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

A 57-year-old woman with acute left leg ischemia due to popliteal artery occlusion and deep T-wave inversion at ECG revealed she had suffered, the day before, from typical chest pain after a confrontational argument; yet, she had not sought medical assistance. Echocardiography showed left ventricular wall motion abnormalities consistent with the diagnosis of emotional stress-induced takotsubo syndrome. Coronary angiography ruled out obstructive atherosclerotic disease and left ventriculography confirmed apical ballooning with evolving thrombosis. Left leg angiography demonstrated diffuse embolisation of the popliteal artery. Ventricular thrombosis is a complication of takotsubo syndrome and has been associated with adverse events supposed to be due to a cardioembolic mechanism, in particular cerebro-vascular accidents. To the best of our knowledge, this is the first direct visualization of systemic cardiogenic embolism in takotsubo syndrome. Physicians should be aware that ventricular thrombosis may be present in the earliest stages of the disease and that emboli dislocation can occur even before wall motion normalization.
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PMID:Systemic embolism in takotsubo syndrome. 1836 70

An aim of the present study was a comparative investigation of a delta-sleep inducing peptide and the drug deltaran on the neural activity of the brain structures involved in emotional processing. Another goal was to analyze the possibility to prevent negative effects of emotional stress on brain ischemia using, along with deltaran, glycine and a delta-sleep inducing peptide. Deltaran and the delta-sleep inducing peptide exert in general similar effect on the burst activity of neurons in the dorsal hippocampus, hypothalamic paraventricular nucleus and ventral anterior thalamic nucleus, inducing amplification of the majority of recorded units. The activation of neuronal activity was seen mostly after the delta-sleep inducing peptide microiontophoresis in the dorsal hippocampus and after the deltaran application in the hypothalamic paraventricular nuclei. The index characterizing blood supply was significantly higher in all rats receiving deltaran as compared to the controls. Animals receiving deltaran survived experimental brain ischemia in 100% cases versus 38% in those not exposed to this drug.
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PMID:[Delta-sleep inducing peptide and the drug deltaran: possible approaches to antistress protection]. 1842 60

Hemoglobin oxygen affinity within the estimated physiological range plays an adaptive antioxidant role during acute cerebral ischemia. This range depends on individual emotional resistance. Brain ischemia induced by common carotid artery occlusion in low resistant Wistar rats increased hemoglobin oxygen affinity by 12% during the acute period. Emotional stress also increased hemoglobin oxygen affinity and determined shifts in this parameter during the development of cerebral ischemia: moderate increase in hemoglobin oxygen affinity (<25%) was followed by further increase in this parameter, while more pronounced shift (>25%) resulted in a significant drop in this parameter due to hemoglobin deoxygenation. Adaptation to stress shifted the upper physiological limit for self-regulation of this process.
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PMID:Effect of emotional stress on hemoglobin oxygen affinity in low resistant animals under normal conditions and during cerebral ischemia. 1864 96

Raynaud's phenomenon, categorized as primary and secondary when occurring isolated or in association with an underlying disease, respectively, is a paroxysmal and recurrent acral ischemia resulting from an abnormal arterial vasospastic response to cold or emotional stress. The key issue in the pathogenesis of Raynaud's phenomenon is presumed to be a dysregulation in the mechanisms of vascular motility resulting in an imbalance between vasodilatation and vasoconstriction. Homocysteine, a non-protein forming sulphured amino acid proposed as an independent risk factor for atherothrombosis in the general population, clearly demonstrated to produce vascular damage through mechanisms also including endothelial injury and modifications in circulating mediators of vasomotion. The rationale for homocysteine involvement in the pathogenesis of Raynaud's phenomenon led some authors to investigate the possible association between mild hyperhomocysteinemia and such a vascular disturbance, particularly in the course of connective tissue disease. Here we review data regarding this putative association and the supposed mechanisms involved, also discussing the emblematic case of a patient with new-onset severe Raynaud's phenomenon and markedly elevated homocysteinemia.
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PMID:Homocysteine and Raynaud's phenomenon: a review. 1968 31

Emotional stress aggravates the course of brain ischemia that has developed in the presence of the former. The investigation studied the functional state of parietooccipital leptomeningeal anastomoses by vital biomicroscopy, as well as the linear blood flow velocity in the a. cerebri media and a. basilaris by high-frequency (38.5 MHz) Doppler ultrasonography before and after occlusion of the common carotid artery in normal (control) Wistar rats and ones that had experienced 18-hour aggressively conflict emotional stress and that were sensitive to the latter. Hemodynamic differences were found in the rats having a varying sensitivity to the used model of cerebral ischemia. Inadequate collateral blood supply along the circle of Willis was shown when this model of brain ischemia was used in the control animals. It was ascertained that in emotional stress, blood flow considerably reduced in the a. basilaris; the contiguous blood supply area displayed evolving brain edema that compressed leptomeningeal anastomoses and prevented the formation of collateral circulation, followed by occlusion of the common carotid arteries. With this, unilateral occlusion was followed by a short-term reduction in systemic blood pressure (BP) that was not seen in the controls and bilateral occlusion was by the development of collapse. Cerebral blood flow became dependent of systemic BP. The obtained experimental data suggest that it is expedient to include antistressor agents into therapy for chronic cerebrovascular diseases. This is particularly relevant to patients with occlusive carotid artery lesion and Willis circle anomalies since emotional stress may be fatal to them.
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PMID:[Hemodynamic mechanisms of negative impact of emotional stress on the development of cerebral ischemia in stressor load-sensitive rats]. 1991 10

The present study was designed to assess the value of the presenting symptom of "typical" anginal pain, "atypical/nonanginal" pain, or the lack of chest pain in predicting the presence of inducible myocardial ischemia using cardiac stress testing in emergency department patients being evaluated for possible acute coronary syndrome. We performed a retrospective observational study of adult patients who were evaluated for acute coronary syndrome in an emergency department chest pain unit. The presenting symptoms were obtained from a structured questionnaire administered before stress testing. Patient chest pain was categorized according to the presence of substernal chest pain or discomfort that was provoked by exertion or emotional stress and was relieved by rest and/or nitroglycerin. Chest pain was classified as "typical" angina if all 3 descriptors were present and "atypical" or "nonanginal" if <3 descriptors were present. All patients underwent serial biomarker and cardiac stress testing before discharge. A total of 2,525 patients met the eligibility criteria. Inducible ischemia on stress testing was found in 33 (14%, 95% confidence interval 10% to 19%) of the 231 patients who had typical anginal pain, 238 (11%, 95% confidence interval 10% to 13%) of the 2,140 patients presenting with atypical/nonanginal chest pain, and 25 (16%, 95% confidence interval 11% to 22%) of the 153 patients who had no complaint of chest pain on presentation. Compared to patients with atypical or no chest pain, patients with typical chest pain were not significantly more likely to have inducible ischemia on stress testing (likelihood ratio +1.25, 95% confidence interval 0.89 to 1.78). In conclusion, in our study, the patients who presented with "typical" angina were no more likely to have inducible myocardial ischemia on stress testing than patients with other presenting symptoms.
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PMID:Comparison of frequency of inducible myocardial ischemia in patients presenting to emergency department with typical versus atypical or nonanginal chest pain. 2049 62

Patients presenting with acute chest pain and suspected acute coronary syndrome (ACS) who have nonobstructive coronary disease on angiography, but new regional wall motion abnormalities are often diagnosed with takotsubo cardiomyopathy (TTC). The cause of TTC is often physical or emotional stress, and this clinical syndrome occurs more often in women than men. When hemodynamically significant mitral regurgitation (MR) accompanies TTC, the mechanism must be carefully elucidated, as systolic anterior motion (SAM) of the mitral valve can cause significant MR and left ventricular outflow tract (LVOT) obstruction. These patients can be conservatively managed, with SAM-associated MR and LVOT obstruction resolving with medical therapy as TTC-associated left ventricular (LV) dysfunction resolves, as opposed to true ACS where further intervention for MR is often necessary. This case report describes 2 cases of TTC presenting with severe MR, who were initially thought to have ACS-associated MR caused by ischemia, but on further echocardiographic interrogation were found to have SAM-associated MR which resolved along with resolution of LV wall motion abnormalities on medical therapy by follow-up echocardiography.
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PMID:Acute mitral regurgitation in suspected acute coronary syndrome: what is the cause? 2402 68

Raynaud's syndrome (RS) is characterized by episodic digital ischemia induced by cold or emotional stress. Pathophysiologic mechanisms include temporary vasospasm and fixed digital artery obstruction. A number of pharmacologic and invasive therapies have been studied to treat RS symptoms; however, there are no specific treatments that are currently approved by the U.S. Food and Drug Administration specifically for RS. Of the available pharmacologic agents, calcium-channel blockers remain the preferred initial treatment for vasospastic RS, although many vasodilators have been studied and found to be efficacious. Vasodilators are less effective in treating digital artery obstruction, and no treatments have been found to be universally beneficial, although the phosphodiesterase V inhibitors have been gaining in popularity. Invasive therapies may have a role in selective cases. In this review, the current evidence of treatment for RS is summarized.
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PMID:Current medical and surgical management of Raynaud's syndrome. 2361 25

Coronary artery disease is the major cause of mortality and morbidity in the industrialized countries; in the United States of America and in Europe, it is responsible for one of every six deaths per year. In the setting of ischemic heart disease, angina pectoris and chest pain, in particular, are the major causes of emergency department accesses. Angina pectoris is a clinical syndrome characterized by discomfort typically in the chest, neck, chin and left arm induced by physical exertion, emotional stress and cold and is relieved by rest or by taking of nitrates. The main targets of treatment of angina pectoris are to improve quality of life by reducing the frequency and the severity of symptoms, to increase functional capacity and to improve prognosis. Ranolazine is a recent antianginal drug with unique methods of action. It was approved by the US Food and Drug Administration in 2006 as add-on therapy in patients symptomatic for stable angina. With the inhibition of the late sodium current, Ranolazine protects against ion deregulation, prevents cellular calcium overload and the subsequent increase in diastolic tension without impacting heart rate and blood pressure. Short term clinical trials and patent research show that add on therapy with Ranolazine in patients with chronic stable angina significantly improves exercise duration, exercise time to angina and reduces the use of nitro glycerine. Long term clinical trials showed no significant differences in the rate of cardiovascular death and myocardial infarction in patients with non-ST segment elevation acute coronary syndromes but a reduction in terms of recurrent ischemia. Ranolazine is generally well tolerated and even if it increases the duration of QTc interval it is not associated with atrial and ventricular arrhythmias. Therefore Ranolazine represents a good therapeutic approach in patients with chronic stable angina still symptomatic, while on optimal anti-ischemic therapy, or intolerant to traditional anti-ischemic drugs.
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PMID:Ranolazine: effects on ischemic heart. 2396 14

Transient global amnesia (TGA) is a sudden and severe anterograde memory disturbance accompanied by various degrees of retrograde amnesia and sometimes executive dysfunction. TGA affects elderly individuals and men and women equally. During the episode, patients cannot recall novel episodic information and therefore repeatedly ask the same questions. They are not fully oriented to space and time. Diagnostic criteria first established in 1985, and elaborated in 1990, demand that there is no clouding of consciousness, other impairments of cognition, or a history of epilepsy or head trauma. An episode of TGA resolves within 24 h leaving a memory gap for the length of the attack. While in rare cases TGA might happen repeatedly, it mostly occurs as a single attack. TGA is considered a benign disorder as memory deficits resolve completely and do not lead to long-term sequelae. In up to 90% of reported TGA cases, a precipitating event - mainly described as physical or emotional stress - is present. The cause of TGA has been a matter of long-standing debate among researchers. In search of an answer, several possible causes (ischemia, migraine, epileptic seizures, or, more recently, a disturbance of venous hemodynamics) have been hypothesized. However, to date there is no scientific proof of any of these mechanisms. By using diffusion-weighted MRI 24-48 h after a TGA episode, small dot-like lesions have been detected in the hippocampus. This has led to the implication that the selective vulnerability of CA1 neurons to metabolic stress might play a role in the pathophysiology of TGA.
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PMID:Transient global amnesia. 2477 37


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