Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1075
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3195
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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Stroke-heart syndrome (SHS) is associated with early mortality in patients with acute ischemic stroke (AIS). However, reliable methods for timely risk stratification remain elusive. Combined monitoring of neurohormonal activation and electrocardiography may help identifying early mortality risk in SHS patients. This study investigates the interaction between elevated BNP and QTc prolongation on short-term mortality in SHS patients. This cohort study included patients with suspected AIS and concomitant SHS. SHS is defined as new-onset cardiac dysfunction after AIS, including acute coronary syndrome, heart failure, and arrhythmias. All patients underwent laboratory tests and electrocardiographic evaluations. Prolonged QTc was defined as &;gt430 milliseconds (ms) in males and &;gt450 ms in females. Patients were followed up for three months, and the study outcomes were all-cause mortality and cardiovascular and cerebrovascular disease (CCVD) mortality. Cox regression models were used to assess the relationship between BNP, QTc interval, and mortality, and the interaction between BNP and the QTc interval on mortality was analyzed. A total of 448 patients were enrolled in this analysis. Prolonged QTc was present in 217 patients (48.44%). Elevated BNP was associated with prolonged QTc (OR 1.90; 95% CI, 1.20-3.01, p=0.006). Elevated BNP, but not prolonged QTc, increased the risk of all-cause and CCVD mortality (HR 5.94; 95% CI, 1.22-29.03, p=0.028 and HR 5.48; 95% CI, 1.01-29.70, p=0.048, respectively). There was a significant interaction between elevated BNP and prolonged QTc on all-cause mortality (p for interaction &;lt0.001). Patients with prolonged QTc and higher BNP had highest risk of all-cause mortality (HR 4.92, 95% CI, 1.03-23.39, p=0.045). This study highlights a significant interaction between prolonged QTc and elevated BNP levels in predicting short-term all-cause mortality among AIS patients with SHS. Prolonged QTc emerges as a critical marker of increased mortality risk, particularly in patients with elevated BNP levels.
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http://dx.doi.org/10.14336/AD.2025.10711 | DOI Listing |