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

The mechanism underlying cardiac arrest in patients with hypertrophic cardiomyopathy (HC) is intriguing. In the clinical setting, myocardial ischemia has long been incriminated, particularly in the young. Among 274 cardiovascular sudden deaths in the young (< or = 35 years), 19 (7.0%), 14 males and 5 females, median age 23 years, had HC. Familial occurrence of HC was ascertained in 3 (16%). SD occurred on effort in 6 (31%). Previous syncope occurred in 5 and palpitations in 3. Basal electrocardiogram (ECG) was abnormal in 7 of 8 available cases. Hypertrophy was septal asymmetric in 14. Gross examination showed large isolated or multiple septal scars in 11 (58%); at histomorphometry, the mean percent area of fibrosis of the septal myocardium was 18.6 +/- 6. Four showed a deep intramyocardial course of the left anterior descending coronary artery. At histology, myocardial disarray involved 30 +/- 16% of the septal myocardium; evidence of acute-subacute myocardial necrosis was present in 14 (74%), 1 of them with a regional acute myocardial infarction. By comparing hearts with (n = 11) and without (n = 8) areas of scar-type fibrosis, we found a statistically significant difference in terms of age (25.5 +/- 5.4 v 15.5 +/- 12.4 years, P = .04), septal thickness (25.4 +/- 5.4 v 15.4 +/- 4.9 mm, P < .001), percent increase of septal thickness versus normal value for age and sex (46.2 +/- 15 v 25.2 +/- 13.6%, P < .01) and mean score of small vessel disease (1.7 +/- 0.4 v 1.2 +/- 0.4, P = .04). Linear regression analysis showed a positive correlation of percent area of replacement fibrosis with septal thickness (P = .01) and with mean score of small vessel disease (P < .01). In conclusion, our pathologic findings of ischemic damage, either acute-subacute or in the form of fibrotic scars, support the clinical evidence that ischemia occurs in the natural history of HC and may contribute to life-threatening electrical instability.
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PMID:Hypertrophic cardiomyopathy and sudden death in the young: pathologic evidence of myocardial ischemia. 1098 48

An internal loop recorder (ILR) implanted to evaluate syncope was activated during an episode of chest pain. Analysis of the recorded event revealed a marked increase in the amount of ST-segment depression over baseline. In addition to rhythm analysis, the ILR may be able to assess myocardial ischemia. Further refinements of filtering may make analysis more accurate.
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PMID:Demonstration of myocardial ischemia by an internal loop recorder. 1106 Aug 84

The evaluation of syncope occurring during exercise or occurring spontaneously in highly trained individuals presents a unique diagnostic challenge. It is of critical importance to exclude potential life-threatening disorders such as hypertrophic cardiomyopathy, long QT syndrome, right ventricular dysplasia, anomalous coronary artery distribution, valvular heart disease, myocarditis, or exercise-induced arrhythmia. This review is not directed towards identifying, treating, or determining athletic eligibility of individuals with such disorders. Rather, we endeavour to discuss the pathophysiology of exercise-induced neurocardiogenic syncope and to address the role of head upright tilt testing in evaluating syncope in athletic individuals in whom proper evaluation has excluded the presence of ischaemic heart disease or primary structural or electrical heart disease.
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PMID:Exercise-induced neurocardiogenic syncope: clinical data, pathophysiological aspects, and potential role of tilt table testing. 1122 99

The long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram. It is associated with precipitation of a polymorphic ventricular tachycardia, torsade de pointes, which may cause sudden death. The syndrome is a disorder of cardiac repolarization caused by the alterations in the transmembrane potassium and sodium currents. Six genetic loci for the congenital forms of the syndrome have been identified; sporadic cases occur because of spontaneous mutations. Acquired causes of the long QT syndrome include drugs, electrolyte imbalance, toxins, marked bradycardia, subarachnoid hemorrhage, stroke, myocardial ischemia, protein-sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease. Clinical symptoms are the result of the precipitation of torsade de pointes and range from such minor symptoms as dizziness to syncope and sudden death. Short-term treatment is aimed at preventing the recurrences of torsade de pointes and includes intravenous magnesium and potassium administration, temporary cardiac pacing, and correction of electrolyte imbalance; rarely, intravenous isoproterenol is indicated. Long-term management includes use of beta-blockers, permanent pacemaker placement, and cardioverter-defibrillator implantation. Asymptomatic patients are treated if under the age of 40 years at the time of diagnosis.
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PMID:Clinical and therapeutic aspects of congenital and acquired long QT syndrome. 1181 8

The prevalence and incidence of atrial fibrillation increase with age. Atrial fibrillation is associated with a higher incidence of coronary events, stroke, and mortality than sinus rhythm. A fast ventricular rate associated with atrial fibrillation may cause tachycardia-related cardiomyopathy. Management of atrial fibrillation includes treatment of underlying causes and precipitating factors. Immediate direct-current cardioversion should be performed in persons with atrial fibrillation associated with acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta-blockers, verapamil, or diltiazem may be used to immediately slow a fast ventricular rate associated with atrial fibrillation. An oral beta-blocker, verapamil, or diltiazem should be given to persons with atrial fibrillation if a rapid ventricular rate occurs a rest or during exercise despite digoxin. Amiodarone may be used in selected persons with symptomatic life-threatening atrial fibrillation refractory to other drug therapy. Nondrug therapies should be performed in persons with symptomatic atrial fibrillation in whom a rapid ventricular rate cannot be slowed by drug therapy. Paroxysmal atrial fibrillation associated with the tachycardia-bradycardia syndrome should be managed with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in persons with atrial fibrillation in whom symptoms such as dizziness or syncope associated with non-drug-induced ventricular pauses longer than 3 seconds develop. Elective direct-current cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than medical cardioversion in converting atrial fibrillation to sinus rhythm. Unless transesophageal echocardiography shows no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective direct-current or drug cardioversion of atrial fibrillation and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer the treatment strategy of ventricular rate control plus warfarin rather than to maintain sinus rhythm with antiarrhythmic drugs, especially in older patients. Digoxin should not be used in persons with paroxysmal atrial fibrillation. Patients with chronic or paroxysmal atrial fibrillation who are at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio (INR) of 2.0 to 3.0. Persons with atrial fibrillation who are at low risk for stroke or who have contraindications to warfarin should receive 325 mg aspirin daily.
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PMID:Atrial fibrillation. 1197 40

A 69-year-old man was admitted with palpitations and syncope. His medical history included hypertension and left ventricular hypertrophy. Arterial pulsation was not palpable on admission. Electrocardiography revealed ventricular tachycardia, and cardioversion restored normal sinus rhythm. An electrophysiological study reproducibly induced polymorphic ventricular tachycardia, so a cardioverter defibrillator was implanted. Echocardiography revealed mid-ventricular obstruction and an apical aneurysm, and Doppler color flow imaging showed a diastolic paradoxic jet from the apex toward the base. Coronary angiography showed no stenosis of the extramural coronary arteries. Ventricular tachycardia on admission showed a right bundle branch block pattern and a superior axis deviation, so the arrhythmia was thought to originate from the apical aneurysm. Apical aneurysm can result from elevated intraventricular pressure or relative myocardial ischemia. This is a rare case of hypertrophic cardiomyopathy with mid-ventricular obstruction complicated with apical aneurysm and polymorphic ventricular tachycardia.
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PMID:[Hypertrophic cardiomyopathy with mid-ventricular obstruction complicated with apical left ventricular aneurysm and ventricular tachycardia: a case report]. 1197 69

Atrial fibrillation (AF) is associated with a higher incidence of mortality, stroke, and coronary events than is sinus rhythm. AF with a rapid ventricular rate may cause a tachycardia-related cardiomyopathy. Immediate direct-current (DC) cardioversion should be performed in patients with AF and acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta blockers, verapamil, or diltiazem may be given to slow immediately a very rapid ventricular rate in AF. An oral beta blocker, verapamil, or diltiazem should be used in persons with AF if a fast ventricular rate occurs at rest or during exercise despite digoxin. Amiodarone may be used in selected patients with symptomatic life-threatening AF refractory to other drugs. Nondrug therapies should be performed in patients with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drugs. Paroxysmal AF associated with the tachycardia-bradycardia syndrome should be treated with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in patients with AF and with symptoms such as dizziness or syncope associated with ventricular pauses greater than 3 seconds that are not drug-induced. Elective DC cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than does medical cardioversion in converting AF to sinus rhythm. Unless transesophageal echocardiography has shown no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective DC or drug cardioversion of AF and should be continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer, especially in older persons, ventricular rate control plus warfarin rather than maintaining sinus rhythm with antiarrhythmic drugs. Digoxin should not be used to treat patients with paroxysmal AF. Patients with chronic or paroxysmal AF at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio of 2.0 to 3.0. Patients with AF at low risk for stroke or with contraindications to warfarin should receive 325 mg of aspirin daily.
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PMID:Management of the older person with atrial fibrillation. 1202 64

The combination of amiodarone and beta-blockers appears superior to amiodarone alone in the prevention of sudden death. At present this combination can be proposed to patients at risk of sudden death in whom a beneficial effect of the implantable defibrillator has not been clearly demonstrated. Therefore, the patients who can be treated with this combination appear the following ones: patients with sustained ventricular tachycardia (VT) causing severe hemodynamic compromise and ejection fraction > 35%; patients with hemodynamically well-tolerated sustained VT; patients with ischemic heart disease, syncope of unknown cause and induction of VT or ventricular fibrillation (VF) during electrophysiologic study; patients with sustained VT or VF and age > 80 years; patients with left ventricular dysfunction, without history of sustained VT or VF, but with "symptomatic ventricular arrhythmias".
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PMID:[The amiodarone-beta blockers combination could represent an alternative treatment in patients at risk for sudden death in which a benefit from implantable defibrillators has not been clearly demonstrated]. 1204 Aug 49

This report describes a case of syncope with an initial ECG that showed ST-segment elevation in the right precordial leads suggestive of Brugada syndrome. Procainamide infusion induced a significant increase in the ST-segment abnormalities, further increasing the suspicion for this syndrome. Cardiac catheterization showed lesions in the proximal left anterior descending artery and distal right coronary artery. Following percutaneous coronary intervention at these sites, the ST-segment abnormalities resolved and a repeat procainamide challenge was negative. Electrophysiological study did not provoke any ventricular arrhythmias. Silent myocardial ischemia may result in ECG changes that resemble those seen in patients with Brugada syndrome.
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PMID:Syncope with ST-segment abnormalities resembling Brugada syndrome due to reversible myocardial ischemia. 1235 80

Dilated cardiomyopathy is a diverse group of heart diseases with variable arrhythmia substrates. The response to programmed stimulation is dependent on spontaneous arrhythmia presentation. In patients with dilated cardiomyopathy, the majority of sustained monomorphic VT is caused by a scar-related reentrant mechanism, similar to that of coronary artery disease. The arrhythmia is uniformly inducible and is often refractory to pharmacologic therapy. Sustained VT is associated with more extensive myocardial fibrosis and non-uniform anisotropy, involving both the endocardium and epicardium, compared to those without sustained reentry. The response to programmed stimulation is more variable in patients presenting with nonsustained arrhythmia, cardiac arrest or syncope. Inducibility of monomorphic VT is much lower compared to those with ischemic heart disease. Other non-reentrant mechanism, such as focal automaticity, can also be observed in patients with monomorphic VT, in the absence of myocardial scar or evidence of slow conduction. The utility of electrophysiology studies to determine prognosis and to guide therapy remains limited in this patient population. The clinical outcome does not correlate with arrhythmia inducibility, and suppression of induced arrhythmia does not predict a good prognosis. The diagnosis of sarcoidosis or Chagas' cardiomyopathy should be considered in patients with dilated cardiomyopathy of unknown etiology, particularly in those with marked regional wall motion abnormalities and inducible VT. Epicardial reentrant circuits may be more prevalent in these cardiomyopathies, especially in those with VT related to chronic Chagas' disease. Although bundle branch reentry VT is a common finding in patients with dilated cardiomyopathy, it can occur in cardiomyopathy of any type and may coexist with other myocardial reentrant VT. It often has a typical bundle branch block QRS pattern during VT and is associated with His-Purkinje conduction delay. Evidence of macroreentry involving the bundle branches can usually be demonstrated, and catheter ablation of the bundle branches provides an effective and specific treatment.
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PMID:Electrophysiology studies in patients with dilated cardiomyopathies. 1243 31


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