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Dyspnea on exertion is a commonly encountered problem in clinical practice. It is usually investigated by resting tests such as pulmonary function tests and echocardiogram, which may at times can be non-diagnostic. Cardiopulmonary exercise testing (CPET) measures physiologic parameters during exercise which can enable accurate identification of the cause of dyspnea. Though CPET has been around for decades and provides valuable and pertinent physiologic information on the integrated cardiopulmonary responses to exercise, it remains underutilized. The objective of this review is to provide a comprehensible overview of the underlying principles of exercise physiology, indications and contraindications of CPET, methodology and interpretative strategies involved and thereby increase the understanding of the insights that can be gained from the use of CPET.

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Cardiac perforation by pacemaker is a rare but potentially fatal complication. Acute perforations occurring within twenty-four hours of insertion of pacemaker can lead to hemopericardium, cardiac tamponade, and death. Hemothorax occurring as an acute complication of pacemaker insertion is reported but extremely rare. Previously, hemothorax and shock as a subacute complication following pacemaker insertion have not been reported. We report the case of an 85-year-old patient who presented with shock from hemothorax caused by pacemaker perforation, two weeks after insertion. Device interrogation showed normal function. Chest X-ray and echocardiogram missed lead dislocation and the diagnosis was made on computed tomogram (CT) of the chest. Following surgical repair, a new ventricular pacemaker was placed transvenously in the right ventricular septum. This case illustrates that CT scan of the chest should be performed in all patients in whom cardiac perforation by pacemaker is suspected but not diagnosed on chest X-ray and echocardiogram. Normal functioning of pacemaker on device interrogation does not exclude perforation.

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The experience with inflammatory bowel disease in a stable, defined population in northeast England is described. In this population, the incidence of inflammatory bowel disease was higher than expected. In particular, a high incidence of colorectal and anal Crohn's disease was found. The literature is reviewed in order to identify some of the factors responsible for this unusual prevalence of inflammatory bowel disease in the study population. No explanation for our unexpected findings can be advanced.

Treatment options for nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D), two conditions which coexist, are limited though weight loss is an important strategy to improve outcomes in either disease. Glucagon-like peptide 1 receptor agonist (GLP1-RA) present a novel option to treat this dual disease by their salutary effects on glycaemic control and weight reduction. Eight randomized controlled trials on T2D and NAFLD from the Cochrane Library, Embase, and PubMed were included in this meta-analysis. The Comprehensive Meta-Analysis Software version 3 was used to calculate the effect size. In a pooled population of 615 patients—297 on GLP1-RA and 318 in the control arm, GLP1-RA produced a significant improvement in alanine aminotransferase [standardised mean difference (SDM), − 0.56, 95% CI − 0.88 to − 0.25, P < 0.01], aspartate aminotransferase (SDM, − 0.44, SE, 95% CI − 0.64 to − 0.24, P < 0.01), gamma glutaryl transaminase (SDM, − 0.60, 95% CI − 0.86 to − 0.34, P < 0.01) and reduction in liver fat content (LFC) (SDM, − 0.43, 95% CI − 0.74 to − 0.12, P < 0.01), as well as glycosylated haemoglobin (SDM, − 0.40, 95% CI, − 0.61 to − 0.19, P < 0.01) and weight (SDM, − 0.66, 95% CI, − 0.88 to − 0.44, P < 0.01), in comparison to standard of care or placebo. Significant improvement in biopsy resolution was also seen in the GLP1-RA arm (Rate Ratio, 6.60, 95% CI 2.67 to 16.29, P < 0.01). This is possibly the first meta-analysis conducted exclusively in patients with T2D and NAFLD which presents a strong signal that GLP1-RA, improve liver function and histology by improving glycaemia, reducing body weight and hepatic fat, which in turn reduces hepatic inflammation.Trial Registration: PROSPERO (ID: CRD42021228824).

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