Pericardial defects are a rare disorder that can be characterized as acquired or congenital. Congenital defects can be further characterized by location and size of the defect, e.g. left- or right-sided and partial or complete absence of the pericardium. While physical examination and electrocardiogram are not diagnostic, chest radiographs and echocardiography have findings that should alert the clinician to the absence of the pericardium as a possible diagnosis. Despite its limitations with visualizing the normal pericardium in areas of minimal adipose, cardiac magnetic resonance is currently the gold standard for diagnosing the congenital absence of the pericardium. Patients have a similar life expectancy to those without pericardial defects; however in certain cases, herniation and strangulation of cardiac chambers can be life threatening and lead to sudden cardiac death. Treatment is tailored to the patient's symptoms, presentation, and the size and location of the defect.

PC consultation appears to be beneficial in the treatment and quality of life of advanced HF patients, independent of their prognosis. This pilot study demonstrated feasibility and sufficient evidence of clinical benefit to warrant a larger randomized clinical trial assessing the benefit of standard involvement by PC in patients with advanced HF, independent of the patient's prognosis or treatment goals.

Acute pericarditis is an acute inflammatory disease of the pericardium, which may occur in many different disease states (both infectious and non-infectious). Usually the diagnosis is based on symptoms (chest pain, shortness of breath), electrocardiographic changes (ST elevation), physical examination (pericardial friction rub) and elevation of cardiac biomarkers. It may occur in isolation or be associated with an underlying inflammatory disorder. In routine clinical practice, acute pericarditis can be associated with myocarditis due to their overlapping etiologies.

Tennis leg is caused by a rupture of the medial head of the gastrocnemius muscle, usually at its distal musculotendinous junction region. However, tears in this muscle and its tendon are also included under the term ‘tennis leg’. It is seen regularly in practice and is an important cause of a painful calf. The common USG findings include: disruption of the pinnate pattern of the distal medial gastrocnemius, usually near the junction of the triceps surae (which is the echogenic line between the gastrocnemius, the soleus, and the plantaris muscles), fluid tracking along the fascia, adjacent hematoma, and intramuscular tears as well as hematomas. USG is useful for confirming the diagnosis, excluding other causes of a painful calf, for assessing the severity of the disease, and in follow-up.

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Pain is a common, underrecognized symptom in patients with chronic but acute decompensated heart failure. Decreased well-being, shortness of breath, and tiredness are the most common and severe symptoms in patients with chronic heart failure, regardless of ejection fraction.

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Key pointsr Intense physical activity, a potent stimulus for sympathetic nervous system activation, is thought to increase the risk of malignant ventricular arrhythmias among patients with hypertrophic cardiomyopathy (HCM).r As a result, the majority of patients with HCM deliberately reduce their habitual physical activity after diagnosis and this lifestyle change puts them at risk for sequelae of a sedentary lifestyle: weight gain, hypertension, hyperlipidaemia, insulin resistance, coronary artery disease, and increased morbidity and mortality.r We show that plasma catecholamine levels remain stably low at exercise intensities below the ventilatory threshold, a parameter that can be defined during cardiopulmonary exercise testing, but rise rapidly at higher intensities of exercise.r These findings suggest that cardiopulmonary exercise testing may be a useful tool to provide an individualized moderate-intensity exercise prescription for patients with HCM.Abstract Intense physical activity, a potent stimulus for sympathetic nervous system activation, is thought to increase the risk of malignant ventricular arrhythmias among patients with hypertrophic cardiomyopathy (HCM). However, the impact of exercise intensity on plasma catecholamine levels among HCM patients has not been rigorously defined. We conducted a prospective observational case-control study of men with non-obstructive HCM and age-matched controls. Laboratory-based cardiopulmonary exercise testing coupled with serial phlebotomy was used to define the relationship between exercise intensity and plasma catecholamine levels. Compared to controls (C, n = 5), HCM participants (H, n = 9) demonstrated higher left ventricular mass index (115 ± 20 vs. 90 ± 16 g/m 2 , P = 0.03) and maximal left ventricular wall thickness (16 ± 1 vs. 8 ± 1 mm, P < 0.001) but similar body mass index, resting heart rate, peak oxygen consumption (H = 40 ± 13 vs. C = 42 ± 7 ml/kg/min, P = 0.81) and heart rate at the ventilatory threshold (H = 78 ± 6 vs. C = 78 ± 4% peak heart rate, P = 0.92).