bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantification of regional myocardial blood flow using 13N-ammonia and reoriented dynamic positron emission tomographic imaging.
Authors: Kuhle W G , Porenta G , Huang S C , Buxton D , Gambhir S S , Hansen H , Phelps M E , Schelbert H R 
Published: June 2012

BACKGROUND
Regional myocardial blood flow has been quantified using transaxial positron emission tomographic (PET) imaging and tracer kinetic modeling. However, the use of transaxial images limits the accuracy of regional partial volume corrections and the localization of the quantified regional flow values. The purpose of the present study was to overcome both problems by calculating regional flows from reoriented short-axis PET images.

METHODS AND RESULTS
Twelve experiments were performed in four dogs. 13N-ammonia was injected intravenously while microspheres were administered into the left atrium during baseline, hyperemic, and low-flow conditions. Serial transaxial frames were acquired with a 15-plane PET scanner and reoriented into short-axis frames. The arterial input function and eight regional myocardial tissue activity curves were derived from the reoriented frames. The arterial input functions were corrected for ammonia metabolites, and the myocardial tissue curves were corrected for spillover of activity, partial volume effects, and heterogeneities in the image's spatial resolution introduced during reorientation. Corrections for regional partial volume were based on estimates of the regional myocardial activity thickness derived from reoriented diastolic images of the heart. The myocardial 13N-ammonia kinetics were described with a two-pool compartmental model. Values of regional myocardial blood flow by PET correlated linearly with those by microspheres (slope, 0.94; y intercept, 0.06 ml/min/g; r = 0.93) over a wide range of flows.

CONCLUSIONS
Regional myocardial blood flow can be measured accurately and noninvasively from serially acquired and reoriented short-axis 13N-ammonia images, thus overcoming limitations inherent to the use of transaxially acquired images and permitting a more complete evaluation of regional blood flows throughout the left ventricular myocardium.
Combined use of time and frequency domain variables in signal-averaged ECG as a predictor of inducible sustained monomorphic ventricular tachycardia in myocardial infarction.
Authors: Nogami A , Iesaka Y , Akiyama J , Takahashi A , Nitta J , Chun Y , Aonuma K , Hiroe M , Marumo F , Hiraoka M 
Published: June 2012

BACKGROUND
Time and frequency domain analyses of signal-averaged ECG (SAECG) have several individual limitations, and the results of the two methods sometimes vary considerably. The purpose of this study was to determine whether the combined use of time and frequency domain variables facilitates identification of patients who will have ventricular tachycardia (VT) induced during programmed ventricular stimulation (PVS).

METHODS AND RESULTS
Nine myocardial infarction (MI) patients with clinically documented sustained monomorphic VT (SMVT), 40 MI patients without clinical VT, and 30 normal healthy control subjects were evaluated. PVS using three extrastimuli and SAECG recording were performed in the MI patients on day 36 +/- 4 after infarction. Of 40 MI patients, SMVT was inducible in 14, sustained polymorphic VT in three, nonsustained monomorphic VT in three, nonsustained polymorphic VT in two, and no inducible arrhythmia was obtained in 18. There were significant differences between MI patients with inducible SMVT and without inducible SMVT in the following SAECG variables: filtered QRS durations (high-pass filter setting, 25, 40, and 80 Hz); low-amplitude signal durations (LAS) under 10, 20, 30, and 40 microV (high-pass filter setting, 40 and 80 Hz); root-mean-square voltages (RMS) of the terminal 20, 30, 40, 50, and 60 msec (high-pass filter setting, 40 and 80 Hz); area ratio (area 20-50 Hz/area 0-20 Hz x 10(5)) of a 120-msec sampling interval starting 20 msec before QRS offset; factor of normality on lead X; and minimum value of the variables on lead X, Y, or Z. Stepwise logistic regression analysis selected only LAS under 30 microV (high-pass filter setting, 80 Hz) and area ratio as independent predictors of inducible SMVT. With these two variables, the predicted probability of inducible SMVT [p(VT)] was expressed as p(VT) = 1/[1+exp (6.2-0.11 LAS-0.01 area ratio)]. This function had 93% sensitivity, 81% specificity, 72% positive predictive value, 95% negative predictive value, and 85% predictive accuracy with greater than or equal to 0.3 as the criterion of a positive test.

CONCLUSIONS
The combined use of time and frequency domain analysis of SAECG can enhance the accuracy of this technique as a screening test for results of PVS in MI patients without clinical VT.
High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnish men.
Authors: Salonen J T , Nyyssönen K , Korpela H , Tuomilehto J , Seppänen R , Salonen R 
Published: June 2012

BACKGROUND
Iron can induce lipid peroxidation in vitro and in vivo in humans and has promoted ischemic myocardial injury in experimental animals. We tested the hypothesis that high serum ferritin concentration and high dietary iron intake are associated with an excess risk of acute myocardial infarction.

METHODS AND RESULTS
Randomly selected men (n = 1,931), aged 42, 48, 54, or 60 years, who had no symptomatic coronary heart disease at entry, were examined in the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD) in Eastern Finland between 1984 and 1989. Fifty-one of these men experienced an acute myocardial infarction during an average follow-up of 3 years. On the basis of a Cox proportional hazards model adjusting for age, examination year, cigarette pack-years, ischemic ECG in exercise test, maximal oxygen uptake, systolic blood pressure, blood glucose, serum copper, blood leukocyte count, and serum high density lipoprotein cholesterol, apolipoprotein B, and triglyceride concentrations, men with serum ferritin greater than or equal to 200 micrograms/l had a 2.2-fold (95% CI, 1.2-4.0; p less than 0.01) risk factor-adjusted risk of acute myocardial infarction compared with men with a lower serum ferritin. An elevated serum ferritin was a strong risk factor for acute myocardial infarction in all multivariate models. This association was stronger in men with serum low density lipoprotein cholesterol concentration of 5.0 mmol/l (193 mg/dl) or more than in others. Also, dietary iron intake had a significant association with the disease risk in a Cox model with the same covariates.

CONCLUSIONS
Our data suggest that a high stored iron level, as assessed by elevated serum ferritin concentration, is a risk factor for coronary heart disease.
Localization of the fast and slow pathways in atrioventricular nodal reentrant tachycardia by intraoperative ice mapping.
Authors: Keim S , Werner P , Jazayeri M , Akhtar M , Tchou P 
Published: June 2012

BACKGROUND
Atrioventricular (AV) nodal reentrant tachycardia is classically described as a reentrant rhythm entirely contained within the compact AV node. Although the concepts of longitudinal dissociation of two intranodal pathways and a distal common pathway are accepted, the proximal portion of the circuit remains undefined. Current reports suggest that the two pathways may be separable by atrial tissue and not contained entirely within the compact node.

METHODS AND RESULTS
We used an ice mapping method to demonstrate the slow and fast pathways of the reentrant circuit and their relation to the atrial septum around the AV node. Six patients with the usual form (slow-fast) of AV nodal reentrant tachycardia were mapped during surgery. In most patients, antegrade slow pathway localization was posterior and inferior to the compact AV node along the tricuspid annulus; in two patients, it was superior along the tendon of Todaro. Retrograde fast pathway localization was anterior or superior to the compact AV node in all patients. In all patients, anatomic distinction was made between the two pathways and the compact node.

CONCLUSIONS
We conclude that no upper common pathway exists within the compact AV node in the usual type of nodal reentrant tachycardia and that the perinodal atrial tissue is a requisite part of the tachycardia circuit.
Effect of ultrasound on tissue-type plasminogen activator-induced thrombolysis.
Authors: Lauer C G , Burge R , Tang D B , Bass B G , Gomez E R , Alving B M 
Published: June 2012

BACKGROUND
The efficacy of fibrinolytic therapy is limited by the small surface area of the clot that is available for the binding of the thrombolytic agent, such as tissue-type plasminogen activator (t-PA). We hypothesized that exposure of the clot to ultrasound during thrombolytic treatment could enhance lysis through perturbation of the thrombus, which would expose additional fibrin binding sites for t-PA.

METHODS AND RESULTS
Whole human blood clots containing radiolabeled fibrinogen were incubated in vitro for 200 minutes with Tris-albumin buffer containing t-PA at concentrations ranging from 3 to 3,000 IU/ml. In paired experiments, one of the clots also was exposed to intermittent ultrasound (1 MHz, 1.75 W/cm2) throughout the experiment. The ultrasound was delivered as a 2-second exposure followed by a 2-second rest interval. The overall difference in mean clot lysis between thrombi receiving ultrasound and those receiving no ultrasound was significant (p less than 0.001) at all concentrations of t-PA. For clots incubated with t-PA at a concentration of 300 IU/ml, ultrasound increased the percent lysis at 200 minutes from 42 +/- 5% (mean +/- SEM) to 64 +/- 10%. In six paired experiments in a rabbit jugular vein thrombosis model, rabbits received 1 mg t-PA alone or t-PA and intermittent ultrasound (1 MHz, 1.75 W/cm2) for 200 minutes. For rabbits receiving ultrasound and t-PA, lysis was 55 +/- 11% at 100 minutes compared with 30 +/- 12% for rabbits receiving only t-PA. Lysis was 6 +/- 10% for rabbits (n = 4) receiving ultrasound alone. No evidence for tissue damage was noted in rabbits exposed to intermittent ultrasound.

CONCLUSIONS
Exposure of whole blood clots in vitro to intermittent ultrasound combined with t-PA caused a significant enhancement of thrombolysis compared with t-PA alone. Intermittent ultrasound also showed a trend toward enhancement of t-PA-induced clot lysis in an animal thrombosis model. These data suggest that noninvasive intermittent ultrasound may be a useful adjunct to thrombolytic therapy.
Restenosis after directional coronary atherectomy. Effects of luminal diameter and deep wall excision.
Authors: Kuntz R E , Hinohara T , Safian R D , Selmon M R , Simpson J B , Baim D S 
Published: June 2012

BACKGROUND
Deep wall excision during directional atherectomy has been reported in one study to increase the risk of subsequent restenosis. On the other hand, we have observed that the probability of late (6-month) restenosis is reduced by maximizing postprocedure luminal diameter. Although such maximal luminal enlargement by directional atherectomy has not increased procedural complications in our experience, it might well increase the incidence of subintimal (deep wall component) recovery. We performed this study to evaluate the relative influences of luminal enlargement and deep wall component excision on postatherectomy restenosis.

METHODS AND RESULTS
Atherectomy resulted in a 7 +/- 15% residual stenosis with < 0.5% incidence of angiographic vessel perforation. The minimal luminal diameter of each lesion was measured before and after intervention in 413 lesions, 389 (94%) of which had histological analysis of the excised specimens. Specimens were categorized by the deepest layer retrieved: type I (recovery of intima alone, n = 141), type II (recovery of media, n = 79), and type III (recovery of adventitia, n = 65). Repeat angiographic measurement of minimal luminal diameter was available for 329 (80%) segments 6 months after atherectomy. Compared with the 32% restenosis rate for type I excision, there was no increase in restenosis (stenosis > 50%) for type II, type III, or types II+III (p = 0.86). Stratification by vessel characteristics also failed to show any association between restenosis and deep wall component recovery in any subgroup, including native coronary (p = 0.85), left anterior descending coronary artery (p = 0.70), right coronary artery (p = 0.51), saphenous graft (p = 0.78), or prior restenosis lesions (p = 0.98). Paradoxically, the recovery of adventitia (type III excision) was associated with a lower late percent stenosis (p = 0.03) and a trend toward less restenosis (p = 0.11) compared with type I excisions. A multiple logistic regression model was constructed that demonstrated immediate postprocedure luminal diameter (p = 0.02) to be an independent determinant of restenosis. In this model, the presence of deep wall components (type II+III) did not adversely affect (p = 0.86) restenosis, but the recovery of adventitia was associated with an independent trend toward reduced restenosis (p = 0.06).

CONCLUSIONS
The immediate goal of directional atherectomy should be to safely provide the largest lumen possible in order to reduce restenosis. The recovery of deep wall components does not appear to jeopardize the beneficial effect that obtaining a large immediate postprocedure lumen diameter has on reducing the incidence of late restenosis.
Real-time NMR beam-directed velocity mapping. V-mode NMR.
Authors: Pearlman J D , Moore J R , Lizak M J 
Published: June 2012

BACKGROUND
Currently available noninvasive techniques for measuring blood flow velocities are constrained by limited view orientations (Doppler ultrasound) or limited time resolution (magnetic resonance imaging, MRI). We describe an MRI technique for measuring flow velocities in real time at arbitrary orientations within a cylindrical volume or "beam": V-mode nuclear magnetic resonance (NMR).

METHODS AND RESULTS
The technique was implemented on a standard 1.5-T clinical NMR imager with no special hardware and was tested on phantoms and human volunteers. The beam can be fired at rates up to 60 times per second, allowing measurements on a time scale that is appropriate for ungated cardiac studies. In phantoms, steady flow velocities were measured with the beam aligned along the direction of flow, and the measured velocities correlated well with the actual velocities (r > 0.99). The radial distribution of velocities in phantoms under constant flow conditions was also determined. In humans, flow of blood in the descending aortas of normal and aortic insufficiency subjects was measured. Distinctive backflow of blood because of aortic insufficiency was readily apparent.

CONCLUSIONS
The V-mode NMR technique is capable of acquiring clinically relevant real-time blood flow information from any desired angle of view with no attenuation at bone or air-tissue interfaces.
Dehydroepiandrosterone sulfate, incidence of myocardial infarction, and extent of atherosclerosis in men.
Authors: LaCroix A Z , Yano K , Reed D M 
Published: June 2012

BACKGROUND
Antiatherogenic effects of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) have been suspected for more than 30 years, yet the available evidence to support or refute such effects in humans is inconclusive. The hypothesis has not been adequately tested in large-scale epidemiological studies.

METHODS AND RESULTS
The present study used a cohort of men initially free of clinically detectable coronary heart disease, stroke, and cancer to compare DHEAS levels measured in sera obtained in 1968-1971 between 238 cases who had definite coronary heart disease during the subsequent 18 years and 476 age-matched controls who survived the follow-up period and remained free of clinically detectable coronary heart disease. In a separate study, the relation of DHEAS levels to extent of atherosclerosis was examined among 82 cohort men who died during the follow-up period and had protocol autopsies. Age-adjusted DHEAS levels were lower among fatal cases of coronary heart disease than among controls (94.7 versus 106.9 micrograms/dl, respectively; p < 0.05). After adjustment for eight coronary risk factors, the odds ratio for fatal coronary heart disease comparing a 100-micrograms/dl difference in DHEAS level was 0.46 (95% confidence intervals, 0.19-1.07). In contrast, age-adjusted DHEAS levels did not significantly differ between nonfatal cases of myocardial infarction and controls (107.2 versus 106.9 micrograms/dl, respectively). Furthermore, DHEAS levels were not related to extent of atherosclerosis at autopsy.

CONCLUSIONS
These findings do not support a role of DHEAS in the development of nonfatal myocardial infarction or the progression of atherosclerosis. The association of DHEAS with fatal coronary heart disease and possibly with death from all causes merits further investigation. These findings suggest continued skepticism that DHEAS has an important role in coronary disease etiology or prevention.
Beneficial effects of atrial natriuretic peptide on exercise-induced myocardial ischemia in patients with stable effort angina pectoris.
Authors: Lai C P , Egashira K , Tashiro H , Narabayashi H , Koyanagi S , Imaizumi T , Takeshita A 
Published: June 2012

BACKGROUND
It has been shown that atrial natriuretic peptide (ANP), an endogenous vasodilator, dilates coronary arteries and decreases coronary vascular resistance. The purpose of this study was to determine whether an intravenous administration of ANP attenuated exercise-induced myocardial ischemia in 14 patients with stable effort angina pectoris.

METHODS AND RESULTS
The first 12 patients (patients 1-12) who had exercise-induced ST segment depression underwent treadmill exercise testing and the last seven patients (patients 8-14) underwent the exercise 201Tl-single-photon emission computed tomography (SPECT) study while synthetic 28-amino acid alpha-human ANP (0.1 micrograms/kg per minute) or saline was intravenously infused in a double-blind, cross-over manner. The duration of exercise testing was the same during ANP and saline infusion, which was determined in preliminary exercise testings in each patient to cause a transient perfusion defect and/or ischemic ST segment depression. During saline infusion, all 12 patients developed exercise-induced ischemic ST segment depression, whereas no significant ST segment depression appeared during ANP infusion. Average ST segment depression during ANP infusion was significantly less (p < 0.01) than that during saline infusion (0.0 +/- 0.0 versus 0.2 +/- 0.1 mV, mean +/- SD). The averaged extent and severity scores assessed by 201Tl-SPECT were smaller (p < 0.05) during ANP infusion than during saline infusion (extent score: 0.22 +/- 0.20 versus 0.42 +/- 0.20; severity score: 18.77 +/- 23.45 versus 38.24 +/- 24.04, respectively). ANP decreased resting systolic blood pressure from 125 +/- 15 to 110 +/- 15 mm Hg (p < 0.01) but did not alter resting heart rate. At peak exercise, systolic blood pressure, heart rate, and the rate-pressure products did not differ during ANP and saline infusion. At peak exercise, plasma ANP increased from 98 +/- 45 to 4,383 +/- 2,782 pg/ml and cGMP increased from 3.6 +/- 1.7 to 34.5 +/- 16.1 pmol/ml during ANP infusion; values were significantly higher than those during saline infusion (from 96 +/- 42 to 133 +/- 66 pg/ml and from 3.4 +/- 1.8 to 4.6 +/- 1.8 pmol/ml, respectively).

CONCLUSIONS
An intravenous administration of ANP attenuated exercise-induced myocardial ischemia in patients with stable effort angina pectoris. Although the mechanism by which ANP attenuated myocardial ischemia was not defined, increased myocardial perfusion to the ischemic region might be an important factor.
Distribution of left ventricular sympathetic afferents demonstrated by reflex responses to transmural myocardial ischemia and to intracoronary and epicardial bradykinin.
Authors: Minisi A J , Thames M D 
Published: June 2012

BACKGROUND
Stimulation of left ventricular (LV) receptors with sympathetic afferents generally results in reflex sympathoexcitatory responses. Stimulation of LV receptors with vagal afferents results in reflex sympathoinhibitory responses. Vagal afferents are known to be preferentially distributed to the inferoposterior (IP) wall of the LV. We tested the hypothesis that there is also a preferential distribution of LV sympathetic afferents.

METHODS AND RESULTS
We measured reflex responses to stimulation of sympathetic afferents located in the anterior and IP LV: We used myocardial ischemia and chemical stimuli to increase the activity of the sensory endings in 15 chloralose-anesthetized, mechanically ventilated dogs with sinoaortic denervation and vagotomy. Reflex responses were assessed by direct recordings of efferent renal sympathetic nerve activity (RSNA). In nine dogs, maximal RSNA changes elicited by transmural anterior myocardial ischemia (22.6 +/- 3.9% increase from baseline nerve traffic) were not significantly different from maximal RSNA changes observed during transmural IP ischemia (27.1 +/- 4.4%). Similar changes in mean arterial and left atrial pressures were noted during transmural anterior and IP ischemia. In eight dogs, maximal changes of RSNA elicited by epicardial or intracoronary bradykinin to the anterior LV were not significantly different from those observed during bradykinin to the IP LV (anterior epicardial bradykinin, 76.7 +/- 11.7%; IP epicardial bradykinin, 72.2 +/- 10.0%; anterior intracoronary bradykinin, 84.6 +/- 21.0%; IP intracoronary bradykinin, 88.8 +/- 17.3%).

CONCLUSIONS
We conclude that cardiac receptors with sympathetic afferents are distributed equally to the IP and anterior regions of the LV.
Tricarboxylic acid cycle activity in postischemic rat hearts.
Authors: Weiss R G , Kalil-Filho R , Herskowitz A , Chacko V P , Litt M , Stern M D , Gerstenblith G 
Published: June 2012

BACKGROUND
Although myocardial oxidative tricarboxylic acid (TCA) cycle activity and contractile function are closely linked in normal cardiac muscle, their relation during postischemic reperfusion, when contractility often is reduced, is not well defined.

METHODS AND RESULTS
To test the hypothesis that oxidative TCA cycle flux is reduced in reperfused myocardium with persistent contractile dysfunction, TCA cycle flux was measured by analyzing the time course of sequential myocardial glutamate labeling during 13C-labeled substrate infusion with 13C nuclear magnetic resonance spectroscopy in beating isolated rat hearts at 37 degrees C. Total TCA cycle flux, indexed by both empirical and mathematical modeling analyses of the 13C data, was not reduced but rather increased in hearts reperfused after 17-20 minutes of ischemia (left ventricular pressure, 73 +/- 5% of preischemic values) compared with flux in developed pressure-matched controls (e.g., total flux, 2.5 +/- 0.4 versus 1.6 +/- 0.1 mumol.min-1.g wet wt-1, respectively; p < 0.01). No TCA cycle activity was detectable by 13C nuclear magnetic resonance in hearts reperfused after 40-45 minutes of ischemia, which lacked contractile recovery and had ultrastructural evidence of irreversible injury.

CONCLUSIONS
These results suggest that TCA cycle activity is not persistently decreased in dysfunctional reperfused myocardium after a brief ischemic episode and therefore cannot account for the reduced contractile function at that time.