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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nitroglycerin (NTG) exercise test can help in detecting ischemia in the presence of right bundle branch block (RBBB), left bundle branch block (LBBB), or digitalis-induced exercise ST changes and in excluding ischemia when a falsely positive test is suspected. This treadmill test has 3-min stages at 10% grade starting at 1.5 mph and progressing in 0.5 mph increments until ST depression is observed. NTG is then given as exercise continues at the ischemia-provoking work load for up to 10 min. Among 3 patients with RBBB, 5 with LBBB, 1 on digitalis and 2 with presumed falsely positive tests, those whose ST depression lessened after NTG had ischemic thallium exercise scans; those with no change in ST depression after NTG had normal thallium images. Additional studies are needed to verify the consistency of these findings among a larger group of patients.
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PMID:The nitroglycerin exercise test. 679 35

To determine the incidence and significance of transient intraventricular conduction abnormalities occurring in association with myocardial ischemia during exercise testing, the recordings of 2,200 consecutive exercise tests were reviewed. Ten patients (0.45%) were identified as having both ischemia and intraventricular conduction abnormalities that developed transiently during the exercise test. In all 10 patients both typical angina and electrocardiographic evidence of ischemia developed during exercise. Among the 10 patients, left anterior hemiblock developed in 4, left posterior hemiblock in 2, right bundle branch block (RBBB) in 2, RBBB with left axis deviation in 1, and left anterior hemiblock progressing to complete left bundle branch block (LBBB) in 1. All 10 patients had cardiac catheterization showing significant obstruction of the left anterior descending (LAD) coronary artery at or before the origin of the first septal branch. Eight patients were treated surgically and 2 medically, all with relief of ischemic symptoms. Nine of the 10 had repeat exercise stress testing without angina or electrocardiographic evidence of ischemia and without recurrence of the transient intraventricular conduction disturbance. It is concluded that the development of transient intraventricular conduction abnormalities associated with myocardial ischemia during exercise testing is an uncommon occurrence (0.45%). When such conduction disturbances do develop, the existence of significant disease in the proximal portion of the LAD coronary artery is strongly suggested. With control of myocardial ischemia, the transient conduction disturbances during exercise are ameliorated.
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PMID:Ischemia-associated intraventricular conduction disturbances during exercise testing as a predictor of proximal left anterior descending coronary artery disease. 683 53

Three cases of radiation-related chronic heart disease are reported. All three patients had been treated for Hodgkin's disease with a mantle technique six to ten years earlier. Ten years after radiation treatment, a 34-year-old woman had dyspnea during exercise. Her heart was enlarged, and an ECG showed a RBBB. An echocardiogram showed pericardial effusion. Right-sided catheterization revealed an infundibular stenosis. A 31-year-old man had chest pain nine years after radiation. An ECG showed complete RBBB and an exercise stress test signs of ischemia; a coronary angiogram showed three proximal stenoses; and an echocardiogram revealed pericardial effusion. A 12-year-old boy had angina pectoris six years after radiation; one year later, he suffered an acute posterior infarction. Two weeks later he died suddenly. An autopsy showed a severe fibrotic and calcified narrowing of the proximal part of the left main coronary artery. Regardless of the patient's age, radiation-related cardiac complications must be kept in mind. Echocardiograms and, in cases of chest pain, exercise stress tests should be a part of routine postradiation follow-up.
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PMID:Radiation-related chronic heart disease. 685 89

From January 1991 to October 1994, 20 Ross procedures were performed. Mean age was 39.70 +/- 7.72 years, range 26 to 56 years. Male/female ratio was 14/6. Nineteen operations were elective, one was semiurgent. Predominant valvular lesion was stenosis in seven patients, aortic regurgitation in four, mixed disease in eight and prosthetic dysfunction in one patient. Twelve pulmonary autografts were implanted in the subcoronary (SC) position, eight as an intraaortic cylinder (inclusion technique (INCL)). Early mortality (< 30 days postoperative) was one (5.0%), there was no late mortality. Reoperation for valve failure occurred in two patients (10.0%). Additional CABG was performed in two patients (10.0%) for technical reasons. Major ECG changes were detected in five patients (three RBBB, two ischemia). No thromboembolic events were reported. Mean follow up was 21.2 months. Aortic insufficiency (AI) at one year was similar in the SC and INCL group. AI grade I in SC: 60%, in INCL: 60%; AI grade II in SC 10%, in INCL: 20%. At two years AI grade I occurred in 100% of the SC group. At three years AI grade I occurred in 75% of the SC group and AI grade II in 25%. No patients of the INCL group had two- or three-year follow up. At discharge slight pulmonary regurgitation was traced in only three patients and it remained stable during the follow up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Three years surgical and clinical experience with the Ross procedure in adults. 758 50

A 41-year-old man was admitted because of chest pain at rest. The exercise test and coronary angiography were performed after all antianginal medication was discontinued for 24 hours. During the graded treadmill exercise stress test using the Bruce protocol, the patient had anginal pain with the electrocardiogram (ECG) showing ST segment elevation in leads V1 and V2. A baseline coronary angiogram disclosed 50% stenosis of the first septal branch of the left coronary artery. After a bolus of 0.1 mg ergonovine was administered into the coronary artery, the patient complained of typical anginal pain. Complete occlusion of the first septal branch was demonstrated, associated with significant ST segment elevation in leads V1-V3, right bundle branch block, and electrical axis deviation to the left on the ECG. The coronary occlusion reversed soon after nitroglycerin administration into the coronary artery. We diagnosed a rare case of angina pectoris caused by spasm of the minor branch of coronary artery, and that serial ECG changes might demonstrate ventricular septal ischemia including the cardiac conduction system. ST segment elevation in leads V1-V3 indicated ischemia of the ventricular septum, and right bundle branch block, axis deviation to the left, and increased amplitude of the precordial R wave might be induced by ischemia of the right bundle branch, left anterior bundle branch and septal branch in the cardiac conduction system supplied by the septal branches of the left anterior descending coronary artery.
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PMID:[Rest angina induced by coronary artery spasm at the first septal artery: a case report]. 816 49

Postoperative conduction disturbances after coronary artery bypass grafting were analyzed in 100 patients who randomly received either blood or crystalloid cardioplegia. Conduction disturbances, mostly transient, developed after termination of cardiopulmonary bypass in 30 of the 100 patients--15 in either group. Ischaemia appeared to be a major determinant for conduction disturbances. Previous inferior myocardial infarction and stenosis of the right coronary artery both exposed the patient to risk of right bundle branch block.
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PMID:Conduction disturbances after blood and crystalloid cardioplegia in coronary bypass surgery. 819 29

A patient with an established LBBB suffered an acute septal myocardial infarction complicated with a 2:1 infranodal AV block. As the ventricular rate decreased, the preexisting LBBB disappeared, and, in its place, a RBBB bradycardia-dependent appeared. Later on, an escape rhythm emerged, and competition between the two rhythms evolved. These disturbances were short-lived, and took place in the first 24 h. It is postulated that an increase in the rate of diastolic depolarization, ischemia related, may cause, in the same area, impairment of conduction and increased automaticity accounting for the findings previously mentioned. In an acute septal infarction conduction disturbances usually are progressive; ischemia rarely may induce hypopolarization rise giving to complex, but reversible, phenomena.
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PMID:[Depressed conduction and increased automaticity in acute septal myocardial infarction]. 902 47

In 1992, Brugada and Brugada described a syndrome characterized by right bundle branch block pattern with ST elevation in leads V1 through V3 and a history of sudden death due to polymorphic ventricular tachycardia or ventricular fibrillation. Since these patients had no evidence of cardiac disease, these findings were ascribed to a distinct clinical entity. Further experience has shown that this same pattern may be mimicked by patients with right ventricular dysplasia, acute ischemia of the right ventricle, other infiltrative cardiomyopathies, as well as tricyclic drug overdose. The pathogenesis of these changes may be due to loss of the dome configuration in the transmembrane potential of right ventricular epicardial cells, which would result in a voltage gradient producing ST elevation. Other explanations involve delayed conduction in a dysplastic right ventricle. The clinical importance of this syndrome is that it calls attention to patients at risk for sudden cardiac death. In addition, these observations have sparked the interest of basic electrophysiologists relative to the relationship of these ECG waveforms and malignant ventricular arrhythmias. Finally, the clinician must exclude other organic diseases before diagnosing this entity.
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PMID:Is the Brugada syndrome a distinct clinical entity? 908 84

In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI, SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: Ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinically course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure cardiogenic shock and malignant ventricular arrthythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.).
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PMID:[In Process Citation] 966 39

In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI. SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinical course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure, cardiogenic shock and malignant ventricular arrhythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.)
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PMID:[Supraventricular arrhythmias and disorders of atrioventricular and intraventricular conduction in patients with acute myocardial infarct]. 991 47


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