Inflammatory-mediated atrial cardiomyopathy diagnosed using multimodality imaging and successfully treated with prednisolone: a case report.

Background: Atrial fibrillation is a common cardiac arrhythmia and often develops secondary to structural cardiac changes. Both the occurrence of atrial fibrillation and/or structural changes of the heart may lead to development of atrial cardiomyopathy and heart failure (HF). However, isolated atrial cardiomyopathy caused by focal atrial thickening is a rare condition, previously only described in case reports as a result of different aetiologies all linked to inflammation. Case summary: A patient with inflammatory-mediated atrial cardiomyopathy causing atrial fibrillation and acute decompensated HF presented as isolated left atrial wall thickening on transoesophageal echocardiography. The diagnosis was confirmed using multimodality imaging with transthoracic and transoesophageal echocardiography, cardiac magnetic resonance imaging, positron emissions tomography/computer tomography scanning and intracardiac echocardiography-guided endomyocardial biopsy. Despite no specific histological aetiology, the observed atrial cardiomyopathy might be associated with type 1 diabetes mellitus. The patient in the present case was successfully treated with prednisolone. Discussion: Diabetes mellitus is an important risk factor for developing atrial fibrillation and diabetic cardiomyopathy, due to reduced levels of anti-inflammatory and increased levels of proinflammatory cytokines causing cardiac inflammatory structural remodelling. The regression of the atrial thickening might be due to prednisolone's anti-inflammatory effects and thereby ability to suppress atrial remodelling and reduce the occurrence of atrial fibrillation. However, the effect of prednisolone might only affect the non-manifested inflammatory-mediated atrial remodelling. Due to the rare occurrence of isolated atrial cardiomyopathy a multiple imaging approach during the diagnostic process and follow-ups are essential to determine the aetiology and effect of the treatment.

The mineralocorticoid receptor blocker spironolactone lowers plasma interferon-γ and interleukin-6 in patients with type 2 diabetes and treatment-resistant hypertension.

BACKGROUND: The mineralocorticoid receptor antagonist spironolactone lowers blood pressure in patients with resistant hypertension despite antihypertensive treatment with angiotensin-converting inhibitors (ACEi) and angiotensin-II receptor blockers (ARB). In preclinical studies, spironolactone suppresses pro-hypertensive interleukin 17A (IL-17A). OBJECTIVES: Plasma samples were analysed from a randomized, double-blind placebo-controlled trial with spironolactone given to patients with type 2 diabetes mellitus (T2DM) and resistant hypertension on three antihypertensive drugs. We tested the hypothesis that spironolactone-induced antihypertensive effects are associated with suppression of IL-17A and related cytokines. METHODS: Interferon-γ (IFN-γ), IL-17A, tumor necrosis factor-α (TNF-α), IL-6, IL-1ß and IL-10 were assessed in plasma with immunoassay in samples before and after 16 weeks of treatment with placebo or spironolactone (12.5-25-50 mg/day). RESULTS: Spironolactone significantly reduced plasma IFN-γ and IL-6 while IL-17A, TNF-α, IL-1ß and IL-10 were unchanged. IL-6 was more sensitive to higher doses of spironolactone. At baseline, serum aldosterone correlated positively with diastolic night blood pressure. Urine albumin/creatinine-ratios correlated positively with plasma IL-6 at baseline. There were no relations between aldosterone and cytokine concentrations at baseline; between cytokine concentration and blood pressure at baseline; and between cytokine concentration decrease and blood pressure decrease, except for IFN-γ, after treatment. The spironolactone-induced elevation in plasma potassium related inversely to blood pressure but not to changes in cytokines. In macrophages in vitro, spironolactone suppressed lipopolysaccharide (LPS)-induced TNF-α, IL-6, IL-1ß and IL-10 levels. CONCLUSION: The antihypertensive action of spironolactone in resistant hypertensive patients is associated with suppressed IFN-γ and IL-6 and not IL-17A. Spironolactone exerts anti-inflammatory actions in vivo on macrophages and T-cells.

Progressive valvular calcifications with critical aortic stenosis in a 25-year-old woman with end-stage renal disease on haemodialysis: a case report.

BACKGROUND: The increased risk of cardiovascular morbidity and mortality in chronic kidney disease (CKD) and end-stage renal disease (ESRD) seems particularly pronounced in patients with concomitant aortic and mitral valvular calcifications. Valvular calcification (VC) is accelerated in patients with CKD and even more so with ESRD and haemodialysis (HD) due to premature endothelial cell dysfunction. Mineral and bone disorder (CKD-MBD) is a common complication of CKD/ESRD and may play a pivotal role in VC. CASE SUMMARY: A 25-year-old woman with congenital hypoplastic kidneys and ESRD on HD from the age of 19 was admitted to the emergency department suffering from chest pain and dyspnoea. Transthoracic echocardiogram (TTE) revealed critical aortic stenosis (AS) with indexed aortic valve area 0.4 cm2/m2, a mean gradient 58 mmHg and a moderate mitral stenosis with a mean gradient 6-8 mmHg developed over the course of 2 years, as a normal TTE was performed at that time. During HD, the patient had longstanding alterations in calcium and phosphate metabolism including secondary hyperparathyroidism that eventually progressed into tertiary hyperparathyroidism. Efforts were made to treat CKD-MBD but patient compliance was low. Subtotal parathyroidectomy was performed 6 months prior to admission. The patient had dual mechanical valve replacement. DISCUSSION: Valvular calcification is common in patients with CKD/ESRD and in particular in patients on HD. Rapid progression of valve disease in this case may be related to the combination of low patient adherence and sustained disturbed calcium and phosphate metabolism with tertiary hyperparathyroidism. Transthoracic echocardiogram should be performed in patients on HD even with minor suspicion of VC and in patients with low adherence and disturbance of calcium and phosphate metabolism.

Body Mass Index, Intensive Blood Pressure Management, and Cardiovascular Events in the SPRINT Trial.

BACKGROUND: It is unclear whether intensive blood pressure management is well-tolerated and affects risk uniformly across the body mass index (BMI) spectrum. METHODS: The randomized, controlled Systolic Blood Pressure Intervention Trial (SPRINT) included 9361 individuals ≥50 years of age at high cardiovascular risk, without diabetes mellitus, with systolic blood pressure between 130 and 180 mmHg. Participants were randomized to intensive vs standard antihypertensive treatment and evaluated for the primary composite efficacy endpoint of acute coronary syndromes, stroke, heart failure, or cardiovascular death. The primary safety endpoint was serious adverse events. We used restricted cubic splines to determine the relationship between BMI, response to intensive blood pressure lowering, and clinical outcomes in SPRINT. RESULTS: Body mass index could be calculated for 9284 (99.2%) individuals. Mean BMI was similar between the 2 treatment groups (intensive group 29.9±5.8 kg/m2 vs standard group 29.8± 5.7 kg/m2; P = 0.39). Median follow-up was 3.3 years (range 0-4.8 years). Body mass index had a significant, J-shaped association with risk of all-cause mortality, stroke, and serious adverse events (P < .05 for all), but these were no longer significant after accounting for key clinical factors (P > .05 for all). Intensive blood pressure lowering reduced the primary efficacy endpoint and increased the primary safety endpoint compared with standard targets, consistently across the BMI spectrum (Pinteraction > .05). CONCLUSION: The overall efficacy and safety of intensive blood pressure lowering did not appear to be modified by baseline BMI among high-risk older adults.

A case report: haemodynamic instability due to true dynamic left ventricular outflow tract obstruction and systolic anterior motion following resuscitation: reversal of haemodynamics on supportive veno-arterial extracorporeal membrane oxygenation.

BACKGROUND: Obstruction of the left ventricular outflow tract (LVOT) as seen in hypertrophic cardiomyopathy is a dynamic condition with a wide range of clinical presentations and symptoms. CASE SUMMARY: We report the use of veno-arterial extracorporeal membrane oxygenation in a female patient who was resuscitated after out-of-hospital cardiac arrest. Soon after admission the patient developed critical haemodynamic compromise due to severe obstruction of the left ventricle outflow tract and systolic anterior motion (SAM) of the mitral valve. Veno-arterial extracorporeal membrane oxygenation restored haemodynamics and was weaned after 4 days without any haemodynamic compromise due to SAM. The patient was discharged from the intensive care unit at Day 13, and after 3 days at the coronary care unit, she was discharged to ambulatory follow-up with no sequelae. DISCUSSION: Veno-arterial extracorporeal membrane oxygenation restored haemodynamic stability in this patient with dynamic severe LVOT obstruction following cardiac arrest.