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)

Hypertrophic cardiomyopathy is the most common cause of sudden death in young individuals who are otherwise healthy. Risk of sudden death is highest in patients who are between 14 and 35 years old. Several mechanisms are involved in sudden death: ventricular arrhythmias, supraventricular arrhythmias leading to cardiac collapse, bradycardias and severe ischemia. Many studies have analyzed how to identify high risk patients. The factors that best identify high risk patients are: previous history of sudden death or syncope, induction in adults of sustained ventricular arrhythmias, the presence of non-sustained ventricular tachycardia in symptomatic patients, the presence of ischemia associated with hypotension in children, the presence of mutations in the beta-myosin heavy chain together with a family history of sudden death and a poor left ventricular ejection fraction. Risk stratification should be done on an individualized basis. In those patients in whom a high risk for sudden arrhythmic death is suspected, the only current effective treatment is the implantable defibrillator.
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PMID:[Sudden death in hypertrophic myocardiopathy]. 992 51

Symptomatic coronary artery fistulas (CAF) are associated with significant morbidity and mortality. With the advent of high-resolution 2-dimensional and color Doppler echocardiography, the detection rate of clinically silent CAF has increased, but their clinical significance and outcome have not been defined. The clinical, echocardiographic, electrocardiographic, and angiographic findings and documented follow-up of 31 patients with an echocardiographic finding of a clinically silent coronary artery fistula from 1986 to 1997 were analyzed. Mean age at diagnosis was 7.2+/-8.4 years. Indications for echocardiography were murmur (n = 23), congenital heart disease (n = 2), cardiomegaly (n = 2), chest pain (n = 1), stridor (n = 1), syncope (n = 1), and chest trauma (n = 1). CAF were detected with color Doppler flow mapping in all patients. The origin of the fistula was from the left coronary artery system (n = 27), right coronary artery system (n = 3), and bilateral (n = 1). The exit sites were the pulmonary artery (n = 18), right ventricle (n = 8), right atrium (n = 2), and left ventricle (n = 3). Global and regional left ventricular function were normal in all patients at presentation and follow-up. Spontaneous closure of the fistula was documented in 7 patients (23%) at mean follow-up of 2.6+/-2.0 years. In 23 patients the fistula persisted without intervention. All patients remained asymptomatic, without adverse clinical events or evidence of ischemia at a mean age at follow-up of 9.3+/-9.1 years (range 4 months to 42.0). Based on this experience, there is no evidence that clinically silent CAF diagnosed incidentally by color Doppler echocardiography are associated with adverse clinical outcome in childhood and adolescence. Conservative management with continued follow-up of these patients appears to be appropriate.
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PMID:Prognostic significance of clinically silent coronary artery fistulas. 1007 33

We present an elderly patient who had syncope, with known coronary artery disease and a conduction abnormality. Because of a possible vasovagal reaction, the patient underwent a tilt table test prior to evaluation of ischemia or her LV function. During the tilt table test on isoproterenol, the patient developed ventricular fibrillation which was corrected immediately by cardioversion. Subsequently, the patient was found to have significant coronary artery disease which was treated with stenting and angioplasty. After treatment, there were no inducible arrhythmias on full dose isoproterenol. This case reports a significant complication that may occur when tilt table testing with isoproterenol and ischemia.
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PMID:Significant complications can occur with ischemic heart disease and tilt table testing. 1023 24

Identification of patients with acute cardiac ischemia (ACI) remains challenging. The object of this study was to examine the role of clinical findings in the diagnosis/triage of emergency department (ED) patients with symptoms suggestive of ACI. The study was designed as a secondary data analysis of a multicenter prospective controlled clinical trial. It was set in 10 midwest, southeast, and northeast U.S. hospitals, and 10,689 patients with chest pain or other symptoms suggesting ACI presenting from May 1993 to December 1993, participated. The results indicated that ACI patients were more likely to have chest pain as a chief complaint or presenting symptom (P = 0.001). The presenting symptom of nausea was more commonly associated with a final diagnosis of ACI (P = 0.003). Shortness of breath as the chief complaint and presenting symptoms of abdominal pain, nausea, dizziness, and fainting were less frequent among patients with a final diagnosis of ACI (P = 0.001). A past history of diabetes mellitus, myocardial infarction, or angina pectoris was more frequently associated with a final diagnosis of ACI (P = 0.001). A lower pulse rate in patients with a final diagnosis of ACI (P = 0.001) was not considered clinically significant. Median first and highest systolic blood pressures (SBPs) were higher, median lowest SBPs were lower, median diastolic blood pressure of the lowest SBPs were lower, and initial and highest pulse pressures were wider in patients with a final diagnosis of ACl (P = 0.001). On arrival, these blood pressure variables in AMI patients, subsequently classified as Killip class 4, were above the threshold for this classification. Rales were more commonly present in patients with a final diagnosis of ACI (P = 0.001). All primary ST-segment abnormalities, Q waves, and T-wave abnormalities, except T-wave flattening, were seen more frequently in patients with a final diagnosis ACI (P = 0.001). Normal ECGs were more frequently associated with a non-ACI final diagnosis, yet 20% of AMI patients and 37% of Unstable Angina Pectoris (UAP) patients had normal ECGs. It can be concluded that certain clinical features can help to identify ED patients with ACI. Initially normal ECGs can be seen in 20% of patients with AMI and 37% of patients with UAP. Patients with ACI can present with "normal" blood pressures and develop cardiogenic shock. Clinical outcome data for ACI patients are presented.
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PMID:Clinical Features of Emergency Department Patients Presenting with Symptoms Suggestive of Acute Cardiac Ischemia: A Multicenter Study. 1075 87

The mechanism underlying cardiac arrest in patients with hypertrophic cardiomyopathy (HC) is intriguing. In the clinical setting, myocardial ischemia has long been incriminated, particularly in the young. Among 274 cardiovascular sudden deaths in the young (< or = 35 years), 19 (7.0%), 14 males and 5 females, median age 23 years, had HC. Familial occurrence of HC was ascertained in 3 (16%). SD occurred on effort in 6 (31%). Previous syncope occurred in 5 and palpitations in 3. Basal electrocardiogram (ECG) was abnormal in 7 of 8 available cases. Hypertrophy was septal asymmetric in 14. Gross examination showed large isolated or multiple septal scars in 11 (58%); at histomorphometry, the mean percent area of fibrosis of the septal myocardium was 18.6 +/- 6. Four showed a deep intramyocardial course of the left anterior descending coronary artery. At histology, myocardial disarray involved 30 +/- 16% of the septal myocardium; evidence of acute-subacute myocardial necrosis was present in 14 (74%), 1 of them with a regional acute myocardial infarction. By comparing hearts with (n = 11) and without (n = 8) areas of scar-type fibrosis, we found a statistically significant difference in terms of age (25.5 +/- 5.4 v 15.5 +/- 12.4 years, P = .04), septal thickness (25.4 +/- 5.4 v 15.4 +/- 4.9 mm, P < .001), percent increase of septal thickness versus normal value for age and sex (46.2 +/- 15 v 25.2 +/- 13.6%, P < .01) and mean score of small vessel disease (1.7 +/- 0.4 v 1.2 +/- 0.4, P = .04). Linear regression analysis showed a positive correlation of percent area of replacement fibrosis with septal thickness (P = .01) and with mean score of small vessel disease (P < .01). In conclusion, our pathologic findings of ischemic damage, either acute-subacute or in the form of fibrotic scars, support the clinical evidence that ischemia occurs in the natural history of HC and may contribute to life-threatening electrical instability.
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PMID:Hypertrophic cardiomyopathy and sudden death in the young: pathologic evidence of myocardial ischemia. 1098 48

A 78-year-old right-handed man with idiopathic orthostatic hypotension and a history of Hashimoto's thyroiditis presented over 2 years with recurrent, stereotyped attacks of bilateral limb shaking and metamorphopsia, which were precipitated by standing more than 3 or 4 minutes, or walking a few meters. These symptoms would resolve upon squatting or lying down and did not occur spontaneously at rest. He did not lose consciousness during the attacks. Speech, power, and sensation were preserved during these attacks. He had no history of seizures or habit of smoking. On examination, his supine blood pressure was 110/60 mmHg, and 62/27 mmHg on standing, with the pulse rate being 61/min and 66/min, respectively. Although he showed orthostatic hypotension, he did not complain of fainting or lightheadedness on standing alone. Magnetic resonance imaging of the brain revealed mild periventricular white matter changes and multiple small ischemic lesions bilaterally in the cerebral deep white matter. An electroencephalogram (EEG) showed mild, generalized slowing of nonspecific feature. EEG monitoring during a limb shaking episode showed no epileptiform abnormalities. Cerebral angiogram revealed a moderate degree of stenosis of the left internal carotid and a mild degree of stenosis of the right internal carotid, the right vertebral arteries and the left vertebral arteries. A single-photon emission computed tomography (SPECT) showed a moderate compromise of perfusion of the left internal carotid territory. After managing both hypotension and orthostatic hypotension with antihypotensive medication and levothyroxine sodium, his symptoms dramatically disappeared. Thus, we diagnosed that transient hemodynamic insufficiency due to combination of vascular stenosis and hypotension was the cause of these symptoms. Limb shaking is a well-described presentation of carotid artery occlusive disease and is usually unilateral. Bilateral limb shaking is rare and only 2 cases have been reported. Metamorphopsia is also a rare symptom of vertebrobasilar ischemia. We suggest that bilateral limb shaking correlates with hypoperfusion in the anterior border zones and metamorphopsia with that in the posterior border zones of both hemispheres. Hemodynamic TIA should be considered as a cause of movement disorders affecting four limbs.
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PMID:[Orthostatic hypotension with repeated bilateral limb shaking and metamorphopsia. A case of hemodynamic transient ischemic attacks]. 1108 97

The involvement of nitric oxide synthase (NOS) in ischemia was evaluated by detecting the expression of neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS) by the immunohistochemical method in the rat model of middle cerebral artery (MCA) occlusion. Transient MCA occlusion (2 hours) was induced in 32 male Wistar rats by extracranial insertion of a 3-0 nylon thread through the internal carotid artery into the MCA. Animals were killed at 0, 6, 24, 72, and 168 hours after MCA occlusion (n = 6, 6, 8, 6, and 6, respectively). The brains were fixed with periodate-lysine-paraformaldehyde, frozen, and sectioned. Sections were stained with polyclonal antibody against nNOS, eNOS, and iNOS. Each section was evaluated by microscopic observation (x100). The number of nNOS-positive neurons was 41.6 +/- 5.8 (mean +/- SD) in the control hemisphere. nNOS was upregulated in the ischemic hemisphere (88.3 +/- 18.9), especially in the border zone at 6 hours after MCA occlusion. However, the number decreased to 36.4 +/- 3.6 and 26.3 +/- 7.3 in the ischemic hemisphere after 72 and 168 hours, respectively. eNOS immunoreactivity was present in the endothelium of major vessels at each time point. eNOS was not detected in the microvessels before ischemia, but faint staining was found in the endothelium at 6 hours after MCA occlusion. Immunostaining became more intense thereafter. Faint iNOS immunoreactivity was seen in the microvessels at 6 hours after MCA occlusion. Macrophages in the ischemic core and astrocytes in the border zone showed immunoreactivity to iNOS at 72 and 168 hours after MCA occlusion. Three types of NOS must be related to different stages of ischemic brain damage. nNOS may be neurotoxic in ischemia in the early phase, like iNOS in the late phase. On the other hand, eNOS seemed to be neuroprotective in all stages. These observations suggest the necessity for tailored therapeutic intervention against NOS isoforms at each stage in patients with ischemic stroke.
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PMID:Time course of expression of three nitric oxide synthase isoforms after transient middle cerebral artery occlusion in rats. 1125 30

A young man had two dangerous episodes of transient loss of consciousness during apnea diving in a swimming pool. Medical and neurologic examination results were normal. Standard autonomic test results (including heart rate variability, baroreflex sensitivity, tilt-table test, and Valsalva ratio) were unremarkable, with the exception of an increased blood pressure decrease during early phase II of the Valsalva maneuver. Syncope with arrhythmic myoclonic jerks could be evoked by a strong straining maneuver. Simultaneous physiologic recordings showed extreme blood pressure and cerebral blood flow velocity decreases and electroencephalographic slowing during syncope. The electrocardiogram showed a continuous sinus rhythm with a progressive tachycardia. The authors' findings were not compatible with baroreflex failure or vasovagal mechanisms (Bezold-Jarisch reflex activation) as the underlying causes. The authors concluded that mechanical factors (strong reduction of blood reflux to the heart) in combination with a reduced threshold of the brain for developing ischemia-related arrhythmic myoclonic jerks were responsible for Valsalva-induced syncope in the patient.
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PMID:Valsalva-induced syncope during apnea diving. 1132 90

We report the case of a 90-year-old man with syncope, arrhythmia, cardiac ischemia, and neurologic deficit after undergoing spinal epidural injection for control of pain related to post-herpetic neuralgia. The diagnosis of arterial gas embolus was made after air was identified in the left ventricle of the heart on an abdominal computed tomographic scan. Emergency physicians should consider and rapidly diagnose this rare but potentially fatal complication of spinal epidural puncture.
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PMID:Documented arterial gas embolism after spinal epidural injection. 1167 75

Bow hunter stroke, which is characterized by transient vertebrobasilar ischemia brought on by head turning, is an unusual condition usually caused by structural abnormalities at the craniocervical junction. The authors present a case in which compression of the left vertebral artery (VA) at the C4-5 level was caused by a laterally herniated intervertebral disc. A 56-year-old man presented with a 6-month history of dizziness and syncope when he turned his head 45 degrees or more to the left. Transcranial Doppler (TCD) ultrasonography demonstrated decreased blood flow through the left VA, and angiography revealed an occlusion of the left VA at the C4-5 level, both when the patient turned his head to the left. Via an anterior cervical approach, the VA canal was unroofed through the transverse foramina to decompress the left VA at C4-5; intraoperatively, the left VA was found to be compressed by a laterally herniated cervical disc fragment. To the best of the authors' knowledge this is the first report of a laterally herniated cervical disc causing bow hunter stroke. The use of TCD may be of value in the diagnosis and management of the disorder, and herniated cervical disc must be included in the roster of potential causes for this rare disease.
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PMID:Bow hunter stroke caused by cervical disc herniation. Case report. 1179 20


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