Association between dietary selenium and zinc intake and risk of dilated cardiomyopathy in children: a case-control study.

BACKGROUND: Dilated cardiomyopathy (DCMP) is characterized by the enlargement and weakening of the heart and is a major cause of heart failure in children. Infection and nutritional deficiencies are culprits for DCMP. Zinc is an important nutrient for human health due to its anti-oxidant effect that protects cell against oxidative damage. This case-control study aimed to investigate the relationship between dietary intake of zinc and selenium and the risk of DCMP in pediatric patients. METHODS: A total of 36 DCMP patients and 72 matched controls were recruited, and their dietary intakes were assessed via a validated food frequency questionnaire. We used chi-square and sample T-test for qualitative and quantitative variables, respectively. Logistic regression analysis was applied to assess the relationship between selenium and zinc intake with the risk of DCMP. RESULTS: After fully adjusting for confounding factors, analyses showed that selenium (OR = 0.19, CI = 0.057-0.069, P trend < 0.011) and zinc (OR = 0.12, CI = 0.035-0.046, P trend < 0.002) intake were strongly associated with 81% and 88% lower risk of pediatric DCMP, respectively. CONCLUSIONS: This study highlights the protective role of adequate dietary intake of selenium and zinc in decreasing the risk of DCMP in children. Malnutrition may exacerbate the condition and addressing these micronutrient deficiencies may improve the cardiac function. Further studies are recommended to detect the underlying mechanisms and dietary recommendations for DCMP prevention.

A Comprehensive Review of Dilated Cardiomyopathy in Pre-clinical Animal Models in Addition to Herbal Treatment Options and Multi-modality Imaging Strategies.

Dilated cardiomyopathy (DCM) is distinguished by ventricular chamber expansion, systolic dysfunction, and normal left ventricular (LV) wall thickness, and is mainly caused due to genetic or environmental factors; however, its aetiology is undetermined in the majority of patients. The focus of this work is on pathogenesis, small animal models, as well as the herbal medicinal approach, and the most recent advances in imaging modalities for patients with dilated cardiomyopathy. Several small animal models have been proposed over the last few years to mimic various pathomechanisms that contribute to dilated cardiomyopathy. Surgical procedures, gene mutations, and drug therapies are all characteristic features of these models. The pros and cons, including heart failure stimulation of extensively established small animal models for dilated cardiomyopathy, are illustrated, as these models tend to procure key insights and contribute to the development of innovative treatment techniques for patients. Traditional medicinal plants used as treatment in these models are also discussed, along with contemporary developments in herbal therapies. In the last few decades, accurate diagnosis, proper recognition of the underlying disease, specific risk stratification, and forecasting of clinical outcome, have indeed improved the health of DCM patients. Cardiac magnetic resonance (CMR) is the bullion criterion for assessing ventricular volume and ejection fraction in a reliable and consistent direction. Other technologies, like strain analysis and 3D echocardiography, have enhanced this technique's predictive and therapeutic potential. Nuclear imaging potentially helps doctors pinpoint the causative factors of left ventricular dysfunction, as with cardiac sarcoidosis and amyloidosis.

A rare cause of dilated cardiomyopathy: hypocalcemia.

Dilated cardiomyopathy (DCM) is characterized by systolic dysfunction and is usually idiopathic. A rare cause of reversible DCM is hypocalcemia. Calcium plays a key role in myocardial contraction. Hypocalcemia can lead to a decrease in contraction, left ventricular systolic dysfunction, and heart failure with reduced ejection fraction (EF). Hypocalcemia-related reversible DCM reports are rare. Herein, we present two cases with heart failure caused by hypocalcemia developed due to hypoparathyroidism. The first case presented with severe heart failure and an extremely low serum calcium level (4.4 mg/dL) due to idiopathic hypoparathyroidism. The second case, which was also admitted with heart failure due to hypocalcemia, had iatrogenic hypoparathyroidism due to a subtotal thyroidectomy. In both cases, patients had reduced left ventricular systolic functions (EF was 33% and 42%, respectively). After calcium replacement and heart failure treatment, calcium levels were normalized. A significant and rapid improvement in heart failure was achieved in both cases (EF 60% and 50%, respectively). Serum calcium levels should always be measured in patients with heart failure, and the etiology of hypocalcemia should be sought. In addition to the standard pharmacotherapy of heart failure with reduced EF, calcium supplementation is essential for treating these patients.

Barth syndrome with severe dilated cardiomyopathy and growth hormone resistance: a case report.

OBJECTIVES: To describe the metabolic and endocrine features of a patient with Barth syndrome who showed evidence of growth hormone resistance. CASE PRESENTATION: A male proband deteriorated rapidly with lactic acidosis after a circumcision at age three weeks and was found to have severe dilated cardiomyopathy. A cardiomyopathy gene panel led to the diagnosis of TAZ-deficiency Barth syndrome. He subsequently experienced hypotonia and gross motor delay, feeding difficulties for the first four years, constitutional growth delay and one episode of ketotic hypoglycaemia. Cardiomyopathy resolved on oral anti-failure therapy by age three years. He had a hormonal pattern of growth hormone resistance, and growth hormone treatment was considered, however height velocity improved spontaneously after age 3½ years. He also had biochemical primary hypothyroidism. CONCLUSIONS: With careful metabolic management with l-arginine supplementation, overnight corn starch, and a prescribed exercise program, our patient's strength, endurance, level of physical activity and body composition improved significantly by age six years.

Management of nonischemic-dilated cardiomyopathies in clinical practice: a position paper of the working group on myocardial and pericardial diseases of Italian Society of Cardiology.

: Nonischemic-dilated cardiomyopathy (NIDCM) is an entity that gathers extremely heterogeneous diseases. This awareness, although leading to continuous improvement in survival, has increased the complexity of NIDCM patients' management. Even though the endorsed 'red-flags' approach helps clinicians in pursuing an accurate etiological definition in clinical practice, it is not clear when and how peripheral centers should interact with referral centers with specific expertise in challenging scenarios (e.g. postmyocarditis and genetically determined dilated cardiomyopathy) and with easier access to second-line diagnostic tools and therapies. This position paper will summarize each step in NIDCM management, highlighting the multiple interactions between peripheral and referral centers, from first-line diagnostic workup and therapy to advanced heart failure management and long-term follow-up.

Treatment of dilated cardiomyopathy caused by coronary microvascular dysfunction with anisodamine: a report of 5 cases.

The management of dilated cardiomyopathy (DCM) is well established. However, a subset of patients does not have recovery from or have recurrences of left ventricular (LV) dysfunction despite receiving optimal medical therapy. Coronary microvascular dysfunction (CMD) can result from structural and functional abnormalities at the intramural and small coronary vessel level affecting coronary blood flow autoregulation and consequently leading to impaired coronary flow reserve. Dilated myocardial phenotype may be responsible for CMD in DCM. Anisodamine can exert a significant effect on relieving microvascular spasm, and improving and dredging the coronary microcirculation. However, whether CMD can be potentially improved with anisodamine to make DCM better remains incompletely understood.

Hypocalcaemic cardiomyopathy: a description of two cases and a literature review.

Hypocalcaemic cardiomyopathy is a rare form of dilated cardiomyopathy. The authors here present two cases in which symptomatic dilated cardiomyopathy was the result of severe hypocalcaemia. First, we report about a 26-year-old woman with primary hypoparathyroidism and then about a 74-year-old man with secondary hypoparathyroidism following a thyroidectomy. In both cases, the left ventricular systolic function improved after calcium supplementation. In the first case, a lack of compliance led to a repeated decrease of both serum calcium level and left ventricular systolic function. The authors also present a comprehensive summary of all cases of hypocalcaemic dilated cardiomyopathy that have been described in literature to date. The mean age of the affected patients was 48.3 years, of which 62% were female patients. The most common causes of hypocalcaemic cardiomyopathy are primary hypoparathyroidism (50%) and post-thyroidectomy hypoparathyroidism (26%). In the post-thyroidectomy subgroup, the median time for the development of hypocalcaemic cardiomyopathy is 10 years (range: 1.5 months to 36 years). Hypocalcaemic cardiomyopathy leads to heart failure with reduced ejection fraction in 87% of patients. Generally, the most common complications of hypoparathyroidism and/or hypocalcaemia are cerebral calcifications, cognitive deficit, and cataracts. Once calcium supplementation is administered, the disease has a good prognosis and, in most individuals, a significant improvement (21%) or even normalization (74%) of the left ventricular systolic function occurs.

Vitamin D deficiency cardiomyopathy in Scotland: a retrospective review of the last decade.

OBJECTIVE: To determine the incidence, demography and prognosis of vitamin D deficiency dilated cardiomyopathy (DCM) in Scotland over the last decade. STUDY DESIGN: A retrospective review of cases of vitamin D deficiency DCM presenting to a national paediatric cardiac centre between 1 January 2008 and 1 January 2018. The departmental database and electronic and paper case notes were used to identify patients and extract data. RESULTS: Six patients were identified (three male), three of whom were Caucasian. Median age at presentation was 206 days (range 2-268.) All six patients had high serum parathyroid hormone levels (median 45 pmol/L, range 27-120 pmol/L), a sensitive marker of total body calcium deprivation secondary to vitamin D deficiency. All patients demonstrated clinical and echocardiographic improvement following high dose vitamin D treatment. No patients required cardiac transplant, and only one patient required extracorporeal life support as a bridge to recovery. After an initial improvement, one child died at 5 months as a result of respiratory infection. Three patients lived within some of the most deprived areas in Scotland. CONCLUSIONS: This case series demonstrates a previously unreported demographic in Scotland, as 50% of cases presented in Caucasian children. Although vitamin D deficiency DCM is relatively rare, it is wholly preventable. Our study confirms that vitamin D deficiency cardiomyopathy is reversible with prompt identification and supplementation. The current implementation of public health policy in the UK is failing to prevent children from developing the most severe manifestation of vitamin D deficiency.

Special topic: The association between pulse ingredients and canine dilated cardiomyopathy: addressing the knowledge gaps before establishing causation.

In July 2018, the Food and Drug Administration warned about a possible relationship between dilated cardiomyopathy (DCM) in dogs and the consumption of dog food formulated with potatoes and pulse ingredients. This issue may impede utilization of pulse ingredients in dog food or consideration of alternative proteins. Pulse ingredients have been used in the pet food industry for over 2 decades and represent a valuable source of protein to compliment animal-based ingredients. Moreover, individual ingredients used in commercial foods do not represent the final nutrient concentration of the complete diet. Thus, nutritionists formulating dog food must balance complementary ingredients to fulfill the animal's nutrient needs in the final diet. There are multiple factors that should be considered, including differences in nutrient digestibility and overall bioavailability, the fermentability and quantity of fiber, and interactions among food constituents that can increase the risk of DCM development. Taurine is a dispensable amino acid that has been linked to DCM in dogs. As such, adequate supply of taurine and/or precursors for taurine synthesis plays an important role in preventing DCM. However, requirements of amino acids in dogs are not well investigated and are presented in total dietary content basis which does not account for bioavailability or digestibility. Similarly, any nutrient (e.g., soluble and fermentable fiber) or physiological condition (e.g., size of the dog, sex, and age) that increases the requirement for taurine will also augment the possibility for DCM development. Dog food formulators should have a deep knowledge of processing methodologies and nutrient interactions beyond meeting the Association of American Feed Control Officials nutrient profiles and should not carelessly follow unsubstantiated market trends. Vegetable ingredients, including pulses, are nutritious and can be used in combination with complementary ingredients to meet the nutritional needs of the dog.

Occurrence of nutritional hypocalcaemic rickets-related dilated cardiomyopathy in a child with concomitant rickets and infantile-onset Pompe disease.

Infantile-onset Pompe disease is a lysosomal storage disorder characterised with hypertrophic cardiomyopathy, respiratory insufficiency, and hypotonia. Dilated cardiomyopathy is an extremely rare and curable complication of nutritional hypocalcaemic rickets. A 3-month-old female infant was referred to our paediatric ICU with a 4-day history of fatigue, tachypnoea, tachycardia, hypoxia, and respiratory failure. According to the laboratory, radiology, and echocardiography findings, she was first diagnosed with nutritional hypocalcaemic rickets-related dilated cardiomyopathy, but vitamin D and elementary calcium supplementation unmasked the underlying infantile-onset Pompe disease. Nutritional hypocalcaemic rickets and infantile-onset Pompe disease must always be kept in mind among the causes of concomitant dilated cardiomyopathy and hypertrophic cardiomyopathy.

Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets.

INTRODUCTION: Golden retrievers are over-represented in cases of taurine-deficient dilated cardiomyopathy and recently a surge in cases has prompted further investigation. OBJECTIVE: To describe the clinical, dietary, and echocardiographic features in golden retrievers diagnosed with taurine deficiency and dilated cardiomyopathy, and to determine specific dietary associations. A second aim was to determine the whole blood taurine concentrations in a representative sample of healthy golden retrievers. ANIMALS: Twenty-four client-owned golden retrievers with documented taurine deficiency and dilated cardiomyopathy and 52 healthy client-owned golden retrievers. METHODS: In this multicenter prospective observational study, baseline and follow-up echocardiographic data, complete diet and medical histories, and whole blood, plasma, or serum taurine concentrations were obtained. Baseline and follow-up echocardiographic data were compared. Associations were evaluated between specific diets and taurine deficiency or congestive heart failure. The prevalence of low whole blood taurine concentrations in the healthy golden retrievers was calculated. RESULTS: Twenty-three of 24 dogs diagnosed with taurine deficiency and dilated cardiomyopathy were fed diets that were either grain-free, legume-rich, or a combination of these factors. None of these diets were feeding trial tested using Association of American Feed Control Officials (AAFCO) procedures. Twenty-three of 24 dogs had significant improvement in their echocardiographic parameters and normalization of taurine concentrations following diet change and taurine supplementation. Nine of 11 dogs diagnosed with congestive heart failure (CHF) had resolution of their congestion at follow-up with five no longer requiring diuretic therapy and four tolerating diuretic dose reduction by >50%. CONCLUSIONS: Certain diets and diet characteristics were associated with the development of taurine deficiency. Taurine deficiency and dilated cardiomyopathy in golden retrievers is likely multifactorial, including a combination of dietary, metabolic, and genetic factors.

Cardiac, bone and growth plate manifestations in hypocalcemic infants: revealing the hidden body of the vitamin D deficiency iceberg.

BACKGROUND: Whilst hypocalcemic complications from vitamin D deficiency are considered rare in high-income countries, they are highly prevalent among Black, Asian and Minority Ethnic (BAME) group with darker skin. To date, the extent of osteomalacia in such infants and their family members is unknown. Our aim was to investigate clinical, cardiac and bone histomorphometric characteristics, bone matrix mineralization in affected infants and to test family members for biochemical evidence of osteomalacia. CASE PRESENTATION: Three infants of BAME origin (aged 5-6 months) presented acutely in early-spring with cardiac arrest, respiratory arrest following seizure or severe respiratory distress, with profound hypocalcemia (serum calcium 1.22-1.96 mmol/L). All infants had dark skin and vitamin D supplementation had not been addressed during child surveillance visits. All three had severely dilated left ventricles (z-scores + 4.6 to + 6.5) with reduced ejection fraction (25-30%; normal 55-70), fractional shortening (7 to 15%; normal 29-40) and global hypokinesia, confirming hypocalcemic dilated cardiomyopathy. They all had low serum levels of 25 hydroxyvitamin D (25OHD < 15 nmol/L), and elevated parathyroid hormone (PTH; 219-482 ng/L) and alkaline phosphatase (ALP; 802-1123 IU/L), with undiagnosed rickets on radiographs. One infant died from cardiac arrest. At post-mortem examination, his growth plate showed a widened, irregular zone of hypertrophic chondrocytes. Histomorphometry and backscattered electron microscopy of a trans-iliac bone biopsy sample revealed increased osteoid thickness (+ 262% of normal) and osteoid volume/bone volume (+ 1573%), and extremely low bone mineralization density. Five of the nine tested family members had vitamin D deficiency (25OHD < 30 nmol/L), three had insufficiency (< 50 nmol/L) and 6/9 members had elevated PTH and ALP levels. CONCLUSIONS: The severe, hidden, cardiac and bone pathology described here exposes a failure of public health prevention programs, as complications from vitamin D deficiency are entirely preventable by routine supplementation. The family investigations demonstrate widespread deficiency and undiagnosed osteomalacia in ethnic risk groups and call for protective legislation.

Is There a Cardiotoxicity Associated With Metallic Head Hip Prostheses? A Cohort Study in the French National Health Insurance Databases.

BACKGROUND: There are four distinguishable types of THA devices in wide use, as defined by the femoral and acetabular bearing surfaces: metal-on-polyethylene (MoP), ceramic-on-polyethylene (CoP), metal-on-metal (MoM), and ceramic-on-ceramic (CoC). Metallic head THAs (MoP and MoM) can potentially induce cardiac toxicity because cobalt species, generated at the head-neck trunnion, and in the case of MoM devices, at the articular surface as well, can be absorbed systemically. However, studies have provided inconsistent results. QUESTIONS/PURPOSES: The purpose of this study was to assess the risk of dilated cardiomyopathy (DCM) or heart failure (HF) associated with metallic head THAs using data from the French national health insurance databases. METHODS: Between 2008 and 2011 in France, 399,968 patients ≥ 55 years had a first THA. A total of 127,481 were excluded after we applied the exclusion criteria regarding arthroplasty and 17,137 as a result of a history of DCM/HF, recorded in the French national health insurance reimbursement databases, between January 1, 2006, and the date of inclusion. The final cohort included 255,350 individuals (43% men; mean age 72 ± 9 years). Of them, 93,581 (37%) had been implanted with MoP, 58,095 (23%) with CoP, 11,298 (4%) with MoM, and 92,376 (36%) with CoC THAs. Patients were followed until December 2015. Patients with incident DCM/HF were identified by a new entitlement to the long-term disease scheme or a first hospitalization with a diagnosis of DCM or HF. MoP and CoP THAs are generally implanted in old patients, whereas MoM and CoC are mostly indicated in young, active male patients. Thus, to consider the specific indications of the bearing couples, analyses were separately performed in two distinct subcohorts, one comprising patients with MoP or CoP and one comprising patients with MoM or CoC THA. In each subcohort, the DCM/HF risk was compared between patients with metallic head versus nonmetallic head THAs (MoP versus CoP, MoM versus CoC). Hazard ratios (adjusted HRs) of incident DCM/HF were estimated using Cox models adjusted for baseline sex, age, THA characteristics (fixation technique with cement, use of a modular femoral neck), and comorbidities at baseline. Cox models were stratified by sex and age. RESULTS: The crude incidence of DCM/HF per 100 person-years was 2.4 in patients with MoP, 1.8 with CoP, 1.2 with MoM, and 1.1 with CoC THAs. Overall, metallic head THAs were associated with a slight increase in DCM/HF risk (MoP versus CoP: adjusted HR, 1.08; 95% confidence interval [CI], 1.05-1.12; p < 0.001; MoM versus CoC: adjusted HR, 1.11; 95% CI, 1.03-1.19; p = 0.007). In the MoM-CoC subcohort, the risk tended to be more pronounced with MoM versus CoC THAs in women (MoM versus CoC: adjusted HR, 1.20; 95% CI, 1.07-1.35; p = 0.002) and patients aged ≥ 75 years (MoM versus CoC: adjusted HR, 1.16; 95% CI, 1.04-1.29; p = 0.009). CONCLUSIONS: Metallic head THAs were associated with a slightly increased DCM/HF risk, especially with MoM in women and older patients. Some caveats should be mentioned: severity of DCM or HF was not available and residual confounding cannot be ruled out despite considering many covariates. Our findings suggest that cardiac function should be regularly monitored in patients with metallic head THAs. Further investigations should be planned on large international cohorts. LEVEL OF EVIDENCE: Level III, therapeutic study.

Severe reversible hypocalcemic cardiomyopathy diagnosed 36 years after subtotal thyroidectomy - a case report.

Chronic hypocalcemia, irrespectively of its etiology, can lead to severe impairment of the left ventricular (LV) contractility manifesting as dilated cardiomyopathy, usually defined as hypocalcemic cardiomyopathy (hypocaCM). This rarely diagnosed type of heart failure (HF), can be completely reversible, when treated properly with calcium and vitamin D supplementation or, in some subjects, with human recombinant parathormone. A CASE REPORT: The authors present a case of a 60-year-old male admitted with advanced pulmonary congestion, recurrent pulmonary edema and pleural effusion. He was refractory to standard HF therapy. One year earlier, the patient was diagnosed with primary dilated cardiomyopathy with ejection fraction decreased to 25% and after coronary angiography, which revealed normal coronary arteries, he received implantable cardioverter-defibrillator (ICD). However, 36 years before, the patient underwent subtotal thyroidectomy, and at the moment presented with multiplicitous symptoms suggestive of profound hypocalcemia. Laboratory investigations confirmed hypocalcemia due to iatrogenic hypoparathyroidism. Improvement of LV function during supplementation with calcium and vitamin D was monitored by echocardiography using two-dimensional longitudinal strain. One should always consider reversible causes of HF, including hypocalcemia, especially when obvious consequences of chronic hypocalcemia as myopathy, depression or cataract are seen. Correct therapy can restore LV function and prevent unnecessary implantation of ICD.

Dilated cardiomyopathy secondary to vitamin D deficiency and hypocalcaemia in the Irish paediatric population: A case report.

We identified three infants with dilated cardiomyopathy (DCM) secondary to severe vitamin D deficieny and hypocalcaemia. All infants were exclusively breast fed, from dark skinned ethnic backgrounds, born and living in Ireland. None of these pregnant mothers or infants received the recommended vitamin D supplementation. Each infant presented in heart failure and required inotropic support as well as calcium and vitamin D replacement. Cardiac function subsequently improved. This highlights the public health issue that many high risk pregnant mothers and infants are not receiving the recommended vitamin D supplementation.

Dilated Cardiomyopathy as the Only Clinical Manifestation of Carnitine Transporter Deficiency.

The authors present a case of carnitine transporter deficiency, which was unmasked after an episode of respiratory distress resistant to treatment with bronchodilators. Chest radiograph showed cardiomegaly; electrocardiogram showed left ventricular hypertrophy and echocardiography revealed dilated cardiomyopathy. Heart failure therapy was initiated and metabolic screening was requested, as family history was indicative of inborn errors of metabolism. Very low levels of free carnitine and carnitine esters in blood were found and genetic testing confirmed the diagnosis of carnitine transporter deficiency. After oral supplementation with L-carnitine, symptoms gradually ameliorated and heart function had fully recovered. Sequence analysis in the SLC22A5 gene revealed the missense mutation c.1319C > T (p.Th440Met) in homozygous state. Homozygous c.1319C > T (p.Th440Met) mutation has not been associated with a pure cardiac phenotype before.

Scar Homogenization Versus Limited-Substrate Ablation in Patients With Nonischemic Cardiomyopathy and Ventricular Tachycardia.

BACKGROUND: Scar homogenization improves long-term ventricular arrhythmia-free survival compared with standard limited-substrate ablation in patients with post-infarction ventricular tachycardia (VT). Whether such benefit extends to patients with nonischemic cardiomyopathy and scar-related VT is unclear. OBJECTIVES: The aim of this study was to assess the long-term efficacy of an endoepicardial scar homogenization approach compared with standard ablation in this population. METHODS: Consecutive patients with dilated nonischemic cardiomyopathy (n = 93), scar-related VTs, and evidence of low-voltage regions on the basis of pre-defined criteria on electroanatomic mapping (i.e., bipolar voltage <1.5 mV) underwent either standard VT ablation (group 1 [n = 57]) or endoepicardial ablation of all abnormal potentials within the electroanatomic scar (group 2 [n = 36]). Acute procedural success was defined as noninducibility of any VT at the end of the procedure; long-term success was defined as freedom from any ventricular arrhythmia at follow-up. RESULTS: Acute procedural success rates were 69.4% and 42.1% after scar homogenization and standard ablation, respectively (p = 0.01). During a mean follow-up period of 14 ± 2 months, single-procedure success rates were 63.9% after scar homogenization and 38.6% after standard ablation (p = 0.031). After multivariate analysis, scar homogenization and left ventricular ejection fraction were predictors of long-term success. During follow-up, the rehospitalization rate was significantly lower in the scar homogenization group (p = 0.035). CONCLUSIONS: In patients with dilated nonischemic cardiomyopathy, scar-related VT, and evidence of low-voltage regions on electroanatomic mapping, endoepicardial homogenization of the scar significantly increased freedom from any recurrent ventricular arrhythmia compared with a standard limited-substrate ablation. However, the success rate with this approach appeared to be lower than previously reported with ischemic cardiomyopathy, presumably because of the septal and midmyocardial distribution of the scar in some patients.

Cardiomyopathy responsive to gluten withdrawal in a patient with coeliac disease.

A 57-year-old man with iron deficiency anaemia developed general malaise, exertional dyspnoea and features of cardiac failure out of proportion to his anaemia (haemoglobin 120 g/L). Investigations showed a severely dilated left ventricle with an ejection fraction of 15%, due to dilated cardiomyopathy. He was treated with high-dose diuretics, ACE inhibitors and ß-blocker therapy. Subsequent investigation into his iron deficiency anaemia revealed a new diagnosis of coeliac disease. After starting a gluten-free diet, his cardiac function improved markedly, with ejection fraction reaching 70%, allowing his cardiac medications to be withdrawn. This case suggests a link between coeliac disease and cardiomyopathy.