bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preinfarction angina prevents left ventricular remodeling in patients treated with thrombolysis for myocardial infarction
Authors: NeŠKOVIÉ Aleksandar N. , Pavlovski KoČO , Bojić Dragana , Popović Zoran , Ota ević Petar , Vlahovićca Alja , Obradovićca Velibor , Putnikovićca Biljana , Vasiljevićca‐Pokraj Zorana , Bojićca Milovan , Popovićca Aleksandar D. 
Published: February 2009

AbstractBackground: It has been shown that preinfarction angina may have beneficial effects on infarct size and mortality. However, there are no studies that have serially assessed the impact of preinfarction angina on left ventricular (LV) function in a large series of patients.Hypothesis: The study was undertaken to determine whether preinfarction angina (within 7 days before infarction) influences LV remodeling.Methods: In all, 119 consecutive patients with acute myocardial infarction were serially evaluated by 2‐dimensional echocardiography (on Days 1, 2, 3, and 7; at 3 and 6 weeks; and at 3, 6, and 12 months following infarction). Left ventricular volumes were determined using Simpson's biplane formula and normalized for body surface area. Wall motion score index and sphericity index were calculated for each study. Coronary angiography was performed before discharge.Results: Preinfarction angina was detected in 39 of 119 patients. Initial echocardiographic and clinical data as well as the incidence of patent infarct‐related artery and collaterals were similar for patients with and without preinfarction angina. In the subset of thrombolysed patients, patients with preinfarction angina showed decrease of LV end‐diastolic and end‐systolic volumes during the follow‐up period (p = 0.033 and p = 0.001, respectively), and improvement of wall motion score index (p < 0.001) and ejection fraction occurred (p = 0.001), without changing of LV shape (p > 0.05); in addition, patients with preinfarction angina had smaller LV volumes and higher ejection fraction than did those without angina, from 3 weeks onward. These favorable effects were not detected in patients not treated with thrombolysis.Conclusions: These data indicate that preinfarction angina has an inhibiting effect on long‐term LV remodeling in patients who underwent thrombolysis for first acute myocardial infarction. It appears that preinfarction angina has no impact on infarct size and early postinfarction LV function.
Increased levels of plasma thrombomodulin in patients with acute myocardial infarction who had thrombolytic therapy and achieved successful reperfusion
Authors: Ileri Mehmet , Hisar Ismet , Yetkin Ertan , KoŞar Feridun , Cehreli Sengül , Korkmaz Sule , Demirkan Deniz 
Published: February 2009

AbstractBackground: There is a growing body of evidence from animal and in vitro studies for the existence of reperfusion injury after thrombolytic therapy for acute myocardial infarction (AMI), but the patient data are limited.Hypothesis: We aimed to examine the plasma thrombomodulin (TM) levels as a marker of endothelial injury and to investigate the effect of successful reperfusion on these levels.Methods: The study included 32 patients who had a first episode of acute myocardial infarction (AMI) and received intravenous streptokinase therapy.Results: Thrombomodulin levels increased significantly at 60 min after thrombolysis compared with the levels before thrombolytic therapy (0 min) in 21 (66%) patients who had successful reperfusion (49.09 ± 10.51 vs. 25.76 ± 5.55 ng/ml, p < 0.001). There was no difference between the TM levels at 0 and at 60 min of thrombolysis in the remaining 11 (34%) patients who could not achieve reperfusion (27.81 ± 6.32 vs. 28.72 ± 7.28 ng/ml, p = 0.35).Conclusion: There was a significant increase in TM levels at 60 min after thrombolysis in a group of patients with AMI who achieved successful reperfusion; this increase may have been caused by the activation/injury of endothelial cells. Data also suggest that the increment in TM levels may be predictive of the potential success of thrombolytic therapy.
Adequacy of anticoagulation in patients with atrial fibrillation: Effect of various parameters
Authors: Cohen Natan , Almoznino‐Sarafian Dorit , Alon Irena , Gorelik Oleg , Koopfer Margarita , Chachashvily Shulamit , Shteinshnaider Miriam , Litvinjuk Vladimir , Modai David 
Published: February 2009

AbstractBackground: Despite reported evidence of the vital importance of appropriate anticoagulation in patients with chronic atrial fibrillation for stroke prevention, this treatment modality still lags behind optimal requirements.Hypothesis: Our objectives were to evaluate various doctor‐or patient‐related factors that influence quality of control and to assess the adequacy of anticoagulation provided by physicians in the community.Methods: In a retrospective study, International Normalized Ratio (INR) values obtained immediately on admission to hospital were considered representative of previous long‐term control.Results: Only 42% of the relevant 385 patient population fell within the protective anticoagulation range of INR 1.91‐4.1. The respective figures for patients with poor (INR < 1.5) or suboptimal (INR 1.51‐1.9) control, as well as those whose INR values risked bleeding (INR > 4.1), were 28.3, 14.1, and 15.6%. Patient involvement in treatment positively influenced quality of control. By contrast, age 70–80 years or absence of congestive heart failure negatively affected quality of anticoagulation [p = 0.07, odds ratio (OR), 1.7 (95% confidence interval, 0.94–3.08), p = 0.014, OR, 2.06 (95% confidence interval, 1.15–3.7) respectively]. The percentage of patients admitted with stroke who had been adequately anticoagulated was significantly lower than that of patients who had no stroke (21 vs. 44.4%). Adequacy of anticoagulation in patients with cardiac prosthetic valves was superior compared with the rest of the patient population (56.7 vs. 42% with optimal, and only 14.5 vs. 28.3% with poor anticoagulation, respectively), indicating that under the same conditions a better quality of treatment could be achieved.Conclusions: Adequacy of anticoagulation in patients with atrial fibrillation lags behind actual recommendations. Better control is required and achievable.
Staged revascularization in critically ill patients with coronary artery disease
Authors: Hayat Nasser Jowhar , Varghese Kiron , Thomas Christus Singh , Khan Nazir Ali 
Published: February 2009

AbstractBackground: Critically ill patients undergoing bypass surgery experience a higher mortality and morbidity.Hypothesis: The study was undertaken to evaluate the efficacy and value of percutaneous transluminal coronary angioplasty (PTCA) as a bridge to coronary artery bypass graft surgery (CABG) in high‐risk patients with refractory unstable angina or cardiogenic shock.Methods: We present 11 seriously unstable patients with severe multivessel coronary artery disease undergoing culprit vessel PTCA. Angioplasty was performed not as a definitive procedure but rather as a bridge to surgical revascularization. All the patients had sustained at least one myocardial infarction prior to catheterization, all had refractory unstable angina, eight patients had only a single patent coronary artery, and five patients were in cardiogenic shock.Results: Following PTCA, all patients enjoyed a stable in‐hospital period. One patient died 12 weeks after successful PTCA while awaiting second CABG. Seven patients subsequently underwent CABG and are doing well. The remaining three patients were also advised to undergo CABG, but elected to continue medical management.Conclusions: Coronary angioplasty of the culprit vessel may play a role as a bridge to surgery in critically ill patients.
Cardiac troponin T Arg92Trp mutation and progression from hypertrophic to dilated cardiomyopathy
Authors: Fujino Noboru , Shimizu Masami , Ino Hidekazu , Okeie Kazuyasu , Yamaguchi Masato , Yasuda Toshihiko , Kokado Hiromasa , Mabuchi Hiroshi 
Published: February 2009

AbstractBackground: Mutations in the cardiac troponin T gene causing familial hypertrophic cardiomyopathy (HCM) are associated with a very poor prognosis but only mild hypertrophy. To date, the serial morphologic changes in patients with HCM linked to cardiac troponin T gene mutations have not been reported.Hypothesis: The aim of this study was to determine the long‐term course of patients with familial HCM caused by the cardiac troponin T gene mutation, Arg92Trp.Results: The Arg92Trp missense mutation was present in 10 individuals from two unrelated pedigrees. They exhibited different cardiac morphologies: three had dilated cardiomyopathy‐like features, five had asymmetric septal hypertrophy with normal left ventricular systolic function, one had electrocardiographic abnormalities without hypertrophy, and one had the disease‐causing mutation but did not fulfill the clinical criteria for the disease. The mean maximum wall thickness was 14.1 ± 6.0 mm. The three patients with dilated cardiomyopathy‐like features had progressive left ventricular dilation. Three individuals underwent right ventricular endomyocardial biopsy. There was a modest degree of myocardial hypertrophy (myocyte diameter: 18.9 ± 5.2 m̈m), and minimal myocardial disarray and mild fibrosis were noted.Conclusion: The Arg92Trp substitution in the cardiac troponin T gene shows a high degree of penetrance, moderate hypertrophy, and early progression to dilated cardiomyopathy in Japanese patients. Early identification of individuals with this mutation may provide the opportunity to evaluate the efficacy of early therapeutic interventions.
Thrombopoietin and mean platelet volume in coronary artery disease
Authors: ŞENARAN HANDAN , Ileri Mehmet , AltinbaŞ Ahmet , KoŞar Ali , Yetkin Ertan , ÖZTÜRK Mustafa , Karaaslan YaŞar , Kirazli Şerafettin 
Published: February 2009

AbstractBackground: Large platelets are shown to be hemostatically more active. It has been suggested that mean platelet volume (MPV) is increased during acute myocardial infarction (AMI) and unstable angina pectoris (USAP). However, the underlying mechanism of the phenomenon remains unclear.Methods: Twenty patients with AMI and 20 patients with USAP were included in this study. Seventeen healthy adult subjects served as controls. Venous blood samples of the subjects were drawn within 12 h after admission. Thrombopoietin levels were measured by ELISA and platelet counts and MPV were assayed by autoanalyzer.Results: Patients with AMI and USAP had higher platelet counts than those in the control group. Although the platelet counts were slightly higher in AMI than in USAP, this did not reach statistical significance. Mean platelet volume and levels of TP were found to be elevated in patients with AMI and USAP compared with control subjects (p < 0.001). Thrombopoietin levels were higher in AMI than USAP, but this was not statistically significant. There was a positive correlation between TP levels and MPV values (p < 0.05).Conclusion: Increased TP levels may increase both platelet counts and platelet size, resulting in hemostatically more active platelets, which may contribute to the development and progression of CAD.
Effect of acute exercise on the raised plasma fibrinogen, soluble P‐Selectin and von willebrand factor levels in chronic atrial fibrillation
Authors: Li‐Saw‐Hee Foo Leong , Blann Andrew D. , Edmunds Eiry , Gibbs Christopher R. , Lip GREGORY Y. H. 
Published: February 2009

AbstractBackground: There is increasing evidence that chronic atrial fibrillation (AF) is associated with a prothrombotic or hypercoagulable state.Hypothesis: This study was undertaken to determine whether short‐term exercise in patients with chronic AF would shift the overall hemostatic balance toward a more prothrombotic state with a reduction in fibrinolytic potential.Methods: We recruited 20 patients (13 men;mean age 65 years ± 11 standard deviation [SD]) with chronic AF who were not treated with antithrombotic therapy and exercised them to exhaustion using a multistage treadmill exercise (standard Bruce) protocol. Blood samples were taken pre exercise, immediately after cessation of exercise, and at 20 min post exercise. The prothrombotic state was quantified by fibrinogen (an index of hemorheology and a coagulation factor), soluble P‐selectin (sP‐sel, marking platelet activation), von Willebrand factor (vWF, an index of endothelial dysfunction), and plasminogen activator inhibitor‐1 (PAI‐1, a regulator of fibrinolytic activity) levels. There were two groups of age‐ and gender‐matched controls in sinus rhythm: (1) healthy controls, and (2) “hospital controls” who were patients with vascular disease.Results: Baseline levels of vWf (p = 0.034) and fibrinogen (p < 0.0001), but not sP‐sel (p = 0.075) were significantly elevated in patients with AF compared with both control groups in sinus rhythm. The PAI‐1 levels were highest in the hospital control patients, but not in chronic AF (p = 0.041). Following treadmill exercise, achieving a mean metabolic equivalent of 4.9 METS (± 1.75 SD) and total exercise duration of 4.9 min (± 2 SD), there was a significant rise in plasma fibrinogen (repeated measures analysis of variance [ANOVA] p = 0.047) and a reduction in PAI‐1 levels (p = 0.025) in patients with AF. There were no significant changes seen in vWf (p = 0.308) or sP‐sel (p = 0.071) levels. No significant changes in these indices were seen in hospital controls (all p = not significant), despite a much longer duration of exercise with greater workload.Conclusion: Patients with chronic AF have increased vWf and fibrinogen levels compared with sinus rhythm. Exercise to exhaustion influences the hypercoagulable state in chronic AF, with a rise in plasma fibrinogen and possible increase in fibrinolytic activity. Nevertheless, acute exercise does not appear to have a significant influence on endothelial dysfunction or platelet activation in patients with AF.
Clinical benefit of noninvasive viability studies of patients with severe ischemic left ventricular dysfunction
Authors: Soto Juan R. , Beller George A. 
Published: February 2009

AbstractThe population of patients who have congestive heart failure of ischemic origin is large and growing. It imposes a heavy burden on human suffering and economic costs such as the chronic use of costly medications, recurrent hospital admissions, and, eventually, death or the necessity of heart transplantation. Therefore, the development of methods for detecting viable myocardium may allow the accurate selection of those patients with coronary artery disease with severe left ventricular dysfunction who are most likely to benefit from revascularization, but also excludes patients who are unlikely to obtain any improvement with revascularization techniques. The presence of reversible dysfunctional myocardium that may improve after revascularization implies the concepts of stunned and hibernating myocardium. Recent evidence suggests that hibernation may not be a stable condition since it might evolve toward an irreversible dysfunction if it is not revascularized at the right moment. The techniques available for viability studies are single‐photon emission computed tomography using thallium‐201 or compounds labeled with technetium‐99m, positron emission tomography, and dobutamine stress echocardiography. Newer and promising techniques are magnetic resonance imaging and contrast echocardiography, whose definitive roles are not clear yet. There is abundant evidence from several important studies showing that patients with a significant amount of viable myocardium have a poor outcome if they are treated medically. Conversely, if these patients are revascularized, their outcomes improve and their symptoms significantly decrease, with less necessity of medication, fewer admissions to the hospital, and even in some cases avoiding heart transplantation. On the other hand, patients with poor or no viability who are revascularized do not obtain significant benefit.
The international EECP patient registry (IEPR): Design, methods, baseline characteristics, and acute results
Authors: Barsness Gregory , Holmes David R. , Feldman Arthur M. , Holubkov Richard , Kelsey Sheryl F. , Kennard Elizabeth D. 
Published: February 2009

AbstractBackground: In 1998, the International EECP Patient Registry (IEPR) was organized to document patient characteristics, safety, and efficacy during the treatment period, and long‐term outcomes. All centers with EECP facilities were invited to join the voluntary Registry. The Registry population comprises all patients starting EECP therapy for treatment of angina pectoris in participating centers.Hypothesis: The study was undertaken to determine whether EECP is a safe and effective treatment for patients with angina pectoris regardless of their suitability for revascularization by more conventional techniques.Methods: After 18 months of operation, 43 clinical centers representing over half of clinical sites using the EECP system contributed cases. The data reported here were collected before the first EECP treatment and upon completion of final treatment. EECP can be used for patients ineligible for either coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI), as well as for those who prefer noninvasive treatment to avoid or delay revascularization. in this report, patients considered to be candidates for revascularization are compared with those not considered suitable.Results: Of the 978 patients analyzed, 70% had Canadian Cardiovascular Society Classification class III or IV angina before starting treatment, and 62% used nitroglycerin. Most (81%) had been previously revascularized, and 69% were considered unsuited for either PCI or CABG at the time of starting EECP. A full treatment course (usually 35 h) was completed in 86%, of whom 81% reported improvement of at least one angina class immediately after the last treatment.Conclusion: In a broad patient population, EECP has been shown to be a safe and effective treatment.
Effect of coronary risk factors on arterial compensatory enlargement in japanese middle‐aged patients with de novo single‐vessel disease—An intravascular ultrasound study
Authors: Isoda Kikuo , Arakawa Koh , Kamezawa Yashuhiro , Nishizawa Ken‐Ya , Nishikawa Ken‐Ichirou , Shibuya Toshio , Ohsuzu Fumitaka , Nakamura Haruo 
Published: February 2009

AbstractBackground: Compensatory enlargement (CE) of atherosclerotic human arteries has been reported; however, the pattern of arterial remodeling in response to plaque formation is not unique.Hypothesis: The study was undertaken to determine the extent of coronary artery compensatory enlargement at stenotic lesions and to correlate the arterial compensatory enlargement with risk factors.Methods: We studied 62 patients with stable angina and de novo single‐vessel disease using intravascular ultrasound and obtained good images in 42 patients (68%). The vessel cross‐sectional area (VA), lumen cross‐sectional area (LA), and plaque cross‐sectional area (PA) were measured at the lesion site and at proximal and distal reference sites. Positive CE was defined as increase in VA of lesion site > 10% compared with that of proximal reference site (CE group, n = 15); shrinkage was defined as reduction in VA of lesion site > 10% compared with that of proximal reference site (S group, n = 14); inadequate CE was defined as intermediate between CE and S (IE group, n = 13). All subjects had coronary risk factors measured before this study.Results: There was no difference in VA, LA, or PA among the three groups at the proximal and distal reference sites, nor in LA at the lesion site; however, VA and PA were significantly smaller in the S group than in the other groups (p < 0.01). Of coronary risk factors, increased systolic blood pressure (SBP), increased diastolic blood pressure (DBP), and decreased high‐density lipoprotein cholesterol (HDL‐c) levels had the strongest association with shrinkage (p < 0.05).Conclusion: Hypertension and decreased HDL level may contribute to the shrinkage response in middle‐aged patients with stable angina.
Homocysteine levels in patients with risk factors for atherosclerosis
Authors: Blum Arnon , Khazim Khaled , Gumanovsky Marina , Yeganeh Shay , Jawabreh Subchi , Lupovitch Sacha , Peleg Aviva 
Published: February 2009

AbstractBackground: Abundant epidemiological evidence has demonstrated that the presence of mild to moderate hyperhomocysteinemia is an independent risk factor for atherosclerosis in the coronary, cerebral, and peripheral vasculature, and for vascular disease, including coronary disease. It has been demonstrated that plasma total homocysteine level is a strong predictor of mortality in patients with angiographically confirmed coronary artery disease.Hypothesis: The study was undertaken to determine the extent of homocysteine levels in patients without documented coronary artery disease, but with at least one risk factor for atherosclerosis.Methods: Fasting blood samples were collected prospectively from 160 consecutive patients (50 women and 110 men, mean age 65 ± 7 years) who had at least one risk factor for atherosclerosis, but had no documented coronary artery disease. Homocysteine levels were measured by an immunoassay method.Results: Of the patients studied, 78 (48.75%) with at least one risk factor for atherosclerosis had high homocysteine levels; 62 patients had mild hyperhomocysteinemia (15–30 μmol/l); and 16 patients had moderate hyperhomocysteinemia (30–100 μmol/l).Conclusions: Our data suggest that hyperhomocysteinemia is highly prevalent in patients with risk factors for atherosclerosis. Homocysteine level (an independent convertible risk factor to atherosclerosis) should be measured routinely in patients with risk factors for atherosclerosis and treated appropriately.
Low‐dose combination therapy with colesevelam hydrochloride and lovastatin effectively decreases low‐density lipoprotein cholesterol in patients with primary hypercholesterolemia
Authors: Davidson Michael H. , Toth Phillip , Weiss Stuart , Mckenney James , Hunninghake Donald , Isaacsohn Jonathan , Donovan Joanne M. , Burke Steven K. 
Published: February 2009

AbstractBackground: Colesevelam hydrochloride is a novel, lipid‐lowering agent that binds bile acids with high affinity. A multicenter, randomized, double‐blind, placebo‐controlled, parallel‐design study was conducted to assess the efficacy and tolerability of combination low‐dose colesevelam and lovastatin treatment in patients with primary hypercholesterolemia.Hypothesis: Combination therapy with low doses of colesevelam and lovastatin decreases low density (LDL) cholesterol with minimal adverse events.Methods: Following a 4‐ to 6‐week dietary lead in, 135 patients were randomized into five groups for a 4‐week treatment period: placebo, colesevelam 2.3 g at dinner, lovastatin 10 mg at dinner, the combination of colesevelam and lovastatin given at dinner (dosed together), and combination treatment with colesevelam given at dinner and lovastatin administered at bedtime (dosed apart).Results: Combination colesevelam and lovastatin treatment decreased LDL cholesterol by 34% (60 mg/dl, p < 0.0001) and 32% (53 mg/dl, p < 0.0001) when colesevelam and lovastatin were dosed together or dosed apart, respectively. Both combination therapies were superior to either agent alone (p < 0.05). Decreases in LDL cholesterol exceeded the combined decreases observed for colesevelam alone (13 mg/dl, 7%) and lovastatin alone (39 mg/dl, 22%). Both combination treatments reduced total cholesterol by 21% (p < 0.0001) and apolipoprotein B by 24% (p < 0.0001). Neither combination treatment significantly altered high‐density lipoprotein cholesterol or triglycerides. Adverse side effects were not significantly different among randomized groups.Conclusions: Combination colesevelam and lovastatin was efficacious and well tolerated, resulting in additive decreases in LDL cholesterol levels whether or not both agents were administered simultaneously.