bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of postreperfusion myocardial hemorrhage using proton NMR imaging at 1.5 T.
Authors: Lotan C S , Bouchard A , Cranney G B , Bishop S P , Pohost G M 
Published: June 2012

BACKGROUND
Intramyocardial hemorrhage occurs frequently after reperfusion of acute myocardial infarction. However, its significance has not yet been established, mainly because of the lack of methods for detecting such hemorrhage. The following ex vivo study was carried out to assess the potential of nuclear magnetic resonance (NMR) imaging to detect and quantitate postreperfusion intramyocardial hemorrhage.

METHODS AND RESULTS
Sixteen adult mongrel dogs underwent 3 hours of coronary occlusion followed by 1 hour of reperfusion, and three dogs underwent 4 hours of occlusion without reperfusion. Radiolabeled microspheres and 51Cr-labeled red blood cells were used to assess flow and evaluate the extent of hemorrhage. These results were later compared with both NMR and histology. Spin-echo NMR imaging was performed on the excised hearts using a 1.5-T system. Macroscopic assessment of the sliced myocardium revealed the existence of hemorrhage in 14 of the 16 dogs that underwent reperfusion but in none of those with occlusion only. In all 16 dogs with reperfusion, zones of increased signal intensity (SI) ratio (1.68 +/- 0.41 compared with control, p less than 0.05) were seen in regions relating to the distribution of the occluded coronary artery, whereas in 13 of the 16 dogs, areas of decreased SI within the zone of increased SI ratio (0.81 +/- 0.16 compared with control, p less than 0.05) were also seen, corresponding to regions with macroscopic hemorrhage. In contrast, in the three dogs without reperfusion, no macroscopic hemorrhage was observed, and likewise, no NMR zones of reduced SI were detected. Hemorrhage size by NMR (decreased SI zones), correlated well with hemorrhage size calculated from tissue slices (r = 0.96, SEE = 0.92%, p less than 0.01), or by 51Cr labeling (r = 0.78, SEE = 1.5, p = 0.1). In the reperfusion group, T2 relaxation times in the infarcted hemorrhagic zone (58 +/- 9 msec) were significantly lower than the infarcted zones without hemorrhage (98 +/- 13 msec, p less than 0.001). In contrast, when compared with control (964 +/- 72 msec), T1 relaxation times were significantly increased in both infarct zones, either with (1,284 +/- 176 msec) or without (1,266 +/- 103 msec) hemorrhage. The selective shortening of T2 relaxation times in the hemorrhagic regions is consistent with the paramagnetic effects of deoxyhemoglobin.

CONCLUSIONS
NMR imaging may provide a noninvasive approach for the detection and quantitation of intramyocardial hemorrhage. This observation may provide a means to further characterize pathological processes associated with acute myocardial infarction and assess the role of myocardial hemorrhage after reperfusion therapy.
Cross-sectional early mitral flow-velocity profiles from color Doppler in patients with mitral valve disease.
Authors: Samstad S O , Rossvoll O , Torp H G , Skjaerpe T , Hatle L 
Published: June 2012

BACKGROUND
Cross-sectional flow-velocity profiles from early mitral flow in 20 patients (10 with mitral regurgitation and 10 with mitral stenosis) were constructed from the velocity data from each point in sequentially delayed two-dimensional digital Doppler ultrasound maps.

METHODS AND RESULTS
The data suggested that the early mitral flow studied in an apical four-chamber view was variably skewed in both patient groups. The maximum flow velocity overestimated the cross-sectional mean velocity at the same time by a factor of 1.12-1.86. The maximum time-velocity integral was 1.13-1.77-fold greater than the cross-sectional mean time-velocity integral. In patients with mitral regurgitation, the cross-sectional flow-velocity profile appeared to be most skewed at the level of the mitral leaflet tips. The level of the mitral annulus appeared to give the most homogenous flow-velocity distribution in both patient groups.

CONCLUSIONS
When calculations of volume flow are based on pulsed Doppler ultrasound recordings with a single sample volume, the possibility of a skewed flow-velocity profile must be taken into account.
Morphological predictors of acute complications after percutaneous excimer laser coronary angioplasty. Results of a comprehensive angiographic analysis: importance of the eccentricity index.
Authors: Ghazzal Z M , Hearn J A , Litvack F , Goldenberg T , Kent K M , Eigler N , Douglas J S , King S B 
Published: June 2012

BACKGROUND
Percutaneous excimer laser coronary angioplasty (ELCA) is a new technique for recanalization of arteries obstructed by coronary atherosclerosis. This study was conducted to assess the complication rate and determine the influence of clinical and angiographic characteristics on complications after ELCA.

METHODS AND RESULTS
A detailed, quantitative, angiographic core laboratory analysis of patients undergoing ELCA was performed by two experienced angiographers who were not the primary laser angioplasty operators. Two hundred patients underwent 203 separate procedures on 220 lesions at three medical centers. Laser success was achieved in 180 lesions (81.8%) and procedural success in 199 (90.5%). Emergency coronary artery bypass graft (CABG) was required in five patients (2.5%). One patient suffered a Q wave myocardial infarction; there were no deaths. Also, acute closure and perforation occurred in 10 (4.5%) and three (1.4%) vessels, respectively. Coronary dissections after laser treatment were seen in 36 vessels (16.4%). Multivariate analysis found two independent preprocedural factors related to complications: eccentricity index, which is the percent deviation of the lesion lumen from the center of the artery (p = 0.0007), and proximal vessel diameter (p = 0.033). In addition, an abrupt proximal face of the lesion was associated with angiographic complications by univariate analysis (p = 0.051). Multivariate analysis showed the eccentricity index (p = 0.032) to be the only independent predictor for the occurrence of any one or more of the important complications (emergency CABG, perforation, acute closure, or Q wave myocardial infarction), whereas lesion angle greater than 45 degrees was a significant univariate predictor (p = 0.029). Other predictors of complications with balloon percutaneous transluminal coronary angioplasty, such as increased lesion length, rough edges, calcification, ulceration, and branch point, were not predictive of complications with the excimer laser.

CONCLUSIONS
The degree of lesion eccentricity is the most powerful predictor of complications after ELCA. This and other morphological predictors may be of benefit in the selection of patients for ELCA as well as directing future development of this new technology.
Anatomical progression of coronary artery disease in humans as seen by prospective, repeated, quantitated coronary angiography. Relation to clinical events and risk factors. The INTACT Study Group.
Authors: Lichtlen P R , Nikutta P , Jost S , Deckers J , Wiese B , Rafflenbeul W 
Published: June 2012

BACKGROUND
At present, there is extensive knowledge on the clinical course of coronary artery disease (CAD), whereas data on the underlying anatomical changes and their relation to clinical events are still limited.

METHODS AND RESULTS
We investigated progression and regression of CAD prospectively over 3 years in 230 patients (average age, 53.2 years) with mild to moderate disease by applying quantitated, repeated coronary angiography. Minimal stenotic diameters, segment diameters, and percent stenosis were analyzed by the computer-assisted Coronary Angiography Analysis System (CAAS). Progression was defined either as an increase in percent stenosis of preexisting stenoses by greater than or equal to 20% including occlusions or as formation of new stenoses greater than or equal to 20% and new occlusions in previously angiographically "normal" segments. At first angiography, we found 838 stenoses greater than or equal to 20% (average degree, 39.3%) and 135 occlusions in the four major coronary branches (4.23 lesions per patient). At second angiography, 82 (9.8%) of the preexisting stenoses had progressed, 15 of them up to occlusion (1.8%; preocclusion degree averaging 46.6%; 29.7-65.6%). In addition, there were 144 newly formed stenoses (average degree, 39.2%) and 10 new occlusions. Hence, 25 (2.6%) of all stenoses had become occluded. Altogether, 129 patients (56.1%) showed progression: 68 (29.6%) with new lesions only, 27 (11.7%) with preexisting lesions, and 34 (14.8%) with both types. Regression (decrease in degree of stenoses greater than or equal to 20%) was present in 29 stenoses (3.6%) and 28 patients (12%). The incidence of new myocardial infarctions was low, with three originating from occluding preexisting stenoses and one from new stenoses; hence, only four (16%) of the 25 new occlusions led to myocardial infarctions. Risk factor analysis showed that cigarette smoking correlated significantly with the formation of new lesions (p = 0.001), whereas total cholesterol correlated with the further progression of preexisting stenoses (p = 0.017) but not with the incidence of new lesions.

CONCLUSIONS
In patients with mild to moderate CAD, the angiographic progression is slow (in this study 18.7% of patients and 7% of stenoses per year) but exceeds regression (4.1% of patients and 1.2% of stenoses per year). Progression is predominantly seen in the formation of new coronary stenoses and less in growth of preexisting ones. Most of the stenoses were of a low degree (less than 50%), clinically not manifest including those going into occlusion and leading to myocardial infarction. Progression was influenced by risk factors, especially cigarette smoking (formation of new lesions) and high cholesterol levels (progression of preexisting stenoses).
Effects of oxygen inhalation on skin microcirculation in patients with peripheral arterial occlusive disease.
Authors: Bongard O , Bounameaux H , Fagrell B 
Published: June 2012

BACKGROUND
Oxygen administration is currently used in clinical medicine to improve peripheral oxygen delivery to tissues threatened by ischemia. However, conflicting results have been reported on the effects of oxygen in ischemic areas. This study was aimed at investigating the effects of 40% oxygen inhalation on the skin microcirculation in the feet of patients with peripheral arterial occlusive disease (PAOD).

METHODS AND RESULTS
Transcutaneous oxygen tension (tc PO2) was measured on the dorsal skin of the foot, and the nailfold microcirculation was investigated by a combination of laser Doppler flowmetry (LDF) and dynamic capillaroscopy (CBV) in the great toes of 17 legs of 11 patients, with 13 legs of eight normal subjects as a control group. Inhalation of oxygen induced a significant decrease of both the total (delta LDF, -307%, p less than 0.02) and nutritional (delta CBV, -17%, p less 0.002) skin microcirculation in normal legs compared with baseline values. A similar response was observed in 10 legs of patients who showed a significant increase of the tc PO2 (greater than or equal to 10 mm Hg) (delta LDF, -14%, NS; delta CBV, -13%, p less than 0.005). By contrast, both the total (+21%, p less than 0.03) and nutritional (+52%, p less than 0.05) circulation significantly increased in the seven legs without significant tc PO2 increase. In addition, the flow motion, which was impaired in the patients, was significantly (p less than 0.05) improved by oxygen inhalation.

CONCLUSIONS
Inhalation of 40% oxygen induces a vasoconstriction in the skin microcirculation of toes of the normal subjects and patients with moderate PAOD but induces an increase of the skin microcirculation in patients with severe PAOD.
Neurophysiological assessment of skeletal muscle fatigue in patients with congestive heart failure.
Authors: Minotti J R , Pillay P , Chang L , Wells L , Massie B M 
Published: June 2012

BACKGROUND
Recent research has demonstrated that patients with congestive heart failure (CHF) exhibit significant functional impairment of skeletal muscle and that these changes may be important determinants of exercise capacity. Although muscle strength may be mildly reduced, the most significant abnormality is markedly enhanced muscle fatigue. The goal of the present study is to determine whether accelerated fatigue is caused by impaired muscle activation, as a result of inadequate central motor drive or neuromuscular transmission, or by a change in the muscle itself.

METHODS AND RESULTS
The study population consisted of nine patients with New York Heart Association class I-III CHF and eight sedentary, age- and sex-matched control subjects. Maximal voluntary contraction force of the foot dorsiflexors (primarily the tibialis anterior) was quantified as a measure of muscle strength, isometric endurance was quantified by the time required for force to decline to 60% of maximal during a sustained maximal contraction, and dynamic endurance was defined as the number of maximal contractions required for force to decline to 60% of maximal under a protocol of six repetitions per minute with an incremental duty cycle. The degree of central motor drive failure was quantified by the degree of force augmentation produced by a superimposed tetanic stimulus delivered to the peroneal nerve during the initial maximal voluntary contraction and at the time when force during the sustained isometric contraction declined to 60% of maximal. Neuromuscular junction transmission was examined by quantifying the amplitude of the compound muscle action potential (M wave) in response to a single nerve stimulus during fatiguing exercise. Muscle strength was relatively preserved in the CHF patients versus the control subjects (93 +/- 41 versus 105 +/- 34 lb; p = NS), but isometric endurance (time to decline to 60%, 34 +/- 15 versus 54 +/- 19 seconds; p less than 0.02) and dynamic endurance (number of repetitions before decline to 60%, 30 +/- 6 versus 43 +/- 7 contractions; p less than 0.001) were both impaired. Tetanic nerve stimulation increased force by similar degrees in the two groups, and the amplitude of the M wave did not decline in either group during exercise.

CONCLUSIONS
These findings indicate that enhanced muscle fatigue in patients with CHF is not caused by impaired central motor drive or an abnormality of neuromuscular junction transmission but rather by an abnormality in the muscle itself.
Coronary endothelial and cardiac protective effects of a monoclonal antibody to intercellular adhesion molecule-1 in myocardial ischemia and reperfusion.
Authors: Ma X L , Lefer D J , Lefer A M , Rothlein R 
Published: June 2012

BACKGROUND
Intercellular adhesion molecule-1 (ICAM-1) is a major ligand on endothelial cells for adherence of activated polymorphonuclear leukocytes (PMNs). The major purpose of this study was to study the effects of RR1/1, a monoclonal antibody against ICAM-1 (i.e., MAb RR1/1), on myocardial injury and endothelial dysfunction associated with myocardial ischemia and reperfusion.

METHODS AND RESULTS
Either MAb RR1/1 (2 mg/kg, n = 7), an antibody that was found to bind selectively to endothelial cells in the cat, or MAb R3.1 (2 mg/kg, n = 7), a nonbinding control antibody, was given as an intravenous bolus 10 minutes before reperfusion. Two hundred eighty minutes later, hearts were excised. The left ventricle area-at-risk (AAR) was similar in MAb RR1/1 (29 +/- 2%) and MAb R3.1 (30 +/- 3%) groups. In MAb R3.1-treated cats, 90 minutes of myocardial ischemia plus 4.5 hours of reperfusion induced a significant myocardial injury (necrotic tissue/AAR, 28 +/- 2%), high myeloperoxidase activity (0.65 +/- 0.16 units/100 mg ischemic tissue), and a marked decrease in endothelium-dependent vasorelaxation in isolated left anterior descending coronary arteries (vasorelaxation to acetylcholine, 29 +/- 3%) with no change in endothelium-independent vasorelaxation (relaxation to NaNO2, 91 +/- 3%). However, cats treated with MAb RR1/1 developed significantly less myocardial necrosis (10 +/- 2% of the AAR, p less than 0.01), lower myeloperoxidase activity in ischemic myocardial tissue (0.2 +/- 0.03 units/100 mg ischemic tissue, p less than 0.01), and enhanced vasorelaxant responses to endothelial-dependent relaxation to acetylcholine (53 +/- 5%) compared with ischemic/reperfused cats treated with Mab R3.1. Furthermore, addition of MAb RR1/1 in vitro significantly inhibited unstimulated PMN adherence to ischemic-reperfused coronary artery endothelium.

CONCLUSIONS
These results suggest that ICAM-1-dependent PMN adherence plays an important role in reperfusion injury, and that PMN adherence and infiltration contribute significantly to coronary endothelial dysfunction.
Cellular mechanisms of differential action potential duration restitution in canine ventricular muscle cells during single versus double premature stimuli.
Authors: Kobayashi Y , Peters W , Khan S S , Mandel W J , Karagueuzian H S 
Published: June 2012

BACKGROUND
We tested the hypothesis that action potential duration (APD) restitution of normal ventricular muscle cells is different during double premature stimuli (S3) compared with a single premature stimulus (S2). We propose a possible ionic mechanism for such a difference.

METHODS AND RESULTS
Action potentials and isometric tension were recorded simultaneously from isolated canine right ventricular trabeculae (2 x 2 x 10 mm) (n = 35). APD and tension restitution curves (APD) and peak tension versus diastolic interval [DI] of S2 and S3 were constructed by the extrastimulus method during pacing at 1,500 msec. The following results were obtained. 1) The APD restitution curve of S2 was different from that of S3. During the restitution of S2, an early biphasic upward hump was present at short DIs. In contrast, a smooth exponential rise was consistently seen during S3 restitution. 2) Peak tension remained significantly (p less than 0.001) lower during the restitution of S2 than during S3 restitution at all DIs tested. 3) The variation of APD during the initial 100 msec of DI was significantly longer during S3 than S2 (22 +/- 5 msec versus 41 +/- 5 msec, p less than 0.001). 4) Caffeine (2 mM, n = 5) and ryanodine (10 microM, n = 5) blocked cyclic variations of tension, presumably by blocking cyclic variations of intracellular calcium ion concentrations ([Ca2+]i), and eliminated the differences in APD restitution between S2 and S3. 5) Nisoldipine at high (5 microM) but not at lower (2 microM, n = 5) concentration eliminated the differences in restitution of both APD and tension between S2 and S3. 6) BAY K 8644 (100 nM, n = 5) had no effect on this difference.

CONCLUSIONS
Greater variations of APD occur during the restitution of S3 than during S2 at short DIs. These differences appear to be caused by cyclic variations in tension and thus in [Ca2+]i. Calcium-sensitive outward currents could explain these differences in APD restitution.
Clinical characteristics and outcome of patients with high defibrillation thresholds. A multicenter study.
Authors: Epstein A E , Ellenbogen K A , Kirk K A , Kay G N , Dailey S M , Plumb V J 
Published: June 2012

BACKGROUND
Successful defibrillation by an implantable cardioverter-defibrillator (ICD) depends on its ability to deliver shocks that exceed the defibrillation threshold. This study was designed to identify clinical characteristics that may predict the finding of an elevated defibrillation threshold and to describe the outcome of patients with high defibrillation thresholds.

METHODS AND RESULTS
The records of 1,946 patients from 12 centers were screened to identify 90 patients (4.6%) with a defibrillation threshold greater than or equal to 25 J. Excluding three patients who received ICDs that delivered greater than 30 J, there were 81 men and six women with a mean age of 59.5 +/- 10.1 years, a mean left ventricular ejection fraction of 0.32 +/- 0.14, and a 76% prevalence of coronary artery disease. Sixty-one patients (70%) were receiving antiarrhythmic drugs, and 45 (52%) were receiving amiodarone. Seventy-one patients (82%) received an ICD. Death occurred in 27 patients--19 of the 71 (27%) with an ICD (eight arrhythmic), and eight of the 16 (50%) without an ICD (four arrhythmic). Actuarial survival for all patients at 5 years was 67%. Actuarial survival rates at 2 years for patients with and without an ICD were 81% and 36%, respectively (p = 0.0024). Actuarial survival at 5 years for the ICD patients was 73%; no patient without an ICD has lived longer than 32 months. Actuarial survival free of arrhythmic death in the ICD patients at 5 years was 84%. Although the only variable to predict survival was ICD implantation (p = 0.003), it is entirely possible that in this retrospective analysis, clinical selection decisions to implant or to not implant an ICD differentiated patients destined to have better or worse outcomes, respectively.

CONCLUSIONS
Antiarrhythmic drug use may be causally related to the finding of an elevated defibrillation threshold. When patients with high defibrillation thresholds receive an ICD, arrhythmic death remains an important risk (42% of deaths in these patients were arrhythmia related, with 16% actuarial incidence at 5 years). Vigorous testing to optimize patch location can potentially benefit patients by enhancing the margin of safety for effective defibrillation.
Highly variable anticoagulant response after subcutaneous administration of high-dose (12,500 IU) heparin in patients with myocardial infarction and healthy volunteers.
Authors: Kroon C , ten Hove W R , de Boer A , Kroon J M , van der Pol J M , Harthoorn-Lasthuizen E J , Schoemaker H C , van der Meer F J , Cohen A F 
Published: June 2012

BACKGROUND
In this study, the anticoagulant response of 12,500 IU heparin s.c. was investigated in patients with myocardial infarction and healthy volunteers to determine variabilities in response and modifying factors.

METHODS AND RESULTS
On the fourth day after thrombolytic therapy, blood samples were taken before and at frequent intervals until 10 hours after the injection of 12,500 IU heparin s.c. Plasma anti-Xa activity, anti-IIa activity, and the activated partial thromboplastin time (APTT) were measured in addition to body weight and thickness of the abdominal subcutaneous fat layer. Contrary to expectations, the increase of anti-Xa activity, anti-IIa activity, and APTT compared with baseline (predrug) levels was very small, with an average maximal APTT of 42.6 seconds (SD, 12.4 seconds; range, 30.4-70.7 seconds). Subsequently, the influence of the length of the injection needle on the anticoagulant effect of 12,500 IU heparin s.c. was studied in 10 healthy volunteers to find a factor that could be responsible for the poor response in the patients. The length of the injection needle did not influence the anticoagulant effect of heparin. Large interindividual and intraindividual variabilities were seen in the volunteers. The majority of volunteers had minimal prolongation of the APTT, but very strong prolongation was also seen (maximal APTT, 163 seconds). There was no correlation between the abdominal skinfold thickness and anti-Xa activity, anti-IIa activity, or APTT (p > 0.05), but in the patient study, there was a correlation between weight and anti-Xa activity and anti-IIa activity (p < 0.05), and in the volunteer study, there was a correlation between weight and anti-Xa activity and APTT (p < 0.05).

CONCLUSIONS
Subcutaneous administration of heparin in a fixed dose for prophylactic and therapeutic purposes may be inadequate because of the large interindividual and intraindividual variations in anticoagulant effect.