Subendocardial Haemorrhage and E.C.G. Changes in Intracranial Bleeding

Koskelo, Pentti; Punsar, Sven; Sipila, W

doi:10.1136/bmj.1.5396.1479

Cited by 127 publications

(40 citation statements)

References 11 publications

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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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“…14 The central role of the insula in the control of cardiovascular function has been supported by a robust experimental and clinical literature. 15,16 Despite the fact that myocardial damage could definitely be produced in animals, until the mid-1960s there was little recognition that this actually occurred in human beings with acute neurological or psychiatric illness until Koskelo and colleagues 17 reported on 3 patients with ECG changes caused by subarachnoid hemorrhage who were noted on postmortem examination to have several small subendocardial petechial hemorrhages. Connor 18 reported focal myocytolysis in 8% of 231 autopsies, with the highest incidence seen in patients who suffered fatal intracranial hemorrhages.…”

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confidence: 99%

The Brain–Heart Connection

2007

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“…Distinctive electrocardiographical abnormalities associated with this intracranial event include a prolonged QT interval (the importance of this change will be discussed later), large upright or deeply inverted T waves, elevation or depression of ST segments, prominent U waves and a marked increase in the amplitude of the U waves in postextrasystolic beats. 3 ' 18 The time course of these abnormalities has not been adequately documented. 10 These ECG changes may closely resemble an acute myocardial infarction.…”

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confidence: 99%

Cardiac Arrhythmias and Sudden Death in Subarachnoid Hemorrhage

Estañol

Marin

1975

Stroke

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Cardiac Arrhythmias and Sudden Death in Subarachnoid Hemorrhage• Life-threatening cardiac arrhythmias can occur in patients with subarachnoid hemorrhage secondary to rupture of intracranial aneurysms. The arrhythmias are secondary to acute dysfunction of the central nervous system and possibly to sudden increase in intracranial pressure. The autonomic nervous system is the mediator in the production of these disorders. The clinical significance of these rhythm disorders is discussed, particularly in regard to the sudden, unexpected death seen in this type of patient. The possible mechanisms of production are analyzed and their therapeutic implications are stressed.

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Subendocardial Haemorrhage and E.C.G. Changes in Intracranial Bleeding

Cited by 127 publications

References 11 publications

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

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

The Brain–Heart Connection

Cardiac Arrhythmias and Sudden Death in Subarachnoid Hemorrhage

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