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Infarction presentation

Pituitary apoplexy (hemorrhagic infarction presenting with sudden severe headache, often followed by pituitary... [Pg.487]

Small deep infarcts in the subcortical white matter of the corona radiata may result from small vessel disease affecting the long medullary perforating arteries extending down from cortical branches of the middle cerebral artery or from embolism. Such centrum semiovale infarcts present as either a lacunar syndrome or, occasionally, as a partial anterior cirulation syndrome with cortical features (Read et al. 1998 Lammie and Wardlaw 1999). They are not, however, easy to classify or to distinguish from border zone infarcts deeper in the white matter lying between the arterial territories of the deep perforators from the first part of the middle cerebral artery and the superficial medullary perforators. [Pg.118]

Sagie A, Sclarovsky S, Strasberg B et al. Acute anterior wall myocardial infarction presenting with positive T waves and without ST segment shift. Electrocardiographic features and angiographic correlation. Chest 1989 95(6) 1211-15. [Pg.321]

O Neill WW, on behalf of the COOL-MI Investigators. Cooling as an adjunct to primary PCI for acute myocardial infarction. Presented at Transcatheter Cardiovascular Therapeutics 2003, Washington, DC, September 2003. [Pg.112]

Widimsky P, Groch L, Zelizko M, Aschermann M, Bednar F, Suryapra-nata H. Multicentre randomized trial comparing transport to primary angioplasty vs. immediate thrombolysis vs. combined strategy for patients with acute myocardial infarction presenting to a community... [Pg.205]

Celik A. ST elevation myocardial infarction presenting after use of pseudoephedrine. Cardiovasc Toxicol 2009 9(2) 103-4. [Pg.329]

Other contraindications for die anticholinergics include tachyarrhythmias, myocardial infarction, and congestive heart failure (unless bradycardia is present). [Pg.230]

FIGURE 4.5 A 72-year-old man with medical history remarkable for hypertension and dyslipidemia presented with posterior circulation infarct (a). CTA and posterior circulation angiography (left vertebral artery injection) performed demonstrated severe mid-basilar artery stenosis (b and c). Left vertebral artery injection demonstrated near-complete reversal of the stenosis after a drug-eluting balloon expandable stent (Cypher, Cordis Johnson Johnson) was deployed (d). [Pg.88]

FIGURE 6.4 (a) Seventy-eight-year-old woman presenting with new onset vertigo and gait unsteadiness. Hypoattenuation of the left cerebellar hemisphere consistent with infarction, (b) Postoperative CT after suboccipital craniectomy and partial resection of the left cerebellar hemisphere. [Pg.131]

In stroke patients presenting to the ED, the first goal of treatment is immediate cardiac and respiratory stabilization. The systemic blood pressure is most often elevated in the setting of an acute stroke as the result of a catecholamine surge, and if the patient is hypotensive, the clinician should consider a concomitant cardiac process, such as myocardial infarction (MI), congestive heart failure (CHF), or pulmonary embolism (PE). [Pg.164]

Cardioembolism Cardioembolism accounts for approximately 30% of all stroke and 25-30% of strokes in the young (age <45 years)." AF accounts for a large proportion of these strokes (15-25%). Symptoms may be suggestive, but they are not diagnostic. Repetitive, stereotyped, transient ischemic attacks (TIAs) are unusual in embolic stroke. The classic presentation for cardioembolism is the sudden onset of maximal symptoms. The size of the embolic material determines, in part, the course of the embolic material. Small emboli can cause retinal ischemic or lacunar symptoms. Posterior cerebral artery territory infarcts, in particular, are often due to cardiac embolism. This predilection is not completely consistent across the various cardiac structural abnormalities that predispose to stroke, and may be due to patterns of blood flow associated with specific cardiac pathologies. [Pg.203]

Among 27 prospective and case-control studies, 16 reported inverse associations between some carotenoids and CVDs, taking plasma or serum concentration as carotenoid biomarkers (11 of 16 studies), dietary intake (5 of 16 studies), or adipose tissue level (1 of 16 studies). With regard to the findings from the studies based on CVD risk, only two of seven presented significant inverse associations of carotenoids, particularly lycopene and P-carotene, whereas five studies of nine showed inverse correlations between myocardial infarcts and lycopene and/or P-carotene the others presented no associations. ... [Pg.133]

Some prospective and case-control studies also investigated the relationship of carotenoids and the evolution of CCA-IMT. Although the EVA study showed no association between total carotenoids and IMT, others like the ARIC study, the Los Angeles Atherosclerosis Study, " and the Kuopio Ischaemic Heart Disease Risk Factor Study demonstrated the protective role of isolated carotenoids such as lycopene, lutein, zeaxanthin, and P-cryptoxanthin on IMT. Thus, findings from prospective and case-control studies have suggested that some carotenoids such as lycopene and P-carotene may present protective effects against CVD and particularly myocardial infarcts and intima media thickness, a marker of atherosclerosis. [Pg.133]

In contrast to the deleterious effects of arginine described by Buisson, L-arginine was shown to decrease infarct size caused by middle cerebral artery occlusion in spontaneously hypertensive rats. L-Arginine is a precursor for NO synthesis by NOS. The authors attributed the protection to dilation of cerebral blood vessels by NO (Morikawa et 1992). These examples illustrate the difficulty that the NO villain/protector paradox presents to us. [Pg.267]

Short-Term Risk of Death or Nonfatal Myocardial Infarction in Patients Presenting With Unstable Angina... [Pg.22]

Risk-stratification of the patient with NSTE ACS is more complex, as in-hospital outcomes for this group of patients varies with reported rates of death of 0% to 12%, reinfarction rates of 0% to 3%, and recurrent severe ischemia rates of 5% to 20%.12 Not all patients presenting with suspected NSTE ACS will even have CAD. Some will eventually be diagnosed with non-ischemic chest discomfort. In general, among NSTE patients, those with ST-segment depression (Fig. 5-1) and/or elevated troponin and/or CK-MB are at higher risk of death or recurrent infarction. [Pg.89]

STE ACS, class I recommendation within the first 24 hours after hospital presentation for patients with anterior wall infarction, clinical signs of heart failure and those with EF less than 40% in the absence of contraindications, class I la recommendation for all other patients in the absence of contraindications. [Pg.95]

Etiologies of VT are presented in Table 6-10. The incidence of VT is variable, depending on underlying comorbidities. Up to 20% of patients who experience acute myocardial infarction... [Pg.125]

MN is a 48-year-old man with a history of hypertension and smoking who presents to the clinic for evaluation of his cholesterol. He denies having chest pain or history of myocardial infarction, stroke, or peripheral artery disease. He has no siblings and both parents are alive with no history of CHD. MN says that he smokes about 1 pack of cigarettes per day. He does not exercise on a regular basis. He has been fasting for approximately 11 hours. [Pg.183]

Signs and symptoms Headache, vomiting, stupor, hemiparesis, aphasia, visual disturbances, and seizure transient ischemic attack is a strong predictor for stroke. Behavioral and performance changes may be present in patients with asymptomatic infarction. [Pg.1007]


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Infarct

Infarction

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