bluuebunny/crossref_metadata_2025_split huggingface dataset:
Aspirin and dipyridamole and their limitations in the therapy of coronary artery disease
Authors: Rowe G. G. , Folts J. D. 
Published: February 2009

AbstractWe have reviewed some of the voluminous literature on the effects of aspirin combined with dipyridamole on coronary thrombosis. There is clear evidence that aspirin is partially effective in preventing platelet aggregation and subsequent thrombosis in experimental constricted and damaged coronary arteries of dogs. Clinical studies show a clear reduction in myocardial infarction in male human subjects who are given aspirin as therapy for unstable angina, or as prophylaxis in asymptomatic individuals. In many studies aspirin and dipyridamole have been combined and are effective. We have not found dipyridamole to be effective in the dog with coronary artery constriction and find no substantial evidence that it is effective in preventing myocardial infarction in man. Until definitive studies show that combining dipyridamole with aspirin is more effective than aspirin alone, we do not recommend its use for prevention of coronary thrombosis.
Reperfusion injury
Authors: Fishbein M. C. 
Published: February 2009

AbstractThis article reviews the early and late morphologic changes associated with reperfusion of ischemic myocardium. If instituted within minutes of coronary artery occlusion, all reversibly injured myocardium is salvaged. Once some irreversibly injured myocardium is present, the usually bland region of coagulation necrosis is transformed into an edematous, hemorrhagic zone with “contraction‐band” necrosis and vascular obstruction (no‐reflow phenomenon). Whether or not these changes occur in otherwise salvageable myocardium is controversial. Data from studies with conflicting results are presented. Popular proposed mechanisms of reperfusion injury include the no‐reflow phenomenon and free radical‐mediated injury. No reflow has been related to direct vascular injury, compression of capillaries by edema fluid, and obstruction of vascular channels by leukocytes. Free radicals, which inactivate enzymes and destroy membranes, are primarily oxygen derived, and produced by neutrophils, endothelial cells, and myocardial cells. Whether or not reperfusion injury exists is still debated; if it does, the mechanism of injury remains to be proven. Ongoing research in this field will augment our knowledge of cell death and interventions to delay or prevent it.
Mexiletine: Pharmacology and therapeutic use
Authors: Manolis A. S. , Deering T. F. , Cameron J. , Markestes N. A. 
Published: February 2009

AbstractMexiletine is a Class IB antiarrhythmic which has basic and clinical electrophysiologic properties similar to lidocaine. Like other Class I antiarrhythmic agents, mexiletine blocks the rapid inward sodium current responsible for phase 0 of the action potential. It has been noted in the clinical electrophysiology laboratory to have minimal effect on sinus node function and AV nodal and His‐Purkinje system conduction. Pharmacokinetic studies have shown that oral absorption is rapid with bioavailability of 80‐90%. Mexiletine is predominantly metabolized by the liver with elimination half‐life of 9 to 12 hours. The antiarrhythmic effects of the primary drug's metabolites remain to be defined. Hemodynamic studies have shown mexiletine to have a lesser negative inotropic effect than procainamide or disopyramide. Although mexiletine as a single agent successfully suppresses 60 to 80% of spontaneous ventricular arrhythmias, it has lower efficacy in suppression of induced ventricular arrhythmias. Multiple studies have shown that as monotherapy mexiletine is effective in preventing the induction of ventricular tachycardia in approximately 20% of patients. When used in combination with a Class IA antiarrhythmic drug for suppression of induced ventricular arrhythmias, multiple investigators have reported greater efficacy. Neurological side effects (tremor, dizziness, memory loss) occur in approximately 10% of patients while gastrointestinal side effects (nausea, anorexia, gastric irritation) occur in up to 40% of patients. Proarrhythmia or other serious toxicity from the drug is uncommon.
An update to silent myocardial ischemia: Pathophysiological, diagnostic, and therapeutic approaches
Authors: Fu L. X. , Hjalmarson Å. 
Published: February 2009

AbstractSilent myocardial ischemia (SMI) is a common ischemic process which can be defined as objective evidence of myocardial ischemia without chest pain or other equivalent indications. SMI can occur in totally asymptomatic patients, as well as in patients who have documented coronary artery disease (CAD) and who, on exercise and/or during Holter monitoring, may show ischemic changes. The precise mechanism for pathogenesis and pathophysiology of SMI remains to be clarified. A great deal has been learned about the role of beta‐adrenergic receptors, adenylyl cyclase, and guanine nucleotide binding proteins (G proteins) in the myocardial ischemic process of SMI. Moreover, standard exercise test and long‐term ECG recordings have proved to be of great value, especially when performed jointly, however, in this field there is still room for expanded knowledge. Pharmacological interventions to date have demonstrated the beneficial effects of beta‐adrenergic receptor antagonists and/or calcium antagonists as contributing substantially to reducing both frequency and duration of SMI episodes. However, therapeutic options to improve the prognosis of SMI appear to be limited.
Metabolic equivalents (METS) in exercise testing, exercise prescription, and evaluation of functional capacity
Authors: Jetté M. , Sidney K. , Blümchen G. 
Published: February 2009

AbstractOne metabolic equivalent (MET) is defined as the amount of oxygen consumed while sitting at rest and is equal to 3.5 ml O2 per kg body weight x min. The MET concept represents a simple, practical, and easily understood procedure for expressing the energy cost of physical activities as a multiple of the resting metabolic rate. The energy cost of an activity can be determined by dividing the relative oxygen cost of the activity (ml O2/kg/min)x by 3.5. This article summarizes and presents energy expenditure values for numerous household and recreational activities in both METS and watts units. Also, the intensity levels (in METS) for selected exercise protocols are compared stage by stage. In spite of its limitations, the MET concept provides a convenient method to describe the functional capacity or exercise tolerance of an individual as determined from progressive exercise testing and to define a repertoire of physical activities in which a person may participate safely, without exceeding a prescribed intensity level.
Heart rate variability
Authors: Malik M. , Camm A. J. 
Published: February 2009

AbstractReduced heart rate variability carries an adverse prognosis in patients who have survived an acute myocardial infarction. This article reviews the physiology, technical problems of assessment, and clinical relevance of heart rate variability. The sympathovagal influence and the clinical assessment of heart rate variability are discussed. Methods measuring heart rate variability are classified into four groups, and the advantages and disadvantages of each group are described. Concentration is on risk stratification of postmyocardial infarction patients. The evidence suggests that heart rate variability is the single most important predictor of those patients who are at high risk of sudden death or serious ventricular arrhythmias.
Aneurysmal coronary sinus associated with severe valvular heart disease
Authors: Wong C. ‐K. , Lau C. ‐P. , Cheng C. ‐H. , Leung W. ‐H. 
Published: February 2009

AbstractWe report a case of aneurysmal coronary sinus complicating severe valvular disease with severe tricuspid regurgitation. Injection in the left superior vena cava outlines the aneurysmal coronary sinus with stasis of the contrast. As this anomaly carries special surgical implication in patients requiring open heart surgery, a correct preoperative diagnosis is mandatory.
Management of the patient following coronary thrombolysis
Authors: Massel D. , Gill J. B. , Cairns J. A. 
Published: February 2009

AbstractMyocardial salvage can be maximized by the early institution of thrombolytic therapy and aspirin. Certain patients may benefit from the administration of intravenous heparin, beta blockers, or nitroglycerin. The routine use of percutaneous transluminal coronary angioplasty (PTCA) or calcium‐channel blockers does not appear to be warranted. Recurrent myocardial ischemia should be vigorously treated with medical therapy and there may be value in cardiac catheterization, followed by PTCA or bypass surgery, depending upon the extent of myocardium at risk and the underlying coronary anatomy. Long‐term morbidity and mortality may be reduced by instituting aspirin and beta blockers as well as by modifying risk factors. There is no evidence for the long‐term benefit from any calcium‐channel blocker. Oral anticoagulation may be warranted in those patients with a mural thrombus, congestive heart failure, or atrial fibrillation. ACE inhibitors may be of value in the presence of left ventricular dysfunction and certainly in the presence of symptomatic congestive heart failure. Antiarrhythmic therapy is generally indicated only for symptomatic or life‐threatening arrhythmias. Residual myocardial ischemia should be sought by exercise testing, and those patients with poor exercise tolerance generally warrant cardiac catheterization in consideration for revascularization.
Infective endocarditis in the 1980s: Experience at a heart hospital
Authors: Mansur A. J. , Grinberg M. , Bellotti G. , Jatene A. , Pileggi F. 
Published: February 2009

AbstractThree hundred episodes of infective endocarditis (IE) in 287 patients were studied from October 1978 to August 1986. The patients were in the age range of 0.2–78 (mean 30.76±16.06) years; 185 (68%) occurred in male patients. The etiologic agents were: Streptococci viridans group (93), enterococci (21), streptococci D group, nonenterococci (19), other streptococci (14), Staphylococcus aureus (59), Staphylococcus epidermidis (14), gram‐negative bacteria (16), other gram‐positive bacteria (16), fungi (4). Etiologic agents were not isolated in 52 (negative cultures). Valvular heart diseases occurred in 231 episodes, congenital heart diseases in 37, other heart diseases in 6. Sixty‐nine occurred in patients with prosthetic heart valves. In 69 there was no previous heart disease. Surgical treatment was performed in 102 episodes (37 with prosthetic valve IE and 65 with native valve IE); 22 patients (21%) died, 12 with prosthetic valve and 10 with native valve IE. The in‐hospital mortality (medical and surgical patients) was 26% (78 patients). Long‐term follow‐up of 206 patients up to 7.1 (mean 2.13±1.68) years revealed that 26 patients died. Thus, IE remains a disease with high mortality and is fatal to a third of the patients, in spite of the progress in therapeutic methods. Its morbidity and mortality continues beyond the microbiological cure.
Atrial natriuretic peptide response to ionic and nonionic contrast left ventriculography
Authors: Salvucci T. J. , Roman C. , Cha S. D. , Maranhao V. 
Published: February 2009

AbstractAtrial natriuretic peptide (ANP) levels were measured prior to and at 1 and 5 minutes postcontrast left ventriculography with an ionic contrast agent (diatrizoate), and a nonionic agent (iopamidol) and the results were compared. Since ionic contrast agents have been found to cause an increase in left ventricular end‐diastolic pressure (LVEDP) and nonionic agents have been found to have less of an effect on LVEDP, we investigated the response of ANP levels, which have been found to increase secondary to increased LVEDP (atrial pressure), with both agents. A group of 38 patients who were scheduled for left heart catheterization for suspected coronary artery disease was included (19 in each group) and blood samples for ANP levels were drawn from the left ventricle. At the same time, heart rate, LVEDP, and left ventricular systolic pressure (LVSP) were also measured. It was found that the LVEDP increased significantly for both agents at 1 minute postventriculography, but no further change occurred at 5 min. Heart rate increased significantly in the diatrizoate group at 1 minute with a return of heart rate to preventriculography levels at 5 min, while the ANP level and LVSP remained unchanged at 1 minute postventriculography with both agents but increased significantly at 5 min in the diatrizoate group only. This difference in ANP response is not correlated with the LVEDP. The response of ANP may be related to heart rate and/or LVSP.
Alpha‐adrenergic blockers: Mechanism of action, blood pressure control, and effects on lipoprotein metabolism
Authors: Nash D. T. 
Published: February 2009

AbstractThe sympathetic nervous system plays a major role in the pathogenesis of essential hypertension and is mediated by the α and β receptors. The α receptor is divided into two types, α1 and α2 based on response to epinephrine and norepinephrine. α1‐Adrenergic receptors have a high affinity for drugs such as prazosin, doxazosin, and terazosin, which act to reduce blood pressure by selective blockade of the receptor. These agents provide a rational approach to the treatment of hypertension by correcting elevated total peripheral resistance, the fundamental hemodynamic abnormality in essential hypertension. In contrast, early α‐adrenergic receptor blockers nonselectively blocked both α1 and α2 receptors and were unsuitable as antihypertensive agents because they induced tachycardia and patients developed a tolerance to them rapidly. α1‐Adrenergic blockers also have beneficial effects on plasma lipoproteins, tending to decrease levels of triglycerides and cholesterol and increase levels of high‐density lipoprotein (HDL) cholesterol and the HDL cholesterol/total cholesterol ratio. β‐Adrenergic blockers, such as propranolol and atenolol, have been shown to have an adverse effect on the lipid profile by tending to increase levels of triglycerides and decrease HDL cholesterol. A number of mechanisms contribute to these effects, in particular, adrenergic modulation of lipoprotein lipase and the triglyceride secretion rate. Doxazosin has been shown to increase the activity of LDL receptors, which may be partly responsible for its beneficial effect on plasma lipids and lipoproteins. Doxazosin is different from other α1 adrenergic inhibitors in that its maximal hypotensive effect occurs within 5 or 6 hours after administration in acute dosing studies, making first‐dose postural hypotension unlikely, and its long half‐life provides 24‐h blood pressure control with once‐daily dosing.
Automatic junctional tachycardia in an adult
Authors: Kumagai K. , Yamato H. , Yamanouchi Y. , Matsuo K. , Tashiro N. , Hiroki T. , Arakawa K. 
Published: February 2009

AbstractWe report an adult patient with junctional ectopic tachycardia, a condition which was initially described in infants, frequently in association with congenital defects. The patient had a rapid, irregular paroxysmal junctional tachycardia with a rate ranging from 160 to 220 beats/min, distinguishing it from the more common nonparoxysmal junctional tachycardia in which a slower heart rate is seen. The electrophysiological study performed during an episode of tachycardia demonstrated periods of atrioventricular dissociation and narrow QRS complexes as well as a junctional ectopic rhythm, which was suggested by a His deflection preceding each ventricular depolarization with a normal HV interval. Both the response to exercise and the results of atrial and ventricular stimulation suggested enhanced automaticity of a high junctional focus. Therapy combining procainamide, verapamil, and digitalis proved to be effective. Thus, junctional ectopic tachycardia can also occur in adults, probably due to enhancement of automaticity.
Limitations of coronary angiography: An underestimated problem?
Authors: Katritsis D. , Webb‐Peploe M. 
Published: February 2009

AbstractAngiographic imaging suffers from many limitations which may distort the diagnostic information obtained from coronary arteriograms. Radiographic features limiting precise coronary stenosis measurement are caused by the x‐ray source, the image intensifier, and the chemical properties of the cinefilm. Biologic variations are introduced by fluctuations in angiographic contrast concentration and flow‐ or contrast‐dependent coronary dilation. Random errors are also introduced by the selection of the radiographic projection and frame to be analyzed and the digitization of cineangiograms. These limitations and their significance in distorting quantitative information obtained from coronary angiograms are discussed in this review.
Pirmenol: An antiarrhythmic drug with unique electrocardiographic features—a double‐blind placebo‐controlled comparison with quinidine
Authors: Salerno D. M. , Fifield J. , Farmer C. , Hodges M. 
Published: February 2009

AbstractPrevious reports have stated that pirmenol is a Class IA antiarrhythmic drug that prolongs the QT interval, but did not use computerized electrocardiography. We randomized 18 patients with frequent ventricular ectopic depolarizations to pirmenol (8 patients) or quinidine (10 patients). Pirmenol was effective and tolerated for suppression of arrhythmia in all 7 patients treated (1 patient withdrew for personal reasons) but quinidine was effective and tolerated for 4 weeks in only 5 of 10 patients (p<0.05). Using computerized 12‐lead electrocardiography, the mean change in PR interval from placebo to treatment was 5 ± 18 ms for quinidine and 5 ± 11 ms for pirmenol (p = NS). The mean change in QRS interval was 5 ± 14 ms for quinidine and 10 ± 5 ms for pirmenol (p = NS). The mean change in QT interval was 46 ± 30 ms for quinidine and 8 ± 9 ms for pirmenol (p<0.01) and the mean change in JT interval was 41 ± 36 ms for quinidine and –2 ± 10 ms for pirmenol (p<0.01). After the double‐blind phase, 4 quinidine patients had computerized electrocardiographic intervals measured on pirmenol; the above findings were confirmed. These electrocardiographic features of pirmenol clearly distinguish it from quinidine, the prototype Class IA drug. However, pirmenol has minimal effect on the PR and QRS intervals, and thus does not appear to be a Class IC drug either. Although its electrocardiographic features are closest to Class IB, its electrophysiology in isolated cells and its antiarrhythmic and side effect profile are atypical for a IB agent. Pirmenol is a unique antiarrhythmic drug that merits further study. Results of this study suggest that the IA‐IB‐IC antiarrhythmic drug classification may be an over‐simplification.
Once‐daily pravastatin in patients with primary hypercholesterolemia: A dose‐response study
Authors: Jones P. H. , Farmer J. A. , Cressman M. D. , Mckenney J. M. , Wright J. T. , Proctor J. D. , Berkson D. M. , Farnham D. J. , Wolfson P. M. , Colfer H. T. , Rackley C. E. , Sigmund W. R. , Schlant R. C. , Arensberg D. , Mcgovern M. E. 
Published: February 2009

AbstractThis multicenter, double‐blind, placebo‐controlled study was conducted to evaluate dose‐response effects and safety of once‐daily administration of pravastatin, a new inhibitor of 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase. Pravastatin 5, 10, 20, 40 mg or placebo was administered at bedtime to 150 patients with primary hypercholesterolemia inadequately controlled on a low‐fat, low‐cholesterol (AHA Phase I) diet. After 8 weeks of treatment, pravastatin produced dose‐dependent reductions in low‐density lipoprotein (LDL) cholesterol of 19.2 to 34.1% (p⩽.001 vs. baseline and placebo) and reductions in total cholesterol of 14.3 to 25.1% (p⩽.01 to p⩽.001 vs. placebo and p⩽.001 vs. baseline). The relationship between the loge dose of pravastatin and decrease in LDL cholesterol was linear (p<0.002). High‐density‐lipoprotein cholesterol increased up to 11.7% and triglycerides decreased by as much as 23.9%. Pravastatin was well tolerated; no patient withdrew from the study as a consequence of treatment‐related adverse events. Despite its relatively short serum half‐life of approximately 2 h, once‐daily administration of pravastatin provides a safe and effective means of reducing elevated LDL and total cholesterol.
Cardiac conduction defects associated with hyponatremia
Authors: Mouallem M. , Friedman E. , Shemesh Y. , Mayan H. , Pauzner R. , Farfel Z. 
Published: February 2009

AbstractCardiac conduction defects have not been previously described in association with hyponatremia, although in patients with congestive heart failure the frequency of ventricular premature beats was found to correlate to the severity of hyponatremia. We describe three patients with second‐degree or complete atrioventricular (AV) block which occurred during or shortly after an episode of severe hyponatremia. The first had thiazide‐induced hyponatremia while on amiodarone. In the second, definite etiology for hyponatremia which was associated with longstanding polydipsia could not be established. The third had ischemic heart disease and intermittent conversion of his first‐degree to second‐degree AV block while hyponatremic after diuretics use. Although it is usually difficult to single out hyponatremia as the cause of conduction defects which usually occur in the presence of cardiac disease, potent medications or other electrolyte abnormalities, we suggest that hyponatremia may play a role in the pathogenesis of conduction defects in the diseased heart.
Metastatic cardiac malignant fibrous histiocytoma presenting as right ventricular outflow tract obstruction
Authors: Kamlow F. J. , Padaria S. F. , Wainwright R. J. 
Published: February 2009

AbstractAn unusual case of metastatic disease of the right ventricle is described in a 74‐year‐old woman who had presented with a malignant fibrous histiocytoma of the right thigh previously treated with surgery and radiotherapy. Two years later she presented with signs and symptoms of tricuspid regurgitation and right ventricular outflow tract obstruction. The diagnosis of right ventricular tumor was made by echocardiographic and angiographic studies and confirmed on postmortem examination.
The relationship between exercise tolerance and quality of life in angina pectoris
Authors: Wiklund I. , Comerford M. B. , Dimenäs E. 
Published: February 2009

AbstractThe relationship between exercise tolerance assessed by a conventional exercise stress test using a standard Bruce protocol and quality of life (QoL) was studied in 50 patients with stable angina pectoris (AP). Before the exercise test, patients completed three self‐administered QoL questionnaires, the Psychological General Well‐Being Index, an Angina‐Specific QoL Questionnaire, and Jenkins' Sleep Dysfunction Scale. Total exercise time (r= ‐0.40) and time until onset of pain (r= ‐0.44) were significantly correlated with perceived physical limitations. Somatic symptoms were related to total time (r= ‐0.38). Apart from a significant correlation between depressed mood and total exercise time (r= 0.36), there was no corresponding correlation with well‐being and sleep disturbance. These results suggest that exercise stress tests do not reflect quality of life in patients with AP.