Cardiac susceptibility artifacts arising from the heart-lung interface.

Cardiac MRI studies often show susceptibility artifacts along the inferoapical myocardial margin in both human and in vivo animal experiments at field strengths of 1.5T and greater. This study was designed to determine the cause of these artifacts in porcine myocardium at 3T. Gradient echo images were obtained under various anatomic and physiologic conditions to systematically study potential sources of local susceptibility gradients. Lung resection in the open-chested, euthanized swine was the only intervention that eliminated the artifact. The data suggest that in the porcine model, the heart-lung interface is the primary cause of these artifacts. Magn Reson Med 45:341-345, 2001.

Cardioplegia and ischemia in the canine heart evaluated by 31P magnetic resonance spectroscopy.

BACKGROUND: Warm continuous blood cardioplegia provides excellent protection, but must be interrupted by ischemic intervals to aid visualization. We hypothesized that (1) as ischemia is prolonged, the reduced metabolic rate offered by cooling gives the advantage to hypothermic cardioplegia; and (2) prior cardioplegia mitigates the deleterious effects of normothermic ischemia. METHODS: Isolated cross-perfused canine hearts underwent cardioplegic arrest followed by 45 minutes of global ischemia at 10 degrees C or 37 degrees C, or 45 minutes of normothermic ischemia without prior cardioplegia. Left ventricular function was measured at baseline and during 2 hours of recovery. Metabolism was continuously evaluated by phosphorus-31 magnetic resonance spectroscopy. RESULTS: Adenosine triphosphate was 71% +/- 4%, 71% +/- 7%, and 38% +/- 5% of baseline at 30 minutes, and 71% +/- 4%, 48% +/- 5%, and 39% +/- 6% at 42 minutes of ischemia in the cold ischemia, warm ischemia, and normothermic ischemia without prior cardioplegia groups, respectively. Left ventricular systolic function, left ventricular relaxation, and high-energy phosphate levels recovered fully after cold cardioplegia and ischemia. Prior cardioplegia delayed the decline in intracellular pH during normothermic ischemia initially by 9 minutes, and better preserved left ventricular relaxation during recovery, but did not ameliorate the severe postischemic impairment of left ventricular systolic function, marked adenosine triphosphate depletion, and creatine phosphate increase. Left ventricular distensibility decreased in all groups. CONCLUSIONS: When cardioplegia is followed by prolonged ischemia, better protection is provided by hypothermia than by normothermia. Prior cardioplegia confers little advantage on recovery after prolonged normothermic ischemia but delays initial ischemic metabolic deterioration, which would contribute to the safety of brief interruptions of warm cardioplegia.

Tissue characterization of atherosclerotic plaque vulnerability by nuclear magnetic resonance.

Developing imaging technologies capable of identifying unstable atheromatous plaques in vivo is a major issue of clinical cardiovascular research. These techniques would permit an earlier surgical or medical therapy and would anticipate acute ischemic syndromes. Plaque vulnerability depends on the relative amount and thickness of its lipid core and fibrous cap. Several means of assessing atherosclerotic plaque composition have been used with nuclear magnetic resonance (NMR): carbon-13 and proton spectroscopy, proton imaging, chemical shift imaging, water diffusion imaging, and magnetization transfer. Recent data have shown that MR allows for accurate in vivo diagnosis and may support large scale prevention studies.

Depressive symptomatology and cocaine-induced pituitary-adrenal axis activation in individuals with cocaine dependence.

The hypothalamic-pituitary-adrenal (HPA) axis plays a role in cocaine dependence and major depressive disorder. The authors examined the correlation between baseline depressive symptomatology and pituitary-adrenal axis activation induced by acute cocaine challenge. Twelve patients with cocaine dependence were administered an iv bolus of cocaine (0.6 mg/kg) and their plasma was assayed for levels of adrenocorticotropic hormone (ACTH) and cortisol. Depressive symptomatology was assessed with total Hamilton rating scale for depression (HRSD) scores and its vegetative and cognitive superfactors. Cocaine produced a mean increase from baseline of 261% for ACTH and 73% for cortisol plasma levels. Changes in ACTH (r=0.69) and cortisol (r=0.59) were positively and significantly correlated with total HRSD scores and its vegetative, but not cognitive, factor symptom cluster. These results suggest that the HPA axis may be involved in affective disturbances associated with the use of cocaine. Implications of these data for the pathophysiology of cocaine dependence are discussed.

Measurement of human myocardial perfusion by double-gated flow alternating inversion recovery EPI.

This paper presents a flow-sensitive alternating inversion recovery (FAIR) method for measuring human myocardial perfusion at 1.5 T. Slice-selective/non-selective IR images were collected using a double-gated IR echoplanar imaging sequence. Myocardial perfusion was calculated after T1 fitting and extrapolation of the mean signal difference SI(Sel - SI(NSel). The accuracy of the method was tested in a porcine model using graded intravenous adenosine dose challenge. Comparison with radiolabeled microsphere measurements showed a good correlation (r = 0.84; mean error = 20%, n = 6) over the range of flows tested (0.9-7 ml/g/min). Applied in humans, this method allowed for the measurement of resting myocardial flow (1.04+/-0.37 ml/g/min, n = 11). The noise in our human measurements (SE(flow) = 0.2 ml/g/min) appears to come primarily from residual respiratory motion. Although the current signal-to-noise ratio limits our ability to measure small fluctuations in resting flow accurately, the results indicate that this noninvasive method has great promise for the quantitative assessment of myocardial flow reserve in humans.

Local relation between oxidative metabolism and perfusion in leg muscles of patients with heart failure studied by magnetic resonance imaging and spectroscopy.

BACKGROUND: We studied the local relation of muscle perfusion and metabolism in patients with severe chronic heart failure. Alterations of skeletal muscle blood flow and oxidative capacity contribute to exercise intolerance in these patients. The interdependence of both parameters has often been questioned. METHODS AND RESULTS: With the use of nuclear magnetic resonance, we quantified leg and muscle perfusion during reactive hyperemia in 7 patients with heart failure (New York Heart Association class III and IV) and 7 age-matched control subjects from the difference in longitudinal relaxation rate (1/T1). By using 31P nuclear magnetic resonance spectroscopy, we assessed oxidative metabolism from the creatine rephosphorylation time constant after a short ischemic exercise. Phosphocreatine recovery is slowed (74.6 +/- 11.3 vs 49.9 +/- 13.9 seconds, p = .002) and reactive hyperemic flow is reduced (48.5 +/- 24.9 vs 113 +/- 30.4 mL/100 mL per minute, p = .0005). CONCLUSIONS: By using a totally noninvasive protocol, we demonstrated that reactive hyperemic flow correlates with oxidative capacity in calf muscles from patients with heart failure, showing that exercise performance and local circulatory dysfunction are decreased in parallel in severe heart failure.

Behavior of atherosclerotic plaque components after in vitro angioplasty and atherectomy studied by high field MR imaging.

AIMS: Using magnetic resonance imaging (MRI), we developed in vitro models to image the response of fatty, fibrous, and calcified plaques to in vitro models of angioplasty and atherectomy, and tested the resistance of collagenous cap and lipid core to radial compression. METHODS AND RESULTS: We studied the effects of balloon compression on 10 fibrous plaques with a complete collagenous cap (group A), 6 fatty plaques without cap (group B), and 5 calcified plaques (group C). Atherectomy was performed on nine other fibrous lesions (group D). In group A, fibrous cap, lipid core, and plaque did not change after radial compression despite a decrease in luminal obstruction due to medial stretching. In group B, a reduction of plaque (-30%) and lipid core (-35%) were observed. Compression dissected calcified plaques at the shoulder level. In group D, atherectomy reduced collagenous cap by 54%, and plaque by 35%. CONCLUSIONS: In these models, MRI shows 1) the high resistance of collagenous caps to radial compression, 2) a stretching effect of compression on disease-free walls, enlarging lumen in case of fibrous plaque, but a reduction and redistribution of lipid cores in case of fatty plaques, 3) the rupture of calcified arteries at the plaque shoulder, and 4) the reduction of fibrous components by atherectomy but not by angioplasty. By characterizing plaque composition, MRI may allow a predictable response of atherosclerotic arteries to interventional procedures.

Imaging perfusion deficits in ischemic heart disease with susceptibility-enhanced T2-weighted MRI: preliminary human studies.

AIM: This feasibility study explores relative myocardial perfusion characterization with an investigational T2/T2 contrast agent. METHODS: Dysprosium-DTPA bis (methylamide) was administered peripherally in six patients with thallium defects. Rest and stress multi-section, gated, T2-weighted images were acquired with a 1.5 T echo-planar imager. Change in transverse relaxation rate was calculated in four segments for each subject. RESULTS: Magnetic resonance (MR) identified five of five instances of ischemia or infarction, at a dose of agent (0.25 mmol/kg) that was comparable to that currently used with clinically approved gadolinium agents. Injection at twice this dose resulted in saturation of the signal change, and the one ischemic segment corresponding to the higher dose was not identified by MR. MR was negative in two segments which, on final diagnosis, were determined to manifest thallium attenuation artifact. CONCLUSION: MR perfusion imaging with high susceptibility agents has the potential to characterize myocardial perfusion deficits.

Acute effects of cocaine on human brain activity and emotion.

We investigated brain circuitry mediating cocaine-induced euphoria and craving using functional MRI (fMRI). During double-blind cocaine (0.6 mg/kg) and saline infusions in cocaine-dependent subjects, the entire brain was imaged for 5 min before and 13 min after infusion while subjects rated scales for rush, high, low, and craving. Cocaine induced focal signal increases in nucleus accumbens/subcallosal cortex (NAc/SCC), caudate, putamen, basal forebrain, thalamus, insula, hippocampus, parahippocampal gyrus, cingulate, lateral prefrontal and temporal cortices, parietal cortex, striate/extrastriate cortices, ventral tegmentum, and pons and produced signal decreases in amygdala, temporal pole, and medial frontal cortex. Saline produced few positive or negative activations, which were localized to lateral prefrontal cortex and temporo-occipital cortex. Subjects who underwent repeat studies showed good replication of the regional fMRI activation pattern following cocaine and saline infusions, with activations on saline retest that might reflect expectancy. Brain regions that exhibited early and short duration signal maxima showed a higher correlation with rush ratings. These included the ventral tegmentum, pons, basal forebrain, caudate, cingulate, and most regions of lateral prefrontal cortex. In contrast, regions that demonstrated early but sustained signal maxima were more correlated with craving than with rush ratings; such regions included the NAc/SCC, right parahippocampal gyrus, and some regions of lateral prefrontal cortex. Sustained negative signal change was noted in the amygdala, which correlated with craving ratings. Our data demonstrate the ability of fMRI to map dynamic patterns of brain activation following cocaine infusion in cocaine-dependent subjects and provide evidence of dynamically changing brain networks associated with cocaine-induced euphoria and cocaine-induced craving.

Water diffusion properties of human atherosclerosis and thrombosis measured by pulse field gradient nuclear magnetic resonance.

Using pulsed field gradient methods combined with magnetic resonance imaging, we calculated the apparent water diffusion coefficient D in different atherosclerotic components to probe the microstructure of normal and diseased arteries by characterizing molecular motion. D was equal to 0.26 +/- 0.13 x 10(-5) cm2.s-1 in plaque lipid core, 1.45 +/- 0.41 x 10(-5) cm2.s-1 in collagenous cap, and 1.54 +/- 0.30 x 10(-5) cm2.s-1 in normal media. Water diffuses isotropically in the atheromatous core of the plaque, suggesting the absence or destruction of confining structures. The comparable diffusion coefficients in collagenous cap and normal media are consistent with similar biophysical barriers in both components. In thrombi, D varies with the aging processes (fresh thrombus, 0.72 +/- 0.11 x 10(-5) cm2.s-1; 1-week-old thrombus, 0.36 +/- 0.08 x 10(-5) cm2.s-1; old occluding thrombus, 1.33 +/- 0.33 x 10(-5) cm2.s-1), consistent with the cross-linking of the fibrin strands occurring in the early phase and the later thrombus organization. Defining an indirect index of arterial lipid infiltration, remodeling, and aging, diffusion imaging provides a new nuclear magnetic resonance characterization of atherothrombosis.

Ischemic intervals during warm blood cardioplegia in the canine heart evaluated by phosphorus 31-magnetic resonance spectroscopy.

OBJECTIVE: Warm blood cardioplegia requires interruption by ischemic intervals to aid visualization. We evaluated the safety of repeated interruption of warm blood cardioplegia by normothermic ischemic periods of varying durations. METHODS: In three groups of isolated cross-perfused canine hearts, left ventricular function was measured before and for 2 hours of recovery after arrest, which comprised four 15-minute periods of cardioplegia alternating with three ischemic intervals of 15, 20, or 30 minutes (I15, I20, and I30). Metabolism was continuously measured by phosphorus 31-magnetic resonance spectroscopy. RESULTS: Adenosine triphosphate level fell progressively as ischemia was prolonged; after recovery, adenosine triphosphate was 99% +/- 6%, 90% +/- 1% (p = 0.0004 vs control), and 68% +/- 3% (p = 0.0002) of control levels in I15, I20, and I30, respectively. Intracellular acidosis with ischemia was most marked in I30. After recovery, left ventricular maximal systolic elastance at constant heart rate and coronary perfusion pressure was maintained in I15 but fell to 85% +/- 3% in I20, (p = 0.003) and to 65% +/- 6% (p = 0.003) of control values in I30, while relaxation (tau) was prolonged only in I30 (p = 0.007). CONCLUSIONS: Hearts recover fully after three 15-minutes periods of ischemia during warm blood cardioplegia, but deterioration, significant with 20-minute periods, is profound when the ischemic periods are lengthened to 30 minutes. This suggests that in the clinical setting warm cardioplegia can be safely interrupted for short intervals, but longer interruptions require caution.

Interrelationship of oxidative metabolism and local perfusion demonstrated by NMR in human skeletal muscle.

Using nuclear magnetic resonance (NMR), we have examined the relationship of high-energy phosphate metabolism and perfusion in human soleus and gastrocnemius muscles. With 31P-NMR spectroscopy, we monitored phosphocreatine (PCr) decay and recovery in eight normal volunteers and four heart failure patients performing ischemic plantar flexion. By using echo-planar imaging, perfusion was independently measured by a local [inversion-recovery (T1-flow)] and a regional technique (NMR-plethysmography). After correction for its pH dependence, PCr recovery time constant is 27.5 +/- 8.0 s in normal volunteers, with mean flow 118 +/- 75 (soleus and gastrocnemius T1-flow) and 30.2 +/- 9.7 ml.100 ml-1.min-1 (NMR-plethysmography-flow). We demonstrate a positive correlation between PCr time constant and local perfusion given by y = 50 - 0.15x (r2 = 0.68, P = 0.01) for the 8 normal subjects, and y = 64 - 0.24x (r2 = 0.83, P = 0.0001) for the 12 subjects recruited in the study. Regional perfusion techniques also show a significant but weaker correlation. Using this totally noninvasive method, we conclude that aerobic ATP resynthesis is related to the magnitude of perfusion, i.e., O2 availability, and demonstrate that magnetic resonance imaging and magnetic resonance spectroscopy together can accurately assess muscle functional status.

Magnetic resonance images lipid, fibrous, calcified, hemorrhagic, and thrombotic components of human atherosclerosis in vivo.

BACKGROUND: Although MRI can discriminate the lipid core from the collagenous cap of atherosclerotic lesions in vitro with T2 contrast, it has not yet produced detailed in vivo images of these human plaque components. METHODS AND RESULTS: We imaged seven lesions from six patients who required surgical carotid endarterectomy and calculated T2 in vivo before surgery in various plaque regions. Using the same acquisition parameters, we repeated these measurements in vitro on the resected fragment and compared MR images with histology. T2 values calculated in vivo correlate with in vitro measurements for each plaque component; the in vitro discrimination we demonstrated previously with T2 contrast can therefore be performed similarly in vivo. CONCLUSIONS: MRI is the first noninvasive imaging technique that allows the discrimination of lipid cores, fibrous caps, calcifications, normal media, and adventitia in human atheromatous plaques in vivo. This technique also characterizes intraplaque hemorrhage and acute thrombosis. This result may support further investigations that include MRI of plaque progression, stabilization, and rupture in human atherosclerosis.

Myocardial intensity changes associated with flow stimulation in blood oxygenation sensitive magnetic resonance imaging.

Functional magnetic resonance imaging exploits deoxygenated blood as an endogenous source for contrast in assessing local changes in tissue perfusion. Intrinsic changes in myocardial signal intensity were measured during dipyridamole induced coronary vasodilatation with T2*-weighted echo planar MRI in healthy volunteers. Concurrently, changes in flow velocity in the left anterior descending coronary artery were measured using a time-of-flight method. Dipyridamole infusion produced 14 +/- 6% increase in myocardial signal intensity (n = 7). Temporal profile of the myocardial signal intensity changes correlated well with the augmentation of coronary flow velocity. The data are consistent with the concept that changes in myocardial deoxyhemoglobin content due to altered flow result in changes in magnetic susceptibility that can be detected on T2*-weighted MR images.

Perfusion changes in human skeletal muscle during reactive hyperemia measured by echo-planar imaging.

Muscle performance is markedly influenced by tissue perfusion. Techniques that allow quantification of microvascular flow are limited by the use of ionizing radiation. In this investigation, we apply an NMR model previously developed by Detre et al. to the measurement of human muscle perfusion during reactive hyperemia. We compare our results with conventional plethysmography adapted to NMR. Using echo-planar imaging, T1 and T2 were measured in 14 subjects during rest, ischemia, and reactive hyperemia. Mean leg muscle T1 in healthy volunteers is 850 ms at rest and 834 ms at reperfusion, leading to a calculated reactive hyperemia flow increase (T1 flow) of 103 +/- 40 ml/100 ml/min. T1 flows correlate well with NMR-plethysmography values. Changes in T2, which are sensitive to both deoxyhemoglobin content and vessel diameter variations, are also correlated with perfusion measurements. T1 changes allow quantification of regional perfusion in human muscle during reactive hyperemia.

Imaging and sizing of atrial septal defects by magnetic resonance.

BACKGROUND: Development of techniques for percutaneous closure of atrial septal defects (ASDs) makes accurate noninvasive sizing of ASDs important for appropriate patient selection. METHODS AND RESULTS: Magnetic resonance (MR) images of ASDs were obtained in 30 patients (mean age, 41 +/- 16 years) by both spin-echo and phase-contrast cine MR imaging. Spin-echo images were obtained in two orthogonal views (short-axis and four-chamber) perpendicular to the plane of the ASD. Spin-echo major and minor diameters were measured, and spin-echo defect area was calculated. Phase-contrast cine MR images were obtained in the plane of the ASD, and cine major diameter and defect area were measured from the region of signal enhancement or phase change due to shunt flow across the defect. MR measurements were compared with templates cut during surgery to match the defect or with ASD diameter determined by balloon sizing at catheterization. ASD size measured from cine MR images (y) agreed closely with catheterization and template standards (x). For major diameter, y = 0.78x + 5.7, r = .93, and SEE = 3.4 mm. On average, spin-echo measurements overestimated major diameter and area of secundum ASDs by 48% and 125%, respectively. CONCLUSIONS: Phase-contrast cine MR images acquired in the plane of an ASD define the defect shape by the cross section of the shunt flow stream and allow noninvasive determination of defect size with sufficient accuracy to permit stratification of patients to closure of the defect by catheter-based techniques versus surgery. Spin-echo images, on the other hand, are not adequate for defining ASD size, because septal thinning adjacent to a secundum ASD may appear to be part of the defect.

T2-weighted contrast for NMR characterization of human atherosclerosis.

We sought to determine whether 1H NMR images without chemical-shift selection can adequately characterize the components of human atheromatous arteries. NMR, as a nondestructive, biochemical imaging tool, has the potential to identify lipids in atherosclerotic plaques but has not yet produced detailed images of atheroma components. Using 1H NMR spectroscopy at 9.4 T, we examined microdissected components of diseased and normal arteries to determine water relaxation constants (T1 and T2) as well as the relative content of mobile lipid. Relaxation times were also measured at 1.5 and 4.7 T. Sections of arteries with atherosclerotic lesions of graded severity were imaged at 1.5 and 9.4 T. The contrast-to-noise ratio (CNR) was used to assess lesion conspicuity. In the atheromatous core, the water NMR signal predominates over that of lipid (lipid-to-water ratio, 0.11). At 9.4 T, T2 is 20.2 ms for the atheromatous core, 30.1 ms for the collagenous cap, and 29.5 ms for normal media. This results in a high CNR on T2-weighted (T2w) images for atheromatous core compared with the collagenous cap and normal media. A similar contrast was measured at lower field strength. Calcifications do not generate appreciable signal due to their low water content but can be detected on T1-weighted (T1w) images. The water T2 contrast allows discrimination of the atheromatous lipid core from collagenous regions. The combination of T1w and T2w sequences permits in vitro identification of the atheromatous core, collagenous cap, calcifications, media, adventitia, and perivascular fat. The discrimination of collagen fibers that overlie lipid deposits permits study of plaque protection and stability at all field strengths and may provide the basis for in vivo microscopy of human atherosclerosis.

Cardiac problems in patients with neurologic disease.

The cardiologist and internist can make a major contribution to the care of patients with neurologic disease, both in terms of treating patients with symptomatic cardiac involvement and reducing mortality. This article highlights the need to recognize ECG abnormalities that may represent purely neurologic disease as well as indicate cardiac pathology that may be part of the neurophysiologic disease process. The role of cardiac emboli in stroke and the essential role of anticoagulation in stroke prevention have been discussed. Additionally, the importance of emboli in relation to endocarditis and the essential role of anticoagulation for stroke prevention in patients with prosthetic valves have been emphasized. Finally, the cardiac manifestations of several neuromyopathic diseases have been indicated, and the importance of cardiac issues in patient management decisions has been shown. The interplay of cardiac and neurologic concerns demonstrates how a collaboration of neurologists and cardiologists can yield rewarding results in resolving some of the more difficult problems in clinical medicine.

13C-NMR spectroscopy of human atherosclerotic lesions. Relation between fatty acid saturation, cholesteryl ester content, and luminal obstruction.

Previous investigations have used 13C-nuclear magnetic resonance (NMR) spectroscopy to demonstrate the similarities between lipoproteins and the mobile lipids of atheroma. In this study, we tested the hypothesis that 13C-NMR changes are related to indices of histological severity. We classified 20 human arteries according to their obstruction ratio (OR), defined as the ratio of the plaque area to the area delimited by the external elastic lamina. In group A, OR was < 40%, and in group B, OR was > 40%. We analyzed at 9.4 T the resonances of unsaturated (UFA) and polyunsaturated (PUFA) carbons, the resonances of the carbons 19 and 21 (C19, C21) of cholesteryl esters (CE), the methine carbon peak of fatty acids (CH2)n, the choline peak from phospholipids (PL), and the glycerol peak from triglyceride (TG). The UFA/PUFA, UFA/(CH2)n, and PUFA/(CH2)n ratios are markers of fatty acid saturation. (C19, C21)/(CH2)n, choline/(CH2)n, and glycerol/(CH2)n are indices of CE, PL, and TG content, respectively. UFA/PUFA in group A is 1.15 +/- 0.34 versus 1.63 +/- 0.32 in group B (P = .005). PUFA/(CH2)n is 0.26 +/- 0.10 in group A versus 0.16 +/- 0.04 in group B (P = .049). C19, C21/(CH2)n in group A is 0.32 +/- 0.15 versus 0.63 +/- 0.23 for group B (P = .003). No significant difference was found in UFA/(CH2)n or in the TG or PL ratios. 13C spectral examination of human atherosclerosis demonstrates decreased resonances for polyunsaturated fatty acyl chains and cholesteryl esters with increasing obstruction.

Warm and cold blood cardioplegia. Comparison of myocardial function and metabolism using 31p magnetic resonance spectroscopy.

BACKGROUND: Standard myocardial protection during cardiac surgery uses hypothermic arrest, but warm heart surgery, recently introduced, is now used in many centers. We hypothesized that warm continuous blood cardioplegia (WCBC) would provide better myocardial preservation than cold continuous blood cardioplegia (CCBC). METHODS AND RESULTS: In isolated cross-perfused canine hearts, left ventricular (LV) function and myocardial O2 consumption (MVO2) were measured at constant LV volume, coronary perfusion pressure, and heart rate before and after 75 minutes of arrest at 37 degrees C or 10 degrees C. Metabolism was evaluated by 31P nuclear magnetic resonance spectroscopy. LV resting tone increased transiently after arrest by CCBC but not WCBC (38 +/- 3.9 versus 2.9 +/- 0.5 mm Hg, P < .0005). Myocardial ATP changed over time differently in the groups (P < .001), declining at the outset of CCBC and returning to control levels during the recovery period after CCBC or WCBC. Intracellular pH rose from 7.17 +/- 0.03 to 7.85 +/- 0.05 during CCBC (P < .0005 versus WCBC). MVO2 declined dramatically during arrest at either temperature but to a lower value during CCBC (P < .0005). LV pressure recovered to 86.1 +/- 5.1% of its prearrest value after CCBC and to 97.2 +/- 7.8% following WCBC (P = NS). After CCBC but not WCBC, there were small but significant increases in LV end-diastolic pressure (by 1.3 mm Hg, P < .05) and in the LV relaxation constant, tau (from 37.3 +/- 1.5 to 42.3 +/- 2.4 milliseconds, P < .05). CONCLUSIONS: The increase in intracellular pH during CCBC is largely accounted for by physicochemical factors. Group differences in ATP over time may be related to rapid cooling contracture during CCBC. The data suggest that CCBC mildly impairs LV function but that WCBC preserves function and metabolism at or near prearrest levels.