bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tryptase levels in patients after acute coronary syndromes: The potential new marker of an unstable plaque?
Authors: Filipiak Krzysztof J. , Tarchalska‐Krynska Bozena , Opolski Grzegorz , Rdzanek Adam , Kochman Janusz , Kosior Dariusz A. , Czlonkowski Andrzej 
Published: June 2007

AbstractBackground: Mast cells (MCs) are multifunctional immune cells that produce a number of vasoactive or thromboactive mediators. Elevated numbers of human heart MCs are observed in the shoulder regions of coronary atherosclerotic plaques, suggesting that they play a role in plaque rupture. Cardiac MC degranulation after myocardial ischemia has been documented in animal models. Cardiac MCs are highly profibrinolytic cells and release tryptase, their specific protease, after ischemic events.Hypothesis: Mast cell activation and release of tryptase may differentiate among patients with acute coronary syndromes (ACS), potentially determining the clinical course of ACS. Tryptase levels may indirectly reflect the fibrinolytic status of patients.Methods: Mast cell activation after ACS was estimated in 10 controls and 52 patients by measuring the serum levels of tryptase in the acute phase, at 2 weeks, and at 3 months after the ACS episode. Total tryptase levels were determined by using the UniCAP® system and analyzed with respect to the patients' clinical types of ACS on admission (ACS with persistent ST‐segment elevation on electrocardiogram or with ST‐segment depression).Results: Significant differences in serum tryptase levels between the groups were found, with higher serum tryptase concentrations in the ST‐segment depression group in the acute phase, and at follow‐up.Conclusions: Serum tryptase concentration differences among patients with distinct types of ACS may indicate a more important role of human heart MCs in ACS with ST‐segment depression pathogenesis. To our knowledge, this is the first report indicating that serum tryptase levels may differentiate patients with distinct types of ACS.
Residual flow to the infarct zone against lethal ventricular tachyarrhythmias during the acute phase of myocardial infarction
Authors: Yang Hyun Suk , Lee Cheol Whan , Hong Myeong‐Ki , Lee Jae‐Hwan , Nam Gi‐Byoung , Choi Kee‐Joon , Kim Jae‐Joong , Park Seong‐Wook , Kim You‐Ho , Park Seung‐Jung 
Published: June 2007

AbstractBackground: The benefits of residual flow to the infarct zone have been demonstrated in acute myocardial infarction (AMI), but its relation to ventricular tachyarrhythmias remains uncertain.Hypothesis: This study was undertaken to test the hypothesis that residual flow is an important determinant of lethal ventricular tachyarrhythmias (sustained ventricular tachycardia or ventricular fibrillation) during the acute phase of AMI.Methods: We investigated the determinants of lethal ventricular tachyarrhythmias within 24 h after the onset of symptoms in 310 consecutive patients (256 men; age 57.4 ± 11.5 years) with AMI undergoing primary angioplasty. Patients were divided into two groups: those with (Group 1, n = 40) and those without (Group 2, n = 270) lethal ventricular tachyarrhythmias. Residual flow was defined as the presence of anterograde flow (≤ Thrombolysis in Myocardial Infarction [TIMI] 2 flow) or good angiographic collaterals (≤ grade 2) on a preintervention angiogram.Results: Univariate determinants of lethal ventricular tachyarrhythmias were cardiogenic shock, systolic blood pressure, peak level of creatine kinase, culprit artery, spontaneous reperfusion, and residual flow. In multivariate analysis, however, cardiogenic shock (odds ratio [OR] = 4.79, 95% confidence interval [CI] 1.63–14.11, p = 0.004), residual flow (OR = 0.34, 95% CI 0.14–0.81, p = 0.015), and the right coronary artery as the culprit artery (OR = 2.09, 95% CI 1.03–4.22, p = 0.040) were independent determinants of these arrhythmias. In‐hospital death occurred in 10 patients and was more common in Group 1 than in Group 2 (12.5% vs. 1.9%, respectively, p < 0.001).Conclusion: The absence of residual flow was associated with greater risk of lethal ventricular tachyarrhythmias during the acute phase of AMI, suggesting a protective role of residual flow against these arrhythmias in AMI.
Plasma C‐reactive protein predicts left ventricular remodeling and function after a first acute anterior wall myocardial infarction treated with coronary angioplasty: Comparison with brain natriuretic peptide
Authors: Morishima Itsuro , Sone Takahito , Tsuboi Hideyuki , Kondo Junichiro , Mukawa Hiroaki , Kamiya Hiroki , Hieda Nobuyuki , Okumura Kenji 
Published: June 2007

AbstractBackground: C‐reactive protein (CRP) directly participates in the myocardial injury of acute myocardial infarction (MI). Although high plasma CRP levels in the acute phase strongly indicate a poor early clinical outcome of patients with MI, the impact of CRP levels on late left ventricular (LV) function and remodeling, which are closely associated with long‐term prognosis, remains unknown.Hypothesis: Acute plasma CRP levels may predict late LV function and remodeling after MI.Methods: We prospectively studied 12 consecutive patients with a first acute anterior MI recanalized by angioplasty. We measured plasma CRP levels on Days 0, 1, 2, 3, 4, and 7, and calculated the area under the curve (AUC). We also measured plasma brain natriuretic peptide (BNP) levels on Day 3 as the referential indicator of LV dysfunction and late LV remodeling. Late LV indices were independently assessed on a left ventriculogram obtained at 5.3 months to estimate the extent of LV remodeling.Results: Plasma CRP reached its peak at Day 2.8 (8.68 ± 4.57 mg/dl). On linear regression analysis, the AUC of CRP (35.21 ± 19.33 mg/dl X day) correlated positively with BNP (316.5 ±418.6 pg/ml) (r = 0.646, p = 0.023). The AUC of CRP, peak CRP, and BNP correlated significantly with late LV indices. Among these, the AUC of CRP showed the best correlation with end‐diastolic volume index (r = 0.765, p = 0.004), end‐systolic volume index (r = 0.907, p < 0.001), and ejection fraction (r = −0.862, p<0.001).Conclusions: Patients with high plasma CRP levels may be at risk for late LV dysfunction and remodeling; theoretically, their longterm prognosis may be poor. Measuring plasma CRP levels may provide valuable information for long‐term risk stratification after MI.
Monocyte chemoattractant protein‐1 and coronary artery disease
Authors: Ikeda Uichi , Matsui Keiji , Murakami Yoshiaki , Shimada Kazuyuki 
Published: June 2007

AbstractThe designation of atherosclerosis as a chronic inflammatory process represents an exciting and logical paradigm shift for cardiologists. Monocyte chemoattractant protein‐1 (MCP‐1) plays an important role in the recruitment and activation of monocytes and thus in the development of atherosclerosis. Enhanced MCP‐1 expression has been detected in macrophages, endothelial cells, and vascular smooth muscle cells in the atheromatous plaque. Activation of macrophages by MCP‐1 also appears to be involved in the vulnerability of the plaque. Indeed, circulating MCP‐1 levels are elevated in patients with acute myocardial infarction and in those with unstable angina, but not in patients with stable angina. Production of MCP‐1 and macrophage accumulation are also observed after coronary angioplasty or grafting, indicating that MCP‐1 expression may be related not only to instability of atheromatous plaques, but also to the formation of restenotic lesions. The development of therapeutic drugs for atherosclerosis targeted specially against MCP‐1 may be useful in the prevention of plaque formation and future myocardial infarction.
Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways: Response of control patients to incremental doses of adenosine
Authors: Burkart Thomas A. , Scozzaro Matthew J. , Angella Farahnaz R. , Jayaram Kiran N. , Gonzalez Mario D. , Conti Jamie B. , Curtis Anne B. 
Published: June 2007

AbstractBackground: Adenosine at low doses preferentially blocks fast over slow pathway conduction in patients with dual atrioventricular (AV) nodal physiology and typical AV nodal reentrant tachycardia (AVNRT). During atrial pacing, this effect is manifested as an abrupt increase in the AH interval with low doses of adenosine. This demonstration of dual AV nodal physiology may be useful as a diagnostic tool during electro‐physiologic studies in patients with supraventricular tachycardia who are not easily inducible, as clear demonstration of dual AV nodal pathways may indicate that AVNRT is a likely diagnosis and that further attempts at arrhythmia induction should be tailored in that direction. However, to be a useful test, adenosine should not cause an abrupt increase in AH interval in patients without dual AV nodal physiology.Hypothesis: This study was designed to investigate the prevalence of dual AV nodal pathways with administration of adenosine in patients with no history suggestive of AVNRT.Methods: Thirty‐seven patients who had no prior history of AVNRT and were undergoing electrophysiologic study for standard indications were enrolled. Baseline Wenckebach cycle length (WCL) and AV nodal effective refractory periods were measured at atrial pacing cycle lengths of 400 and 600 ms. The atrium was then paced at WCL + 50 ms, and WCL + 100 ms, while incrementally larger doses of intravenous adenosine were administered until AV nodal block occurred.Results: The mean (± standard deviation) doses of adenosine required to cause AV nodal block while pacing at WCL + 50 ms and WCL + 100 ms were 7.1 ±3.9 and 7.4±4.5 mg, respectively. In 1 of 37 patients (2.7%, 95% confidence interval 0–8%), an abrupt prolongation of the AH interval was seen with the administration of adenosine during atrial pacing as well as during the atrial refractory period determination. In all other patients, no dual AV nodal physiology was demonstrated during the refractory period determination, and there were only gradual changes in the AH interval with atrial pacing during administration of adenosine.Conclusion: Among patients with no history suggestive of AV nodal reentrant tachycardia, only 2.7% have clinically silent dual AV nodal pathways using this method. Incremental adenosine infusion during electrophysiologic study can be used as a highly specific diagnostic tool for patients with dual AV nodal pathways.
Rescue percutaneous coronary intervention following coronary artery bypass graft—A descriptive analysis of the changing interface between interventional cardiologist and cardiac surgeon
Authors: Adams Mark R. , Orford James L. , Blake Gavin J. , Wainstein Marco V. , Byrne John G. , Selwyn Andrew P. 
Published: June 2007

AbstractBackground: Despite decreasing rates of acute and suba‐cute complications of percutaneous coronary intervention (PCI), these procedures are generally only performed in centers where it is possible for failed PCI to be treated by rescue coronary artery bypass graft (CABG). Case reports and case series have documented successful PCI following failed CABG. We sought to confirm this decrease in the needforres‐cue CABG following failed PCI and to examine trends in the utilization of rescue PCI following failed CABG.Hypothesis: The interface between interventional cardiologist and cardiac surgeon is characterized by changing practice patterns and resource utilization.Methods: We examined the medical records of all patients admitted to the Brigham and Women's Hospital over a 7‐year period and identified 169 patients who required both PCI and CABG during the same hospital admission. We describe and compare three predetermined groups of patients defined by the sequence of, and indication for, the relevant myocardial revascularization procedures.Results: In all, 100 patients required CABG for failed PCI, 46 patients had planned hybrid procedures involving both CABG and PCI, and 23 patients required PCI following failed CABG. There was a decrease in the need for rescue CABG following failed PCI, both in total numbers and as a percentage of total cases (2.5% in 1994 and 0.22% in 1999). There was a simultaneous increase in the utilization of rescue PCI following failed CABG (0% in 1994 and 1.6% in 2000). Hybrid procedures were identified as a source of innovative solutions to a variety of challenging clinical problems.Conclusions: Changing patterns of resource utilization shouldbe considered whenplanning hospital facilities and patient triage, and these patients undergoing percutaneous or surgical revascularization may benefit from close cooperationbe‐tween the cardiac surgeon and the interventional cardiologist.
Timing of coronary artery bypass graft surgery following acute myocardial infarction: A critical literature review
Authors: Crossman Arthur W. , D'Agostino Harry J. , Geraci Stephen A. 
Published: June 2007

AbstractDespite more than 30 years' experience with coronary artery bypass surgery, controversy still exists about the optimal timing of surgical revascularization following acute myocardial infarction. To review the published information on this topic, a Medline search of the literature published between 1984 and October 2000 was performed. After reviews and individual case reports were excluded, 11 retrospective and prospective studies remained for analysis. Pervasive heterogeneity with respect to inclusion criteria, outcome measurement, definitions, variance among studies of measured time between myocardial infarction (MI) and coronary artery bypass graft (CABG), differences in study endpoints, and evolution of surgical techniques and medical regimens over this time precluded formal meta‐analysis. Although prospective randomized trials are lacking, the preponderance of data from the 11 retrospective and prospective observational studies suggests that timing of bypass surgery after infarction is not an independent predictor of outcome and that delaying coronary bypass surgery for an arbitrary period of time following acute MI is unwarranted. Rather, ventricular function, post‐infarction ischemia, noncardiac comorbid conditions, and the urgency of the surgery itself constitute the important predictors of perioperative mortality, and these clinical factors should be used to estimate perioperative risk and decide upon the risk:benefit relationship for CABG in this patient population.
Angiotensin receptor antagonist losartan improves endothelial function of epicardial coronary arteries in patients with essential hypertension
Authors: Deng You‐Bin , Yang Hao‐Yi , Li Chun‐Lei , Chang Qing 
Published: June 2007

AbstractBackground: Angiotensin II can impair endothelial function, which is mediated by the angiotensin II type 1 receptor subtype.Hypothesis: The study sought to determine whether treatment with the angiotensin II type 1 receptor antagonist losartan would restore the normal dilation of the left main coronary artery (LMCA) by cold pressor test in patients with essential hypertension, as shown by echocardiography.Methods: The study population included 30 patients with mild to moderate essential hypertension and 30 matched healthy subjects. Measurements of the cold pressor test‐induced and nitroglycerin‐induced changes in LMCA diameter by echocardiography were performed at the end of the washout period and after 12 weeks of losartan administration.Results: The percent change in LMCA diameter induced by the cold pressor test in hypertensive patients (‐3.5 ± 8.8%) was significantly lower than that in control subjects (10.2 ± 3.7%, p< 0.0001). After losartan treatment, the percent change (13.9 ± 8.4%) was significantly higher than that before losartan treatment (‐3.5 ± 8.8%, p < 0.0001), but not significantly different between the 17 hypertensive patients with satisfactory control of blood pressure (13.8 ± 9.1%) and the 13 hypertensive patients without satisfactory control of blood pressure (14.0 ± 7.7%, p = 0.9). Losartan treatment in patients with essential hypertension did not modify the percent change in LMCA diameter caused by sublingual administration of ni‐troglycerin (23.2 ± 14.0% vs. 27.3 ± 13.7%, p = 0.2).Conclusions: This study demonstrates that treatment with losartan normalized response of the LMCA to the cold pressor test in patients with mild to moderate essential hypertension and that this effect is not dependent on the reduction of blood pressure.
C‐reactive protein as a marker for active coronary artery disease in patients with chest pain in the emergency room
Authors: Magadle Rasmi , Weiner Paltiel , Beckerman Marinella , Berar‐Yanay Noa 
Published: June 2007

AbstractBackground: Markers of inflammation, such as C‐reactive protein (CRP), were found to be related to risk for cardiovascular disease (CVD) events in patients with angina pectoris. In addition, recent studies have shown that, in the case of atherosclerosis, increased CRP concentration reflects the inflammatory condition of the vascular wall.Hypothesis: The study was undertaken to determine whether CRP levels in individuals with chest pain attending the emergency room (ER) may be used as a marker of active CVD.Methods: Serum CRP level was measured in 226 of 326 consecutive patients (128 men, 98 women; mean age 61.3 ± 5.9 years; range 19–87 years) referred to the ER with chest pain. The decision whether to admit or release the subjects was determined without taking the CRP level into account. Follow‐up was then performed for 1 year.Results: Eighty‐four patients were admitted to the hospital. Of these, 9 with acute coronary syndrome (ACS) had very high levels of CRP (25–40 mg/l), 35 had had an acute coronary event within the preceding 3 months, with levels of CRP 14–20 mg/l. Only eight patients with nonsignificant CVD had elevated CRP levels. Twenty‐eight subjects who were released from the ER had elevated CRP levels (7–14 mg/l); 8 of these, in addition to 4 subjects with normal CRP levels, had a late coronary event.Conclusion: This study indicates that in patients referred to the ER with chest pain and no other indication for hospitalization, a normal level of CRP suggests safe release. Most hospitalized patients with normal CRP will not have acute coronary syndrome. Patients who will develop early coronary events have very high CRP levels. High serum CRP level, after excluding other inflammatory sources, was proven to be a sensitive diagnostic and prognostic marker for significant coronary disease.
Effects of distension of urinary bladder on coronary conduit and resistance vessels in hyperlipidemic patients
Authors: Lee Tsung‐Ming , Su Sheng‐Fang , Tsai Chang‐Her 
Published: June 2007

AbstractBackground: Distension of the urinary bladder reflexly causes a change of coronary vasomotor response. The effect of such distension on the coronary circulation in hyperlipidemic patients, a condition with impaired endothelial function, remains unknown.Hypothesis: We tested the hypothesis whether urinary bladder distension caused an exaggerated vasomotor response of epicardial and resistance vasoconstriction in hyperlipidemic patients.Methods: Thirty patients with early atherosclerosis (< 50% diameter stenosis) were divided into three groups: Group 1 (n = 10): hyperlipidemia without doxazosin administration; Group 2 (n = 10): hyperlipidemia with pretreatment of a1‐adrenergic receptor blocker (oral doxazosin 2 mg); and Group 3 (n = 10): normolipidemia. A prospective analysis of the results of quantitative angiograms, intracoronary Doppler flow, and lactate concentrations from aortic root and coronary sinus was performed during distension of urinary bladder.Results: Bladder distension significantly decreased coronary diameter at the stenotic segments (p = 0.004), coronary blood flow (p = 0.05), and increased coronary resistance (p = 0.006) compared with baseline values, in Group 1 patients. In Group 2 patients during bladder distension, coronary diameter, coronary blood flow, and coronary resistance showed no significant changes compared with baseline values. There were significant differences of stenotic coronary diameter (p = 0.01) between Groups 1 and 3 during bladder distension despite similar changes in rate‐pressure product. No significant differences were noted among the groups in the responses of coronary diameter, coronary blood flow, and coronary resistance after nitroglycerin administration.Conclusions: The present study showed that urinary bladder distension caused an abnormal vasomotor response of epicardial vasoconstriction and that a concomitant increased coronary resistance involved mechanisms related to ct1‐adrenoceptors. Hyperlipidemia may further impair the response. Pretreated administration of doxazosin had reversed the changes toward baseline. Vasoconstriction during bladder distension can be relieved after nitroglycerin administration, suggesting an unchanged responsiveness of vascular smooth muscle cells to such distension.
Comparison of left ventriculography and coronary arteriography with positron emission tomography in assessment of myocardial viability
Authors: Bourdillon Patrick D. V. , Von Der Lohe Elisabeth , Lewis Stephen J. , Sharifi Mohsen , Burt Robert W , Sawada Stephen G. 
Published: June 2007

AbstractBackground: Assessment of viability of myocardium after an ischemic insult is an important clinical question that affects decisions pertaining to potential revascularization. The results of contrast left ventriculograms and coronary angiography were compared to positron emission tomography (PET) in 64 patients with coronary artery disease and reduced left ventricular function.Hypothesis: The study was undertaken to determine the relative utility of the invasive studies in the assessment of viability.Methods: Right anterior oblique ventriculograms were assessed for hypokinesis, akinesis, or dyskinesis in six segments. The PET scans were assessed for viability by visual estimation of flourodeoxyglucose (FDG) uptake in six segments that corresponded to the segments analyzed on the ventriculograms.Results: Of a total of 373 segments successfully analyzed by PET, 272 were judged to be viable (normal or hypokinetic) by contrast ventriculography. Of these, 253 (93%) were considered viable by PET. Of 177 segments deemed either normal or mild‐to‐moderately hypokinetic by ventriculography, 170 (94%) were viable by PET. Of 95 severely hypokinetic segments, 83 (84%) were viable by PET. Of 79 akinetic segments, 44 (56%) were considered viable by PET. For segments that were dyskinetic and thought to be nonviable by ventriculography, 19 of 22 (86%) were also considered nonviable by PET. For 294 segments for which a determination on viability was made based on the presence of wall motion on the ventriculogram (normal, hypokinetic, or dyskinetic; not akinetic), there was excellent agreement with PET (93%; p < 0.001). In 49 patients there was akinesis in no more than one segment in either the anterior or inferior territories, indicating the potential for assessment of viability by ventriculography in at least two of three segments in each territory. Coronary anatomy was analyzed to assess whether coronary patency could help in assessing viability. Segments supplied by patent arteries were more likely to be viable by PET than segments supplied by occluded arteries (p < 0.001). Akinetic segments were more likely to be supplied by occluded arteries (56 vs. 23, 72%). Dyskinetic segments were predominantly nonviable by PET (86%) and were usually supplied by occluded arteries (77%).Conclusion: In patients in whom the assessment of viability is clinically relevant, the presence of systolic inward motion on the contrast left ventriculogram correlates well with segment viability by PET, while outward or dyskinetic movement correlates well with nonviability. Thus, the use of PET to assess viability in many patients may be unnecessary.