bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stress‐induced arrhythmic disease of the heart‐Part I
Authors: Meerson Felix Z. 
Published: February 2009

AbstractThis review deals with the following principal concepts: (1) Heart injuries in single severe stress episodes manifested primarily in disturbances of membrane lipid bilayer, sarcolemmal Na, K‐pump, and sarcoplasmic Ca‐pump with concurrent limited disturbances of the heart energy supply, namely, of the creatine kinase and glycolysis systems. These disturbances cause small focal myocardial lesions and reduce cardiac electrical stability: the fibrillation threshold falls and ectopic activity increases. in repeated stress, this damage, localized mainly in the richly innervated conduction system, accumulates to cause even more pronounced disturbances of electrical stability and severe arrhythmias. (2) Severe stress and beta‐adrenergic effects on the heart regularly result in coronary vasodilation and increased coronary blood flow. However, the entire primary complex of stress‐induced injuries and disturbances of the heart's electrical stability occurs despite the increased coronary blood flow. Thus, beta‐adrenergic stress‐induced injuries may indeed develop as primary stress damage to cardiomyocytes without any relation to ischemia. (3) The main factor determining high vulnerability or, on the contrary, resistance of the heart to stress is the state of stress‐limiting systems, namely, the opioidergic, GABAergic, cholinergic, adenosinergic, and other systems. Activation of these systems by adaptation to repeated stress or other factors prevents serious injuries to the heart in severe stress. Conversely, genetically determined or acquired dysfunction of these systems predisposes to severe arrhythmias and sudden death. Thus, in stress‐induced arrhythmic disease as well as in ischemic heart disease, the main pathogenetic links are outside the heart, but they differ from those observed in ischemia. (4) The clinical picture of stress‐induced arrhythmic disease, that is, alterations in electrocardiogram, coronarogram, and patient responses to stress, physical loads, and tranquilizers differ, as do pathologic alterations in the heart. These differences are summarized at the end of this review.
Pathology of mitral valve stenosis and pure mitral regurgitation—Part II
Authors: Waller Bruce F. , Howard Jane , Fess Stephen 
Published: February 2009

AbstractThis two‐part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. in Part I, conditions producing mitral valve stenosis were reviewed. in over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenitally malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. in Part II, conditions producing pure mitral regurgitation are discussed. in contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendineae.
Prognosis, severity of symptoms, and aspects of well‐being among patients in whom myocardial infarction was ruled out
Authors: Karlson Bjöurn W. , Wiklund Ingela , Bengtson Ann , Herlitz Johan 
Published: February 2009

AbstractIn a high proportion of patients hospitalized due to suspected acute myocardial infarction (AMI) the diagnosis cannot be confirmed. The majority of these patients have ischemic heart disease and are at risk for subsequent cardiac events. The aim of this study was to describe the severity of symptoms and various aspects of well‐being 1 year after hospitalization due to suspected AMI in surviving patients in whom the diagnosis was not confirmed, and to relate the observations to those found among survivors of a confirmed AMI. All patients admitted to Sahlgrenska Hospital, Göteborg, due to suspected AMI and who were alive after 1 year were asked to answer a questionnaire including questions regarding cardiovascular, psychiatric, and psychological symptoms. Patients in whom AMI was not confirmed reported more cardiovascular symptoms, for example, chest pain (p <0.001), dyspnea (p <0.01), palpitations (p <0.001), and fatigue (p <0.01) when compared with patients who suffered confirmed AMI. The majority of psychosomatic and psychological parameters evaluated were also more frequently reported by these patients and their quality of life seems to be worse compared with survivors of AMI.
Congenital heart disease and pregnancy
Authors: Perloff Joseph K. 
Published: February 2009

AbstractIn Europe and North America, a dramatic fall in the incidence of rheumatic fever and rheumatic heart disease has coincided with advances in medical and surgical management of congenital heart disease and has resulted in a shift in the relative incidence of these two categories of cardiac disorders in women of child‐bearing age. This review deals with pregnancy and congenital heart disease—unoperated and operated. Central to this topic is the intricate interplay between maternal circulatory and respiratory physiology and maternal congenital heart disease, and the effects of this interplay upon the fetus which is exposed to risks that threaten its intrauterine viability and to risks that subsequently express themselves as developmental defects or transmitted congenital malformations of the heart or circulation.
Neuroendocrine activation in relation to left ventricular function in chronic severe congestive heart failure: A subgroup analysis from the cooperative north scandinavian enalapril survival study (CONSENSUS)
Authors: Eriksson S. V. , Eneroth P. , Kjekshus J. , Offstad J. , Swedberg K. 
Published: February 2009

AbstractLeft ventricular (LV) function and plasma levels of cardiovascular hormones were examined in patients with severe chronic congestive heart failure (CHF), randomized to placebo or enalapril, in addition to conventional therapy. M‐mode echocardiography and plasma hormone concentrations were available at baseline and after 6 weeks of treatment. There was a significant relationship between LV systolic function and levels of angiotensin‐II and norepinephrine. Enalapril increased LV fractional shortening (FS%) (13.3±5.6 to 15.4±5.8, p<0.05) and decreased the systolic time interval index (0.58±0.14 to 0.48 ± 0.15, p < 0.05) concurrent with a significant decrease in angiotensin‐converting enzyme activity and in aldosterone, angiotensin‐II, and norepinephrine concentrations after 6 weeks. No changes were found in the placebo group. However, there was no direct relationship between the amount of change in neurohormones and improvement in LV function after 6 weeks.These findings indicate that in patients with severe chronic CHF, severe LV systolic dysfunction is associated with high plasma levels of angiotensin‐II and norepinephrine, which can be favorably modified by enalapril. This may be of importance for prolonging life in severe heart failure. The lack of relationship between changes in individual hormones and systolic function suggests complex dynamic interaction. It is, therefore, not sufficient to predict changes in LV function by measuring changes in only one hormone.
Artificial intelligence versus logistic regression statistical modelling to predict cardiac complications after noncardiac surgery
Authors: Lette Jean , Colletti Bruce W. , Cerino Michel , Mcnamara Daniel , Eybalin Marie‐Claire , Levasseur André , Natnel Stanley 
Published: February 2009

AbstractThe traditional approach to developing models predictive of cardiac events has been to perform logistic regression (LR) analysis on a variety of potential predictors. An alternative is to use an artificial intelligence system called a neural network (NN) which simulates biological intelligence. To evaluate the potential applicability of the latter method, we compared the ability of LR and NN techniques to predict cardiac events after noncardiac surgery. A total of 200 patients (training group) underwent cardiac risk assessment before major noncardiac surgery using 17 clinical parameters and 7 quantitative indices based on dipyridamole‐thallium imaging. There were 21 postoperative myocardial infarctions and/or cardiac deaths. Data from the training group were used to develop two predictive models: one based on backward stepwise LR multivariate statistical analysis and the other one using a neural network. Both models were then validated on a second group of 160 consecutive patients also referred for preoperative risk stratification (validation group). The NN consisted of 14 input, 29 hidden, and 1 output neurons and used a back‐propagation algorithm (learning rate 0.2, training tolerance 0.5, sigmoid transfer function). The sensitivity, specificity, positive and negative predictive accuracies for the prediction of postoperative events in the validation group of 160 patients were, respectively, 67% (6/9), 82% (124/151), 18% (6/33), and 98% (124/127) for LR, and 67% (6/9), 96% (145/151), 50% (6/12), and 98% (145/148) for the NN, with a difference in specificity which attained statistical significance (p < 0.01). Artificial intelligence may provide a useful alternative to conventional LR statistical analysis for the purpose of preoperative cardiac risk assessment.
Regression of left ventricular hypertrophy with long‐term treatment of nifedipine in systemic hypertension
Authors: Yamakado Tetsu , Teramura Shinobu , Oonishi Takahiro , Maeda Mitsugu , Nakano Takeshi 
Published: February 2009

AbstractWe investigated the regression of left ventricular (LV) hypertrophy with long‐term treatment of nifedipine in patients with systemic hypertension. Echocardiograms of the LV were obtained in nine patients before and at a mean of 50 months (13‐105 months) after nifedipine monotherapy (30‐60 mg/day). Nifedipine significantly reduced both systolic and diastolic blood pressures (BP) by a mean of ‐46 mmHg and ‐21 mmHg, respectively. With systemic BP reduction, LV mass was significantly reduced by a mean of ‐ 15%, associated with a decrease in LV posterior wall thickness and end‐diastolic dimension. There was no significant change in LV fractional shortening. We conclude that nifedipine may cause regression of LV hypertrophy in systemic hypertension, and that reversal of the increase in LV mass could be maintained during long‐term nifedipine treatment.
Amyloid disease of the heart
Authors: Hackel Andrea J. , Wagner Galen S. , Reimer Keith , Hackel Donald B. 
Published: February 2009

AbstractA 70‐year‐old woman with a history of hypertension had been well until 3 years before when she developed atrial fibrillation and subsequently congestive heart failure. The heart failure became worse and she had three fainting spells. Low voltage on electrocardiogram and global hypokinesis on echocardiography were suggestive of cardiac amyloidosis. The patient died suddenly of intractable ventricular fibrillation. Autopsy confirmed heavy infiltration of the myocardium by amyloid.
Clustered lipid droplets in the endomyocardial biopsies from a patient with neuroleptic malignant syndrome
Authors: Watanabe Kenichi , Inomata Takayuki , Miyakita Yasushi , Masani Fumiaki , Shibata Akira , Izumi Tohru 
Published: February 2009

AbstractNeuroleptic malignant syndrome is caused by serious adverse effects of antipsychotic agents and occurs only rarely. Endomyocardial biopsies documented unique clustered lipid droplets in a Japanese man with this disease. After administration of haloperidol, he had symptoms of high fever, respiratory dysfunction, and cardiogenic shock, and subsequently suffered from multiple organ failure. Fortunately, he was completely cured with intensive therapy. in the convulsant stage, left ventricular endomyocardial biopsies were performed that yielded the interesting discovery of unique clustered lipid droplets among the myofibrils. It was suggested that although the pathomechanism of neuroleptic malignant syndrome is unknown, this disease may be characterized by a lipid metabolic disorder of the cardiac muscle cell.
Percutaneous transvenous mitral commissurotomy for restenosis after surgical mitral valvotomy
Authors: Bahl Vinay K. , Chandra Subhash , Talwar Kewal K. , Sharma Sanjiv , Kaul Upendra , Wasir Harbans S. 
Published: February 2009

AbstractPercutaneous transvenous mitral commissurotomy (PTMC) was performed in 350 patients. Of these patients, 51 (15%) (30 women and 21 men, aged 32 ± 11 years) had restenosis 11 ± 4 years following surgical valvotomy. Forty (79%) patients were in New York Heart Association (NYHA) class III and 11 (21 %) were in class IV. PTMC resulted in an increase in mitral valve area from 0.82 ± 0.3 to 1.9 ± 0.2 cm2 (p < 0.001), an increase in cardiac index from 1.9 ± 0.4 to 2.8 ± 0.51/min/m2 (p < 0.001), and a decrease in mean transmitral gradients from 29 ± 4 to 6 ± 4 mmHg (p < 0.001). The results did not differ from those observed in 299 patients without prior surgical valvotomy. On univariate analysis, the subvalvular fibrosis, assessed angiographically, and the duration from prior surgery were not found to influence the overall outcome. At 24 weeks, 46 of 48 (96%) patients in whom clinical follow‐up was available, were found to be in NYHA class I and 2 (4%) patients were in class II. Thus, PTMC is a safe and effective procedure for patients with mitral restenosis following surgical valvotomy.
A clinical and in vitro study on the possible interaction of intravenous nitrates with heparin anticoagulation
Authors: Pye Maurice , Oldroyd Keith G. , Hutton Ian , Cobbe Stuart M. , Conkie James A. 
Published: February 2009

AbstractIt has been reported that intravenous nitrates inhibit the anticoagulant effect of heparin. This possible interactior has potentially serious implications for the management of patients with acute coronary ischemic syndromes. This possible interaction was assessed prospectively in a clinical and in an in vitro study involving 24 patients receiving both drugs for the management of unstable angina pectoris. There was a small in hibitory effect of intravenous glyceryl trinitrate or isosorbide dinitrate on the anticoagulant effect of heparin in 3 of 24 case in vivo, as assessed by activated partial thromboplastin time measurements. Nitrates or propylene glycol had no effect or heparin activity in vitro. It was concluded that there may be an inhibitory effect of nitrates on anticoagulation in a small miority of patients, but close attention to detail in monitoring heparin anticoagulation is far more important.
High cardiac output state in patients with multiple myeloma: Case report and review of the literature
Authors: Kosinski Daniel J. , Fraker Theodore D. , Grubb Blair P. , Roush Kenneth 
Published: February 2009

AbstractA high cardiac output state, with or without congestive heart failure, has recently been recognized in patients with multiple myeloma. This case report deals with a 62‐year old man with multiple myeloma refractory to treatment, a high cardiac output state, and life‐threatening pulmonary edema In addition, a brief review of the literature is presented.
Influence of the infarct site on the identification of patients with ventricular tachycardia after myocardial infarction based on the time‐domain and spectral turbulence analysis of the signal‐averaged electrocardiogram
Authors: Kulakowski Piotr , Hnatkova Katerina , Bashir Yaver , Heald Spencer C. , Staunton Anne , Malik Marek , Camm A. John 
Published: February 2009

AbstractIn a significant proportion of patients with sustained ventricular tachycardia (VT) following anterior myocardial infarction, the areas of slow conduction are activated early during cardiac depolarization. Therefore, they may not be detected by the standard time‐domain analysis of the signal‐averaged electrocardiogram (SAECG) which is limited to the terminal part of the QRS complex. Spectral turbulence analysis of the SAECG is a new frequency domain technique which examines the whole QRS complex and may improve identification of patients with sustained VT following anterior infarction. We compared the results of time‐domain and spectral turbulence analyses of the SAECG in 53 postinfarction patients with sustained VT and in 53 age‐, gender‐ and infarct site‐matched patients without VT. The receiver operator characteristic curves have shown that the time‐domain analysis resulted in better identification of patients with VT following inferior than following anterior infarction (e.g., at the sensitivity level of 90%, the corresponding values of specificity were 96 and 90%, respectively), whereas the spectral turbulence analysis performed better in the anterior site of infarction. When both time‐domain and spectral turbulence analyses were combined, the accuracy of the SAECG for identification of patients with VT following anterior infarction improved, reaching a specificity of 97% at the sensitivity level of 90%. In conclusion (1) spectral turbulence analysis of the SAECG results in better identification of patients with VT following anterior than following inferior infarction, and (2) the combination of time‐domain and spectral turbulence analyses of the SAECG may improve identification of patients with VT following anterior infarction.
Evaluation of QRST isointegral maps in detecting posterior myocardial infarction with and without conduction disturbance
Authors: Agetsuma Hirotaka , Suzuki Akira , Hiral Makoto , Sano Hiroaki , Tomita Yasushi , Ichihara Yoshio , Adachi Masayoshi , Takatsu Fumimaro , Hayashi Hiroshi 
Published: February 2009

AbstractWe investigated the usefulness of QRST isointegral maps (I‐maps) for detecting posterior myocardial infarction (MI) with and without conduction disturbance. The I‐maps were recorded during sinus rhythm and right ventricular (RV) pacing, which simulated left bundle‐branch block (LBBB) in 19 patients with and in 20 patients without MI. Data on 608 normal subjects were used as controls. The “‐2 SD area,” where the QRST integral value was less than the lower limit of the normal range, was assessed by ΣDM (sum of QRST integral values below the normal range). Posterior MI was diagnosed with a sensitivity of 84%, a specificity of 90%, and a diagnostic accuracy of 87%, assuming that MI was present if ΣDM exceeded 50 mVms. During simulated LBBB, when the criterion ΣDM more than 250 mVms was used, the sensitivity, specificity, and diagnostic accuracy were 79, 75, and 77%, respectively. Thus, I‐maps may be useful in detecting posterior MI in patients with and without an intraventricular conduction disturbance.
Emergency intracardiac defibrillation for refractory ventricular fibrillation
Authors: Haught W. Herbert , Conti Jamie B. , Tucker Kelly J. , Curtis Anne B. 
Published: February 2009

AbstractHemodynamically unstable ventricular arrhythmias induced during electrophysiologic testing almost always respond to prompt application of direct current transthoracic shocks. In rare cases, however, ventricular fibrillation may be refractory to conventional treatment. Recently, a technique of intracardiac defibrillation has been successfully used to resuscitate patients with ventricular fibrillation refractory to transthoracic defibrillation. We describe two patients with a history of myocardial infarction and left ventricular dysfunction who were admitted with symptomatic episodes of ventricular tachycardia. Both had inducible sustained monomorphic ventricular tachycardia. During a repeat electrophysiologic study in Patient No. 1 on procainamide and at the initial study in Patient No. 2, right ventricular burst pacing to terminate ventricular tachycardia resulted in ventricular fibrillation refractory to resuscitation efforts, including transthoracic defibrillation with 360 J. Emergency intracardiac defibrillation with 200 and 360 J, respectively, successfully converted both patients to sinus rhythm. Both patients were subsequently discharged from the hospital on amiodarone. These cases illustrate the life‐saving capabilities of intracardiac defibrillation.
Prevalence, characteristics, and risk stratification of electrocardiographic and symptomatic silence of myocardial ischemia despite scintigraphically evidenced ischemia in symptomatic patients presenting with severe coronary artery stenosis
Authors: Zehender Manfred , Kasper Wolfgang , Granzow Heike , Just Hanjörg , Krause Thomas , Moser E. , Olschewski Manfred 
Published: February 2009

AbstractSymptoms of angina pectoris and transient ST‐segment depression are most commonly used to evidence acute myocardial ischemia during exercise testing. However, the diagnostic accuracy of either or both criteria in relation to clinical characteristics and the patient's exercise response has been a subject of controversy. The prevalence and severity of symptoms of angina pectoris and/or ST‐segment depression were studied prospectively in 147 consecutive patients with a history of daily angina pectoris, scintigraphic evidence of exercise‐induced myocardial ischemia, and coronary artery stenosis >75%. Logistic regression analysis was applied to determine absence of any or both criteria by the clinical characteristics or exercise response of the patient. During exercise testing, ST‐segment response failed to prove scintigraphically evidenced myocardial ischemia in 14/147 patients (10%) and 35/147 patients (24%) when ST‐segment depression ≥0.1 in either ≥1 or ≥2 ECG leads was chosen. Symptoms of angina pectoris were found to be absent in 69/147 patients (47%). Only 58 patients (40%) suffered from angina and met the ECG criterion at the time of scintigraphic myocardial ischemia. Absence of ST‐segment depression was best predicted by clinical variables such as large myocardial infarction (increase: 2.6 times, p = 0.007), number of stenoses ≥2 (2.0 times, p = 0.023), and presence of diabetes mellitus (4.3 times, p = 0.035). Painless myocardial ischemia was only determined by blood response to exercising. Thus, a double product > 23 increased the risk of painless myocardial ischemia by 1.5 times (p = 0.017). In multivariate analysis, only blood pressure response, infarction size, and the number of diseased vessels were found to be independent predictors of the absence of angina pectoris or ST‐segment depression during myocardial ischemia.