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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dynamic, long-term electrocardiography by the Holter technique has gained a definite and important role in cardiac diagnosis. Indications for its application include the diagnosis of ischemic heart disease, the assessment of antiarrhythmic therapy, the evaluation of function of artificial pacemakers, the investigation of physiologic correlates of known arrhythmias, the evaluation of the efficacy of antianginal therapy, and the assessment of the natural history of cardiac arrhythmias in various conditions. In our hands, the technique has proved most fruitful in the uncovering of arrhythmic correlates of transient neurologic disturbances or syncope, and in the precise characterization of patients suspected of having the sick sinus syndrome.
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PMID:Holter monitoring in the diagnosis and management of cardiac rhythm disturbances. 94 79

Recurrent electromechanical dissociation, eventually fatal, presented as Stokes-Adams-like syncope in a patient with severe underlying coronary heart disease. Mechanical function was probably suppressed because of myocardial ischemia due to recent occlusion of the proximal right main coronary artery; the left main coronary artery had been occluded previously. Spasm of the proximal right coronary artery may have accounted for his recurrent attacks of pain and syncope. It is suggested that this clinical picture has a grave prognosis, demanding urgent therapeutic measures. While these measures are likely to be more hazardous than usual, the grave prognosis and potential for therapeutic success make them well worth the risk.
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PMID:Recurrent electromechanical dissociation due to severe underlying coronary heart disease. 95 83

This paper reports the results of a retrospective study carried out with special reference to the survival rate in a series of 101 selected cases including patients with complete heart block (CHB) combined or not combined with Adams-Stokes attacks and patients with arrhythmic syncope without ECG evidence of CHB. All these patients were treated in our Department during 1958-68, none being artificially paced. Twenty-seven patients were alive at the end of the follow-up, i,e 6-15 years after admission to this Department on account of syncopal episodes or CHB. The survival rate--higher in females than males--was lower in the cases of CHB combined with Adams-Stokes attacks than in the cases of asymptomatic CHB. This applied also to the instances in which a complicating disease such as ischaemic heart disease (IHD), hypertension, diabetes, digitalis intoxication or cardiac enlargement coexisted. The survival rate in the 68 cases of CHB was higher at one year (68%) as well as at 5 years (37%) than that reported by other investigators. When assessing the survival rate in cases treated with artificial pacemakers, it is important to study the individual case histories with special reference to a previous or coexisting condition such as IHD, hypertension, diabetes or the presence of cardiac enlargement. The present results support the view that the indications for treatment with artificial pacing should be wide, albeit that the prognosis in this series was more favourable than might have been anticipated from observations by others.
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PMID:Prognosis of patients with complete heart block or arrhythmic syncope who were not treated with artificial pacemakers. A long-term follow-up study of 101 patients. 101 54

The cardiovascular effects of prolonged administration of levodopa were studied in 54 men and women with Parkinson's disease; 23 of them were younger than 70 and 31 were 70 or older. The patients were evaluated clinically before treatment was started and at regular intervals thereafter. The average optimal dosage of levodopa for both age groups was 3.0 and 2.5 gm per day, respectively, during an average treatment period of 20.7 months. Eleven patients showed hypotension (systolic BP of 105 mm Hg or less) that was not related to dosage; in only 6 did the drug have to be permanently discontinued because of syncope; 3 of this group had an associated psychiatric disorder. Four patients had pretreatment hypertension; in 3 the BP fell to normal during therapy; in the remaining patient the hypertension persisted and was successfully treated by an antihypertensive drug. In 5 patients an occasional atrial or ventricular ectopic beat was noted both before and during levodopa therapy but no therapeutic intervention was required. Thirty of the 46 patients with adequate ECG follow-up did not show any significant changes; 5 others showed an increase, and 11 a decrease in myocardial ischemia. Thus the administration of levodopa in elderly patients with or without heart disease is a relatively safe procedure. The only exception would be patients over 70 years of age with a history of previous myocardial infarction. In this group there seems to be a higher incidence of clinically significant hypotension. In such patients, levodopa therapy should be carried out with great caution.
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PMID:Cardiovascular effects of levodopa in aged versus younger patients with Parkinson's disease. 125 82

Ninety five patients with a mean age of 39 +/- 19 years, 82 of whom were symptomatic, having an accessory atrioventricular bidirectional conduction pathway (WPW syndrome: 77; "concealed": 18) were followed up for an average of 7.3 +/- 2.6 years. The objectives were to analyse: the incidence and causes of death and the possible predictive factors of death due to the WPW syndrome--the influence of medical treatment and type of medication on survival and symptoms. Of the 8 cardiac deaths, 6 seemed to be related to the WPW syndrome, a prevalence of 7.8% and an annual incidence of 1.1/1000. The main risk factors which were identified were: age 62 +/- 8 years versus 37 +/- 15 years in survivors; p < 0.02--associated organic heart disease, especially ischaemic heart disease (5/6)--the description of severe symptoms, in particular recurrent syncope--documented malignant spontaneous or induced arrhythmias (5/6)--anterograde AV conduction with an effective refractory period < or = 230 msec in 4, though it was only 270 msec in the other 2 patients, indicating that this parameter is not specific--amiodarone (6/6) did not prevent the fatal outcome in this particular group of patients. In the "benign" forms, only betablocker drugs could significantly reduce the frequency and severity of symptoms, especially when compared with Class I or IC antiarrhythmics. These results suggest that the indications of radical treatment should be widened in high risk patients, especially when elderly and with associated coronary artery disease. They also suggest that the role of betablocker drugs should be reevaluated in the so-called "benign" symptomatic forms.
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PMID:[Long-term outcome of a hospital series of patients with atrio-ventricular accessory pathway]. 136 71

The cause of the syncope in aortic stenosis has been the subject of controversy partly because only a few patients have been monitored during their syncopal episodes. Among the mechanisms proposed are hypersensitive carotid sinus, complete A-V block, ventricular arrhythmias, and ischemic myocardial depression. It is now accepted that the syncope is caused by a vasodepressor response from stimulation of left ventricular baroceptors, resulting in reflex hypotension and bradycardia. This case report describes a patient who developed a syncopal episode during stress testing. Although the mechanism for the syncope is consistent with the vasodepressor response, ischemic changes were observed in the electrocardiogram before the development of syncope. Review of literature shows that, although different mechanisms for syncope have been described, all reported patients manifested myocardial ischemia before the development of their syncopal episodes even when the syncope was nonexertional and clearly caused by a vasodepressor response. The authors conclude that, independent of the mechanism proposed, myocardial ischemia is overlooked as an important substrate in which the syncopes are precipitated in aortic stenosis.
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PMID:Case report: myocardial ischemia: an overlooked substrate in syncope of aortic stenosis. 153 5

Patients with infrequent recurrent syncope undiagnosed after extensive noninvasive and invasive testing pose a diagnostic and therapeutic dilemma. The purpose of this pilot study was to assess the feasibility of using an implanted, long-term monitor as an aid to diagnosis in these patients. This was done using commercially available pacemakers with monitoring functions. Sixteen patients (eight males and eight females), aged 59.7 +/- 17 years who had unexplained syncope despite a 12-lead electrocardiogram, repeated Holter monitoring, exercise testing, echocardiography, an electrophysiological study, and a tilt test (n = 6), were entered into the study. Patients had experienced a mean of 3.1 +/- 1 episodes of syncope in the 12 months prior to the study. All provided a history suggestive of Stokes-Adams attacks and were referred for consideration of pacemaker implantation. Two patients had ischemic heart disease and one patient had a long QT interval. Patients had an Intermedics Nova II or Medtronic Quintech DPG pulse generator capable of recording sensed and paced events implanted with a single right ventricular lead. Syncope or presyncope occurred in ten patients (62%) 4.9 +/- 4.2 months after pacemaker implantation. Bradycardia was detected in six patients and four patients had no arrhythmia. In addition to bradycardia, one patient also had tachycardia detected. Pacing therapy resulted in symptom relief in all six patients with syncope or presyncope due to bradycardia. Complications of pacemaker implantation (lead insulation failure) occurred in two patients. One of these patients subsequently had an infection of the generator pocket with associated systemic sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Feasibility of long-term electrocardiographic monitoring with an implanted device for syncope diagnosis. 171 65

Invasive electrophysiological testing has contributed importantly to the objective evaluation and management of patients at high risk for sudden cardiac death. The clinical application of the technique is based on the hypothesis that the reproducible induction of ventricular arrhythmias by programmed cardiac stimulation constitutes a marker of risk for spontaneous ventricular arrhythmias and sudden death as well as an objective end point to guide the selection of antiarrhythmic therapy. The value of electrophysiological testing is well established in patients with ischemic heart disease and a history of sustained ventricular tachycardia or fibrillation and in some subsets of patients with unexplained syncope. More recently, the technique has been used by some investigators to identify individuals at high risk for sudden death among patients with recent myocardial infarction and those with left ventricular dysfunction and recurrent nonsustained ventricular tachycardia. The predictive value of the technique in patients with nonischemic heart disease is unknown. In addition to its use as an objective end point in the selection of antiarrhythmic drug therapy, invasive electrophysiological testing has advanced our knowledge of the mechanisms of life-threatening ventricular arrhythmias and contributed importantly to the development of new therapies, such as implantable arrhythmia control devices and catheter ablation techniques.
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PMID:Role of invasive electrophysiological testing in the evaluation and treatment of patients at high risk for sudden cardiac death. 172 98

Sudden death is an important facet of the natural history of hypertrophic cardiomyopathy. Issues related to the nature and etiology of sudden death and the prospective identification of those patients at increased risk have been the subject of intense study, and consequently, our concepts and knowledge have continued to evolve. Occurrence of sudden death has been reported to be about 2-3% per year in a hospital-based referral population and, although described in most age groups, is most common in older children and young adults. The typical profile is that of a young asymptomatic patient with substantially increased left ventricular wall thickness who dies while performing sedentary or modest physical activities; however, a substantial minority die suddenly during or just after severe exertion, including those participating in competitive athletics. Other risk factors that have been identified in patients with hypertrophic cardiomyopathy include nonsustained ventricular tachycardia on ambulatory electrocardiogram, a strong family history of sudden death, and prior occurrence of syncope (or cardiac arrest). Electrophysiological studies have shown that most patients judged at increased risk for sudden death have sinoatrial or His-Purkinje conduction disease or inducible supraventricular or ventricular tachycardia; inducibility of a sustained ventricular arrhythmia is associated with prior occurrence of syncope or cardiac arrest. Hemodynamic and electrophysiological studies in patients with hypertrophic cardiomyopathy have demonstrated several potential mechanisms for cardiac arrest or sudden death, including atrial arrhythmias associated with hypotension, bradyarrhythmias, and ventricular tachyarrhythmias, all of which can be exacerbated in the presence of left ventricular outflow tract obstruction or myocardial ischemia.
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PMID:Sudden cardiac death in hypertrophic cardiomyopathy. 172 6

One patient with chronic exertional angina, not significant electrocardiographic signs of myocardial ischemia at exercise stress test and recent onset of angina at rest underwent coronary arteriography. A second one with known severe aortic stenosis underwent cardiac catheterization and coronary arteriography because of effort chest pain and syncope. A single coronary artery originating respectively from the right and from the left sinus of Valsalva but without significant coronary stenosis was detected in both patients. This entity is a quite uncommon finding of relevant interest if surgical treatment is required and good prognosis if not associated with additional cardiac anomalies.
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PMID:Anomalous coronary arteries: a report of 2 cases of single coronary artery. 175 57


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