Myocarditis has numerous aetiologies, and Celiac Disease (CD) has been described as a rare cause. CD has received little attention in current guidelines and may be underdiagnosed. We report a case involving a 28-year-old male with myocarditis causing severe left ventricular dysfunction and dilatation that was probably related to CD. This case highlights the importance of screening for CD in patients presenting with myocarditis and signs of malabsorption when other common causes are excluded. Besides optimal medical treatment and cardiac resynchronization therapy, a gluten-free diet and immunosuppression may also be effective measures in the management of CD-related myocarditis.

doi: https://doi.org/10.12669/pjms.38.4.6129 How to cite this:Myrmel GMS, Lunde T, Saeed S. Clinical spectrum of Celiac disease from a cardiology perspective. Pak J Med Sci. 2022;38(4):782-784. doi: https://doi.org/10.12669/pjms.38.4.6129

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Severe hypertension has numerous etiologies. When accompanied by bradycardia, the spectrum of differential diagnoses is greatly narrowed and is commonly seen in patients with increased intracranial pressure. However, other etiologies such as bradycardia-induced hypertension are rarely mentioned. Here we report the case of a 73-year-old woman presenting with symptoms of heart failure, severe hypertension, and bradycardia with a 2:1 atrioventricular block. Echocardiography demonstrated increased left ventricular filling secondary to bradycardia and prolonged diastole, leading to greater ventricular stretch, increased contractile force and greater stroke volume (Frank-Starling mechanism), which subsequently caused elevated systolic blood pressure (BP), low diastolic BP and a wide pulse pressure. Treating the bradycardia by pacing led to an immediate and substantial BP reduction, although complete BP normalization had a slower time course and was probably due to the concomitant effect of the antihypertensive treatment initiation. This pathophysiological mechanism has received little attention in the literature. Further, stimulation of sympathetic afferents located in the heart by distension of the cardiac walls as well as the role of vagally innervated cardiopulmonary receptors due to the increased pressure in the heart and the pulmonary artery should also be kept in mind as alternative hypotheses.

Background Patients who present with acute chest pain who are not diagnosed with acute myocardial infarction (AMI) may still carry an increased cardiovascular risk. Growth differentiation factor-15 (GDF-15) has earlier been shown to be a strong prognostic marker in the general population and after AMI. However, the prognostic value in the chest pain population without AMI is unknown. Purpose The objective of this study was to investigate the prognostic power of GDF-15 in patients presenting with acute chest pain without myocardial infarction. Methods A total of 984 patients admitted with suspected NSTE-ACS were included. After excluding patients with AMI the remaining 849 patients were followed for median 722 days (range 1 to 1112 days). The primary endpoint was all-cause mortality. The secondary endpoint was all-cause mortality or AMI. GDF-15 was measured in biobanked admission samples, and patients were divided into two groups based on GDF-15 levels (1: ≤1800 pg/ml, 2: >1800 pg/ml). Kaplan-Meier survival curves according to GDF-15 concentrations ≤1800 pg/ml or >1800 pg/ml were generated. Cox proportional hazards regression analysis was used to estimate unadjusted and adjusted hazard ratios, the latter using age, sex, hypercholesterolemia, current smoking, diabetes, hypertension, BMI, previous myocardial infarction and eGFR <60ml/min/1.73m2 as covariates. The incremental prognostic value of adding GDF-15 to cardiac troponin T was estimated. Results GDF-15 concentrations were strongly associated with outcome. GDF-15 concentration were higher in non-survivors than survivors (median 2572 pg/ml vs. 910 pg/ml, p<0,001). In the category with GDF-15 >1800 pg/ml, 28 (17.9%) died, and 49 (31.4%) patients met the secondary endpoint, whereas in the category with GDF-15 levels <1800 pg/ml, only 12/693 (1.7%) died and 25 (3.6%) reached the secondary endpoint, respectively. GDF-15 >1800 pg/ml was associated with an increased risk of death with an unadjusted hazard ratio (HR) of 10.9 (95% CI: 5.6 – 21.5, p: 0.001) and an adjusted HR of 5.2 (95% CI: 1.4 – 19.4, p: 0.014). The risk of death or AMI in patients with GDF-15 >1800 pg/ml was also increased with an unadjusted HR of 9.5 (95% CI 5.9 – 17.7 p: 0.001) and an adjusted hazard ratio of 4.6 (95% CI: 1.7–12.27, p: 0.002). Adding GDF-15 to troponin T led to an increase in C-statistic from: 0.80 (95% CI: 0.73- 0.88) to 0.86 (95% CI 0.79 – 0.91) in predicting all-cause mortality. The optimal cut-off value for predicting the primary endpoint was estimated to be 1818 pg/ml, resulting in a Youden Index of 0.55 with a specificity of 85% and sensitivity of 70%. Conclusion GDF-15 is a strong prognostic marker in patients presenting with acute chest pain without AMI and may aid identifying those patients with high cardiovascular risk who require further diagnostics and treatment. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Western Norway Regional Health Authority