Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ventricular preexcitation, as seen in Wolff-Parkinson-White syndrome, results in a high frequency of positive exercise electrocardiographic responses. Why this occurs is unknown but is not believed to reflect myocardial ischemia. Exercise thallium testing is often used for noninvasive assessment of coronary artery disease in patients with conditions known to result in false-positive electrocardiographic responses. To assess the effects of ventricular preexcitation on exercise thallium testing, 8 men (aged 42 +/- 4 years) with this finding were studied. No subject had signs or symptoms of coronary artery disease. Subjects exercised on a bicycle ergometer to a double product of 26,000 +/- 2,000 (+/- standard error of mean). All but one of the subjects had at least 1 mm of ST-segment depression. Tests were terminated because of fatigue or dyspnea and no patient had chest pain. Thallium test results were abnormal in 5 patients, 2 of whom had stress defects as well as abnormally delayed thallium washout. One of these subjects had normal coronary arteries on angiography with a negative ergonovine challenge, and both had normal exercise radionuclide ventriculographic studies. Delayed thallium washout was noted in 3 of the subjects with ventricular preexcitation and normal stress images. This study suggests that exercise thallium testing is frequently abnormal in subjects with ventricular preexcitation. Ventricular preexcitation may cause dyssynergy of ventricular activation, which could alter myocardial thallium handling, much as occurs with left bundle branch block. Exercise radionuclide ventriculography may be a better test for noninvasive assessment of coronary artery disease in patients with ventricular preexcitation.
 ...
PMID:Exercise thallium testing in ventricular preexcitation. 357 50

The case reported herein illustrates an unusual form of nonobstructive hypertrophic cardiomyopathy which was associated with Wolff-Parkinson-White syndrome, myocardial ischemia and necrosis despite normal coronary arteries. The patient is unique since the hypertrophied myocardial segment was localized exclusively to the posterolateral free wall. Quantitative thallium-201 scintigraphy demonstrated reversible ischemia that corresponded precisely with this region of posterolateral hypertrophy. While the exact mechanism for ischemia in patients with hypertrophic cardiomyopathy and normal coronary arteries remains controversial, a functional rather than anatomic disturbance of blood flow seems likely.
 ...
PMID:Hypertrophic cardiomyopathy and myocardial ischemia with normal coronary arteries. 360 9

We compared the parameters describing the defibrillation threshold in patients with normal hearts and in patients with ischemic heart disease, using a special electrode system and sequential pulses of current. Twenty-eight patients consented to the study (mean age: 36.6 +/- 10.1 years; mean mass: 80.7 +/- 13.8 kg). Twenty-one patients underwent surgery for Wolff-Parkinson-White syndrome (relatively normal hearts). Six patients had a history of previous myocardial infarction and aneurysm or coronary artery disease; and one patient had been resuscitated from an episode of sudden death, without evidence of consequent myocardial damage. For 26 patients, defibrillation thresholds were determined intraoperatively by passing sequential pulses through a catheter electrode and epicardial mesh electrode. For 2 patients defibrillation thresholds were determined during electrophysiologic study, after ventricular fibrillation was induced by programmed stimulation, by passing sequential pulses through a catheter and skin-patch electrode. Parameters for sequential pulse defibrillation thresholds between the two groups did not differ appreciably. Total energy for patients with normal hearts averaged 9.9 +/- 6.3 J compared to 8.9 +/- 4.6 J for patients with cardiac disease. No patient with cardiac disease had defibrillation parameters that exceeded the range of the normal patients. These results suggest that the presence of cardiac disease may not significantly alter the parameters necessary for successful defibrillation when using sequential pulses for delivery of energy.
 ...
PMID:Sequential pulse defibrillation in man: comparison of thresholds in normal subjects and those with cardiac disease. 361 39

Eleven critically ill patients with life-threatening cardiac arrhythmias refractory to currently approved antiarrhythmic drugs were treated with intravenous amiodarone. Two patients had acute myocarditis, five had acute myocardial infarction, two had left ventricular failure secondary to ischemic heart disease, one had Wolff-Parkinson-White syndrome, and one manifested postoperative atrial fibrillation. Eight of the patients had severe cardiac failure and five had hypotension requiring intravenous dopamine. Five patients were treated for recurrent ventricular fibrillation, two for recurrent ventricular tachycardia, and four for recurrent atrial arrhythmias. Six patients had repeated cardioversions. The arrhythmias had lasted a mean of 88.3 hours resistant to a mean of 2.7 different intravenous antiarrhythmic drugs. The ventricular arrhythmias did not recur after commencing intravenous amiodarone, but some minor atrial arrhythmias occurred for 24 hours. One patient died of intractable left ventricular failure, chronic obstructive lung disease, and respiratory arrest during treatment. The dose of amiodarone was 150 mg over 5 minutes, followed by 600 mg/24 hr for 3 to 4 days; one patient on total parenteral nutrition required intravenous amiodarone for 20 days. Hypotension, cardiac failure, and bradyarrhythmias were not induced by this treatment. Intravenous amiodarone can be used safely in critically ill patients with impaired left ventricular function to control life-threatening refractory cardiac arrhythmias.
 ...
PMID:Intravenous amiodarone in the treatment of refractory life-threatening cardiac arrhythmias in the critically ill patient. 395 53

A case with transient WPW syndrome during silent acute myocardial infarction is presented. Although the clinical picture and laboratory data were non contributory and the surface electrocardiogram showed delta and not Q waves, myocardial perfusion scintigraphy showed typical area of acute necrosis. Abnormal accessory connections probably occur or latent such pathways become functional during acute myocardial ischemia.
 ...
PMID:Silent acute myocardial infarction masked by transient WPW syndrome. 651 92

The aim of this third part is to discuss the nature and origin of the destructive lesion of the conduction system. A total of 53 hearts of patients dying from av-block was available for this study, and in morbid anatomy the commonest pattern of lesions responsible for av-block is destruction of the branching bundle and the origin of both bundle branches. The pathological processes found in the heart and conduction system are as follows: ischemic heart disease (49%), surgical lesions (15%), calcificatory destruction (6%), inflammatory destruction (6%), various distinct causes (11%), and primary av-block (13%). Main interest is focused on the group with primary heart block. Morphologically our series shows little fibrosis but an unexplained loss of conduction fibers and strikingly atrophic elements (filiform fibers). At attempt is made to explain the loss of conduction fibers as a consequence of the natural developing process which separates the atria from the ventricles, a separation essential for electrical stability of the heart. It is accepted that the accessory muscle bundles which characterize the Wolff-Parkinson-White syndrome are a failure in reduction of the muscle fibers running from the atria to the ventricles at an early embryological stage. If this same process runs to excess, the result must be an av-block. We consider a part of the so-called primary av-block to be a consequence of this process.
 ...
PMID:[Sudden cardiac death due to conduction disorder. III. Is the so-called idiopathic AV block caused by a congenital abnormality?]. 728 Jun 20

The Wolff-Parkinson-White syndrome has been studied in a group of healthy aviation personnel over the past 15 years. The incidence of this electrocardiographic pattern has been determined in 22,500 healthy individuals and found to be 0.25%. The prevalence of documented tachyarrhythmias in this group of individuals was found to be only 1.8% while in a group of referred patients the prevalence was 20%. The limitations of the widely accepted classification into Type A and Type B patterns was borne out by our inability to categorize 45% of subjects with the WPW pattern. Q waves as QS or QR complexes in the inferior limb leads were found in 16.7% of subjects, but in all there was Q wave-T wave vector discordance. The limited value of stress testing in these individuals was reflected by 30% of our patients who demonstrated false positive signs of ischaemic heart disease. A discussion of the incidence, classification, differential diagnosis, mechanism of tachyarrhythmias, associated cardiovascular anomalies, and treatment follows.
 ...
PMID:The Wolff-Parkinson-White pattern in health aircrew. 728 6

Sotalol is a nonselective beta-adrenoceptor antagonist which prolongs cardiac repolarisation independently of its antiadrenergic action (class III antiarrhythmic properties). The antiarrhythmic action of sotalol appears to arise predominantly from its class III properties, and the drug exhibits a broader antiarrhythmic profile than the conventional beta-blockers. Sotalol is effective in controlling paroxysmal supraventricular tachycardias and the ventricular response to atrial fibrillation/flutter in Wolff-Parkinson-White syndrome, in maintaining sinus rhythm after cardioversion of atrial fibrillation/flutter, and in preventing initiation of supraventricular tachyarrhythmias following coronary artery bypass surgery. Sotalol shows promise in the control of nonmalignant and life-threatening ventricular arrhythmias, particularly those associated with ischaemic heart disease. It is effective in suppressing complex forms of ventricular ectopy, displaying superior antiectopic activity to propranolol and metoprolol. The acute efficacy of sotalol in preventing reinduction of sustained ventricular tachyarrhythmias and suppressing spontaneous episodes of these arrhythmias on Holter monitoring is translated into long term prophylactic efficacy against arrhythmia recurrence in approximately 55 to 85% of patients with refractory life-threatening ventricular arrhythmias. In addition, sotalol offers the advantage over the class I agents of reducing cardiac and all-cause mortality in the high risk population with life-threatening ventricular arrhythmias. The adverse effects of sotalol are primarily related to its beta-blocking activity and its class III property of prolonging cardiac repolarisation. Sotalol is devoid of overt cardiodepressant activity in patients with mild or moderate left ventricular dysfunction. The overall arrhythmogenic potential is moderately low, but torsade de pointes may develop in conjunction with excessive prolongation of the QT interval due to bradycardia, hypokalaemia or high plasma concentrations of the drug. In summary, sotalol displays a broad spectrum of antiarrhythmic activity, is haemodynamically well tolerated, and confers a relatively low proarrhythmic risk. It is likely to prove particularly appropriate in the treatment and prophylaxis of life-threatening ventricular tachyarrhythmias.
 ...
PMID:Sotalol. An updated review of its pharmacological properties and therapeutic use in cardiac arrhythmias. 750 52

We treated 10 cases of thoracic malignancy accompanied with cardiovascular disease. Among thoracic malignancy, 7 cases were lung cancer and 3 were esophageal cancer. Accompanied cardiovascular diseases were ischemic heart disease (2 cases), valvular disease (3 cases), WPW syndrome (1 case), aortic aneurysm (4 cases). The mean age was 66, ranged from 51 to 79. The simultaneous occurrence of the two lesions were observed in 6 cases and thoracic malignancy was diagnosed after a varying interval of time following surgery of cardiovascular disease in 4 cases. In cases of thoracic malignancy accompanied with heart disease, the treatment of heart disease should precede the operation of malignant disease to reduce the risk of surgery. For the patient with esophageal cancer, posterior mediastinal esophagostomy should be applied who may have heart surgery in future. In cases of coexisting malignancy and aortic aneurysm, the priority of treatment should be determined considering the size of aneurysm. If the transverse diameter of aneurysm is larger than 7 cm, there is a high risk of rupture, so surgery for the aneurysm precedes operation of malignant diseases. It is desirable to avoid concomitant operation of malignancy and cardiovascular disease.
 ...
PMID:[Treatment of thoracic malignancy accompanied with cardiovascular disease]. 823 Sep 1

The utility of body surface potential mapping to improve interpretation of electrocardiographic information lies in the presentation of thoracic surface distributions to characterize underlying electrophysiology less ambiguously than that afforded by conventional electrocardiography. Localized cardiac disease or abnormal electrophysiology presents itself electrocardiographically on the body surface in a manner in which pattern plays an important role for identifying or characterizing these abnormalities. Thus, in myocardial infarction, transient myocardial ischemia, Wolff-Parkinson-White syndrome, or ventricular ectopy, observation of electrocardiographic potential patterns, their extrema, and their magnitudes permits localization and quantization of the abnormal activity. Conventional electrocardiography assesses pattern information incompletely and does not use information of distribution extrema locations or magnitudes. Thus, increases or decreases in the magnitudes of electrocardiographic features (ST-segment potential displacement, amplitude, or morphology of Q, R, S, or T waves) associated with changes in cardiac sources (ischemia, infarction, conduction abnormalities, etc.) as measured from fixed leads have a high likelihood of being misinterpreted if the distribution itself is changing. In this study, the authors demonstrate the utility of estimating distributions from small numbers of optimally selected leads, including conventional leads, to reduce uncertainty in the interpretation of electrocardiographic information. This issue is highly relevant when thresholds are used to detect significance of potential levels (exercise testing, detection of myocardial infarction, and continuous monitoring to assess ST-segment changes). Significance of this work lies in improved detection and characterization of abnormal electrophysiology using conventional or enhanced leadsets and methods to estimate thoracic potential distributions.
 ...
PMID:Estimating ECG distributions from small numbers of leads. 865 36


<< Previous 1 2 3 Next >>