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)

Anomalous origin of right coronary artery from the left sinus of Valsalva is a uncommon congenital anomaly which is difficult to demonstrate angiographically. For many years pathologists classified it as a minor anomaly of no clinical significance. It has only recently been associated with significant manifestations of myocardial ischemia. These manifestations have included acute myocardial infarction, angina pectoris, syncope, ventricular tachycardia and fibrillation, and sudden death. Two patients with this anomaly are reported. One patient had angina pectoris in the absence of significant atheromatous coronary lesions. In the second patient the aberrant origin of the right coronary artery was associated to aortic valve disease. The possible physiopathology mechanisms responsible for manifestations of myocardial ischemia in patients with this anomaly are analyzed.
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PMID:[Anomalous origin of the right coronary artery from the left sinus of Valsalva. Apropos of 2 cases]. 177 7

Torsades de pointes (TdP) is a life-threatening ventricular tachycardia that occurs in the setting of a prolonged QT interval and is most frequently related to administration of antiarrhythmic drugs. Patients with organic heart disease, with low serum electrolyte levels, with a previous episode of TdP and with bradycardia or baseline QT prolongation may be at increased risk of developing TdP. After initiation of a QT prolonging therapy, the dosage should be modified if the QT interval reaches 560-600 ms. Cessation of medication and immediate hospitalization are indicated in the presence of lightheadedness, syncope, or increased frequency and complexity of ventricular premature beats. The conventional therapy of TdP with isoproterenol or cardiac pacing, although usually effective, has certain disadvantages. Isoproterenol is contraindicated in patients with hypertension or ischemic heart disease, whereas institution of cardiac pacing requires skilled personnel and fluoroscopy. Recently, infusion of magnesium sulfate has been shown to abolish TdP both in the clinical and experimental setting. Compared with conventional therapy, magnesium sulfate has the advantage of safety and simplicity of its administration. In doubtful cases, if does not aggravate a ventricular tachycardia that is not TdP, as may occur with isoproterenol. This advantage and the prompt effectiveness of the drug in four clinical series, including 31 patients, support the use of magnesium sulfate as the first line of therapy for TdP.
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PMID:Torsades de pointes: prevention and therapy. 185 60

Heart muscle perfusion was studied by exertion scintigraphy Tal-201 in 24 patients, 16M and 8F, aged 16-45 years, means--28 +/- 7.4 years with hypertrophic cardiomyopathy. The relationship between perfusion disturbances and sudden death risk factors occurring in this group of patients was evaluated. Disturbances of heart muscle perfusion were found in 20 pts (83%); 2 pts had permanent perfusion defects, in 18 pts these defects were completely or partially reversible at rest. Only 4 pts (17%) had normal heart muscle perfusion. In patients with perfusion disturbances there was found a significantly more frequent occurrence of the following sudden death risk factors: 1. syncope (p less than .01) 2. ventricular arrhythmia of IV b class according to Lown (p less than .01) 3. advanced hypertrophy of intraventricular septum (p less than .01) 4. sudden death in patients families (p less than .05) The evaluation of the heart muscle perfusion confirmed the occurrence of myocardial ischemia in most of the examined patients. Normal coronaro-angiography in all the patients over 35 years as well as the young age of the other patients exclude atherosclerosis as the cause of myocardiac ischemia in the group under study. This is a confirmation of nonatherosclerotic etiology of myocardiac ischemia in hypertrophic cardiomyopathy patients. The correlation between perfusion disturbances and sudden death risk factors points to the role of ischemia in the natural course of disease and the value of exertion scintigraphy TI-201 in prognosing patients with hypertrophic cardiomyopathy.
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PMID:[Disturbances of myocardial perfusion by exertion scintigraphy in patients with hypertrophic cardiomyopathy and their relationship with sudden death risk factors]. 194 60

The records of 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack- (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA-related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41%). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow-up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.
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PMID:Transient ischemic attack-related syncope. 204 43

The purpose of the study was to describe the clinical picture in patients with ischemic heart disease (IHD) and verifying severity of ventricular arrhythmias. The study included 856 patients with IHD aged 23-88 years (mean = 55.3), including 659 men and 197 women. Holter monitoring was performed in all patients. Ventricular arrhythmias were graded according to Lown. The patients were divided into five groups: group 1-349 patients with Lown's grade 1 and 2; group 2-95 patients with grade 3; group 3-152 patients with grade 4a and 4b; group 4-11 patients with grade 5; group 5-507 patients (selected from groups 2, 3 and 4) with Lown's grade 3 and 4 or 5. Arterial hypertension was found in 17.1%, myocardial infraction in 66%, and syncope in 12.3% of the patients. The patients with complex ventricular arrhythmias versus Lown's grade 1 and 2 show significant differences especially in respect to: the frequency of previous anterior myocardial infraction, the incidence of pain at rest, loss consciousness, the frequency of ventricular tachycardia and fibrillation, anginal pain and exercise-related arrhythmias. The patients with Lown's ventricular arrhythmia grade 3-5 do not differ significantly in their clinical manifestations of IHD from the patients with ventricular arrhythmias grade from 3 to 5. The development of silent myocardial ischemia during exercise stress testing is typical also for the patients with complex ventricular arrhythmias. A decreased contractility index, ejection fraction and dyskinesis are significantly more frequent in the patients with complex ventricular arrhythmias.
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PMID:[Complex ventricular arrhythmias in ischemic heart disease]. 208 68

A 64-year-old woman with a history of hypertension for ten years and of syncope 18 month previously visited our Division of Cardiology on 12 June, 1989. The S4 and mitral regurgitation were audible at the apex, and her electrocardiogram showed ST-depression in leads II, aVF, V5-6 and prominent U-wave (PU) in V1-3 when first seen. Then, she was thought to have a posterior myocardial ischemia. PU in V1-3 diminished whereas T-wave increased after nitrate and Ca++ blocker. Ergometer exercise ECG showed ST-depression in II, III, aVF, V4-6 and PU with decreased T-wave in V2-3 with no apparent symptoms. Simultaneously, Tl-201 myocardial imaging demonstrated a transient posterior defect. A silent posterior myocardial ischemia was, therefore, confirmed. Coronary arteriograms demonstrated subtotal obstruction of the proximal left circumflex artery, and the peripheral site was filled by collaterals from the right coronary artery. Angina-induced PU in the right precordial leads proved to be useful in detection of posterior myocardial ischemia, and this marker may also improve the possibility of detection of silent posterior ischemia.
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PMID:[A case of silent posterior myocardial ischemia/left circumflex artery obstruction detected by prominent U-wave in right precordial leads]. 228 23

Sustained ventricular tachyarrhythmias and sudden death are particularly prevalent in patients with idiopathic dilated cardiomyopathy (IDC). In contrast to patients with ischemic heart disease, the value of electrophysiological stimulation (EPS) in patients with IDC has not yet been established. To clarify the role of EPS in these patients, we studied 19 patients (58 +/- 11 years) with IDC who had symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF). The mean left ventricular ejection fraction was 26 +/- 9%. Ten patients had survived out-of-hospital cardiac arrest, eight had documented sustained monomorphic VT and one patient had non-sustained VT associated with syncope. Thirteen of the 19 patients (68%) had their clinical ventricular tachyarrhythmias induced at EPS (12 VT, 1 VF). In nine of 13 patients (69%), the arrhythmias were subsequently suppressed during serial electrophysiological drug testing. During 17 +/- 11 months of follow-up, 10/19 (53%) patients experienced recurrence of their arrhythmias and nine out of 19 (47%) patients died; six died suddenly and three secondary to heart failure. There was no difference in arrhythmia recurrence between patients with and without inducible ventricular tachyarrhythmias at initial study. Furthermore, suppression of arrhythmia during serial testing did not predict outcome; recurrences were observed in five out of nine patients whose arrhythmias were suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiological evaluation of sustained ventricular tachyarrhythmias in idiopathic dilated cardiomyopathy. 245 34

Ambulatory electrocardiographic monitoring and the frequent use of stress electrocardiography have been important tools in characterizing the prevalence and prognostic importance of ventricular ectopic activity in both healthy persons and patients with organic heart disease. These studies have demonstrated that ventricular ectopy is not uncommon in persons with no evidence of heart disease. However, it is rarely of high density or repetitive, and even when frequent or repetitive, or both, carries little, if any, risk of sudden death in patients without syncope. However, in patients with organic heart disease and in certain clinical settings, frequent and repetitive ventricular ectopy identifies a population at high risk for arrhythmia-induced syncope or sudden death. These rhythm disturbances have particular prognostic importance in ischemic heart disease with depressed left ventricular function and hypertrophic cardiomyopathy. Patients with presyncope or syncope and structural heart disease who demonstrate frequent and repetitive ventricular ectopy are also a high-risk group. Therefore, individual risk stratification is important in deciding whether and how to treat patients with ventricular ectopy.
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PMID:Ventricular ectopic activity: prevalence and risk. 248 Jul 10

Our study group included 12 patients (4 males, 8 females), mean age 60 yr, with symptomatic or threatening tachyarrhythmias (Lown classes IV A, B, V); 2 patients were suffering from mitral valve prolapse syndrome, 2 from ischemic heart disease; 4 from cardiac insufficiency caused by hypertensive or ischemic heart disease; 4 had no evident clinical signs of cardiopathy. Patients suffering from: cardiac insufficiency (F.C. III e IV NYHA); II and III degree BAV; atrial flutter and fibrillation; long QT syndrome; acute ischemic heart disease were excluded from the study. During short-term treatment, patients received placebo for four days and subsequently flecainide 200 mg daily for four days. During medium-term treatment patients received flecainide 200 mg daily (for six months). Several Holter/24-hour monitorings were performed for evaluation of therapy. No significant reduction in the number of ectopic ventricular beats (B.E.V.) was found with placebo whereas reductions of B.E.V. number (97% and 95%, respectively) were found during short and medium-term treatment with flecainide. Flecainide produced: changes in Lown class: from IV A, B and V to II and I; a marked reduction of subjective symptoms (dyspnea, giddiness syncope, precordial pain); ECG changes: increases in: PR: 5-25%; QRS: 11-12%; QT: 11-22%. Flecainide produced no pro-arrhythmic effects or changes in echocardiographic ventricular function index. Flecainide can be considered one of the most effective new antiarrhythmic drugs.
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PMID:[Short- and medium-term treatment of ventricular hyperkinetic arrhythmia with flecainide]. 252 12

The natural history of the patient with hypertrophic cardiomyopathy is characterized by slow progression of symptoms and left ventricular hypertrophy; severe functional limitation is unusual and encountered only in about 20%. Most of the deaths are sudden and occur irrespective of the functional status of the patient and there are no routine electrocardiographic or hemodynamic measurements indicative of poor prognosis. Sudden death may be associated with syncope and young age at diagnosis as well as with a family history of sudden death. The mechanisms underlying the cause of sudden death have not been clearly elucidated. Although complete heart block may complicate myotomy or myectomy, the development, in an unoperated patient, of symptomatic conduction disease is uncommon. Preexcitation syndromes may be present in a small subpopulation (about 2%), but this appears seldom responsible for sudden death. Outflow tract spasm has also been postulated as a causal factor but the fact that proportionately an equal number of patients with and without ventricular outflow gradients die suddenly, suggests that other mechanisms must be important. Further hypotheses, currently however, without substantiation, have implicated acute changes in diastolic filling or acute myocardial ischemia as causes of sudden death. Recently published studies have stressed the importance of ventricular arrhythmias as a cause of sudden death. Ventricular tachycardia occurs in about 30% of such patients and can be found significantly more frequent in adult patients who die suddenly. In children and adolescents, since they have a lesser incidence of ventricular tachycardia, possibly, other mechanisms are involved. In general, episodes of ventricular tachycardia are asymptomatic and self-limited; the main ventricular rate recorded during 135 episodes in 30 of our patients was 142 beats per minute with an average duration of eight beats. Variable QRS morphology suggests different sites of origin. Due to the marked spontaneous variability, the probability of missing ventricular tachycardia with a single 24-hour continuous ambulatory ECG is 54%; on 96 hours of continuous ECG monitoring the probability can be reduced to 8%. Accordingly, continuous ambulatory ECG monitoring should be carried out for at least 48 to 72 hours. At the time of diagnosis, approximately 7% of the patients have atrial fibrillation. On three days of continuous 24-hour ECG monitoring, about 40% will be found to have atrial fibrillation or supraventricular arrhythmias. The correlation between supraventricular arrhythmias and sudden death is weaker than that of the latter with ventricular arrhythmias.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Arrhythmias in hypertrophic cardiomyopathy. Significance and therapeutic consequences]. 258 Jul 67


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