When amiodarone-induced thyroiditis meets cardiomyopathy with excessive trabeculation: a case report.

Introduction: Amiodarone is a potent antiarrhythmic medication used to treat life-threatening ventricular arrhythmias; however, its well-established adverse effect is a thyroid disorder. Amiodarone-induced thyroiditis (AIT), a clinical entity involving two types with different etiopathology and treatment approaches, may occur at the beginning or even several years after amiodarone treatment discontinuation. The toxicity profile of amiodarone becomes especially important in young patients with lifelong cardiac disorders, which are often refractory to other antiarrhythmic drugs. Herein, we report the first case of non-sustained ventricular tachycardia (NSVT), an unusual presentation of type II AIT, in a young male patient who was previously diagnosed with left ventricular cardiomyopathy with excessive trabeculation. Case report: A 36-year-old male non-athlete presented with tiredness during regular follow-up. Continuous electrocardiographic monitoring (cECG) revealed NSVT, whereas echocardiography and cardiac magnetic resonance imaging detected discrete structural and functional changes that could not fully explain the observed cECG report. Conversely, an unmeasurably low thyrotropin level on admission and previous exposure to amiodarone pointed the diagnostic pathway in the direction of the thyroid gland. Elevated free thyroxine and undetectable autoantibody titers with unremarkable sonographic findings raised clinical suspicion of type II AIT. Scintigraphic imaging with 99mTc-2-methoxyisobutylisonitrile (sestamibi) revealed decreased thyroid uptake; hence, prednisone was introduced for treatment. Clear improvements in both biochemical and electrocardiographic parameters were observed after immunomodulatory treatment of type II AIT in this young patient with cardiomyopathy and excessive trabeculation. Conclusion: Treatment of reversible causes of cardiac rhythm abnormalities such as type II AIT should be considered before choosing other treatment modalities, particularly in patients with structural cardiac disorders. The importance of a multidisciplinary approach in complex cases such as the one reported, thus, cannot be emphasized enough.

Study of vitamin D receptor gene polymorphisms in a cohort of myocardial infarction patients with coronary artery disease.

BACKGROUND: Vitamin D deficiency is associated with cardiovascular diseases, including coronary artery diseases (CAD). As vitamin D manifests its biological function through its vitamin D receptor (VDR), VDR gene polymorphisms potentially affect VDR functionality and vitamin D activity. Therefore, the objective of this study was to analyze three well-studied VDR gene polymorphisms-Fok1 (rs2228570), BsmI (rs1544410) and Taq1 (rs731236)-in a cohort of CAD patients after acute myocardial infarction. METHODS: In the presented cross-sectional study, 155 participants with CAD after acute myocardial infarction and 104 participants in a control group without CAD were enrolled. The participants in both groups were Caucasians of European origin. The genotyping of VDR polymorphisms rs2228570, rs1544410 and rs731236 was assessed by RT-PCR. RESULTS: The results show an association between the T/T genotype of the BsmI (rs1544410) and the G/G genotype of the Taq1 (rs731236) VDR polymorphism and CAD patients after acute myocardial infarction. There was no association between the Fok1 (rs2228570) VDR polymorphism and CAD patients after acute myocardial infarction. CONCLUSION: The presented results suggest a potential association of the BsmI (rs1544410) and Taq1 (rs731236) VDR polymorphisms with CAD patients after myocardial infarction.

Vitamin D-binding protein (rs4588) T/T genotype is associated with anteroseptal myocardial infarction in coronary artery disease patients.

BACKGROUND: Cardiovascular diseases (CVD) are among leading causes of death worldwide and amongst CVD, coronary artery disease (CAD) accounts for almost half of all cardiovascular deaths as the most common cause of death in the developed world. Vitamin D and the vitamin D-binding protein (VDBP) have been studied as possible CAD pathogenesis factors but literature data provide opposing evidence on their role in CAD. Herein we aimed to present novel evidence on the association of two VDBP polymorphisms (rs4588) and (rs7041) with CAD in patients after acute myocardial infarction and study possible correlations of these polymorphisms with 25-hydroxyvitamin D [25(OH)D] serum levels. METHODS: The cross-section genotyping study included 155 subjects with CAD upon acute myocardial infarct and 104 control subjects. All patients and control group were Caucasians of European descent. VDBP polymorphisms (rs4588) and (rs7041) were studied by use of RT-PCR. Liquid chromatography, tandem mass spectrometry (LC-MS/MS) method was used for measurement of vitamin D in the serum. RESULTS: Association of the VDBP (rs4588) T/T genotype with CAD patients after acute MI and correlation of VDBP (rs4588) genotype G/G with higher levels of total vitamin D were found. No correlation of 25(OH)D serum levels with CAD were established but the multivariate logistic regression modelling enabled association of total vitamin D level and VDBP (rs4588) T/T genotype with CAD and anteroseptal myocardial infarction (ASMI) CAD occurrence. CONCLUSIONS: Obtained data speak in favor to the VDBP (rs4588) T/T genotype as a susceptibility factor for anteroseptal myocardial infarction where the same genotype showed to be generally more prevalent in smokers.

Correlation between immunological-inflammatory markers and endothelial disfunction in the early stage of coronary heart disease.

Classical risk factors for endothelial dysfunction (ED), such as age, gender, total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, and smoking history are utilised for the Framingham score and Systemic Coronary Risk Estimation (SCORE) for evaluation of the 10-year cardiovascular risk in routine practice. Nonetheless, pro-inflammatory mediators are deeply involved in the initiation and the progression of ED and coronary artery disease (CAD), and act additionally or independently of metabolic factors before clinical manifestations of the disease appear. C-reactive protein, a marker of intimal thickening of the myeloid-related protein 8/14 heterodimer, monocyte chemotactic protein 1, interleukin-15, the cytotoxic mediator, granulysin, and the matrix metalloproteinase 9 could be valuable, single, fast, and non-invasive laboratory tools for ED deterioration degree assessment. We propose to investigate the impact of pro-inflammatory biomarkers on ED, measured by previously established clinical methods in patients with yet undiagnosed CAD and at medium risk for an acute coronary event. It could be useful to measure and correlate the concentration of particular inflammatory markers in peripheral blood samples and the results of the Framingham and SCORE charts, multi-slice computed tomography coronary angiography, echocardiography, brachial artery flow-mediated dilatation, carotid-femoral pulse wave velocity, ankle-brachial index, carotid wall thickening, myocardial perfusion scintigraphy, and particularly, cardiac magnetic resonance imaging. The goal would be that the degree of correlation between particular inflammatory markers and the results of some methods for the assessment of ED or cardiac ischaemic imaging could be emphasised and pro-inflammatory markers positioned in the pathogenetic algorithm of CAD.