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The baseline data from GLORIA-AF phase 2 demonstrate that in newly diagnosed nonvalvular atrial fibrillation patients, NOAC have been highly adopted into practice, becoming more frequently prescribed than VKA in Europe and North America. Worldwide, however, a large proportion of patients remain undertreated, particularly in Asia and North America. (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients With Atrial Fibrillation [GLORIA-AF]; NCT01468701).

To determine the better method of measuring pericardial constraint, pericardial pressure was recorded by a liquid-filled open-ended catheter and a liquid-containing flat balloon in six open-chest anesthetized dogs. Left ventricular pressure was measured by a micromanometer-tipped catheter and left ventricular anteroposterior diameter was measured by sonomicrometry. Left ventricular end-diastolic pressure was raised to 20 +-1.7 (mean -+ SD) mm Hg by intravenous saline. Left ventricular diastolic pressure-diameter loops were constructed (1) with incremental amounts of saline (0 to 50 ml) in the resealed pericardium, (2) with several small holes in the pericardium, and (3) pressure is familiar to cardiovascular physiologists and can be measured by connecting a manometer to any fluid-filled space as with a liquid-filled catheter. The concept of surface pressure is more difficult; it is the force per unit surface area exerted by, for example, the left ventricular surface on the overlying parietal pericardial membrane. The difference between the pericardial liquid pressure and surface pressure is the compressive contact stress7 developed between the surfaces.4The oft-quoted work by Kenner and Wood' supports the common view that pericardial pressure is approximately equal to intrathoracic pressure and unchanged by alterations in cardiac volume. They dilated the heart substantially by aortic and pulmonary artery constriction without importantly raising pericardial (liquid) pressure. Thus, the aim of the present study was to determine whether an open-ended catheter or a flat, liquid-containing balloon could accurately measure pericardial constraint. To arrive at a "gold standard" of pericardial pressure we postulated a simple, static-equilibrium concept: at a given left ventricular end-diastolic size (diameter) the correct pericardial pressure is that pressure which must be added to left ventricular transmural pressure to equal the intracavitary left ventricular pressure. We measured left ventricular transmural pressure directly as a function of left ventricular diameter at the end of the experiment after removal of the pericardium with the chest widely open and the lungs retracted. Thus, we defined the calculated pericardial pressure as the difference between the left ventricular end-diastolic pressure measured when the pericardium was closed and the left ventricular end-diastolic pressure measured at the same diameter when the pericardium was removed. To determine the dependence of the measured pericardial pressure on the volume of pericardial liquid we infused saline into the resealed pericardial cavity. To test the hypothesis that even a netlike pericardium would induce a measurable, physiologically significant constraint on left ventricular diastolic filling, measurements were repeated after several small holes had been cut in the pericardium. MethodsAnimal preparation. Experiments were done in six mongrel dogs (22 to 33 kg). Anesthesia was induced by 25 mg/kg iv sodium thiopental (Pentothal, Abbott Labora...

SUMMARY To determine the relationship of phase changes and abnormalities of ventricular contraction and conduction, we performed phase image analysis of blood pool scintigrams in 29 patients. Eleven patients had no evidence of blood pool contraction or ECG conduction abnormalities, four had contraction abnormalities, seven had abnormal conduction and seven had abnormalities of both variables.The phase delay generally related to the degree of contraction abnormality. The mean phase delay in hypokinetic segments differed from that in normokinetic segments in the same patient (p < 0.025), the phase delay of akinetic and dyskinetic segments differed from that in normokinetic segments (p < 0.001) and the phase delay in dyskinetic segments differed from that in akinetic segments (p < 0.005), but there was a significant overlap in the phase delay in normal and hypokinetic segments. Also, in patients with conduction abnormalities, the minimal associated regional phase delay presented a phase dispersion and a pattern of contraction consistent with the pattern of conduction and different from normal.A single study performed both at rest and with stress demonstrated the effect of heart rate on phase assessment and confirmed the independent effects of contraction and conduction on phase delay. Acquisition and analytic methods should add significantly to the resolution of the phase method.EQUILIBRIUM multiple-gated blood pool scintigraphy is an accurate noninvasive method for determining ventricular size and function.1' 2 Analytic methods that use digital computer manipulation have been applied to the blood pool study to extract additional data.8' 4 Such manipulation produces functional images as the ejection fraction image, which color-codes the end-diastolic frame of the blood pool scintigram in terms of regional ejection fraction, while the stroke volume image color-codes the end-diastolic frame in terms of regional stroke volume. Recently, the phase image has been developed. MethodsPhase image analysis was performed on two series of consecutive patients, in whom blood pool scintigraphy was required clinically for the noninvasive assessment of ventricular size and function. One group included patients with a normal ejection fraction and segmental wall motion and without electrocardiographic conduction delay. A second consecutive series of patients had reduced left ventricular ejection fraction and obvious contraction abnormalities on qualitative visual blood pool assessment or significant electrocardiographic intraventricular conduction delay with QRS > 0.12 second. All patients were in normal sinus rhythm.The history of each patient was reviewed for infarction, and a 12-lead ECG was obtained on the day of scintigraphy. Electrocardiographic abnormalities were noted. Evidence of infarction was confirmed historically and supported by the presence of ECG Q waves . 0.04 second in duration. Conduction abnormalities, including evidence of left bundle branch block and right bundle branch block,7 were documented and pacemaker ar...

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