Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
To investigate the underlying mechanisms of the left ventricular (LV) apical ballooning syndrome, we evaluated the functional responsiveness to dobutamine stimulation in patients with the syndrome. Over a 22-month period, 11 consecutive patients with the apical ballooning syndrome were referred to our institution. All 11 patients were women and 57 to 85 years of age (mean 73 +/- 10). Among them, 10 patients underwent low-dose dobutamine echocardiography within 24 hours after admission (17 +/- 8 hours). Echocardiography was repeated in the convalescent phase (48 +/- 33 days) to assess functional outcome. In the resting state, all patients showed akinetic wall motion in the midportion of the left ventricle and apical left ventricle. After low-dose dobutamine infusion, akinetic wall motion detected at rest did not show any improvement despite the hypercontractile basal LV wall. In the convalescent phase, LV dysfunction was not observed on echocardiography in all 11 patients. The LV apical ballooning syndrome has a unique feature that reversible dysfunction lacks functional amelioration during dobutamine administration. In conclusion, this finding suggests that the pathophysiologic mechanisms of the syndrome appear to be distinct from those of myocardial stunning after transient ischemia, and catecholamine-mediated cardiac toxicity may play a role in the development of the syndrome.
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Source |
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http://dx.doi.org/10.1016/j.amjcard.2007.06.057 | DOI Listing |
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