Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 10-20% of patients dying suddenly and unexpectedly do not have structural heart disease. The major causes of sudden death in this population are acute ischemia, the syndrome of right bundle branch block, and ST-elevation from V1 to V3, the long QT-syndrome, and the Wolff-Parkinson-While syndrome. In some patients, none of these syndromes can be recognized and ventricular fibrillation is classified as idiopathic. There are good preventive and therapeutic methods against acute ischemia and there are also curative treatments for the Wolff-Parkinson-White syndrome. Patients with idiopathic ventricular fibrillation cannot be recognized beforehand. However, there are electrocardiographic and genetic markers for the Brugada syndrome and the long QT syndrome. It is, therefore, justified to discuss the possible role of the prophylactic defibrillator to prevent sudden death in these 2 syndromes for which no effective treatment exists. Patients with Brugada syndrome have a high incidence of sudden death, and prophylactic defibrillators are indicated in patients with inducible arrhythmias at electrophysiologic study, irrespective of symptoms. On the contrary, the incidence of sudden death in the long QT syndrome is very low, making prophylactic defibrillator implantation not cost-effective.
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PMID:Use of the prophylactic implantable cardioverter defibrillator for patients with normal hearts. 1008 49

Brugada syndrome is characterized by ST segment elevation in the right precordial leads, V1-V3 (unrelated to ischemia or structural disease), normal QT intervals, apparent right bundle branch block, and sudden cardiac death, particularly in men of Asian origin. An autosomal dominant mode of inheritance with variable expression has been described. The only gene thus far linked to the Brugada syndrome is the cardiac sodium channel gene, SCN5A. The possible cellular and ionic basis for these features of the Brugada syndrome are discussed. Strong sodium channel block, among other modalities, has been shown to be capable of inducing epicardial and transmural dispersion of repolarization, thus providing the substrate for the development of phase 2 and circus movement reentry, which underlies ventricular tachycardia/ventricular fibrillation.
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PMID:Ion channels and ventricular arrhythmias: cellular and ionic mechanisms underlying the Brugada syndrome. 1035

We report on the case of a 33-year-old man with recurrent syncopes appearing suddenly due to sustained monomorphic ventricular tachycardias. The electrocardiogram (ECG) showed a right bundle branch block pattern and ST segment elevation in the precordial leads V1 to V2, not explained by ischemia, electrolyte disturbances, toxic ingestion, or structural heart disease (coronary and right ventricle angiograms as well as biopsies of the right ventricle were normal). ECG image was compatible with the so-called Brugada syndrome, first described in 1992. This entity is very rare. Missed diagnosis can be disastrous because life-threatening ventricular arrhythmias often develop in patients.
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PMID:A young man with recurrent syncopes, right bundle branch block and ST segment elevation. 1053 May 45

The Brugada syndrome is characterized by ST-segment elevation in the right precordial leads, V1-V3 (unrelated to ischemia or structural disease), normal QT intervals, RBBB pattern, and sudden cardiac death, particularly in men of Asian origin. An autosomal dominant mode of inheritance with variable penetrance is generally observed. The only gene mutations thus far linked to the Brugada Syndrome appear in the alpha subunit of the gene that encodes for the cardiac sodium channel, SCN5A. An outward shift in the balance of currents contributing to phase 1 of the right ventricular action potential is thought to underline to electrocardiographic manifestation of the syndrome. Strong sodium channel block, among other modalities, can accentuate the action potential notch in right ventricular epicardial cells, eventually leading to loss of the action potential dome. This results in the development of a large dispersion of repolarization within epicardium as well as between epicardium and endocardium, providing the substrate for the development of phase 2 and cirus movement reentry, which underline VT/VF. Therapy is directed at restoring the balance of current via inhibition of the transient outward current, Ito, and/or stimulation of inward calcium using beta adrenergic agonists, among several strategies.
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PMID:Cellular and ionic mechanisms responsible for the Brugada syndrome. 1126 34

We describe the case of a patient with coronary artery disease who developed transient ST-segment depression, right bundle branch block (RBBB), left anterior hemiblock, ST-segment elevation +ST), and "giant" T-waves in her electrocardiogram (ECG), an assortment of ECG patterns heretofore unreported in conjunction with exercise stress testing (EST). The amplitude of the +ST was modulated by the superimposed RBBB, as was shown by its augmentation after the abrupt disappearance of RBBB. Following recession of the latter "giant" T-waves, which usually are encountered in the hyperacute phase of myocardial infarction, developed and persisted late in the recovery period. Cardiac enzymes after EST were negative, and arteriography revealed a stenotic left anterior descending coronary artery. The present case indicates that a variety of ECG expressions of severe transmural ischemia or myocardial infarction can also be manifest in the course of EST; this also suggests a common pathophysiological mechanism in severe EST-triggered ischemia and the early phase of myocardial infarction.
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PMID:Unusual ECG responses to exercise stress testing. 1145 18

Right bundle branch block (RBBB) is independently associated with all-cause mortality in patients referred for noninvasive evaluation of coronary artery disease. However, further stratification of risk in these patients has not been specifically addressed. The aim of this study was to risk stratify patients with RBBB who were referred for stress echocardiography. The study population was comprised of 343 patients (267 men; age 66 +/- 9 years) with RBBB who underwent pharmacologic stress echocardiography (231 dipyridamole, 112 dobutamine) for evaluation of suspected or known coronary artery disease. Overall mortality was the only end point. Stress echocardiography was positive for ischemia in 109 patients (32%). During follow-up (38 +/- 32 months), 36 deaths occurred. Seventy-three patients underwent revascularization and were censored. Ischemia at stress echocardiography (hazard ratio [HR] 2.9, 95% confidence interval [CI] 1.5 to 5.5, p=0.002), left anterior fascicular block (LAFB) (HR 2.8, 95% CI 1.4 to 5.6, p = 0.002), age >65 years (HR 2.1, 95% CI 1.0 to 4.3, p=0.047), and wall motion score index at rest (HR 2.5, 95% CI 1.0 to 6.5, p=0.057) were multivariate predictors of mortality. On the basis of stress echocardiographic result and presence and/or absence of LAFB, 3 levels of risk were identified: (1) low-risk, in cases of no ischemia and no LAFB (49% of the entire study population); (2) intermediate-risk, in cases of ischemia or LAFB only; and (3) high-risk, in cases of ischemia and LAFB. Clinical data, electrocardiography at rest, and stress echocardiographic results can provide effective stratification of risk in patients with RBBB.
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PMID:Prediction of mortality in patients with right bundle branch block referred for pharmacologic stress echocardiography. 1467 79

Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow-up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction. One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first-degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.
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PMID:Electrocardiographic follow-up of biventricular pacemakers. 1584 37

The T-wave of the electrocardiogram (ECG) is generated both from the left and the right ventricles of the heart. Each ventricle may produce a normal, an "ischemic", or a "secondary" T-wave, depending on segmental perfusion, intraventricular pressure, or QRS complex duration. The direction of the T-wave is determined by the particular inward rectifier potassium channels recruited by various layers and segments in the two ventricles. The observed T-wave in the clinical ECG is the summation of the left and right ventricular T waves, and is thus biventricular. Clinical observations in right bundle branch block (RBBB) and in right ventricular hypertensive states such as pulmonary embolism suggest that many ECG's interpreted as inferior or anterior left ventricular ischemia are in fact examples of abnormal potassium channel recruitment in the right ventricle. Consideration of the right ventricular component of the T-wave in every electrocardiographic interpretation improves diagnostic understanding and accuracy, as the possible right ventricular origin of observed anterior or superior T waves will not be overlooked.
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PMID:T waves are independently generated in both right and left ventricles: the clinically recorded T is a summation of two separate repolarizations, and is thus always biventricular. 1608 69

A 75-year-old man with a past history of bilateral thalamic hemorrhage was scheduled for cholecystectomy and cholelithotomy under general anesthesia. Although the preoperative ECG showed a complete right bundle branch block, the echocardiogram revealed no abnormality. Anesthesia was induced with thiopental and vecuronium, and maintained with sevoflurane in oxygen. Soon after changing to the left decubitus position for the insertion of an epidural catheter, ECG showed complete atrioventricular block, which did not respond to atropine. Adrenalin was transiently effective, but arrhythmia continued. After administration of dopamine, norepinephrine and isoproterenol, we inserted a temporary transvenous pacemaker catheter, and the hemodynamics became stable by ventricular pacing. The operation was postponed. Subsequent cardiologic examination showed no ischemia. The atrioventricular block disappeared 7 hours after the induction of general anesthesia. We should be very careful with the anesthetic management of a patient with a complete right bundle branch block.
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PMID:[A case of complete atrioventricular block after induction of general anesthesia]. 1629 74

Uncommon association of left anterior fascicular ventricular tachycardia (VT) with a healed myocardial infarction (MI) is described. A 55-year-old man with a history of anteroseptal MI had verapamil-sensitive VT. The VT exhibited a right bundle branch block configuration and right-axis deviation. The VT exit was located at the left ventricular anterolateral wall. At the mid-anterior left ventricular septum, delayed Purkinje potentials were seen during sinus rhythm, and the optimal pace map was obtained with pace delay. During the VT, diastolic and systolic Purkinje potentials were simultaneously recorded at the same site. Ablation targeting the delayed potentials during sinus rhythm prolonged the time between QRS onset and the delayed potentials, and the VT no longer became inducible when the delayed potentials were completely eliminated. Left anterior fascicular VT develops in post-MI patients; ischemia-injured His-Purkinje system may be involved in the mechanism of the VT.
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PMID:Verapamil-sensitive left anterior fascicular ventricular tachycardia associated with a healed myocardial infarction: changes in the delayed Purkinje potential during sinus rhythm. 1854 67


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