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Published on: May 31, 2016
A case of massive dystrophic cardiac calcinosis with increased bone resorption markers: a novel pathophysiologic
Vedat Davutoglu1, Selim Kervancioglu, Yusuf Sezen
1Department of Cardiology, Sahinbey Medical Center, Gaziantep University, Gaziantep, Turkey. davutoglu@gantep.edu.tr
Insights
Increased bone resorption may cause cardiac calcification and intractable heart failure in elderly patients. This case highlights a novel mechanism linking osteoporosis to severe cardiac dysfunction.
Area of Science:
- Cardiology
- Endocrinology
- Geriatrics
Background:
- A 72-year-old male presented with severe congestive heart failure refractory to treatment.
- The patient had a history of anterior myocardial infarction 20 years prior.
Observation:
- Echocardiography and CT revealed extensive cardiac calcification (myocardium, chordae, mitral annulus, aortic valve).
- No chronic renal insufficiency or hypercalcemia were noted.
- Elevated bone resorption markers and severe osteoporosis were diagnosed.
Findings:
- A novel mechanism is proposed: increased bone resorption leads to calcium deposition in avascular heart tissues.
- This calcification is exacerbated by high left ventricular end-diastolic pressure.
Implications:
- Dystrophic cardiac calcinosis, linked to bone resorption, may cause cardiomyopathy and intractable heart failure.
- This suggests a potential link between osteoporosis and age-related cardiac dysfunction, warranting further investigation.
Abstract:
We report a 72-year-old man who presented to our emergency room with congestive heart failure that was resistant to initial medical therapy. He had suffered from anterior myocardial infarction 20 years prior. Echocardiography and computed tomography revealed marked cardiac calcification including myocardium, chordal structures, mitral annulus, and aortic valve. Neither chronic renal insufficiency nor hypercalcemia were present in our patient. Bone resorption markers were increased and bone mineral density was consistent with severe osteoporosis. We suggested a novel mechanism, that increased bone resorption may lead to accumulation of calcium into avascular tissues in the heart (ie, chordal structures, mitral annulus, aortic valve, and fibronecrotic myocardium) especially in the setting of high left ventricular end-diastolic pressure. Dystrophic cardiac calcinosis, an age-related cardiomyopathy, is associated with elevated bone resorption markers and it may cause alterations in cellular calcium hemostasis with initiation of deleterious events leading to aggravate dilated and restrictive cardiomyopathy and may result in intractable congestive heart failure. The implication of this case report needs to be reemphasized.
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