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Updated: Jun 12, 2026

In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
[Assessment of myocardial perfusion and function in victims of scorpion envenomation using gated-SPECT]
Alexandre Baldini de Figueiredo1, Palmira Cupo, Antônio O Pintya
1Hospital das Clínicas, Faculdade de Medicina de Ribeirão Preto, USP, São Paulo, SP, Brasil.
Insights
Scorpion envenomation frequently causes myocardial perfusion abnormalities and impaired left ventricular function. Recovery of heart function correlates with improved perfusion, suggesting its role in acute ventricular failure.
Area of Science:
- Cardiology
- Toxicology
- Medical Imaging
Background:
- Scorpion envenomation can lead to severe cardiac complications like cardiogenic shock and pulmonary edema.
- The exact pathophysiological mechanisms underlying these cardiac issues in scorpion envenomation are not fully understood.
Purpose of the Study:
- To investigate the relationship between abnormalities in myocardial perfusion and left ventricular contractile function in patients affected by scorpion stings.
- To assess the recovery of cardiac function following scorpion envenomation.
Main Methods:
- Utilized ECG-gated myocardial perfusion scintigraphy (gated SPECT) on 15 patients within 72 hours and 15 days post-envenomation.
- Analyzed images using semi-quantitative visual perfusion and motion scores (SPS, SMS) and calculated left ventricular ejection fraction (LVEF).
Main Results:
- At baseline, 12 of 15 patients showed abnormal myocardial perfusion and contractility, with low LVEF (44.6%).
- Significant correlations were found between perfusion scores (SPS) and motion scores (SMS), and between SPS and LVEF.
- Follow-up revealed significant recovery in global and segmental contractility (LVEF, SMS) and perfusion (SPS).
Conclusions:
- Myocardial perfusion defects are common in scorpion envenomation and are topographically linked to contractile dysfunction.
- The reversibility of perfusion defects correlates with the recovery of cardiac contractility.
- These findings highlight the role of myocardial perfusion abnormalities in the pathophysiology of acute ventricular failure due to scorpion envenomation.
Background:
Cardiogenic shock and acute pulmonary edema are the major causes of death of patients with scorpion envenomation, whose pathophysiological mechanism remains controversial.
Objective:
To investigate the correlation between myocardial perfusion abnormalities and left ventricular contractile function in victims of scorpion envenomation.
Methods:
Fifteen patients underwent ECG-gated myocardial perfusion scintigraphy (gated SPECT) within 72 hours of, and 15 days after scorpion envenomation. Images were analyzed by means of a semi-quantitative visual perfusion score (0 = normal, 4 = absent) and motion score (0 = normal, 4 = akinesia), using the 17-segment model. Summed perfusion (SPS) and summed motion (SMS) scores were calculated for each patient. Ejection fraction (LVEF) was calculated by a commercially available software.
Results:
At baseline, 12 out of the 15 patients presented abnormal myocardial perfusion and contractility. Mean values of SPS, SMS and LVEF were 12.5 A+/- 7.3, 17.0 A+/- 12.8, and 44.6 A+/- 16.0%, respectively. A positive correlation between SPS and SMS (r = 0.68; p = 0.005) and negative correlation between SPS and LVEF (r = -0.75; p = 0.0021) were found. The follow-up studies showed recovery of global contractility (LVEF of 68.9 A+/- 9.5, p = 0.0002), segmental contractility (SMS of 2.6 A+/- 3.1, p = 0.0009) and perfusion (SPS of 3.7 A+/- 3.3, p = 0.0003). Improvement of LVEF correlated positively with improvement of SPS (r = 0.72; p = 0.0035).
Conclusions:
Myocardial perfusion abnormalities are common in scorpion envenomation and correlate topographically with the contractile dysfunction. Recovery of contractility correlates with reversibility of perfusion defects. These findings suggest the participation of myocardial perfusion abnormalities in the pathophysiology of this form of acute ventricular failure.
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