2000
DOI: 10.1007/bf02682032
|View full text |Cite
|
Sign up to set email alerts
|

Structural and metabolic changes in cardiac conducting system during massive pulmonary embolism

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

0
2
0
1

Year Published

2003
2003
2015
2015

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 5 publications
(3 citation statements)
references
References 1 publication
0
2
0
1
Order By: Relevance
“…[19][20] When atrial fibrillation develops in the context of pulmonary embolism it is thought to be secondary to acute right-sided pressure overload with stretching of the right atrium, which is usually accompanied and aggravated by tricuspid regurgitation. [21][22] The finding of increased mortality among patients who leave the hospital in atrial fibrillation vs. normal sinus rhythm is hypothesis generating and deserves further study. It is plausible that this subset of patients in whom therapies failed, or were not considered, has a different substrate to develop and maintain atrial fibrillation such as subclinical cardiac dysfunction, infection or allograft rejection.…”
Section: Discussionmentioning
confidence: 99%
“…[19][20] When atrial fibrillation develops in the context of pulmonary embolism it is thought to be secondary to acute right-sided pressure overload with stretching of the right atrium, which is usually accompanied and aggravated by tricuspid regurgitation. [21][22] The finding of increased mortality among patients who leave the hospital in atrial fibrillation vs. normal sinus rhythm is hypothesis generating and deserves further study. It is plausible that this subset of patients in whom therapies failed, or were not considered, has a different substrate to develop and maintain atrial fibrillation such as subclinical cardiac dysfunction, infection or allograft rejection.…”
Section: Discussionmentioning
confidence: 99%
“…Последние наблюдения демонстрируют, что острую перегрузку правых отделов сердца при ТЭЛА крупных сосудов можно обнаружить по уровню кардиального тропонина [72][73][74][75][76][77][78], который повышается за счет по вреждения миокарда правого желудочка [79,80]. Хо тя этот показатель может иметь прогностическое значение [77,78], его роль в диагностике ограниче на, и при тромбоэмболии мелких ветвей легочной артерии он не имеет диагностической ценности [81].…”
Section: клинические рекомендацииunclassified
“…9 It has also been shown that massive PE can be accompanied by inhibition of glycolytic enzymes in the conducting cardiomyocytes of both ventricles, resulting in structural and electrophysiologic impairment of the conducting cardiomyocytes. 10 This study was designed to evaluate whether pulmonary emboli were associated with abnormal cardiac enzymes and whether the presence of chest pain had any important diagnostic implications in predicting RV myocyte damage and elevated cardiac enzymes. We also evaluated to discern whether patients with PE who had a history of coronary artery disease (CAD) had a higher incidence of chest pains and whether RV dysfunction on echocardiogram was associated with chest pain.…”
mentioning
confidence: 99%