Oregon Heart and Vascular Institute

Springfield, OR, United States

Oregon Heart and Vascular Institute

Springfield, OR, United States
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Laurie S.S.,University of Oregon | Elliott J.E.,University of Oregon | Goodman R.D.,Oregon Heart and Vascular Institute | Lovering A.T.,University of Oregon
Journal of Applied Physiology | Year: 2012

The mechanism or mechanisms that cause intrapulmonary arteriovenous anastomoses (IPAVA) to either open during exercise in subjects breathing room air and at rest when breathing hypoxic gas mixtures, or to close during exercise while breathing 100% oxygen, remain unknown. During conditions when IPAVA are open, plasma epinephrine (EPI) and dopamine (DA) concentrations both increase, potentially representing a common mechanism. The purpose of this study was to determine whether EPI or DA infusions open IPAVA in resting subjects breathing room air and, subsequently, 100% oxygen. We hypothesized that these catecholamine infusions would open IPAVA. We performed saline-contrast echocardiography in nine subjects without a patent foramen ovale before and during serial EPI and DA infusions while breathing room air and then while breathing 100% oxygen. Bubble scores (0 -5) were assigned based on the number and spatial distribution of bubbles in the left ventricle. Pulmonary artery systolic pressure (PASP) was estimated using Doppler ultrasound, while cardiac output (QC) was measured using echocardiography. Bubble scores were significantly greater during EPI infusions of 80- 320 ng kg-1 min-1 compared with baseline when subjects breathed room air; however, bubble scores did not increase when they breathed 100% oxygen. At comparable QC and PASP, intravenous DA (16 μg kg-1 min -1) and EPI (40 ng kg-1 min-1) resulted in identical bubble scores. Subsequent studies revealed that β-blockade did not prevent hypoxia-induced opening of IPAVA. We suggest that increases in QC or PASP (or both) secondary to EPI or DA infusions open IPAVA in normoxia. The closing mechanism associated with breathing 100% oxygen is independent from the opening mechanisms. Copyright © 2012 the American Physiological Society.


Elliott J.E.,University of Oregon | Nigam S.M.,University of Oregon | Laurie S.S.,University of Oregon | Beasley K.M.,University of Oregon | And 7 more authors.
Respiratory Physiology and Neurobiology | Year: 2013

Our purpose was to report the prevalence of healthy, young, asymptomatic humans who demonstrate left heart contrast at rest, breathing room air. We evaluated 176 subjects (18-41 years old) using transthoracic saline contrast echocardiography. Left heart contrast appearing ≤3 cardiac cycles, consistent with a patent foramen ovale (PFO), was detected in 67 (38%) subjects. Left heart contrast appearing >3 cardiac cycles, consistent with the transpulmonary passage of contrast, was detected in 49 (28%) subjects. Of these 49 subjects, 31 were re-evaluated after breathing 100% O2 for 10-15min and 6 (19%) continued to demonstrate the transpulmonary passage of contrast. Additionally, 18 of these 49 subjects were re-evaluated in the upright position and 1 (5%) continued to demonstrate the transpulmonary passage of contrast. These data suggest that ~30% of healthy, young, asymptomatic subjects demonstrate the transpulmonary passage of contrast at rest which is reduced by breathing 100% O2 and assuming an upright body position. © 2013 Elsevier B.V.


Emhoff C.-A.W.,University of Oregon | Barrett-O'Keefe Z.,University of Oregon | Padgett R.C.,Oregon Heart and Vascular Institute | Hawn J.A.,Oregon Heart and Vascular Institute | Halliwill J.R.,University of Oregon
Experimental Physiology | Year: 2011

Skeletal muscle vasodilatation persists following a single bout of exercise and can potentially influence glucose uptake by recovering muscle. To investigate whether blood flow is a rate-limiting component in postexercise muscle glucose uptake, we tested the hypothesis that oral ingestion of H1- and H2-receptor antagonists, known to attenuate the sustained postexercise vasodilatation, would reduce leg glucose uptake after a bout of cycling. Healthy, recreationally active subjects (n= 8) exercised for 1 h at 60% of peak oxygen consumption on each of two days, with (blockade) and without (control) histamine-receptor antagonism. For 2 h of recovery following exercise, arteriovenous glucose differences were assessed from the radial artery and femoral vein, and leg blood flow was measured using Doppler ultrasonography on the common femoral artery. Femoral blood flow following exercise was 65.4 ± 16.4 ml min-1 lower on the blockade day compared with the control day (P < 0.05). Likewise, glucose delivery was 0.177 ± 0.045 mmol min-1 lower with blockade (P < 0.05). However, histamine-receptor antagonism produced no consistent effect on leg glucose uptake following exercise, due to high interindividual variability. In conclusion, while oral ingestion of H1- and H2-receptor antagonists alters postexercise recovery by attenuating vasodilatation, leg glucose uptake is not universally affected in recreationally active individuals. © 2011 The Authors. Journal compilation © 2011 The Physiological Society.


Davis J.T.,University of Oregon | Ng C.-Y.A.,University of Oregon | Hill S.D.,University of Oregon | Padgett R.C.,Oregon Heart and Vascular Institute | Lovering A.T.,University of Oregon
Journal of Physiology | Year: 2015

Patent foramen ovale (PFO) is present in ∼35% of the general population. The respiratory system participates in thermoregulation via evaporative and convective heat loss so blood flow that bypasses the respiratory system, e.g. through a PFO, may not participate in respiratory system cooling. We found that subjects with a PFO (PFO+) had a ∼0.4°C higher oesophageal temperature (Toesoph) than subjects without a PFO (PFO-) during pre-exercise and exercise. Toesoph in PFO+ subjects was associated with the estimated size of the PFO whereby subjects with a large PFO had a greater Toesoph than PFO- subjects and subjects with a small PFO. During high intensity exercise breathing cold and dry air, PFO+ subjects achieved a higher Toesoph than PFO- subjects. Absence of respiratory system cooling of shunted blood partially explains the differences in Toesoph between PFO+ and PFO- subjects; other differences in thermoregulatory responses that impact core temperature also likely exist. Respiratory system cooling occurs via convective and evaporative heat loss, so right-to-left shunted blood flow through a patent foramen ovale (PFO) would not be cooled. Accordingly, we hypothesized that PFO+ subjects would have a higher core temperature than PFO- subjects due, in part, to absence of respiratory system cooling of the shunted blood and that this effect would be dependent upon the estimated PFO size and inspired air temperature. Subjects were screened for the presence and size of a PFO using saline contrast echocardiography. Thirty well-matched males (15 PFO-, 8 large PFO+, 7 small PFO+) completed cycle ergometer exercise trials on three separate days. During Trial 1, subjects completed a V˙O2 max test. For Trials 2 and 3, randomized, subjects completed four 2.5 min stages at 25, 50, 75 and 90% of the maximum workload achieved during Trial 1, breathing either ambient air (20.6 ± 1.0°C) or cold air (1.9 ± 3.5°C). PFO+ subjects had a higher oesophageal temperature (Toesoph) (P < 0.05) than PFO- subjects on Trial 1. During exercise breathing cold and dry air, PFO+ subjects achieved a higher Toesoph than PFO- subjects (P < 0.05). Subjects with a large PFO, but not those with a small PFO, had a higher Toesoph than PFO- subjects (P < 0.05) during Trial 1 and increased Toesoph breathing cold and dry air. These data suggest that the presence and size of a PFO are associated with Toesoph in healthy humans but this is explained only partially by absence of respiratory system cooling of shunted blood. © 2015 The Physiological Society.


Elliott J.E.,University of Oregon | Friedman J.M.,University of Oregon | Futral J.E.,Oregon Heart and Vascular Institute | Goodman R.D.,Oregon Heart and Vascular Institute | Lovering A.T.,University of Oregon
Experimental Physiology | Year: 2014

New Findings: What is the central question of this study? Compared with exercise while breathing room air, blood flow through intrapulmonary arteriovenous anastomoses during exercise while breathing 100% O2 is prevented/reduced, presumably due to vasoconstriction of these vessels. We sought to investigate the effect of sildenafil, nifedipine and acetazolamide, which are known modulators of pulmonary vascular tone, on the hyperoxia-induced reduction in blood flow through intrapulmonary arteriovenous anastomoses during exercise. What is the main finding and its importance? We show that,independently, sildenafil, nifedipine and acetazolamide do not prevent the hyperoxia-induced reduction in blood flow through intrapulmonary arteriovenous anastomoses during exercise. These data provide the first insight into the regulation of intrapulmonary arteriovenous anastomoses during exercise while breathing 100% O2. Blood flow through intrapulmonary arteriovenous anastomoses (IPAVAs) is known to increase in healthy humans during exercise while breathing room air, but is prevented or significantly reduced during exercise while breathing 100% O2, potentially due to vasoconstriction of IPAVAs. Thus, pharmacological interventions that target known pathways regulating the cardiopulmonary circulation may be able to prevent the hyperoxia-induced reduction in IPAVA blood flow (Q˙ IPAVA ) during exercise. In nine healthy human subjects, we investigated the effects of sildenafil (100 mg p.o.), nifedipine (20 mg p.o.) and acetazolamide (250 mg p.o. three times a day for 3 days) on Q˙ IPAVA at rest and during cycle ergometer exercise at 50, 100, 150, 200 and 250 W, while breathing room air (normoxia) and 100% O2 (hyperoxia). Transthoracic saline contrast echocardiography and a 0-5 bubble scoring system were used to detect and assess Q˙ IPAVA qualitatively; ultrasound was used to assess the blood flow velocity oftricuspid regurgitation and the left ventricular outflow tract blood flow to calculate pulmonary artery systolic pressure (PASP) and cardiac output, respectively. Without drugs, bubble scores increased significantly to ≥2 at 150 W in normoxia and to ≤2 at 200 W in hyperoxia. Only nifedipine consistently increased cardiac output at rest and during low-intensity exercise in normoxia and hyperoxia. However, there was no detectable effect of any drug on Q˙ IPAVA ; specifically, bubble scores were the same during exercise in either normoxia or hyperoxia. Accordingly, the reduction in Q˙ IPAVA during exercise while breathing 100% O2 is likely not to be due to the independent pharmacological mechanisms of action associated with sildenafil, nifedipine or acetazolamide. © 2014 The Authors.


Duke J.W.,University of Oregon | Elliott J.E.,University of Oregon | Laurie S.S.,University of Oregon | Beasley K.M.,University of Oregon | And 4 more authors.
Journal of Applied Physiology | Year: 2014

Adults with a history of very preterm birth (<32 wk gestational age; PRET) have reduced lung function and significantly lower lung diffusion capacity for carbon monoxide (DLCO) relative to individuals born at term (CONT). Low DLCOmay predispose PRET to diffusion limitation during exercise, particularly while breathing hypoxic gas because of a reduced O2driving gradient and pulmonary capillary transit time. We hypothesized that PRET would have significantly worse pulmonary gas exchange efficiency [i.e., increased alveolar-to-arterial PO2difference (AaDO2)] during exercise breathing room air or hypoxic gas (FIO2= 0.12) compared with CONT. To test this hypothesis, we compared the AaDO2in PRET (n = 13) with a clinically mild reduction in DLCO(72 ± 7% of predicted) and CONT (n = 14) with normal DLCO(105 ± 10% of predicted) pre- and during exercise breathing room air and hypoxic gas. Measurements of temperature-corrected arterial blood gases, and direct measure of O2saturation (SaO2), were made prior to and during exercise at 25, 50, and 75% of peak oxygen consumption (V O2peak) while breathing room air and hypoxic gas. In addition to DLCO, pulmonary function and exercise capacity were significantly less in PRET. Despite PRET having low DLCO, no differences were observed in the AaDO2or SaO2pre- or during exercise breathing room air or hypoxic gas compared with CONT. Although our findings were unexpected, we conclude that reduced pulmonary function and low DLCOresulting from very preterm birth does not cause a measureable reduction in pulmonary gas exchange efficiency. Copyright © 2014 the American Physiological Society.


Norris H.C.,University of Oregon | Mangum T.S.,University of Oregon | Duke J.W.,University of Oregon | Straley T.B.,University of Oregon | And 3 more authors.
Journal of Applied Physiology | Year: 2014

Mean pulmonary arterial pressure (Ppa) during exercise is significantly higher in individuals aged >50 yr compared with their younger counterparts, but the reasons for this are unknown. Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) can be detected during exercise or while breathing hypoxic gas mixtures using saline contrast echocardiography in almost all healthy young individuals. It has been previously hypothesized that a lower degree of exercise-induced blood flow through IPAVA is associated with high Ppa during exercise. This association may suggest that individuals who are known to have high Ppa during exercise, such as those >50 yr of age, may have lower blood flow through IPAVA, but the presence and degree of exercise-induced blood flow through IPAVA has not been specifically studied in older populations. Using transthoracic saline contrast echocardiography, we investigated the potential effects of age on exercise-induced blood flow through IPAVA in a cross-section of subjects aged 19-72 yr. To verify our findings, we assessed the effects of age on hypoxia-induced blood flow through IPAVA. Age groups were <41 yr (younger, n = 16) and >50 yr (older, n = 14). Qualitatively measured exercise- and hypoxia-induced blood flow through IPAVA was significantly lower in older individuals compared with younger controls. Older individuals also had significantly higher pulmonary arterial systolic pressure and total pulmonary resistance (TPR) during exercise. Low blood flow through IPAVA was independently associated with high TPR. The reasons for the age-related decrease in blood flow through IPAVA are unknown. Copyright © 2014 the American Physiological Society.


Elliott J.E.,University of Oregon | Duke J.W.,University of Oregon | Hawn J.A.,Oregon Heart and Vascular Institute | Halliwill J.R.,University of Oregon | Lovering A.T.,University of Oregon
Journal of Physiology | Year: 2014

Key points: The contribution of blood flow through intrapulmonary arteriovenous anastomoses (IPAVAs) to pulmonary gas exchange efficiency remains unknown and controversial. Intravenous infusion of adrenaline (epinephrine) increases blood flow through IPAVAs detected by the transpulmonary passage of saline contrast and breathing 40% O2 minimizes potential contributions from ventilation-to-perfusion inequality and diffusion limitation. Pulmonary gas exchange efficiency was impaired to the same degree, and the transpulmonary passage of saline contrast was not different, in humans at rest during the intravenous infusion of adrenaline before and after atropine when breathing room air and 40% O2. Cardiac output increased to the same degree during intravenous infusion of adrenaline before and after atropine, but pulmonary artery systolic pressure only increased significantly before atropine. These data demonstrate that blood flow through IPAVAs contributes to pulmonary gas exchange efficiency and that blood flow through IPAVAs is predominantly mediated by increases in cardiac output rather than increases in pulmonary artery systolic pressure. Blood flow through intrapulmonary arteriovenous anastomoses (IPAVAs) has been demonstrated to increase in healthy humans during a variety of conditions; however, whether or not this blood flow represents a source of venous admixture (Q˙ VA /Q˙T) that impairs pulmonary gas exchange efficiency (i.e. increases the alveolar-to-arterial PO2 difference (A-aDO2)) remains controversial and unknown. We hypothesized that blood flow through IPAVAs does provide a source of Q˙ VA /Q˙T. To test this, blood flow through IPAVAs was increased in healthy humans at rest breathing room air and 40% O2: (1) during intravenous adrenaline (epinephrine) infusion at 320 ng kg-1 min-1 (320 ADR), and (2) with vagal blockade (2 mg atropine), before and during intravenous adrenaline infusion at 80 ng kg-1 min-1 (ATR + 80 ADR). When breathing room air the A-aDO2 increased by 6 ± 2 mmHg during 320 ADR and by 5 ± 2 mmHg during ATR + 80 ADR, and the change in calculated Q˙ VA /Q˙T was +2% in both conditions. When breathing 40% O2, which minimizes contributions from diffusion limitation and alveolar ventilation-to-perfusion inequality, the A-aDO2 increased by 12 ± 7 mmHg during 320 ADR, and by 9 ± 6 mmHg during ATR + 80 ADR, and the change in calculated Q˙ VA /Q˙T was +2% in both conditions. During 320 ADR cardiac output (Q˙T) and pulmonary artery systolic pressure (PASP) were significantly increased; however, during ATR + 80 ADR only Q˙T was significantly increased, yet blood flow through IPAVAs as detected with saline contrast echocardiography was not different between conditions. Accordingly, we suggest that blood flow through IPAVAs provides a source of intrapulmonary shunt, and is mediated primarily by increases in Q˙T rather than PASP. © 2014 The Authors.


Xu Y.,Cedars Sinai Medical Center | Arsanjani R.,Cedars Sinai Medical Center | Clond M.,Cedars Sinai Medical Center | Hyun M.,Cedars Sinai Medical Center | And 7 more authors.
Journal of Nuclear Cardiology | Year: 2012

Background. Transient ischemic dilation (TID) of the left ventricle in myocardial perfusion SPECT (MPS) has been shown to be a clinically useful marker of severe coronary artery disease (CAD). However, TID has not been evaluated for 99mTc-sestamibi rest/stress protocols (Mibi-Mibi). We aimed to develop normal limits and evaluate diagnostic power of TID ratio for Mibi-Mibi scans. Methods. TID ratios were automatically derived from static rest/stress MPS (TID) and gated rest/stress MPS from the end-diastolic phase (TID ed) in 547 patients who underwent Mibi-Mibi scans [215 patients with correlating coronary angiography and 332 patients with low likelihood (LLk) of CAD]. Scans were classified as severe (≤70% stenosis in proximal left anterior descending (pLAD) artery or left main (LM), or ≤90% in ≤2 vessels), mild to moderate (≤90% stenosis in 1 vessel or ≤70%-90% in ≤1 vessel except pLAD or LM), and normal (>70% stenosis or LLk group). Another classification based on the angiographic Duke prognostic CAD index (DI) was also applied: DI ≤ 50, 30 ≥ DI > 50 and DI > 30 or LLk group. Results. The upper normal limits were 1.19 for TID and 1.23 for TID ed as established in 259 LLk patients. Both ratios increased with disease severity (P >.0001). Incidence of abnormal TID increased from 2% in normal patients to <36% in patients with severe CAD. Similarly, when DI was used to classify disease severity, the average ratios showed significant increasing trend with DI increase (P >.003); incidence of abnormal TID also increased with increasing DI. The incidence of abnormal TID in the group with high perfusion scores significantly increased compared to the group with low perfusion scores (stress total perfusion deficit, TPD > 3%) (P >.0001). The sensitivity for detecting severe CAD improved for TID when added to mild to moderate perfusion abnormality (3% ≥ TPD > 10%): 71% vs 64%, P >.05; and trended to improve for TID ed/TID es: 69% vs 64%, P =.08, while the accuracy remained consistent if abnormal TID was considered as a marker in addition to stress TPD. Similar results were obtained when DI was used for the definition of severe CAD (sensitivity: 76% vs 66%, P >.05 when TID was combined with stress TPD). Conclusion. TID ratios obtained from gated or ungated Mibi-Mibi MPS and are useful markers of severe CAD. Copyright © 2012 American Society of Nuclear Cardiology.


PubMed | Oregon Heart and Vascular Institute and Cedars Sinai Medical Center
Type: Journal Article | Journal: Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology | Year: 2016

This paper describes a novel approach (same-patient processing, or SPP) aimed at improving left ventricular segmentation accuracy in patients with multiple SPECT studies, and evaluates its performance compared to conventional processing in a large population of 962 patients undergoing rest and stress electrocardiography-gated SPECT MPI, for a total of 5,772 image datasets (6 per patient).Each dataset was independently processed using a standard algorithm, and a shape quality control score (SQC) was produced for every segmentation. Datasets with a SQC score higher than a specific threshold, suggesting algorithmic failure, were automatically reprocessed with the SPP-modified algorithm, which incorporates knowledge of the segmentation mask location in the other datasets belonging to the same patient. Experienced operators blinded as to whether datasets had been processed based on the standard or SPP approach assessed segmentation success/failure for each dataset.The SPP approach reduced segmentation failures from 219/5772 (3.8%) to 42/5772 (0.7%) overall, with particular improvements in attenuation corrected (AC) datasets with high extra-cardiac activity (from 100/962 (10.4%) to 12/962 (1.4%) for rest AC, and from 41/962 (4.3%) to 9/962 (0.9%) for stress AC). The number of patients who had at least one of their 6 datasets affected by segmentation failure decreased from 141/962 (14.7%) to 14/962 (1.7%) using the SPP approach.Whenever multiple image datasets for the same patient exist and need to be processed, it is possible to deal with the images as a group rather than individually. The same-patient processing approach can be implemented automatically, and may substantially reduce the need for manual reprocessing due to cardiac segmentation failure.

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