bluuebunny/crossref_metadata_2025_split huggingface dataset:
Refining the treatment of women with unstable angina—A randomized, double‐blind, comparative safety and efficacy evaluation of integrelin™ versus aspirin in the management of unstable angina
Authors: Goldschmidt‐Clermont Pascal J. , Schulman Steven P. , Chandra Nisha C. , Grigoryev Dmitriy , Dise Kirk R. , Sagar Manish , Fox Robert J. , Coleman Lindsay D. , Ouyang Pamela , Baughman Kenneth L. , Gerstenblith Gary , Bray Paul F. , Richardson Christine , Dorsey Frank C. , Du Mee Charles , Kitt Michael M. ,   on behalf of the Investigators of the Study
Published: February 2009

AbstractBackground: Although women typically develop coronary artery disease several years after men, once they have symptomatic disease their thromboembolic complications are worse than in men. The mechanism mediating this gender difference in outcome after thromboembolic events is unknown. We previously studied platelet functions in siblings from patients with premature coronary artery disease. We observed that platelets from women are more responsive than their male counterparts. In particular, platelets from women stimulated ex vivo with various agonists bind more fibrinogen molecules than platelets from men.Hypothesis: We hypothesized that in patients with acute coronary events, the control of platelet activity might require stronger antagonists in women than in men.Methods: To test this hypothesis, we investigated retrospectively the results of a trial on Integrelin™ in unstable angina.Results: We report that platelet aggregation and Holter‐de‐tected ischemic episodes are significantly reduced in women with unstable angina treated with the specific GPIIb‐IIIa inhibitor, Integrelin, compared with the standard platelet inhibitor aspirin. In contrast, both platelet aggregation and Holter‐detected ischemic events are well controlled in men with unstable angina treated with standard therapy including aspirin. Conclusion: Integrelin does provide protection in men, but, in contrast with women, not beyond what can be achieved with aspirin. Our data are consistent with the concept that the platelets from women require stronger and more specific inhibitors to limit their activity, and that platelets may play a more important role in women with acute coronary syndromes than in men. Most important, specific GPIIb‐IIIa inhibitors may represent a therapeutic option which provides as much suppression of ischemic events in women as they do in men with coronary artery disease.
Interference of cellular phones with implanted permanent pacemakers
Authors: Chen Wai‐Hong , Lau Chu‐Pak , Ho David Sai‐Wah , Lee Iris Siu‐Fong , Leung Sum‐Kin 
Published: February 2009

AbstractBackground and hypothesis: Occasional reports have suggested that cellular phones may interfere with permanent pacemakers. Our investigation sought to determine systematically the effects of commercially available cellular phones on the performances of different pacing modes and sensing lead configurations of permanent implanted pacemakers.Methods: We conducted the study in 29 patients implanted with single‐ or dual‐chamber bipolar rate‐adaptive permanent pacemakers (a total of nine different models and six different sensors: minute ventilation, activity sensing using either accelerometer or piezoelectric crystal, QT and oxygen saturation sensing) from four different manufacturers. Three different cellular phones with analog or digital coding with maximum power from 0.6 to 2 W were used to assess the effect of pacemaker interference. Each cellular phone was positioned at (1) above the pacemaker pocket, (2) the ear level ipsilateral to the pacemaker pocket, and (3) the contralateral ear level. Surface electrocardiograms, intracardiac electrograms, and marker channels were recorded where possible during the following maneuvers at each position: (1) calls made by a stationary phone to a cellular phone, and (2) calls made from the cellular phone to a stationary phone. A total of eight different pacing modes [DDD(R), VDD(R), AAI(R) and VVI(R)] in both unipolar and bipolar sensing configurations was tested.Results: Interference was demonstrated during cellular phone operation in 74 of 2,418 (3.1%) episodes in eight patients. Three types of interference were observed: inhibition of pacing output, rapid ventricular tracking in DDD(R) or VDD(R) mode, and asynchronous pacing. All were observed only with the cellular phone positioned above the pacemaker pocket. Interference occurred prior to and after the termination of the ringing tone of the cellular phone in 57% of cases. Cellular phones with either digital or analog technology could cause interference. Unipolar atrial lead was most susceptible to interference (relative frequency of interference: unipolar 1.8%, bipolar 0.4%, p<0.05;atrial 2.9%, ventricular 1 %, p <0.05). There was no sensor‐driven rate acceleration during all tests. In all patients, reprogramming of the sensitivity level successfully prevented cellular phone interference.Conclusions: Commercially available cellular phones can cause reversible interference to implanted single‐ or dual‐chamber permanent pacemakers. The effect is maximal with high atrial unipolar sensitivity, especially in single pass VDD(R) systems. Both digital and analog cellular phones can lead to interference. Pacemaker interference can occur prior to a warning sign (ringing tone) of the phone and may have significant implications in patient safety.
Severe right heart failure in a patient with grave's disease
Authors: Xenopoulos Nicholaos P. , Braden Gregory A. , Applegate Robert J. 
Published: February 2009

AbstractThis brief report presents a patient with isolated right heart failure and two rare underlying causes, hyperthy‐roidism and dysplastic tricuspid valve. Repair of the tricuspid valve and treatment of the hyperthyroidism were both essential for successful treatment of the right heart failure. Most important, recrudescence of hyperthyroidism in this patient was associated with reappearance of florid right heart failure. This report provides further information about a potential linkage of hyperthyroidism and severe right heart failure.
The iron hypothesis—Does iron cause atherosclerosis?
Authors: Meyers David G. 
Published: February 2009

AbstractWomen experience only 30–50% of the coronary heart disease (CHD) incidence and mortality of age‐matched men. Since oxidation of low‐density lipoprotein (LDL) cholesterol is important in atherosclerosis, and oxidation is catalyzed by iron, it has been hypothesized that the lower iron stores of women reduce their risk of CHD through lessened lipid peroxide. The biochemistry of oxidation is well described in the literature and involves iron as a catalyst in the formation of powerful free radicals which subsequently modify LDL cholesterol. Chelating iron with desferrioxamine stops oxidation. Iron is present in atherosclerotic gruel and this gruel stimulates lipid peroxidation. Serum deficient in iron has minimal oxidative capacity which increases with iron repletion. At least seven epidemiologic studies have found a positive association between CHD and various indicators of body iron. Conversely, 18 epidemiologic studies have found a negative or no association. While biochemically appealing, the iron hypothesis remains unproven.
QT interval change with age in an overtly healthy older population
Authors: Reardon Michael , Malik Marek 
Published: February 2009

AbstractBackground: Prolonged QT interval on the surface electrocardiogram (ECG) is known to be associated with arrhythmias, coronary heart disease, and sudden cardiac death. Increased QT dispersion has also been related to arrhythymias which are more frequent in the elderly.Hypothesis: This study investigated the relationship between aging, QT interval, and QT dispersion.Methods: Normal resting ECGs were recorded from 96 healthy subjects (73 women, age range 40‐102 years). No subject had symptoms or signs of heart disease and none was on medication affecting cardiac function. All had normal heart size on chest x‐ray and normal electrolytes. Using a digitizing board, the RR and QT intervals were measured on each lead of each ECG, excluding only the leads in which the T wave was not visible. Mean RR, mean QT interval, and heart rate‐adjusted QTc interval (standard Bazet's formula) were obtained from these measurements. Further, QT dispersion was calculated for each ECG as (1) the difference between the maximum and minimium QT interval, and (2) as the coefficient of variance of QT interval of all measurable leads.Results: A significant correlation between aging and prolonged QTc was noted in the total population (r = 0.43, p <0.05), as well as in men (r = 0.4, p <0.05) and women (r = 0.23, p<0.05) separately. There was no association between QT dispersion and increasing age regardless of the method of calculation (r= ‐0.04, r= ‐0.08 respectively, both NS).Conclusion: The rate‐adjusted QT interval is prolonged with increasing age and may contribute to the increased risk of ventricular arrhythmias and cardiac mortality in elderly patients.
Mechanism of left a trial enlargement related to ventricular diastolic impairment in hypertension
Authors: Matsuda Masako , Matsuda Yasuo 
Published: February 2009

AbstractBackground and hypothesis: Systemic hypertension is the leading cause of left ventricular (LV) hypertrophy. The present study aimed to investigate the mechanism of left atrial (LA) enlargement in patients with hypertensive heart disease during cardiac catheterization.Methods: Data were obtained from eight control subjects and seven patients with hypertensive heart disease. Left atrial and LV pressures from catheter‐tip micromanometer, and LA and LV volumes from biplane cineangiograms were analyzed during the same cardiac cycle.Results: Left atrial maximal volume were 93 ± 26 ml in patients with hypertensive heart disease and 63 ± 12 ml in control subjects (p<0.05). In patients with hypertensive heart disease, time constant of LV relaxation was significantly greater than that in controls (54 ± 18 vs. 31 ± 16 ms, respectively p<0.01). Left atrial maximal volume correlated with time constant of LV relaxation (r = 0.86, p<0.01). The ratio of LV filling volume before LA contraction to LV stroke volume in patients with hypertensive heart disease was significantly lower than that in control subjects (65 ± 13 vs. 76 ± 7%, respectively p<0.05). On the other hand, the ratio of LV filling volume during LA contraction to stroke volume in patients with hypertensive heart disease was significantly higher than that in controls (35 ± 13 vs. 24± 7%, respectively p<0.05). Left atrial volume before LA contraction in patients with hypertensive heart disease was significantly larger than that in controls (74 ± 22 vs. 47 ± 10 ml, respectively, p<0.01). During LA contraction, LA work was significantly increased in patients with hypertensive heart disease compared with that in controls (274 ± 101 vs. 94 ± 42 mmHg. ml, respectively p<0.001). Left atrial work showed significant correlation with LA volume before LA contraction (r = 0.75, p <0.01).Conclusion: Left ventricular diastolic filling was impaired in patients with hypertensive heart disease. Enlargement of left atrium might be attributed to the impairment of blood flow from left atrium to left ventricle due to the increased LV stiffness.
Biochemical markers of coagulation activation in mitral stenosis, atrial fibrillation, and cardiomyopathy
Authors: Ikeda Uichi , Yamamoto Keiji , Shimada Kazuyuki 
Published: February 2009

AbstractAdvances in the understanding of the biochemistry of the mechanism of hemostasis have led to the development of sensitive methods for determining levels of markers which reflect thrombin activity (thrombin‐antithrombin III complex, fibrinopeptide A, F1+2 fragment), active fibrinolysis (D‐dimer, plasmin‐α2‐plasmin inhibitor complex), and platelet activity (platelet factor 4, ß‐thromboglobulin) in vivo. Measurement of these markers may be useful in identifying patients with various cardiovascular disorders at high risk of thromboembolism.
Transesophageal pulsed doppler echocardiographic evaluation of left atrial systolic performance in hypertrophic cardiomyopathy: combinEd analysis of transmitral and pulmonary venous flow velocities
Authors: Oki Takashi , Íuchi Arata , Tabata Tomotsugu , Yamada Hirotsugu , Manabe Kazuyo , Kageji Yoshimi , Abe Miho , Ito Susumu , Fukuda Nobuo 
Published: February 2009

AbstractBackground: Hypertrophic cardiomyopathy (HC) is characterized by impaired left ventricular (LV) diastolic function due to an increase in LV wall thickness. The severity of this disease varies depending on the localization and extent of the hypertrophied myocardium and the presence and extent of myocardial disarray or fibrosis.Hypothesis: The purpose of this study was to examine the background of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole in patients with HC using pulsed Doppler echocardiography.Methods: Hemodynamic abnormalities between the left atrium and left ventricle during atrial systole were evaluated in patients with HC using transmitral flow (TMF) and pulmonary venous flow (PVF) velocities obtained by transesophageal pulsed Doppler echocardiography. The study population included 50 patients with HC, including 39 with asymmetric septal hypertrophy and 11 with apical hypertrophy, and showing fractional shortening of the left ventricle ≥ 30%. They were classified into three groups: (1) Group A (n = 11): the ratio of the late to early TMF velocity < 1, and peak atrial systolic PVF velocity (PVA) < 25 mm/s;(2) Group B (n = 13): their ratio < 1, and PVA ≥ 25 mm/s;and (3) Group C (n = 26): their ratio ≥ 1. The mean age of patients in Group A was lower than that in Groups B and C.Results: Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Furthermore, left atrial volume changes during atrial systole in Group B were significantly smaller than those in the other HC groups and the control group. Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C. The duration of the atrial systolic waves of the TMF and PVF in Group B was significantly shorter and longer, respectively, than that in Group A. Left ventricular end‐diastolic pressure (LVEDP) decreased in descending order with Group B > Group C > Group A. In all patients there was a significant positive correlation between the LVEDP and peak atrial systolic PVF velocity or the difference in duration between the atrial systolic waves of PVF and TMF. Plots of these values shifted toward the left and inferiorly in Group A, and toward the right and superiorly in Group B.Conclusion: Peak velocity and duration of TMF and PVF during atrial systole by transesophageal pulsed Doppler echocardiography are useful indices of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole, particularly a forceful atrial contraction mismatched to the left atrial afterload and severity of LV diastolic dysfunction, in HC.
Creatine kinase isoforms as circulating markers of deterioration in idiopathic dilated cardiomyopathy
Authors: Hossein‐Nia Mojgan , Holt David W. , Mckenna William J. , Baig Kamran , Goldman Jonathan H , Keeling Philip J , Caforio Alida L.P. 
Published: February 2009

AbstractBackground: A proportion of patients with dilated cardiomyopathy (DCM) may have ongoing myocardial damage secondary to viral or immune mediated myocardial inflammation.Hypothesis: The prognostic determinants identify patients with decreased survival but do not provide a measure of myocardial damage. To obtain an objective assessment of myocardial damage in DCM, we measured plasma levels of creatine kinase (CK), its isoenzymes (CK‐MM and CK‐MB), and separated the isoforms of CK‐MM and CK‐MB.Methods: The cohort consisted of 77 consecutive patients (61 men, 16 women) with DCM (World Health Organization criteria), aged 49 ± 14 years (range 19–60). Patients had been symptomatic for 29 ± 38 months (range 0.5–200 months) with 48 in New York Heart Association class I/II and 29 in class III/IV at the time of diagnosis. During median follow‐up of 27 months from diagnosis (range 0.6–165), 50 patients remained clinically stable and 27 had deteriorated.Results: A significantly higher proportion of patients with DCM had abnormal MB2/MB1 ratio compared with normal volunteers (11,14% vs. 1, 1%, p = 0.003). Patients who deteriorated had higher MB2/MB1 ratio, (1.22 ± 0.62 vs. 0.85 ± 0.56;p = 0.01), and more frequently had abnormal MB2/ MB1 ratio (8,30% vs. 3,6%;p=0.004) and CK and CK‐MM activities (5, 19% vs. 2, 4%;p = 0.03) than those who remained stable. Patients with DCM with high CK‐MB activity had 3.13‐fold increased odds of sudden death or need for cardiac transplantation (95% confidence interval 1.53–6.40, p = 0.008). Thus, CK measurements, in particular CK‐MB isoforms, are markers of myocardial damage in a subset of patients with DCM and could be useful in investigating the possibility of persistent myocardial damage in these patients.
Relation of iodine‐123 metaiodobenzylguanidine myocardial scintigraphy to endomyocardial biopsy findings in patients with dilated cardiomyopathy
Authors: Murata Katsutoshi , Kusachi Shozo , Murakami Takashi , Nogami Kunio , Murakami Masahiro , Hirohata Satoshi , Tominaga Youkou , Komatsubara Issei , Tsuji Takao 
Published: February 2009

AbstractBackground:Iodine‐123 metaiodobenzylguanidine (123I‐MIBG) concentrates in adrenergic neurons and has been developed for evaluation of the sympathetic nervous system. Recent studies have demonstrated that the normal heart is clearly visualized by123I‐MIBG cardiac scintigraphy, whereas abnormal123I‐MIBG myocardial uptake and washout have been demonstrated in patients after myocardial infarction and in patients with congestive cardiomyopathy, long QT syndrome, and ventricular tachycardia.Hypothesis:Based on evidence from recent studies, it can be hypothesized that123I‐MIBG uptake is related to histopathologic changes in the myocardium.Methods:The relation of123I‐MIBG uptake to the histologic findings for the heart was studied in 24 patients with dilated cardiomyopathy (DCM). The study group did not include patients with complicating disorders that primarily affect the adrenergic nervous system. The123I‐MIBG uptake was visually assigned one of four grades using the two criteria of the mean score for six regional uptake grades (mean score) and the global score obtained by visual evaluation of the entire image (global score). The123I‐MIBG uptake score was also determined for the region at which the biopsy specimen was obtained (biopsy region score). The histologic findings were evaluated by assigning one of four grades for each of the following five factors: myocyte hypertrophy, myocardial fibrotic change, myocyte degeneration and necrosis, mononuclear cell infiltration, and myocyte disarray. The sum for all grades was defined as the total score, and the global score was also assigned to the overall histologic findings.Results:All of the global, mean, and biopsy region scores for123I‐MIBG uptake correlated significantly with the global and total scores for the histologic findings. Among the histologic factors, myocyte degeneration showed score correlated with all global, mean, and biopsy region scores for the uptake. Myocyte hypertrophy was associated weakly with the123I‐MIBG uptake scores.Conclusion:These results indicate that123I‐MIBG uptake imaging is associated with histopathologic abnormalities in patients with DCM.
Dynamic three‐dimensional echocardiography in the assessment of cor triatriatum
Authors: Melzer Christoph , Bartel Thomas , Müller Silvana , Kleber Franz Xaver , Baumann Gert 
Published: February 2009

AbstractClassic cor triatriatum sinistrum is a rare cardiac malformation to be found in the adult. One year after surgical correction of an atrial septal defect in a 55‐year‐old man, cor triatriatum sinistrum was diagnosed by transesophageal echocardiography. We compared transthoracic echocardiography, transesophageal echocardiography, and cardiac catheterization to dynamic three‐dimensional echocardiography (3‐D echo) which offers a new, noninvasive approach to determine the opening size between the accessory and the true left atrium. The findings by 3‐D echo, confirmed by left heart catheterization, showed that the accessory membrane was not stenosing. Surgical correction was therefore not indicated in this patient.
The vital role of papillary muscles in mitral and ventricular function: echocardiographic insights
Authors: Madu Ernest C. , D'Cruz Ivan A. 
Published: February 2009

AbstractThe two left ventricular (LV) papillary muscles are small structures but are vital to mitral valve competence. Partial or complete rupture, complicating acute myocardial infarction, causes severe or even catastrophic mitral regurgitation, potentially correctable by surgery. Papillary muscle dysfunction is a controversial topic in that the role of the papillary muscle itself, in causing mitral regurgitation post infarction, has been seriously questioned; it is less confusing if this syndrome is attributed not only to papillary muscle but also to adjacent LV wall ischemia or infarction. Papillary muscle calcification is easily and frequently detected on echocardiography, but its clinical significance remains uncertain. Papillary muscle hypertrophy accompanies LV hypertrophy of varied etiology and may have a significant role in producing dynamic late‐systolic intra‐LV obstruction in hypertrophic cardiomyopathy and other hyperdynamic hypertrophied LV chambers. All the above abnormalities can be adequately assessed by 2‐D echocardiography and the Doppler modalities. In selected cases, transesophageal echocardiography can provide additional valuable data by improving visualization of papillary muscles and mitral apparatus.
Depression and coronary heart disease: A review for cardiologists
Authors: Carney Robert M. , Freedland Kenneth E. , Sheline Yvette I. , Weiss Edward S. 
Published: February 2009

AbstractMajor depression is a common comorbid condition in patients with coronary heart disease (CHD). Although mild emotional distress may be a normal reaction to myocardial infarction or other manifestations of CHD, major depression should not be considered a normal reaction, nor should it be ignored. Major depression is a debilitating comorbid disorder that can seriously complicate recovery and increase the risks of further cardiac morbidity and mortality. Fortunately, it is one that can be successfully treated in the majority of cases. The purpose of this review is to present the evidence for the negative prognostic effects of depression in cardiac patients and to discuss methods for assessing and treating depression in these patients.