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Updated: Aug 7, 2026
Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Acute left ventricular dysfunction of severe scorpion envenomation is related to myocardial perfusion disturbance
Palmira Cupo1, Alexandre B Figueiredo, Antonio P Filho
1Pediatrics Division, Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil. pcupo@fmrp.usp.br
Insights
Severe scorpion envenomation can cause heart failure. Myocardial perfusion scintigraphy revealed temporary myocardial ischemia contributes to left ventricular dysfunction in children with scorpion envenomation.
Area of Science:
- Cardiology
- Toxicology
- Pediatrics
Background:
- Scorpion envenomation (SE) can lead to severe cardiac dysfunction, including acute pulmonary edema and cardiogenic shock.
- The exact pathophysiology of SE-induced heart failure remains debated.
- This study investigates the role of myocardial ischemia in left ventricular dysfunction following SE.
Purpose of the Study:
- To assess the contribution of myocardial ischemia to left ventricular dysfunction in children with severe scorpion envenomation.
- To utilize 99mTc-Sestamibi myocardial perfusion scintigraphy (MPS) to evaluate cardiac function post-envenomation.
Main Methods:
- Prospective study of 12 children with severe Tityus serrulatus envenomation.
- Myocardial perfusion scintigraphy (MPS) performed acutely (within 72h) and at follow-up (15 days).
- Echocardiography assessed left ventricular ejection fraction (EF) and regional wall motion (WM); MPS evaluated myocardial perfusion (MP).
Main Results:
- Initial echocardiography revealed significant left ventricular (LV) wall motion abnormalities (mean score 31.4+/-13.9) and reduced EF (36+/-16%).
- All patients showed myocardial perfusion defects (mean uptake score 14.6+/-7.8).
- A strong correlation was found between myocardial perfusion and wall motion abnormalities (p<0.0001), and between summed WM and MP scores (R=0.68, p=0.016).
Conclusions:
- Findings support transitory myocardial ischemia as a key mechanism in acute cardiac dysfunction from severe scorpion envenoming.
- Microvascular spasm, potentially due to catecholamine surge, is implicated in triggering myocardial perfusion disturbances.
- Follow-up showed significant improvement in LV function and normalization of myocardial perfusion.
Background:
Scorpion envenomation (SE) may present severe cardiac dysfunction with acute pulmonary edema and cardiogenic shock. The pathophysiology of this acute heart failure is still controversial. We aimed at assessing the contribution of the myocardial ischemia to the left ventricular dysfunction in SE by using 99mTc-Sestamibi myocardial perfusion scintigraphy (MPS).
Methods:
Twelve children (7 males, 1-12 years old) presenting severe Tityus serrulatus envenomation were prospectively submitted to MPS within 72 h (acute) and 15 days (follow-up) after the event. MPS images were interpreted using a visual semi-quantitative uptake score (0 = normal, 4 = absent). Echocardiography was used for the assessment of left ventricular (LV) ejection fraction (EF) and regional wall motion (WM) by using a semi-quantitative score (0 = normal, 4 = akinesia). A 16-segment LV model was used.
Results:
Initial echocardiography showed marked WM abnormalities with a mean score of 31.4+/-13.9, and a reduced EF (36+/-16%). All patients exhibited myocardial perfusion (MP) defects. The mean MP uptake score was 14.6+/-7.8. A significant topographic association between MP and WM changes was obtained (p<0.0001, Fischer exact test). A positive correlation was obtained between the summed WM and MP scores (R=0.68, p=0.016). Follow-up evaluation showed a significant improvement of LVEF (65+/-10%) and WM score (3.9+/-4.2), parallel to the normalization of MP.
Conclusions:
These observations strongly support the participation of transitory myocardial ischemia in the mechanism of the acute cardiac dysfunction caused by severe scorpion envenoming. Micro vascular spasm related to the catecholamine over stimulation may be the pathophysiologic link triggering the myocardial perfusion disturbance in this syndrome.
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