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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spasm of coronary arteries can cause chest pain indistinguishable from classic angina pectoris in patients without atherosclerosis of these vessels or recognizable heart disease. Associated electrocardiographic changes usually correspond to the coronary artery affected and disappear when the attack of pain ends. Sublingual nitrates are excellent agents for the control of the episodic anginal symptoms. There have been scattered reports of myocardial infarction occurring in patients with normal coronary arteries; a role of arterial spasm in these cases in speculative.
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PMID:Myocardial ischemia from coronary arterial spasm. 0 82

Although both sudden death and acute myocardial infarction are almost always associated with long-standing obstructive coronary artery disease, both may originate in the myocardium. Spasm has been suggested as a factor contributing to sudden death. Not all persons dying of acute myocardial infarction have narrowed coronary arteries, nor do all persons with obstructed arteries die of heart disease. The first phase of acute myocardial infarction may well involve myocardial necrosis, followed by stasis and collapse of collateral circulation and occasionally by coronary occlusion.
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PMID:Sudden death and acute myocardial infarction: clues to differences in pathophysiology. 70 7

A case of Prinzmetal angina refractory to classic medical treatment, in which the angina attacks were suppressed with the administration qf reserpine is presented. The possible physiopathologic mecanisms of this entity are reviewed. The possibility of coronary spasm due to an alteration in the regulation of the coronary arterial tone from an autonomic.nervous system illness is established, an abnormal coronary vascular reactivity is also reviewed. It is emphasized that the Prinzmetal angina is an original entity, idfferent from the coronary arteriosclerotic heart disease, which may coexist with it but which cannot be treated in the same way, because its physiopathologic mecanisms are different.
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PMID:[Prinzmetal's angina. Response to the treatment with reserpine. Review of its physiopathological mechanisms]. 88 60

Iliac and femoral arteries previously exposed to percutaneous catheterization were examined by angiography in conjunction with re-catheterization in 44 infants and children, most of them with heart disease. Frequency and extension of thrombotic changes were analysed, as well as the relationship between occurrence of thrombotic complications and age, haematocrit value, catheterization time, and tendency to arterial spasm. Only age and arterial spasm were significant for the occurrence of thrombotic complications. Injury of the intima was considered to be the primary cause of these complications.
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PMID:Angiography of the femoral artery following percutaneous catheterization in infants and children. 98 61

The influence of percutaneous catheterization of the femoral vessels on the arterial peak flow (APF) and the venous emptying rate (VER) of the calves was studied with strain gauge plethysmography in 112 children 2-16 years of age, who underwent arterial (49 cases) or venous catheterization, mostly because of heart disease. The conditions on the catheterized side were compared with those on the other side, and the pre-catheterization values were compared with those obtained after completed catheterization. The catheterization procedure was proved to have no general influence on APF or VER, although it may have an effect in individual patients. APF was not affected at arterial or venous catheterization in children older than 8 years of age. In the younger children, APF was slightly decreased on the catheterized side after arterial as well as venous catheterization. This was considered to be caused by arterial spasm. On the following day APF was normal. A few patients in this age group had a marked reduction in APF caused by intense spasm or thrombotic occlusion after arterial catheterization. These patients will be accounted for separately. VER on the catheterized side was not significantly influenced after venous or arterial catheterization, irrespective of the age of the patients.
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PMID:Percutaneous catheterization of the femoral vessels in children. I. Influence on arterial peak flow and venous emptying rate in the calves. 123 37

The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.
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PMID:High prevalence of coronary artery spasm in survivors of cardiac arrest with no apparent heart disease. 841 43

Twenty-one patients were successfully resuscitated from cardiac arrest. Electrocardiograms (ECG) during cardiac arrest were recorded in 14 patients with ventricular fibrillation in 7, ventricular tachycardia in 4, cardiac standstill in three, Torsade de Points in one and atrial fibrillation with rapid ventricular response in 1. Thirteen patients (group I) had structural heart disease or primary ECG abnormality and 8 patients (group II) had no apparent heart disease. Electrophysiologic study (EPS) was performed in 12 patients of group I and 5 of group II. In group I, ventricular tachycardia was induced in 7, and His-ventricular conduction disturbance was demonstrated in 2, and 2 patients with Wolff-Parkinson-White (WPW) syndrome had an effective refractory period of the antegrade accessory pathway less than 250 msec. No patients in group II showed abnormal EPS findings. Spasm provocation test was performed in 8 patients (2 in group I and 6 in group II). Coronary spasm was induced in 5 patients (1 in group I and 4 in group II). Two patients in group II had positive results of upright-tilt testing. During the follow-up period, 2 patients died suddenly in group I and 1 patient whose cause of cardiac arrest was unknown had a recurrence of cardiac arrest. In group II, all patients whose etiology could be demonstrated by serial examinations had good prognosis. In conclusion, EPS is useful in evaluation of the cause of cardiac arrest especially when patients have structural heart disease, and coronary spasm may be involved in patients with cardiac arrest without apparent heart disease.
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PMID:Role of electrophysiologic testing and coronary spasm provocation test in survivors of cardiac arrest. 157 5

Myocardial perfusion scintigraphy with thallium-201 was performed in 33 subjects (mean age 45 years, range 28-61) with exercise-induced, rate-dependent left bundle branch block (LBBB) in order to assess both the value of Thallium-201 myocardial imaging for the diagnosis of coronary artery disease (CAD) and the pathogenesis (ischaemic or not) of the conduction defect. Of the 33 patients evaluated, 16 had chest pain suggestive of CAD and 17 were asymptomatic. None had a history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 b.min-1. Eighteen patients showed repolarization abnormalities (ST segment depression with deep inverted T waves) compatible with ischaemia, after QRS normalization. Thallium-201 myocardial uptake was normal in 12 subjects; in the remaining 21, reversible Thallium-201 defects were demonstrated in the septum (18 patients), septum and apex (2), and septum and infero-apical wall (1). No patient had irreversible defects and all had normal coronary angiography, with negative ergonovine tests for coronary artery spasm. The patients were followed up for a mean of 43 months (range 16-80). One patient died from sudden death, but no cardiac event occurred in the other patients. In conclusion, exercise Thallium-201 myocardial scintigraphy showed a high prevalence (64%) of reversible perfusion defects in a group of patients with exercise-induced LBBB without any evidence of CAD at angiography or coronary spasm at ergonovine test. Moreover, follow-up showed a relatively low rate of major cardiac events.
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PMID:Assessment of myocardial perfusion with thallium-201 scintigraphy in exercise-induced left bundle branch block: diagnostic value and clinical significance. 164 85

Results of earlier experiments suggested that hamsters with inherited heart disease were at a higher risk of succumbing to stress during the vasospastic, lesion-forming period of their lives rather than later when the process of congestive heart failure had begun. To test this hypothesis, we stressed cardiomyopathic hamsters (CMH) whose ages differed by about 3 months; the younger of the two groups of stressed hamsters was in the vasospastic phase of the disease. The stressor was cold immobilization in which stressor intensity was manipulated using two durations of cold exposure. Log rank survival curves revealed no difference in mortality with the more intense stressor. However, significantly fewer of the older hamsters succumbed to the less intense stressor (46% as compared with 85% of the younger CMHs). Examination of the hearts in the experiment where mortality rate was the same for both groups revealed evidence of cardiac dilatation, indicative of heart failure, only in the older hamsters following stress. Since the younger hamsters did not show these changes and since they, but not the older animals, have coronary microvascular spasm and an increased susceptibility to stress, it would appear that the process of coronary vasospasm should be viewed as an independent and additional risk factor in determining the consequences of stress. Because of the effects of stress in the younger cardiomyopathic hamster, we believe that a neural link--which can be activated by stress--may be involved in the pathogenetic process of coronary vasospasm.
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PMID:Hamsters with coronary vasospasm are at increased risk from stress. 188 13

A 52 year old patient presenting with spontaneous anginal chest pain for 4 days was admitted to hospital for a more intense and prolonged chest pain associated with signs of left ventricular failure (gallop, pulmonary crepitations, hypoxemia). Coronary angiography showed marked septal hypokinesia and spontaneous localised spasm of the left anterior descending and marginal arteries with a variable degree of luminal narrowing of the other segments of these two arteries and of the right coronary artery. These changes regressed after intracoronary injection of molsidomine. The signs of left ventricular failure disappeared in 48 hours. The wall motion abnormality, monitored by 2D echocardiography, regressed slowly over 3 days. On the other hand, the electrocardiogram, which showed anterior wall subendocardial ischaemia with prolongation of the QTc interval during the spasm, remained abnormal for a long time. Therefore, in the absence of organic heart disease, coronary spasms associated with vasoconstriction can induce a sufficiently severe and durable alteration of left ventricular function to create clinical signs of cardiac failure and profound and prolonged ST-T wave changes on the electrocardiogram.
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PMID:[Coronary spasm and diffuse coronary vasoconstriction responsible for transient left ventricular insufficiency]. 192 21


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