scholarly journals QRS–ST–T triangulation with repolarization shortening as a precursor of sustained ventricular tachycardia during acute myocardial ischemia

2015 ◽  
Vol 31 (2) ◽  
pp. 118-120 ◽  
Author(s):  
Velislav N. Batchvarov ◽  
Elijah R. Behr
1985 ◽  
Vol 26 (1) ◽  
pp. 11-22
Author(s):  
Kazuya FUJINO ◽  
Yutaka NAKAYA ◽  
Hiroyoshi MORI ◽  
Yoshikazu HIASA ◽  
Takatoshi ISHIDA ◽  
...  

2011 ◽  
Vol 301 (3) ◽  
pp. R775-R782 ◽  
Author(s):  
Heidi L. Lujan ◽  
Sandhya Krishnan ◽  
Stephen E. DiCarlo

The response to myocardial ischemia is complex and involves the cardio-cardiac sympathetic reflex. Specifically, cardiac spinal (sympathetic) afferents are excited by ischemic metabolites and elicit an excitatory sympathetic reflex, which plays a major role in the genesis of ventricular arrhythmias. For example, brief myocardial ischemia leads to ATP release, which activates cardiac spinal afferents through stimulation of P2 receptors. Clinical work with patients and preclinical work with animals document that disruption of this reflex protects against ischemia-induced ventricular arrhythmias. However, the role of afferent signals in the initiation of sustained ventricular tachycardia has not been investigated. Therefore, we tested the hypothesis that cardiac spinal deafferentation reduces the susceptibility to sustained ventricular tachycardia in adult (12–15 wk of age), conscious, male Sprague-Dawley rats. To test this hypothesis, the susceptibility to ventricular tachyarrhythmias produced by occlusion of the left main coronary artery was determined in two groups of conscious rats: 1) deafferentation (bilateral excision of the T1-T5 dorsal root ganglia) and 2) control (sham deafferentation). The ventricular arrhythmia threshold (VAT) was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. Results document a significantly higher VAT in the deafferentation group (7.0 ± 0.7 min) relative to control (4.3 ± 0.3 min) rats. The decreased susceptibility to tachyarrhythmias with deafferentation was associated with a reduced cardiac metabolic demand (lower rate-pressure product and ST segment elevation) during ischemia.


2016 ◽  
Vol 97 (6) ◽  
pp. 913-917
Author(s):  
A I Abdrakhmanova ◽  
N B Amirov ◽  
N A Tsibul’kin ◽  
E B Frolova ◽  
O Yu Mikhoparova ◽  
...  

Recent publications devoted to the etiology, diagnosis and treatment of cardiogenic syncope were reviewed. The analysis of the current state of views on a pathogenesis, classification and features of a clinical picture of syncope of cardiogenic etiology was performed. Cardiogenic syncope has a 20-30% mortality. The highest risk is characteristic for the age more than 45 years, heart failure, history of ventricular tachycardia, nonspecific changes on ECG. With three and more risk factors the probability of a sudden cardiac death within the next year can reach 80%. The cause of cardiogenic syncope is reduction of cerebral blood flow. Cardiogenic syncope can be caused by a fall in blood pressure, cardiac output and total peripheral vascular resistance. Cardiogenic syncope may be the result of bradycardia and asystole, supraventricular and ventricular tachycardia, pulmonary embolism, dissecting aortic aneurysm, structural defects and cardiac anomalies, presence of myxoma or mobile atrial clot, cardiac tamponade, constrictive pericarditis, acute myocardial ischemia, abnormalities of the coronary arteries, dysfunction of prosthetic valve and cardiac pacemakers. In the diagnosis of cardiogenic syncope anamnesis and data received on physical examination are important. Instrumental examination should include electrocardiography, detection of comorbid conditions, exercise stress tests such as cycle ergometry or treadmill test, Holter ECG monitor, echocardiography, and coronary angiography for suspected acute myocardial ischemia.


1978 ◽  
Vol 40 (02) ◽  
pp. 407-417
Author(s):  
Michael J Saliba ◽  
Richard J Pavalec

SummaryIntestinal mucosa heparin (IMH) and beef lung heparin (BLH) were infused into dogs subjected to myocardial ischemia by intermittent coronary artery occlusions. The IMH was from a mixture of beef, sheep, and pig intestinal mucosa. Initial control occlusion and recovery was followed by a second occlusion with 60,000 units of IMH or BLH added. Electrocardiographic S-T segment elevations (ST) were measured acutely. There were no significant differences in ST in non-ischemic myocardium before occlusions or with occlusions. In ischemic myocardium, IMH significantly lowered control ST 84% in amount (t = 6.1 p <0.00005), and 76% in number (t = 11.6 p <0.00001). BLH lowered control ST a significant, lesser, 36% in amount (t = 3.6 p <0.008), and 35% in number (t = 3.2 p <0.01). The difference between IMH and BLH in ischemic myocardium was a significant 48% in amount (t = 4.0 p <0.0007), and 41% in number (t = 2.0 p <0.06). Myocardial adenosine triphosphate (ATP) levels were assayed after 90 min. ATP levels were 31% higher in both ischemic and non-ischemic myocardium in IMH-treated dogs than in BLH- treated. It was concluded that IMH and BLH are functionally different, and IMH was significantly more effective.


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