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Updated: Apr 12, 2026

Ultrasonic Assessment of Myocardial Microstructure
Published on: January 14, 2014
Ultrastructural calcium distribution and myocardial calcium content in human idiopathic dilated cardiomyopathy
H G Olbrich1, H Michaelis1, G Vandeplassche
1Zentrum der Inneren Medizin, Universität Frankfurt, Germany.
Insights
This study found no evidence of global myocardial calcium overload in end-stage dilated cardiomyopathy patients. Mitochondrial calcium deposits, a marker of cellular calcium overload, were similar in failing and non-failing hearts.
Area of Science:
- Cardiology
- Cell Biology
- Biochemistry
Background:
- Myocardial calcium overload in chronic heart failure remains a debated topic.
- Understanding intracellular calcium handling is crucial for heart failure research.
Purpose of the Study:
- To investigate myocardial calcium content and intracellular calcium distribution in end-stage dilated cardiomyopathy.
- To determine if cellular calcium overload occurs in failing human hearts.
Main Methods:
- Atomic absorption spectrophotometry for myocardial calcium and magnesium content.
- Phosphate-pyroantimonate method for ultrastructural calcium distribution.
- Morphometric analysis of mitochondrial calcium deposits.
Main Results:
- No significant differences in myocardial calcium and magnesium content were found across heart ventricles and septum.
- Calcium precipitates were observed in sarcolemma, T-tubules, intercalated disks, and mitochondria in both failing and non-failing hearts.
- Mitochondrial calcium deposits did not differ between dilated cardiomyopathy and non-failing hearts.
Conclusions:
- The study suggests no global myocardial calcium overload in end-stage dilated cardiomyopathy.
- Mitochondrial calcium buffering capacity appears maintained in failing hearts.
Abstract:
Myocardial calcium overload in chronic heart failure is still a debatable issue. The aim of this study was to investigate the myocardial calcium content and intracellular calcium distribution in end-stage dilated cardiomyopathy. The explanted hearts of 13 patients (9 male, 4 female, mean age 49 ± 12 years) undergoing heart transplantation because of end-stage dilated cardiomyopathy were examined. Samples were obtained from the right and left ventricular free wall and from the septum. Calcium and magnesium content were measured by atomic absorption spectrophotometry. Ultrastructural calcium distribution was examined in dilated cardiomyopathy using the phosphate-pyroantimonate method. Ultrastructural calcium distribution was also examined in left ventricular biopsies obtained from 3 patients (male, mean age 47 ± 3.6 years) with nonfailing hearts. The number of mitochondrial calcium precipitates was estimated morphometrically by a point counting method. Myocardial calcium and magnesium content in dilated cardiomyopathy did not differ significantly among the right and left ventricles and septum ranging from 8.5 to 10.8 mmol/kg dry weight. The phosphate-pyroantimonate method visualized calcium precipitates being confined to the sarcolemma, T-tubules, intercalated disks, and mitochondria in both nonfailing myocardium and dilated cardiomyopathy. Because mitochondria may act as buffers of cytoplasmic calcium, mitochondrial calcium precipitates served as a criterion for a possible cellular calcium overload. No differences in the amount of mitochondrial calcium deposits were observed between dilated cardiomyopathy and nonfailing hearts. The data suggest that there is no global myocardial calcium overload in human eng-stage dilated cardiomyopathy.
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