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)

Cardiac memory is an uncommonly recognized entity in which T wave inversions on electrocardiogram (EKG) appear consistent with ischemia. Persistent deep T wave inversions are seen after return of normal depolarization in leads where the T waves were normal before pacing. These changes are generally recognized to occur in association with artificial pacemakers but may occur with other entities with intrinsic ventricular ectopic focus of depolarization, such as intermittent left bundle branch block. Although consideration of ischemia should be given priority, awareness of the benign nature of cardiac memory may allow some patients to avoid unnecessary work-up and admission. Sometimes the diagnosis cannot be confirmed definitively in the Emergency Department (ED) because many patients who have pacemakers also have coronary artery disease and only after a negative work-up for ischemia can one retrospectively presume cardiac memory as the likely etiology.
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PMID:Cardiac memory-persistent T wave changes after ventricular pacing. 1235 90

Electrocardiographic (ECG) evidence of cardiac ischemia or infarction is difficult to detect in the presence of left bundle branch block (LBBB). Traditional ECG indicators of ischemia, such as ST- segment elevation, are common in LBBB and may not indicate acute ischemia. Proper evaluation of the initial ECG is crucial in selecting candidates for early thrombolysis, because the earlier reperfusion treatment is administred, the better are the results. Individuals with LBBB are particularly important stratum of patients to identify. This is true not only because they have a high baseline mortality and receive the greatest incremental improvement in survival when given thrombolytic agents but also because it is tendency to undertreat them. The criteria of Sgarbosa are too insensitive to be used as screening (roule out) test to determine which patients with an LBBB do not have an AMI. The Sgarbosa criteria are, however, highly specific and can be used reliably as confirmatory test to rule in AMI in patients with LBBB. ECG alone doesn't support the diagnosis of AMI. Elevated value of biochemical markers of myocardial necrosis in the presence of LBBB confirms the diagnosis. Despite the recently updated joint practical guidelines of American Heart Association (AHA) and American College of Cardiology (ACC) which defines that all patients having symptoms consistent with acute MI and LBBB should be treated like ST-segment elevation, only minority of them receive thrombolytic therapy, particularly the elderly (only 4%). In the absence of definitive diagnosis of AMI doctors withhold from decision to administer thrombolytic treatment because of risk of haemorrhagic complications. There are not perfect diagnostic tools allowing early diagnostic of AMI in patients having LBBB. Currently the best justified strategy is to follow AHA/ACC recommended guidelines to administer thrombolysis to all patients with LBBB presenting with chest pain, particularly if serum biomarkers are elevated.
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PMID:[The importance of left bundle branch block in the diagnosis of acute myocardial infarction]. 1257 61

A 53-year-old male patient with a previous diagnosis of situs inversus with mirror-image dextrocardia underwent thallium-201 (Tl-201) stress-redistribution myocardial perfusion single photon emission computed tomography (SPECT). Electrocardiogram (ECG) obtained on right hemithorax revealed constant complete left bundle branch block. Tl-201 stress-redistribution SPECT images revealed abnormal perfusion with reversible ischemia in the anteroseptal, septal and inferoseptal walls. Coronary angiography performed 1 month after SPECT study was normal. This case illustrates that false positive reversible perfusion defects can be seen in patients with mirror-image dextrocardia associated with constant complete left bundle branch block. To our knowledge, this is the first reported case of mirror-image dextrocardia and constant complete left bundle branch block with false positive Tl-201 SPECT findings.
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PMID:Thallium-201 myocardial SPECT in a patient with mirror-image dextrocardia and left bundle branch block. 1457 88

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

Postsystolic motion (PSM) is a delayed ejection motion of the myocardium occurring after the aortic valve closure, during a generally prolonged isovolumic relaxation time (IVRT). In this review we analyze the physiopathologic mechanisms underlying PSM and the contribution of tissue Doppler for its understanding. By using various techniques, this phenomenon has been described in experimental observations and related to myocardial ischemia produced by gradual or abrupt coronary occlusion. In clinical studies, it is associated with recovery of regional myocardial function. Tissue Doppler, providing a velocity map of myocardial motion, allows an easy, noninvasive detection of PSM in the clinical setting. PSM, as identified by tissue Doppler, appears a hallmark of myocardial ischemia and viability but it may occur also in nonischemic conditions as left ventricular (LV) hypertrophy and volume overload, left bundle branch block and even in normal individuals. Strain and strain rate (SR), obtainable by off-line color tissue Doppler, may be useful to identify the mechanisms underlying PSM since these measurements reflect, respectively, the intrinsic rate and the percentage of deformation of a given myocardial segment, and are relatively independent of both overall cardiac movement and tethering of the neighboring LV segments. By using SR imaging, the ratio of PSM to regional systolic longitudinal strain can be used to separate ischemic from nonischemic PSM and appears the best quantitative parameter to identify ischemia during dobutamine stress. A method to detect LV wall asynchrony and immediate benefit of cardiac resynchronization therapy has been developed combining the assessment of tissue-tracking (TT) derived delayed longitudinal contraction and of SR-derived PSM.
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PMID:Myocardial postsystolic motion in ischemic and not ischemic myocardium: the clinical value of tissue Doppler. 1596 39

Most patients with ST depression during adenosine infusion have reversible perfusion defects by single-photon emission computed tomographic (SPECT) perfusion images. Occasionally ST depression is observed in the setting of normal perfusion images. The outcome of such patients is controversial. We identified 65 patients who underwent gated SPECT perfusion imaging with adenosine as the stress agent. These patients were selected based on the following criteria: none had previous myocardial infarction or coronary revascularization, all were in sinus rhythm, and none had left bundle branch block. The 65 patients had normal SPECT images but ischemic ST response (>or=1 mm ST depression). There were 52 women and 13 men who were 66 +/- 13 years of age. History of diabetes mellitus was present in 16 patients (25%) and hypertension in 48 patients (74%). At a mean follow-up of 24 months, there were no cardiac deaths or myocardial infarctions, and there were 6 coronary revascularization procedures (2 coronary artery bypass graftings and 4 coronary stentings of 1-vessel coronary disease). One patient died of cancer. In conclusion, patients with no previous myocardial infarction or coronary revascularization who have normal SPECT images have a benign outcome despite the presence of ST depression (0% for death or myocardial infarction and 4.6%/year for coronary revascularization). Balanced ischemia could not be a common cause for discordant perfusion and ST response.
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PMID:Outcome of patients with adenosine-induced ST-segment depression but with normal perfusion on tomographic imaging. 1702 61

In patients with acute myocardial infarction, early reperfusion and sustained patency of the culprit artery are important determinants of survival. The 12-lead electrocardiogram (ECG) is considered the noninvasive gold standard for identification of acute ST-elevation myocardial infarction. Nurses play a critical role in the process of obtaining, interpreting, and communicating ECG findings. This study evaluates nurses' ability to differentiate ischemic from nonischemic ECG patterns, to detect affected ECG leads and location of ischemia, and assesses skill level by hospital unit type. Seventy-five nurses were given a set of 6 patient scenarios, each with a corresponding 12-lead ECG, and asked to identify the presence or absence of ischemia. Fourteen (19%) of the 75 nurses correctly identified the presence or absence of ischemia in all 6 scenarios. Of the 3 ECGs with a myocardial infarction pattern, 59 (79%) of the nurses identified all 3 as ischemic; however, no one was able to determine the correct leads, location, or amplitude of ST-segment elevation. For the 3 nonischemic ECGs, 37 (49%) of the nurses identified a normal ECG as ischemic, 47 (63%) determined that an early repolarization pattern was ischemic, and 34 (45%) indicated that a left bundle branch block pattern was ischemic. These results not only identify educational opportunities but also provide important information for researchers implementing clinical trials evaluating the use of bedside ECG monitoring systems for detection of acute myocardial ischemia.
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PMID:Interpreting 12-lead electrocardiograms for acute ST-elevation myocardial infarction: what nurses know. 1754 21

Pharmacologic stress agents (dipyridamole, adenosine and dobutamine) allow virtually all patients to be safely assessed for ischemic heart disease. These agents have mild but significant side effects, mandating a thorough knowledge of indications, contraindications, side effects and management before their use. Adjunctive exercise improves image quality in vasodilator pharmacologic myocardial perfusion imaging. Diabetics, especially women, have a much higher cardiac event rate than nondiabetics for an equal amount of ischemia. They also have a higher incidence of asymptomatic ischemia. There is growing support for screening with myocardial perfusion imaging (MPI) for asymptomatic ischemia in diabetics. The ability of MPI to identify hypocontractile but viable myocardium, thus predicting improvement in myocardial function after revascularization, is one of the most powerful uses of the modality. Vasodilator MPI should be used as the initial test in patients with left bundle branch block or paced ventricular rhythm, even if they are able to exercise.
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PMID:Pharmacologic stress myocardial perfusion imaging. 1794 36

In order to develop simple technique of combination of transesophageal echocardiography (TEE) and transesophageal pacing, to create algorithm and protocol of transesophageal stress-echocardiography, and to study possible complications and methods of their elimination we examined 39 subjects (mean age 50 +/- 7.2 years) with suspected ischemic heart disease (IHD), 22 patients with arterial hypertension, 11 patients with episodes of ischemic changes on 24 hour ECG. In 11 patients with high blood pressure (BP) and 2 patients with frequent ventricular extrasystoles veloergometry was contraindicated, and in 3 patients veloergometry was not informative due to complete left bundle branch block. We suggested a device for simultaneous transesophageal echocardiography (TEE) and transesophageal pacing which consisted of transesophageal multiplane ultrasound cardiological transducer and electrode for transesophageal pacing. During test pacing frequency was increased stepwise from 120 140 and to 160 beats per min until appearance of ischemia or achievement of submaximal heart rate (HR). During intubation of esophagus HR and systolic BP increased from 80.2 +/- 11.5 to 102 +/- 12.5 b/min and from 130 +/- 23.6 to 149.1 +/- 17.5 mm Hg, respectively. Magnitude of double product rose from 104.4 +/- 29.4 to 149.4 +/- 32.3. This served as additive stress factor, facilitating more precise diagnosis of IHD. As a result various derangements of regional myocardial contractility were revealed in 14 patients (36%). These derangements were accompanied with ischemic ECG changes in 72% and with mitral regurgitation - in 43% of cases. The test was stopped prematurely in 1 patient because of paroxysm of reciprocal atrioventricular tachycardia. Simplicity of the proposed device, lack of complications allow to recommend it for clinical application. Anatomical proximity of esophagus and the heart, average 20 mm Hg elevation of BP, rising cumulative myocardial oxygen requirements augment reliability of the method in diagnostics of IHD.
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PMID:[Novel diagnostic possibilities of transesophageal stress echocardiography with electrical atrial pacing]. 1826 Aug 88

We present a 46-year-old patient who suffered from cardiac arrest and subsequently underwent placement of an implantable cardioverter defibrillator (ICD). The patient underwent a cardiac catheterization which revealed no significant coronary artery disease. About 1 year later he experienced appropriated and frequent ICD discharges due to monomorphic ventricular tachycardia (VT) with left bundle branch block morphology. His prodromal symptoms were mild dizziness and lightheadedness with no chest pain. Amiodarone, mexiletine, sotalol and dofetilide as well as ablation of two inducible ventricular tachycardias in the electrophysiology studies were unsuccessful in controlling the arrhythmias and ICD discharges. During the last episode, he experienced a mild burning sensation in his chest and was given nitroglycerin 0.4 mg sublingually, which relived his symptoms and aborted the VT. This led to a second cardiac catheterization to investigate whether the VT was being induced by myocardial ischemia. This second coronary angiogram spontaneously revealed significant coronary vasospasm and simultaneously, the patient's cardiac rhythm showed short runs of VT with left bundle branch block morphology. Intracoronary nitroglycerine relieved the coronary vasospasm and terminated the arrhythmia. The patient was treated with isosorbide mononitrate and diltiazem. He remained symptom free with no ICD discharges and no VT in ICD interrogations for more than 2 years. Coronary vasospasm may be silent and with no chest pain which creates a difficult clinical situation particularly if it is associated with ventricular tachycardia and sudden cardiac death. The mechanisms of VT in the setting of coronary vasospasm are not known and increased automaticity, focal discharges, functional unidirectional block with reentry, or a combination of these mechanisms may contribute to inducing the VT during the transient ischemia or rarely in the reperfusion phase. It is important to perform provocative tests to diagnose silent coronary vasospasm in unexplained sudden cardiac arrests.
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PMID:Multiple episodes of ventricular tachycardia induced by silent coronary vasospasm. 1829 82


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