bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dose-dependent smooth muscle cell proliferation induced by thermal injury with pulsed infrared lasers.
Authors: Douek P C , Correa R , Neville R , Unger E F , Shou M , Banai S , Ferrans V J , Epstein S E , Leon M B , Bonner R F 
Published: June 2012

BACKGROUND
Recently, laser-heated and radio frequency-heated balloon angioplasty techniques have been proposed as a means to treat or minimize dissection and elastic recoil but have been associated with a high rate of clinical restenosis. Similarly, pulsed laser angioplasty techniques proposed to minimize thermal injury while ablating obstructing atheroma have failed to reduce clinical restenosis. Because "hot balloon" and pulsed laser angioplasty create both mechanical and thermal injury, it has been difficult to discern the cause of the smooth muscle cell (SMC) proliferation resulting in restenosis and whether such magnitude of proliferation is predictable and dose related. This study was undertaken to explore these issues.

METHODS AND RESULTS
Localized thermal lesions accompanying efficient ablation were created with a pulsed Tm:YAG laser in nine rabbit aortas, which consistently led to a focal proliferation of SMC that filled the ablated region by 4 weeks. Transcutaneous Ho:YAG pulsed laser irradiation at multiple independent sites of 24 central rabbit ear arteries without ablation led to brief approximately 30 degrees C thermal transients and thermal damage to the artery wall resulting in significant neointimal proliferation by 3 weeks and a mean cross-sectional narrowing of 59 +/- 17% at a dose of 390 mJ/mm2. Acute and chronic responses to varying total energy deposition were studied by histology after the rabbits were killed at 2 hours to 4 weeks. Arterial segments midway between laser injuries were unaffected and served as internal controls. Neointimal proliferation at 3 weeks after laser injury exhibited a clear dose dependence. Mean cross-sectional narrowing increased from 34 +/- 10% to 85 +/- 15% as laser fluence increased from 240 mJ/cm2 to 640 mJ/cm2 (r = 0.84). Similarly, cross-sectional narrowing caused by SMC neointimal proliferation increased from 20 +/- 10% to 77 +/- 17% for a fixed surface irradiation as the depth of the most superficial arterial media decreased from 600 microns to 330 microns (r = 0.94).

CONCLUSIONS
Thermal injury to the arterial wall is a potent stimulus for SMC proliferation and may necessitate reduction in laser or thermal energy used for angioplasty. Moreover, a dose-response relation exists between the degree of thermal injury and SMC proliferative response. Hence, this technique could be used as a practical model of restenosis suitable for screening therapies for inhibition of SMC proliferation.
Randomized trial of late elective angioplasty versus conservative management for patients with residual stenoses after thrombolytic treatment of myocardial infarction. Treatment of Post-Thrombolytic Stenoses (TOPS) Study Group.
Authors: Ellis S G , Mooney M R , George B S , da Silva E E , Talley J D , Flanagan W H , Topol E J 
Published: June 2012

BACKGROUND
After thrombolytic therapy for patients with acute myocardial infarction (MI), percutaneous transluminal coronary angioplasty (PTCA) is frequently performed because of the presence of a "significant" infarct vessel stenosis demonstrated at predischarge coronary angiography. Several studies have shown PTCA performed early after thrombolysis to be unnecessary or even harmful. However, PTCA in these trials was generally performed 1-3 days after MI, when the milieu in the infarct artery may be unsuited for PTCA, and the incidence of major ischemic complications was high. To date, no trial has assessed whether delayed PTCA (4-14 days) should be performed in patients without evidence of ischemia on stress testing.

METHODS AND RESULTS
To test the hypothesis that delayed PTCA might provide clinical benefit compared with medical therapy alone, 87 patients treated within 6 hours of chest pain onset with thrombolytic therapy and with negative functional test were randomized between PTCA to be performed 4-14 days after MI versus no PTCA. Both groups received medical therapy. Patients with postinfarct angina or prior Q wave infarction in the infarct distribution were excluded. The primary study end point was increase in left ventricular ejection fraction with exercise measured by radionuclide studies 6 weeks after MI, a parameter known from other studies to correlate inversely with future ischemic events. Clinical outcome was also monitored for 12 months. There were no differences between the study groups for any prerandomization variable recorded. Mean age was 57 +/- 10 years, 84% of patients were male, 21% had prior MI, 36% had anterior MI, 7% had multivessel disease, and the infarct stenosis measured 70 +/- 17% before randomization. PTCA was successful in 38 of 42 patients (88%) but resulted in non-Q wave MI due to acute closure of the treated site in three of 42 (9.5%). There was no difference in 6-week resting ejection fraction or increase in ejection fraction with exercise between the two groups (47 +/- 12% and 6 +/- 8%, respectively, in the PTCA group; 49 +/- 10% and 5 +/- 9% in the no-PTCA group; p = NS for both.) There were no deaths in either group. Actuarial 12-month infarct-free survival was 97.8% in the no-PTCA group and 90.5% in the PTCA group (p = 0.07).

CONCLUSIONS
There was no functional or clinical benefit from routine late PTCA after MI treated with thrombolytic therapy in this relatively low-risk cohort of patients. These data strongly suggest that patients with an uncomplicated MI after thrombolytic therapy, even if they have a "significant" residual stenosis of the infarct vessel, should be treated medically if they are without evidence of ischemia on stress testing before hospital discharge.
Radiofrequency catheter ablation of left lateral accessory pathways via the coronary sinus.
Authors: Haissaguerre M , Gaita F , Fischer B , Egloff P , Lemetayer P , Warin J F 
Published: June 2012

BACKGROUND
The purpose of this study was to describe a new technique for catheter ablation of left lateral accessory pathways (APs) by radiofrequency energy applied at the epicardium through the coronary sinus wall using a unipolar configuration.

METHODS AND RESULTS
In an overall group of 212 patients with left lateral APs, multiple endocardial ablation attempts of the AP were unsuccessful in eight patients. The mean +/- SD cumulative duration of previous attempts was 12 +/- 9 hours, using DC shocks and/or radiofrequency energy applied both at the atrial and/or ventricular AP insertions. Epicardial AP insertion was determined by bipolar and unipolar unfiltered distal electrograms by scanning the coronary sinus with a steerable 6F or 7F catheter with a 4-mm distal electrode. The local atrial to ventricular electrogram amplitude ratio was 0.3-1.6. At the ablation site, the catheter tip was slightly deflected toward the annulus to increase both the ventricular component of electrograms and contact with the epicardium. In four patients, epicardial electrogram timings were earlier than endocardial ones. The AP was ablated in seven of the eight patients with 20-30 W applied for 10-60 seconds. No complications occurred except a marked nonspecific pain during radiofrequency energy application; however, the catheter remained adherent to the coronary sinus wall, and its withdrawal was performed during a new radiofrequency application to decrease the risk of coronary sinus rupture. After ablation, echocardiograms, coronary artery angiograms, and levophase coronary sinus angiograms showed no abnormality in all patients except two who had a probable mural thrombus in the coronary sinus. AP conduction remained abolished for 1-10 months of follow-up in seven patients.

CONCLUSIONS
Radiofrequency catheter ablation of left lateral APs can be achieved effectively and relatively safely via the mid or distal coronary sinus when endocardial approaches are unsuccessful.
Clinical outcomes after the arterial switch operation for transposition. Patient, support, procedural, and institutional risk factors. Congenital Heart Surgeons Society.
Authors: Kirklin J W , Blackstone E H , Tchervenkov C I , Castaneda A R 
Published: June 2012

BACKGROUND
As the probability increases that the arterial switch operation is optimal treatment for transposition, detailed information about outcomes and the circumstances in which they are suboptimal becomes important.

METHODS AND RESULTS
A multi-institutional prospective study with annual detailed follow-up included 513 neonates with simple transposition or transposition and ventricular septal defect entering for diagnosis and treatment at < 15 days of age and undergoing an arterial switch repair. The 1-month and 1- and 5-year survivals were 84%, 82%, and 82%, respectively. The hazard function for death had a rapidly declining single phase that approached zero by 12 months after surgery. Among the eight patients who died > or = 3 months after the operation, four had severe ventricular dysfunction, probably related to imperfect coronary arterial transfer. Coexisting single ventricular septal defect was not a risk factor for death. Origin of the left main coronary artery or only the left anterior descending or the circumflex artery from the right posterior sinus (sinus 2) was a risk factor that was even stronger when an intramural course was present; multiplicity of ventricular septal defects was a risk factor. Longer global myocardial ischemic time and total circulatory arrest time were risk factors. Certain institutions were shown to be risk factors for death; the results in some improved with increasing experience, in some they did not, and in some they worsened.

CONCLUSIONS
Good early and intermediate-term clinical outcomes can be obtained in neonates with simple transposition and transposition and ventricular septal defect by use of the arterial switch operation. Certain coronary artery patterns and certain institutions lessen the goodness of outcome.
Transcatheter closure of patent foramen ovale after presumed paradoxical embolism.
Authors: Bridges N D , Hellenbrand W , Latson L , Filiano J , Newburger J W , Lock J E 
Published: June 2012

BACKGROUND
Many have proposed a relation between presence of a patent foramen ovale, with or without atrial septal aneurysm, and cryptogenic stroke. The effect of foramen ovale closure on the risk for subsequent strokes is unknown.

METHODS AND RESULTS
Transcatheter closure of a patent foramen ovale was undertaken in 36 patients with known right-to-left atrial shunting and presumed paradoxical emboli (31 strokes, 25 transient neurological events, four systemic arterial emboli, and two brain abscesses). Individual patients had between one and four such events. None had a left heart or carotid source of embolism; 31 of 35 had no known risk factors for stroke. Events occurred in 12 patients while they were taking warfarin. At cardiac catheterization, patent foramina ovalia were significantly larger than predicted for age in 67% of the patients. Implantation of a double-umbrella device in the patent foramen ovale was achieved in all without serious procedural complications. Of 34 who have returned for follow-up, one has a residual atrial communication that may be clinically important, five had trivial leaks, and 28 have complete closure. There have been no strokes during a mean follow-up of 8.4 months.

CONCLUSIONS
Transcatheter closure of a patent foramen ovale can be accomplished with little morbidity and may reduce the risk of recurrence. Further investigations directed toward identifying the population at risk and assessing the effect of intervention are warranted.
Parallel cardiac and vascular adaptation in hypertension.
Authors: Roman M J , Saba P S , Pini R , Spitzer M , Pickering T G , Rosen S , Alderman M H , Devereux R B 
Published: June 2012

BACKGROUND
Although vascular damage in the noncoronary circulation is a major cause of complications in hypertension, relatively little is known of the in vivo geometry and function of the arterial circulation in patients with uncomplicated hypertension or of their relation to left ventricular hypertrophy, a marker of enhanced risk of cardiovascular complications.

METHODS AND RESULTS
Wall thickness and internal diameter of the common carotid artery and the presence of atherosclerosis within the extracranial carotid arteries were determined by ultrasound in 43 asymptomatic hypertensive patients and 43 normotensive subjects matched for sex, age, and body size. Vascular stiffness was estimated from simultaneous superimposed carotid pressure waveforms obtained with an external solid-state transducer. Left ventricular size and function were determined echocardiographically. Compared with normal subjects, hypertensive patients had greater left ventricular absolute and relative wall thicknesses, left ventricular mass, and carotid absolute and relative wall thicknesses (p < 0.005). Carotid intimal-medial thickness exceeded the 95th percentile of normal values in 28% of hypertensive patients (p < 0.01). Carotid atherosclerosis was equally prevalent within the two blood pressure groups and was associated with older age, larger left ventricular and carotid wall thicknesses, and carotid diameter. Despite similar carotid pulse pressures, vascular stiffness was significantly increased in the hypertensive patients. Among the population as a whole, significant relations existed between cardiac and vascular wall thicknesses and internal dimensions. In multivariate analyses, these relations were statistically independent of age and blood pressure.

CONCLUSIONS
The present study documents the presence of geometric and functional changes within the common carotid artery in uncomplicated hypertension that parallel findings within the left ventricle. The potential contribution of these changes to the cardiovascular complications of hypertension, particularly in the setting of left ventricular hypertrophy, is unknown.
Myocardial cell hypertrophy after myocardial infarction with reperfusion in dogs.
Authors: Kambayashi M , Miura T , Oh B H , Murata K , Rockman H A , Parra G , Ross J 
Published: June 2012

BACKGROUND
The potential role of myocardial cell hypertrophy in the ischemic zone in the mechanism of late recovery of regional contractile function after myocardial infarction followed by reperfusion has not been examined.

METHODS AND RESULTS
Eight chronically instrumented, conscious dogs were subjected to 90-120 minutes of circumflex coronary artery occlusion followed by reperfusion. The thickness and function of the anterior (AT) and posterior (PT) walls was measured by ultrasonic gauges at control, during occlusion, and after reperfusion. After 3 weeks, cross-sectional areas of surviving cells were determined from subepicardial (epi), midwall (mid), and subendocardial (endo) regions in six dogs and compared with those from six animals without infarction, including three sham-operated control dogs. PT systolic wall thickening showed dyskinesia during occlusion but recovered after reperfusion to 48% of control at 1 week and 67% at 3 weeks. End-diastolic thickness of the PT wall increased markedly after reperfusion, but AT and PT walls were only slightly thicker (p = NS) than in control dogs at 3 weeks. Cross-sectional areas of reperfused dogs in the infarct region averaged 279 (PTepi), 291 (PTmid), and 317 microns 2 (PTendo) and were significantly larger than in control animals (237 [PTepi], 241 [PTmid], and 233 microns 2 [PTendo]). PT cell areas were significantly larger than AT cells, ENDO cell areas were larger than EPI cells (both p < 0.05), and ENDO cells of the AT wall were larger than those of noninfarcted dogs (p < 0.05).

CONCLUSIONS
In dogs with myocardial infarction followed by reperfusion, the cross-sectional areas of cells in the infarcted PT wall were larger than those in the noninfarcted AT wall, and within both the infarcted and noninfarcted zones, cell areas were larger in the endocardial than the epicardial region. In all regions of the infarcted wall and in the ENDO region of the noninfarcted wall, cell areas were generally larger than those of control dogs without infarction, and the control dogs showed no transmural differences in cell areas. The mechanisms responsible for this significant remodeling of the reperfused infarcted zone, which involves myocardial cellular hypertrophy, are unknown, but it is possible that hypertrophy of surviving regions of the infarcted wall played a role in the late recovery of regional function that accompanied this hypertrophic response.
Critical analysis of the signal-averaged electrocardiogram. Improved identification of late potentials.
Authors: Lander P , Berbari E J , Rajagopalan C V , Vatterott P , Lazzara R 
Published: June 2012

BACKGROUND
This study performed a critical analysis of signal-averaging methods. The objective was to optimize detection of late potentials.

METHODS AND RESULTS
We studied two patient populations: a low-arrhythmia-risk group with no evidence of heart disease and a group with clinically documented ventricular tachycardia (VT). Filtered QRS duration (QRSD) and terminal QRS amplitude (RMS40) were measured from the vector magnitude. A QRS duration based on the latest detectable ventricular activity in any of the three individual XYZ leads was also measured. Because of improved signal-to-noise ratio, both individual lead analysis and extended (600-versus 200-beat) averaging yielded significant changes in signal-averaged ECG parameters. Both approaches gave an increased sensitivity for VT identification. Sensitivity, specificity, and accuracy were evaluated as functions of critical values of QRSD and RMS40. RMS measurements in the terminal QRS, ranging from 20 to 100 msec and including RMS40, did not contribute to maximizing sensitivity and were highly correlated with QRSD. Our results from the low-arrhythmia-risk group suggest that age and sex should be considered in the definition of late potentials.

CONCLUSIONS
We propose a VT risk stratification scheme using signal-averaged ECG parameters obtained from both individual lead and vector magnitude analysis. This allows definition of four categories of VT risk derived statistically from the study data. This definition is based on combined measures of sensitivity, specificity, and negative and positive predictive value.
Association of early-onset coronary heart disease in South Asian men with glucose intolerance and hyperinsulinemia.
Authors: McKeigue P M , Ferrie J E , Pierpoint T , Marmot M G 
Published: June 2012

BACKGROUND
Rates of coronary heart disease are higher in South Asians (Indians, Pakistanis, and Bangladeshis) settled overseas than in other ethnic groups. We tested the hypothesis that this excess risk results from metabolic disturbances associated with insulin resistance.

METHODS AND RESULTS
There were 1,421 South Asian men and 1,515 European men aged 40-69 years in London examined in the Southall Study. Prevalence of ischemic ECG abnormalities was higher in South Asians than in Europeans (17% versus 12%, p < 0.001), with an excess of major Q waves (Minnesota codes 1-1 or 1-2) in younger South Asian men (p = 0.01 for the age-ethnicity interaction). Major Q waves were strongly associated with glucose intolerance and hyperinsulinemia in younger South Asians; these factors accounted statistically for 73% of major Q waves in those aged 40-54 years. Age-standardized prevalence of a positive history of coronary heart disease was similar in South Asians and Europeans (8.5% versus 8.2%, NS), and positive history without Q waves was not associated with glucose intolerance or hyperinsulinemia in South Asians. Smoking rates and average plasma cholesterol were lower in South Asians than in Europeans; in a logistic model controlling for smoking and cholesterol, the odds ratio for major Q waves in South Asians compared with Europeans was 2.4 (95% CI, 1.5-3.8). Adjusting for glucose intolerance and hyperinsulinemia reduced this ratio to 1.5 (95% CI, 0.9-2.5).

CONCLUSIONS
These results are consistent with the hypothesis that insulin resistance underlies the high coronary risk in South Asian people and strengthen the evidence for a fundamental role of this metabolic pattern in the etiology of coronary heart disease.
Accuracy of exercise 201Tl myocardial scintigraphy in asymptomatic young men.
Authors: Schwartz R S , Jackson W G , Celio P V , Richardson L A , Hickman J R 
Published: June 2012

BACKGROUND
Little is known about the diagnostic usefulness of 201Tl scintigraphy for detecting asymptomatic coronary artery disease in apparently healthy men. We thus evaluated planar 201Tl exercise myocardial scintigraphy in 845 asymptomatic male military aircrew undergoing coronary arteriography because of abnormal noninvasive tests suggesting possible myocardial ischemia.

METHODS AND RESULTS
Patients were stratified by prior disease risk into six subgroups using age (< 45 and > or = 45 years) and ratio of total to high density lipoprotein cholesterol (< 4.5, 4.5-6.0, and > 6.0). Significant coronary artery disease (> or = 50% diameter stenosis in any major coronary artery) was present in 143 (16.9% prevalence). Overall sensitivity and specificity of 201Tl scintigraphy adjusted for verification bias were estimated to be 45 +/- 4% and 78 +/- 1%, respectively. These values are lower than corresponding values accepted for clinical populations. Positive and negative predictive values varied across subgroups. A normal thallium scan indicated low risk of disease, but an abnormal test was likely to be a false-positive result. A logistic equation was retrospectively fit to the data for estimating the probability of disease given age, cholesterol ratio, and thallium results. Within each quintile of estimated risk, the average risk did not differ significantly from the observed disease prevalence.

CONCLUSIONS
Exercise 201Tl scintigraphy is limited by the frequent occurrence of false-positive tests in detecting asymptomatic, anatomic coronary artery disease in young men in accordance with Bayesian probability theory.