Heart Damage Associated with Intracranial Lesions

Connor, Richard C.

doi:10.1136/bmj.3.5609.8

Cited by 114 publications

(43 citation statements)

References 17 publications

(10 reference statements)

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“…[11][12][13] Troponin T increases above the cutoff value in clinical situations with trace amounts of injured myocardial tissue; it increases in 19% to 64% of patients with unstable angina pectoris, whereas CK-MB usually remains normal. 8 Likewise, troponin T but not CK-MB increases after endomyocardial biopsy, in which small amounts of tissue (12 to 14 mm 3 ) are removed.…”

Section: Discussionmentioning

confidence: 99%

Creatine Kinase-MB Elevation After Stroke Is Not Cardiac in Origin

Arsava

Sarıbaş

2002

Stroke

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Background and Purpose-Creatine kinase-MB (CK-MB) increases in some patients with stroke, with no clear evidence of an acute coronary syndrome. Its elevations have been suggested to represent a biological marker for stroke-related myocardial injury. Troponin T has superior sensitivity and specificity to CK-MB in revealing minor myocardial injury. Therefore, we studied troponin T levels after stroke to determine whether troponin T increases in parallel to CK-MB. Methods-We made daily measurements of CK-MB, myoglobin, total creatine kinase (total CK), and troponin T levels up to day 5 in 32 patients with large hemispheric infarction and with no history of coronary heart disease. The daily enzyme levels were compared with those of a control group of 22 patients with neurological diseases other than stroke. Results-Serum CK-MB, myoglobin, and total CK levels were elevated above the cutoff value in 11, 26, and 20 patients with stroke, respectively. These enzyme levels gradually increased within the first 3 days and declined afterward. Troponin T did not exceed the reference range in any patients. One patient had elevated myoglobin and 3 had elevated total CK in the control group. The difference between groups was significant for CK-MB, myoglobin, and total CK at various time points. Conclusions-Troponin T, a more specific biochemical marker of myocardial injury, does not increase after stroke.Normal troponin T along with elevated CK-MB signifies that CK-MB is not the biological marker for myocytolysis. CK-MB elevations in stroke patients are likely to be noncardiac in origin.

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Section: Discussionmentioning

confidence: 99%

Creatine Kinase-MB Elevation After Stroke Is Not Cardiac in Origin

Arsava

Sarıbaş

2002

Stroke

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“…1 ' 9 Greenhbot and Reichenbach 10 reported 6 fatal cases of SAH in which recent subendocardial hemorrhages and myofibrillar degeneration were evident at postmortem. Conversely, Connor 11 demonstrated that the cause of death in 13 of 18 patients with focal myocytolysis was intracranial hemorrhage.…”

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confidence: 99%

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Benedict¹,

Loach²

1978

Stroke

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SUMMARYIn patients with subarachnoid hemorrhage there were increased concentrations of plasma epinephrine and norepinephrine when compared with those concentrations in a group of patients admitted to hospital with other illness.Reassessment after a variable period showed that in patients whose eventual clinical result was poor the plasma epinephrine and norepinephrine concentrations increased further while in those with a good result those concentrations showed a decline. No such changes were evident in plasma dopamine-,8-hy droxylase activities which were within normal range.In a sub-group of patients who had neurosurgery after admission for clipping an aneurysm, the post-operative changes of plasma epinephrine and norepinephrine concentrations were related to the clinical condition of the patients.

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“…1 ECO changes could be demonstrated in animals six days after intraeranial haemorrhage, a and in men two days after such trauma. 2 In cases of recovery from subarachnoid haemorrhage such ECC abnormalities returned to normal.…”

Section: Heart Damage Associated With Intracranial Lesionsmentioning

confidence: 79%