Myocardial Calcification Research Articles

Full calcium jacket: massive idiopathic myocardial calcification by cardiovascular magnetic resonance and cardiac CT

A 57-year-old gentleman with a history of persistent atrial fibrillation for the past year was admitted with heart failure attributed to poor control of the heart rate. Chest X-ray revealed a marked calcification of the cardiac silhouette. The echocardiogram was inconclusive because of a very deficient echocardiographic window. The CMR scan revealed several intramyocardial masses widespread all over the segments of the left ventricle. They restricted the thickening of the …

Vitamin D

Vitamin D is a fat-soluble vitamin that is naturally found in very few foods, is added to others, and is available as a dietary supplement. It is produced endogenously when ultraviolet light strikes the skin. Recent epidemiologic and experimental evidence has suggested that low vitamin D levels may play a role in various cardiovascular conditions, including coronary artery disease, congestive heart failure, valvular calcification, stroke, hypertension, and cognitive decline. Low vitamin D may lead to vascular smooth muscle cell proliferation, endothelial cell dysfunction, vascular and myocardial cell calcification, and increased inflammation. However, the data supporting a cardioprotective effect of vitamin D supplementation are very weak, and the large, controlled clinical trials now in progress should resolve this issue.

Porcelain Heart: Rapid Progression of Cardiac Calcification in a Patient with Hemodialysis

Cardiac calcification usually occurs in patients with end-stage renal disease. However, rapid progression of cardiac calcification is rarely associated with secondary hyperparathyroidism of end-stage renal disease. We report a patient with end-stage renal disease who showed moderate left ventricular hypertrophy at the first echocardiography, and showed severe myocardial calcification and severe mitral valve stenosis 4 years later. We suspected a rapid progression 'porcelain heart' cardiomyopathy secondary to hyperparathyroidism of end-stage renal disease. The patient underwent parathyroidectomy, and considered mitral valve replacement.

Nephrogenic Calcific Arteriopathy

Vascular calcification in chronic kidney disease (CKD) is extremely common and contributes to significant morbidity and mortality among these patients. The pathogenesis is complex and involves multiple factors, including elevated calcium x phosphorus product as well as deficiencies in circulating or locally produced inhibitors of calcification, parathyroid hormone, hyperlipidemia and inflammation. Similarly, valvular heart calcifications as well as myocardial and pulmonary calcifications of fatal consequences can also occur, presumably related to the same pathogenetic factors (Figures 1, 2). Other forms of extraskeletal tissue calcification of nonfatal consequences but leading to incapacity can also develop in CKD patients (Figure 3). These complications may be prevented by awareness and early intervention directed towards correcting some of the aforementioned participating mechanisms.

Ghrelin reduces rat myocardial calcification induced by nicotine and vitamin D3 in vivo

Ghrelin, a newly discovered bioactive peptide, initially was identified as a strong stimulant for the release of growth hormone (GH) and that has improved cardiac function in patients suffering from end-stage chronic heart failure. Increasing evidence has demonstrated that ghrelin may have myocardial protective effects. However, the role of ghrelin in the pathogenesis of cardiovascular diseases remains unclear. In this study, an in vivo model of rat myocardial calcification induced by vitamin D3 and nicotine was used to study the possible mechanism in the regulatory action of ghrelin on the calcified myocardium. Calcification increased total Ca2+ content and 45Ca2+ deposition in the myocardium and alkaline phosphatase (ALP) activation in the plasma. Compared with the control group, ghrelin mRNA expression was up-regulated and the myocardium calcium content was significantly increased in vitamin D3 and nicotine-treated rats. Rats were subcutaneously injected with 1 or 10 nmol/kg ghrelin. Rats treated with both low- and high-dose ghrelin decreased total Ca2+ content and 45Ca2+ deposition in cardiac muscle and inhibited ALP activation in the myocardium and plasma, in a concentration-dependent manner. In addition, osteopontin (OPN) mRNA expression significantly decreased and that of endothelin (ET-1) significantly increased with myocardial calcification. Ghrelin treatment increased OPN expression at the mRNA level and reduced ET-1 mRNA expression in a dose-dependent manner. These results indicate that exogenous administration with ghrelin attenuates myocardial calcification induced by nicotine and vitamin D3, and that the possible mechanism is via the ghrelin-induced increase in the OPN mRNA levels and decrease in the ET-1 mRNA expression in the myocardium.

Left ventricular aneurysm with massive myocardial calcification

A 68-year-old man with mild shortness of breath was referred for computed tomography angiography (CTA). When he was 40 years old, he had been admitted to another hospital because of acute anterior myocardial infarction. His chest X-ray showed curvilinear shaped calcification along the cardiac contour (Fig. 1a). Volume rendering reconstruction imaging showed a large area of high-attenuation density in the territory of the obstructed left anterior descending coronary artery (Fig. 1b). Multiplanar reconstruction imaging revealed marked thinning of the left ventricular myocardium with fine myocardial calcification in the anteroseptal-lateral segments (Fig. 2). Cine images of CTA showed absent regional wall thickening (Movies 1 and 2). Myocardial calcification is usually classified as either dystrophic or metastatic [1]. Dystrophic calcification usually occurs in areas of transmural myocardial infarction and develops in areas of ventricular aneurysm. Cardiac CTA is well suited to depict the extent of postischaemic changes to the myocardium including calcification by evaluating both morphological and functional information. Fig. 1 a The lateral view of chest X-ray showing curvilinear shaped calcification along the cardiac contour; b Volume rendering reconstruction image of the CTA showing the calcified myocardium located on the territory of left anterior descending coronary artery ... Fig. 2 Multiplanar reconstruction image of CTA showing marked thinning of the left ventricular myocardium with fine myocardial calcification in the anteroseptal-lateral segments (Left: horizontal long-axis image, Movie 1,) (Right: short-axis image, Movie 2)

Extensive Radiation-Induced Heart Disease in an Adult Patient Treated for Lymphoma as a Child

Cardiovascular complications are the second leading cause of late mortality in survivors of Hodgkin's lymphoma (HL) exposed to mediastinal radiotherapy. Symptomatic cardiac disease following classic thoracic irradiation for HL is reported in 10%-30% of patients at 5-10 years of follow-up. We present the case of a 44-year-old man with a history of left cervical nodular lymphocyte predominant HL treated at childhood with 40 Gy extended field thoracic irradiation (Mantle) who presented with mixed aortic and mitral valve disease, coronary artery stenosis, myocardial and aortic calcifications, and mediastinal fibrosis. Despite extensive cardiac surgery, the postoperative course was complicated and resulted in the patient's death. We review herein the typical cardiac involvement related to mediastinal radiotherapy and the controversies surrounding its surgical approach.

Incidence of focal myocardial 18F-FDG uptake and correlation with coronary calcifications by PET/CT

ObjectiveTo evaluate the incidence of 18F-FDG focal uptake in the myocardium as well as its correlation with coronary vessel calcifications. Material and methodsA total of 130 patients who underwent an oncological PET/CT study were reviewed retrospectively. Sixty-five had undergone a myocardial perfusion study because of clinical suspicion of coronary artery disease (group 1). There were no significant differences in age and gender regarding another group of the same series (n = 65; group 2). Focal myocardial 18F-FDG uptake and the presence of coronary vessel calcifications were identified by 2 independent observers. ResultsGroup 1: in 18 out of 65 patients (28%) focal myocardial 18F-FDG uptake was identified (5 had 2 foci; total: 23 foci). In 43 out of 65 studies (66%), calcification was identified in the coronary vessels. Group 2: in 6 out of 65 patients (9%) focal myocardial 18F-FDG uptake was identified (1 had 2 foci; total: 7 foci). In 17 out of 65 studies (26%), calcification was identified in the coronary vessels.Comparative analysis: focal myocardial 18F-FDG uptake and coronary vessel calcifications were more frequent in the group 1 patients (p < 0.01).There was no correlation between the presence of coronary vessel calcifications and focal myocardial 18 F-FDG uptake in individual patients in both groups (group 1: p = 0.7; group 2: p = 0.163). ConclusionsPET/CT allows simultaneous assessment of focal myocardial 18F-FDG uptake and myocardial vessel calcifications. Patients with clinical suspicion of coronary artery disease have a higher incidence of focal myocardial 18F-FDG uptake and coronary calcifications. However, 18F-FDG focal uptake is often observed in sites remote from those with calcification.

Incidencia de focos miocárdicos de captación de 18F-FDG y su relación con la presencia de calcificaciones coronarias por PET/TC

Objective To evaluate the incidence of 18F-FDG focal uptake in the myocardium as well as its correlation with coronary vessel calcifications. Material and methods A total of 130 patients who underwent an oncological PET/CT study were reviewed retrospectively. Sixty-five had undergone a myocardial perfusion study because of clinical suspicion of coronary artery disease (group 1). There were no significant differences in age and gender regarding another group of the same series (n = 65; group 2). Focal myocardial 18F-FDG uptake and the presence of coronary vessel calcifications were identified by 2 independent observers. Results Group 1: in 18 out of 65 patients (28%) focal myocardial 18F-FDG uptake was identified (5 had 2 foci; total: 23 foci). In 43 out of 65 studies (66%), calcification was identified in the coronary vessels. Group 2: in 6 out of 65 patients (9%) focal myocardial 18F-FDG uptake was identified (1 had 2 foci; total: 7 foci). In 17 out of 65 studies (26%), calcification was identified in the coronary vessels. Comparative analysis: focal myocardial 18F-FDG uptake and coronary vessel calcifications were more frequent in the group 1 patients (p < 0.01). There was no correlation between the presence of coronary vessel calcifications and focal myocardial 18F-FDG uptake in individual patients in both groups (group 1: p = 0.7; group 2: p = 0.163). Conclusions PET/CT allows simultaneous assessment of focal myocardial 18F-FDG uptake and myocardial vessel calcifications. Patients with clinical suspicion of coronary artery disease have a higher incidence of focal myocardial 18F-FDG uptake and coronary calcifications. However, 18F-FDG focal uptake is often observed in sites remote from those with calcification.

Endomyocardial nodular calcification as a cause of heart failure

Massive cardiac calcification is rare, occurring in association with chronic diseases or more commonly with previous myocardial infarction. We present an intriguing case of massive myocardial calcification of the left ventricle in a young patient with restrictive cardiomyopathy and progressive heart failure who required transplantation. The patient's history and clinical presentation did not reveal the etiology of the myocardial calcification.

Unexpected massive myocardial calcification

Unexpected massive myocardial calcification

“Porcelain heart” cardiomyopathy secondary to hyperparathyroidism: Radiographic, echocardiographic, and cardiac CT appearances

We report the radiographic, echocardiographic and cardiac CT appearances of 'porcelain heart' in an 85-year-old woman who presented with progressive heart failure. The extensive myocardial calcification was secondary to hyperparathyroidism with renal failure.

Myocardial Calcification and Hypertension following Chronic Renal Failure and Ameliorative Effects of Furosemide and Captopril

Objectives: The aim of this study was to prevent metastatic myocardial calcification and hypertension following chronic renal failure (CRF). Methods: A total of 50 male Sprague-Dawley rats were allocated to one of five groups: the control group (sham), the NxNT group (nephrectomized rats receiving no treatment), the NxFuro group (nephrectomized rats treated with furosemide), the NxCap group (nephrectomized rats treated with captopril) and the NxFuroCap group (nephrectomized rats treated with furosemide and captopril). Surgery (5/6 nephrectomy) was performed to induce CRF. Oral treatment with furosemide (20 mg/kg) and/or captopril (0.05 mg/kg) was given twice daily for 5 weeks. Parameters were studied after 5 weeks. Results: In the NxNT group, arterial blood pressure was significantly increased compared with the controls. Monotherapy with furosemide or captopril and both in combination maintained blood pressure to near or below control. Myocardial and remnant-kidney calcification was detected in NxNT rats, but calcification was absent in the NxFuroCap rats. Cardiac hypertrophy and fibrosis was observed in the NxNT group but not in treatment groups. Both plasma inorganic phosphate and Ca²⁺ significantly increased in the NxNT group, but the difference was not significant in the treatment groups. Conclusion: Furosemide, either alone or in combination with captopril, is capable to prevent myocardial calcification, cardiac hypertrophy and hypertension, maintaining blood Ca²⁺ and phosphate levels by slowing CRF.

Idiopathic massive myocardial calcification: a case report and review of the literature

We report a rare case of massive myocardial calcification in a 42-year-old male who presented with symptoms of congestive heart failure and arrhythmia. Myocardial calcification is most commonly associated with myocardial infarction or, less commonly, hypercalcemia. This case is particularly unusual due to the lack of any known predisposing risk factors, including normal coronary arteries, normal renal function, and normal serum calcium levels. Alternative etiologies are discussed accompanied by a review of the literature.

Unexpected massive myocardial calcification

A 62-year-old female with a history of hypertension, atrial fibrillation and pulmonary embolism was admitted for dyspnoea.

A premature infant with fetal myocardial and abdominal calcifications and factor V Leiden homozygosity

We present a premature male neonate with confirmed factor V Leiden deficiency diagnosed prenatally with cardiac and abdominal calcifications. Our patient's findings suggest that clinicians consider thromboembolic conditions when multiple fetal calcifications are visualized.

Disruption of the aortic elastic lamina and medial calcification share genetic determinants in mice.

Disruption of the elastic lamina, as an early indicator of aneurysm formation, and vascular calcification frequently occur together in atherosclerotic lesions of humans. We now report evidence of shared genetic basis for disruption of the elastic lamina (medial disruption) and medial calcification in an F(2) mouse intercross between C57BL/6J and C3H/HeJ on a hyperlipidemic apolipoprotein E (ApoE(-/-)) null gene, known to mediate myocardial calcification. Using transgenic complementation, we show that Abcc6 also contributes to aortic medial calcification. Our data indicate that calcification, though possibly contributory, does not always lead to medial disruption and that in addition to aneurysm formation, medial disruption may be the precursor to calcification.

Mitral valve disease as well as uncommon extensive epipericardial and intramyocardial calcification secondary to massive mitral annular calcification

A 71-year-old woman with a history of childhood pulmonary tuberculosis was admitted to our hospital for exertional dyspnoea (NYHA functional class II). Transthoracic and transoesophageal echocardiography demonstrated moderate to severe mixed mitral valve disease due to massive mitral annular calcification (MAC) and extensive infiltrative calcification of the atrioventricular groove. In addition, a very uncommon intramyocardial calcification of the ventricular septum and the lateral free wall was diagnosed. This case demonstrates a rare combination of mitral valve disease secondary to MAC, and a small hypertrophied left ventricle, as well as epipericardial and myocardial calcification likely due either to the massive MAC with myocardial extension or to former tuberculous perimyocarditis. The multidimensional imaging approach, which has been used in this particularly case, provided an excellent visualization and clinical evaluation of this rare finding.

Cardiac calcified amorphous tumor in a patient presenting for ventricular tachycardia ablation: intracardiac echocardiogram diagnosis and management

Calcified amorphous tumors (CAT) of the heart are rare primary cardiac tumors characterized by heavy myocardial and valve apparatus calcification. The relationship of the entity with ventricular arrhythmia, if any, is unknown. We describe a case of cardiac CAT in a 58-year-old woman with prior cardiac arrest and recurrent ventricular tachycardia who presented for radiofrequency ablation. Pre-ablation intracardiac echocardiogram revealed the characteristic endomyocardial calcific pattern associated with this tumor that precluded catheter manipulation in the left ventricle. The imaging characteristics and management are described.

Myocardial calcification in a patient with end‐stage renal disease

Myocardial calcification in a patient with end‐stage renal disease