was the best discriminator between a sufficient and an insufficient antiplatelet response to clopidogrel. The full linear regression model including all of these parameters could only explain 11.5% of the antiplatelet response (5.2% by CYP2C19*2 carrier status alone).
Conclusions: The authors concluded that in patients critically dependent on adequate platelet inhibition, genotyping alone or in combination with clinical factors cannot replace phenotyping of platelet function.
Perspective: The primary finding of this analysis is that the CYP2C19*2 loss-of-function polymorphism and several clinical variables (diabetes mellitus, age, and body mass index) show a statistical highly significant association with high on-clopidogrel residual platelet aggregation. However, despite confirming the strong impact of the CYP2C19 loss-of-function polymorphism on antiplatelet effect of clopidogrel, the current data suggest that genotyping for CYP2C19 is insufficient for clinical decision-making without platelet function testing. Furthermore, addition of clinical variables could not fully correct this shortcoming. Based on all available data, it seems reasonable to integrate both genotyping and platelet function measurement to assess ischemic risk and to guide antiplatelet therapy in appropriate high-risk patients. Debabrata Mukherjee, M.D., F.A.C.C.
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