EXERCISE INDUCED NONSUSTAINED VENTRICULAR TACHYCARDIA-A SIGNIFICANT MARKER OF CORONARY ARTERY STENOSIS?

2001 ◽  
Vol 33 (5) ◽  
pp. S272
Author(s):  
M Fejka ◽  
K A. Skelding ◽  
R A. Corpus ◽  
J Arends ◽  
W W. O??Neill ◽  
...  
1987 ◽  
Vol 10 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Richard J. Peterson ◽  
Spencer B. King ◽  
William A. Fajman ◽  
John S. Douglas ◽  
Andreas R. Grüntzig ◽  
...  

2011 ◽  
Vol 4 (2) ◽  
pp. 176-186 ◽  
Author(s):  
Shanmugam Uthamalingam ◽  
Hui Zheng ◽  
Marcia Leavitt ◽  
Eugene Pomerantsev ◽  
Imad Ahmado ◽  
...  

2015 ◽  
Vol 61 (4) ◽  
pp. 387-390
Author(s):  
Rudzik Roxana ◽  
Şuş Ioana ◽  
Hadadi László ◽  
Şerban Răzvan Constantin ◽  
Dobreanu Dan

AbstractIntroduction: Coronary vasospasm is a possible cause of ventricular tachyarrhythmias and is frequently associated with atherosclerotic lesions. The revascularization of mild to moderate coronary artery stenosis which causes symptoms only due to associated vasospasm is still a matter of debate, as the standard treatment of Prinzmetal angina is represented by the long term administration of calcium-channel blockers.Case presentation: We present the case of a 46 year old woman with an intermediate severity coronary artery stenosis complicated by vasospastic angina and subsequent polymorphic ventricular tachycardia. Although the functional significance of the fixed coronary artery lesion was equivocal at invasive fractional flow reserve measurement, a combined pharmacologic and interventional treatment strategy was chosen with stent implantation and long acting calcium channel blocker administration with a symptom-free, good clinical outcome.Conclusion: Patients with vasospastic angina and intermediate severity atherosclerotic coronary artery stenoses are at risk of malignant ventricular arrhythmias, therefore myocardial revascularization should be considered in addition to the standard medical treatment.


1992 ◽  
Vol 70 (18) ◽  
pp. 1407-1411 ◽  
Author(s):  
Andreas P. Michaelides ◽  
Harisios Boudoulas ◽  
Gregory P. Vyssoulis ◽  
Charalambos Skouros ◽  
Pavlos K. Toutouzas

1976 ◽  
Vol 37 (1) ◽  
pp. 153 ◽  
Author(s):  
Paul L. McHenry ◽  
Stephen N. Morris ◽  
John F. Phillips

1992 ◽  
Vol 263 (2) ◽  
pp. H392-H398 ◽  
Author(s):  
D. C. Homans ◽  
R. Asinger ◽  
T. Pavek ◽  
M. Crampton ◽  
P. Lindstrom ◽  
...  

This study was designed to test the hypothesis that the oxygen free radical scavengers superoxide dismutase (SOD) and catalase may reduce myocardial “stunning” after exercise-induced ischemia. To test this hypothesis, 8 mongrel dogs performed treadmill exercise for 10 min in the presence of a flow-limiting coronary artery stenosis. Regional left ventricular function was measured with ultrasonic microcrystals implanted to measure regional wall thickening. Regional myocardial perfusion was measured with radioactive microspheres. The combination of SOD (5 mg/kg iv) and catalase (5 mg/kg iv) did not affect heart rate, blood pressure, coronary artery flow, or regional myocardial blood flow at rest, during exercise, or in the postexercise period. SOD and catalase had no effect on regional wall thickening at rest before exercise. During exercise in the absence of a coronary artery stenosis, thickening was slightly lower during SOD and catalase infusion (27 +/- 11.0 vs. 30.8 +/- 11.5%, SOD vs. control P = 0.05). During exercise in the presence of a coronary artery stenosis, there was no difference in thickening. Infusion of SOD and catalase affected neither the transient rebound function occurring early after exercise nor the prolonged period of stunning. These results indicate that the myocardial stunning that follows exercise-induced ischemia is unlikely to be mediated by oxygen free radicals.


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