Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a 42-year-old man with Brugada syndrome (BRS) mimicking acute coronary syndrome. Chest pain, near-syncope, and electrocardiographic changes were thought initially to be due to ischemia. Cardiac catheterization was performed. The coronary arteries and left ventricular function were normal. Careful review of his electrocardiogram suggested a diagnosis of BRS. BRS may be confused with acute coronary syndrome; early recognition of this syndrome is essential, as implantable cardioverter-defibrillator therapy may be life-saving.
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PMID:Brugada syndrome mimicking acute coronary syndrome. 1614 80

Congenital anomalous origins of the coronary arteries represents a rare but well-described cause of myocardial ischemia and sudden death. Left coronary artery (LCA) arising from the right sinus of Valsalva is a rare congenital coronary anomaly that seems to be commonly associated with sudden death in young trained athletes. The possibility of a coronary artery anomaly should always be considered in young individuals with a history of chest pain or syncope, particularly if the episodes are triggered by exercise. We describe a case of congenital LCA anomaly in an asymptomatic 10-year-old girl with no family history of sudden death; no previous unexplained syncopal episodes or exercise-induced symptoms were reported. She experienced a cardiac arrest while she was resting at school and was not recoverable despite early emergency department admission and intensive prolonged cardiopulmonary resuscitation attempts. Post-mortem pathological findings revealed a single origin from the right sinus of Valsalva for both right and left coronary arteries. The LCA was compressed between the aorta and the pulmonary trunk. Histologic features suggested recent ischemia. Although sudden death can be the first manifestation of this condition, it is important to be particularly aware of prodromic symptoms: exertional dyspnea, chest pain, syncope or dizziness. Recognition during life of this coronary anomaly is mandatory to prevent the risk of sudden death and to plan surgical correction if clinically indicated.
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PMID:Exercise-unrelated sudden death as the first event of anomalous origin of the left coronary artery from the right aortic sinus. 1624 3

Myocardial bridging (MB) is a rare coronary anomaly in children that is typically associated with hypertrophic cardiomyopathy or left ventricular hypertrophy. Several reports, mainly in adults, have suggested an association between MB and sudden death or ischemia without other cardiac abnormalities. In this report, we describe an 11-year-old girl with syncope and manifestations of cardiac ischemia associated with MB of the middle segment of the left anterior descending artery. The coronary anomaly was not associated with left ventricular hypertrophy. Surgical unroofing of the affected coronary artery segment resulted in complete recovery. MB should be included in the differential diagnosis of children presenting with syncope and signs of ischemia even in the absence of ventricular hypertrophy.
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PMID:Symptomatic myocardial bridging in a child without hypertrophic cardiomyopathy. 1639 Sep 19

Symptoms of ipsilateral carotid artery compression secondary to an elongated styloid process or calcified stylohyoid ligament may be seen in Eagle syndrome. The patient will typically experience cervicofacial pain due to stimulation of the arterial nervous plexus. In addition, symptoms directly attributable to compression of the carotid artery may be seen, including visual symptoms and syncope. We report here the case of a patient who developed symptoms consistent with left hemispheric ischemia within 15 seconds of turning his head to the left. These symptoms were completely reversible on returning the head to the neutral position. No long-term sequelae were detected clinically or radiographically.
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PMID:Reversible left hemispheric ischemia secondary to carotid compression in Eagle syndrome: surgical and CT angiographic correlation. 1721 44

Cardiac tumors other than myxomas are rare. We report a series of 10 intracavitary polypoid myofibroblastic proliferations in children and young adults emphasizing gross, histologic, and clinical features. There were 6 females and 4 males, with a mean age of 10 years (range 5 wk to 21 y). All lesions were endocardial-based, located in the right atrium (1), right ventricular inflow/tricuspid valve (1), right ventricular outflow (3), mitral valve (3), aortic valve/left coronary sinus (1), and left ventricular free wall (1). Symptoms included shortness of breath or dyspnea (3), syncope (2), chest pain (1), transient ischemic attacks (1), and fever with myalgias (1). All tumors were surgical resections, except 1 tumor that resulted in sudden coronary death and that was diagnosed at autopsy, and 1 tumor that embolized into the coronary artery and was treated by cardiac transplant. Two tumors, present in the aortic and mitral valves, respectively, caused cardiac ischemia. The tumors were polypoid or filiform and histologically resembled inflammatory myofibroblastic tumors of extracardiac sites, with loose spindle cell growth with sparse inflammation. Although there were frequent collagen bundles interspersed among the tumor cells, there were no large areas of dense fibrosis. Surface fibrin was present on the polypoid projections in 7 cases. Symptoms resulted from prolapse into coronary ostia or embolization, but no patient developed metastasis. Long-term follow-up in 2 patients demonstrated no evidence of disease or recurrence. Although metastatic potential was not identified, these tumors may result in serious symptoms, including myocardial infarct, syncope, and sudden death. These cardiac myofibroblastic tumors are readily distinguished from other endocardial-based cardiac tumors, including papillary fibroelastoma and myxoma, which may present clinically in the same manner.
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PMID:Cardiac inflammatory myofibroblastic tumor: a "benign" neoplasm that may result in syncope, myocardial infarction, and sudden death. 1759 79

Approximately 20% of coronary artery anomalies produce sudden death or life-threatening symptoms, including arrhythmias, syncope, and myocardial infarction. The most common clinical symptom of coronary artery anomaly is angina or exertional syncope. Physical examination is usually unrevealing in the absence of myocardial infarction or symptoms of ongoing ischemia. The rapid advent of cardiac computed tomography (CT) technology has made it an important adjunct to the diagnosis of coronary anomalies by angiography. The authors describe the case of a 54-year-old white man who presented with gangrenous toes. He had severe peripheral vascular disease, a femoral-popliteal bypass graft, residual hemiparesis from an ischemic stroke, hypertension, deep vein thrombosis, and a recent myocardial infarction. He underwent a 64-slice cardiac CT angiogram, which showed an interarterial course of the left main coronary artery between the aorta and the pulmonary trunk.
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PMID:Evaluation of anomalous aortic origins of the coronaries by 64-slice cardiac computed tomography. 1793 19

1,4-Dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic acid methyl 6-(5-phenyl-3-pyrazolyloxy)hexyl ester (CV159) exhibits selective blocking of Ca(2+)/calmodulin and inhibits Ca(2+) overloading in living organisms. The effects of this antagonist in mice with hepatic ischemia-reperfusion injury were investigated using electron paramagnetic resonance imaging (EPRI) and ex vivo EPR (x-band EPR) techniques. The EPRI determined that the 3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl half-life in CV159-treated mice was significantly shorter than that in untreated mice and was almost equal to that in the sham group. Both the cytosolic and the mitochondrial superoxide scavenging activities in CV-treated mice were significantly higher than that in untreated mice. Faint staining of the anti-superoxide dismutase antibody and strong staining of anti-inducible nitric oxide synthase antibody were observed in the liver of control group. In contrast to these findings, immunostaining of these antibodies in the liver of CV159-treated mice were reversed compared to control group. Western blotting showed that CV159 contributed to the high superoxide dismutase expression and low expression of inducible nitric oxide synthase. The alanine aminotransferase level in CV159-treated mice significantly decreased in comparison to that observed in the untreated mice. We conclude that CV159 retains its organ-reducing activity against radicals in hepatic reperfusion injury, which is mediated by the inhibition of Ca(2+) overloading.
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PMID:Effect of CV159-Ca(2+)/calmodulin blockade on redox status hepatic ischemia-reperfusion injury in mice evaluated by a newly developed in vivo EPR imaging technique. 1806 26

Patients with acute alcohol intoxication often present with pathological electrocardiographic (ECG) changes. The changes are more frequent and prognostically more significant in chronic alcoholics, in patients with ischaemic heart disease (IHD), in alcohol cardiomyopathy or another organic heart disease, but they can also occur in young and healthy individuals. The typical ECG changes in inebriety are disturbances of heart rate having the nature of electric impulse generation disorder or of impulse conduction pathology. In persons without clinical evidence of heart disease, they are classified as 'holiday heart syndrome'. The most frequent tachyarrhythmia is atrial fibrillation; less frequent but prognostically much more significant is torsades de pointes (TdP) polymorphous ventricular tachycardia. Among bradyarrhythmias, the most significant is alcohol-induced sinus bradycardia which may be manifested by recurrent syncope. The higher the blood alcohol concentration, the higher the occurrence of a significant extension of ECG intervals with possible manifestation of latent conduction disturbance or even sudden cardiac death. Apart from heart rate disturbances, ECG picture very often shows non-specific repolarisation changes. Ischaemia, which is mostly asymptomatic in the form of silent myocardial ischaemia, is worsened in alcohol-intoxicated IHD patients. The resulting ECG may be to a large extent influenced by states which often associate with inebriety, such as hypothermia, hypoglycaemia or electrolyte imbalance. ECG changes similar to those due to acute alcohol intoxication are also present in acute abstinence syndrome, especially in delirium tremens. There is convincing evidence that not only chronic alcoholism, but also single episodes of excessive alcohol consumption are associated with increased cardiovascular mortality.
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PMID:[ECG changes in alcoholic intoxication]. 1863 Jun 9

Hypertrophic cardiomyopathy (HCM) is classified as a primary cardiomyopathy. HCM is a clinically heterogeneous but relatively common autosomal dominant genetic heart disease that probably is the most frequently occurring cardiomyopathy. HCM is characterized morphologically and defined by a hypertrophied, nondilated left ventriculum (LV) in the absence of another systemic or cardiac disease that is capable of producing the magnitude of wall thickening evident (e.g., systemic hypertension, aortic valve stenosis). Most HCM patients have the propensity to develop dynamic obstruction to LV outflow under resting or physiologically provocable conditions, produced by systolic anterior motion of the mitral valve with ventricular septal contact. The phenotypic features of HCM may develop at any age from infancy to adulthood, and are characterized by a great heterogeneity in the extent, magnitude, and distribution of left ventricular hypertrophy. Hypertrophic obstructive cardiomyopathy (HOCM) often leads to heart failure, severe ischemia, severe symptoms and death. Determination of the exact site of the hypertrophy and of the obstruction of the left ventricular outflow tract, in asymmetric septal hypertrophy, establishes which is the best treatment strategy. In the treatment of HOCM, drug therapy with negatively inotropic drugs, percutaneous transluminal septal myocardial ablation by alcohol-induced septal branch occlusion, surgical myectomy and DDD pacemaker therapy are considered the therapeutical options. We present a case of an obstructive hypertrophic cardiomyopathy in an 84-year-old Italian woman with a left ventricular outflow tract (LVOT) peak gradient with the Valsalva maneuver of 188 mm Hg and with a history of first episode of syncope.
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PMID:Revelation of an obstructive hypertrophic cardiomyopathy in an elderly patient. 1918 3

It has been widely outlined by our group the possibility that a sufferance of the inner ear can take place as a consequence of hemodynamic imbalance which could affect young and healthy people and recognize a merely functional origin. As reported in previous papers, an altered reaction of the autonomic nervous system could actually jeopardize the labyrinthine perfusion even in absence of other damages. From this standpoint, the hypothesis that a hyperactivity of the vagal response to an acute sympathetic drive may result in an inner ear sufferance deserves to be explored. A mechanism which appears to fit to this model is represented by the Bezold-Jarisch reflex (BJR), which is considered to be responsible for vasovagal syncope and is characterized by a dynamic reasonably compatible with our findings. According to these premises, especially considering that the inner ear has a less active protective mechanism against ischemia as compared to brain, in predisposed subjects tinnitus, when considered as an initial symptom of inner ear hypoperfusion, can represent a warning able to prevent the lack of consciousness related to the syncope.
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PMID:Tinnitus as a warning for preventing vasovagal syncope. 1944 64


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