Manganese-enhanced Magnetic Resonance Imaging in Dilated Cardiomyopathy and Hypertrophic Cardiomyopathy.

Patients with dilated cardiomyopathy (n= 10) or hypertrophic cardiomyopathy (n= 17) underwent both gadoliniumand manganese contrast-enhanced magnetic resonance imaging and were compared with healthy volunteers(n= 20). Differential manganese uptake (Ki) was assessed using a two-compartment Patlak model. Compared withhealthy volunteers, reduction in T1 with manganese-enhanced magnetic resonance imaging was lower in patientswith dilated cardiomyopathy [mean reduction 257 ± 45 (21%) vs. 288 ± 34 (26%) ms,P< 0.001], with higher T1 at40 min (948 ± 57 vs. 834 ± 28 ms,P< 0.0001). In patients with hypertrophic cardiomyopathy, reductions in T1 wereless than healthy volunteers [mean reduction 251 ± 86 (18%) and 277 ± 34 (23%) vs. 288 ± 34 (26%) ms, with andwithout fibrosis respectively,P< 0.001]. Myocardial manganese uptake was modelled, rate of uptake was reducedin both dilated and hypertrophic cardiomyopathy in comparison with healthy volunteers (meanKi19 ± 4, 19 ± 3,and 23 ± 4 mL/100 g/min, respectively;P= 0.0068). In patients with dilated cardiomyopathy, manganese uptake ratecorrelated with left ventricular ejection fraction (r2= 0.61,P= 0.009). Rate of myocardial manganese uptake demon-strated stepwise reductions across healthy myocardium, hypertrophic cardiomyopathy without fibrosis and hyper-trophic cardiomyopathy with fibrosis providing absolute discrimination between the healthy myocardium andfibrosed myocardium (meanKi23 ± 4, 19 ± 3, and 13 ± 4 mL/100 g/min, respectively;P< 0.0001)

Characterizing heart failure with preserved and reduced ejection fraction: An imaging and plasma biomarker approach.

IntroductionThe pathophysiology of heart failure with preserved ejection fraction (HFpEF) remains incompletely defined. We aimed to characterize HFpEF compared to heart failure with reduced ejection fraction (HFrEF) and asymptomatic hypertensive or non-hypertensive controls.Materials and methodsProspective, observational study of 234 subjects (HFpEF n = 140; HFrEF n = 46, controls n = 48, age 73±8, males 49%) who underwent echocardiography, cardiovascular magnetic resonance imaging (CMR), plasma biomarker analysis (panel of 22) and 6-minute walk testing (6MWT). The primary end-point was the composite of all-cause mortality and/or HF hospitalization.ResultsCompared to controls both HF groups had lower exercise capacity, lower left ventricular (LV) EF, higher LV filling pressures (E/E', B-type natriuretic peptide [BNP], left atrial [LA] volumes), more right ventricular (RV) systolic dysfunction, more focal and diffuse fibrosis and higher levels of all plasma markers. LV remodeling (mass/volume) was different between HFpEF (concentric, 0.68±0.16) and HFrEF (eccentric, 0.47±0.15); pConclusionsHFpEF is a distinct pathophysiological entity compared to age- and sex-matched HFrEF and controls. HFpEF and HFrEF are associated with similar adverse outcomes. Inflammation is common in both HF phenotypes but cardiomyocyte stretch/stress is greater in HFrEF

Gross right heart dilatation secondary to Ebstein's anomaly.

Gross right heart dilatation secondary to Ebstein's anomaly

The curious case of an invisible dog: a patient with non-psychiatric visual hallucinations.

A 74-year-old man reported experiencing hallucinations of a dog standing on his right side, following a recent episode of infective endocarditis. There was no history of reduced conscious level, psychosis or substance misuse. Neurological examination revealed an isolated right inferior quadrantopia, and the hallucinations were visible only in the area of the visual defect. A computed tomography scan confirmed a left occipital lobe infarct, congruent with the clinical signs. The infarct was deemed to be have originated from a septic embolus of his infected aortic valve and he was diagnosed with Charles Bonnet's syndrome (CBS). CBS is characterized by the presence of stereotyped visual hallucinations on a background of partial sight and in the absence of any psychotic illness. Early recognition can prevent wrongful diagnosis of a psychiatric condition, which may provide comfort to patients. Management is centred on reassurance and counselling, with medical therapies reserved only for patients experiencing distressing hallucinations

Myocardial Calcium Handling in Type 2 Diabetes: A Novel Therapeutic Target

Type 2 diabetes (T2D) is a multisystem disease with rapidly increasing global prevalence. Heart failure has emerged as a major complication of T2D. Dysregulated myocardial calcium handling is evident in the failing heart and this may be a key driver of cardiomyopathy in T2D, but until recently this has only been demonstrated in animal models. In this review, we describe the physiological concepts behind calcium handling within the cardiomyocyte and the application of novel imaging techniques for the quantification of myocardial calcium uptake. We take an in-depth look at the evidence for the impairment of calcium handling in T2D using pre-clinical models as well as in vivo studies, following which we discuss potential novel therapeutic approaches targeting dysregulated myocardial calcium handling in T2D

Competing interests in a lung cancer with metastasis to the pituitary gland: syndrome of inappropriate ADH secretion versus diabetes insipidus.

Metastases to the pituitary gland are rare; cancers that most commonly metastasize to the pituitary are breast and lung cancers. No specific computed tomography or magnetic resonance imaging features reliably distinguish primary pituitary masses from metastases. A combination of a detailed clinical assessment together with specialist endocrine and neuroradiology support is essential to make the rare diagnosis of a pituitary metastasis. We present the case of a man with metastatic lung cancer, initially presenting as hypopituitarism. Subtle features in the history, together with neuroimaging findings atypical for pituitary adenomas, provided clues that the diagnosis was one of the pituitary metastases. Treatment of diabetes insipidus (DI) with replacement antidiuretic hormone (ADH) was complicated by extreme difficulties in achieving a satisfactory sodium and water balance. This was the result of coexistent DI and syndrome of inappropriate ADH secretion perpetuated by the patient's primary lung cancer, a phenomenon not previously described in the literature