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Electrocardiograph mortalities

Thierstein ST, Hanigan JJ, Faaul MD, et al. 1960. Trichloroethylene anesthesia in obstetrics Report of 10,000 cases, with fetal mortality and electrocardiographic data. Obstet Gynecol 15 560-565. [Pg.293]

On the basis of the information derived from the GUSTO trial, Hathaway (1998a,b) reported a nomogram, for the quantification of involved area and to stratify the 30-day mortality risk, on the basis of the ST-segment abnormalities (elevation or depression) at the time of hospital admission (between 1 and 4 h from the onset of pain). Also, electrocardiographic (QRS complex width) and clinical (age, risk factors, Killip class, etc.) data were included (Table 8.4). From a practical point of view, an ST-segment deviation (upward or downward deviation)above 15 mm is supposed to indicate the existence of a large area of myocardium at risk (see Risk stratification ) (p. 257). [Pg.224]

Table 8.4 Nomogram for estimating 30-day mortality from initial clinical and electrocardiographic variables (Hathaway et al. JAMA 1998). Table 8.4 Nomogram for estimating 30-day mortality from initial clinical and electrocardiographic variables (Hathaway et al. JAMA 1998).
Cardiac ruptures are much less frequent with the currently available therapies. However, they may still be found in 2-3% of Q-wave infarctions and are still an important cause of mortality in the acute phase (Figueras et al, 1995). Additionally, cardiac rupture may occur without prodromal signs in patients with evolving Q-wave or equivalent infarction, sometimes small and for that their occurrence is even more dramatic. Therefore, it is extremely important to assess correctly the subtle premonitory data, such as some electrocardiographic details. Contrary to what occurs in primary VF, which may be virtually always resolved in the coronary care unit, cardiac rupture requires urgent surgical treatment. The mortality rate is only below that of cardiogenic shock secondary to a massive infarction. Fortunately, also the latter is much less frequent with the currently available therapies. [Pg.245]

Diercks GF, Hillege HL, van Boven AJ et al. Microalbuminuria modifies the mortality risk associated with electrocardiographic ST-T segment changes. J Am Coll Cardiol 2002 40 1401. [Pg.313]

Rautaharju PM, Kooperberg C, Larson JC, LaCroix A. Electrocardiographic abnormalities that predict coronary heart disease events and mortality in postmenopausal women the Women s Health Initiative. Circulation 2006 113 473. [Pg.320]

Sutherland SE, Gazes PC, Keil JE, Gilbert GE, Knapp RG. Electrocardiographic abnormalities and 30-year mortality among white and black men of the Charleston Heart Study. Circulation 1993 88 2685. [Pg.322]

Zimetbaum PJ, Buxton AE, Batsford W, et al. Electrocardiographic predictors of arrhythmic death and total mortality in the multicenter unsustained tachycardia trial. Circulation 2004 110(7) 766-9. [Pg.20]

Cardiovascular Effects. A number of studies in humans and animals have examined the effects of zinc on serum cholesterol and triglycerides. These data are discussed below under Other Systemic Effects. However, no studies regarding the direct relationship between excessive zinc intake and cardiac mortality were located. No effects on electrocardiographic results were found in a group of elderly subjects (>65 years of age) taking zinc supplements of up to 2 mg zinc/kg/day (Hale et al. 1988) or 0.71 mg zinc/kg/day (Czerwinski et al. 1974). There was also no effect on the frequency of cardiovascular disease (heart attack, heart failure, hypertension, or angina) in elderly subjects (>67 years of age) taking up to 2 mg zinc/kg/day (Hale et al. 1988). [Pg.33]

Conclusions Some antiepileptic drugs, mainly carbamazepine, in particular circumstances, can affect the cardiac repolarization cycle and predispose to SUDEP, but data are still elusive. The susceptibility factors that are most consistently associated with SUDEP include poor seizure control, antiepileptic drug poly therapy, and a long duration of epilepsy [46 ]. In particular, seizure control seems to be of paramount importance in the prevention of SUDEP. In fact, some studies have shown that in a considerable proportion of people with chronic epilepsy, shortly after seizures, some electrocardiographic features occur that may predict an increase in the risk of cardiac mortality or sudden cardiac death [47 ]. Hence, antiepileptic drugs as a class may have a protective effect against SUDEP, since they prevent seizures or reduce their number. [Pg.89]


See other pages where Electrocardiograph mortalities is mentioned: [Pg.263]    [Pg.281]    [Pg.148]    [Pg.508]    [Pg.352]    [Pg.430]    [Pg.468]   
See also in sourсe #XX -- [ Pg.507 ]




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