May 2020 Br J Cardiol 2020;27(2) doi: 10.5837/bjc.2020.010
Xenophon Kassianides, Adil Hazara, Sunil Bhandari
The current President of the United States once stated that “the kidney has a very special place in the heart”; despite the questionable anatomical reference, the truth is that the kidneys and heart are intertwined, affected by common pathophysiological processes and sharing many of the same disease-causing risk factors. Ronco and colleagues have previously classified the complex array of inter-related derangements that simultaneously involve both organs, and this serves as a useful starting point in understanding their important physiological and pathophysiological inter-dependence.1
May 2020 Br J Cardiol 2020;27(2) doi: 10.5837/bjc.2020.011
Yuen W Liao, James Redfern, John D Somauroo, Robert M Cooper
The health benefits of physical activity are well documented. Patients with hypertrophic cardiomyopathy (HCM) are often discouraged from participating in physical activity due to a perceived increase in the risk of sudden cardiac death (SCD). As a result, only 45% of patients with HCM meet the minimum guidelines for physical activity, and many report an intentional reduction in exercise following diagnosis. Despite most SCD being unrelated to HCM, guidelines traditionally focused on the avoidance of potential risk through restriction of exercise, without clear recommendations on how to negate the negative health impact of inactivity. Retrospective reviews have demonstrated that the majority of cardiac arrests in patients with HCM occurred at rest or on mild exertion and that the overall incidence of HCM-related SCD is significantly lower than previously reported. We will discuss current international guidelines and recommendations and consider the outcomes of various studies that have investigated the effects of exercise of different intensities on patients with HCM. In light of the growing evidence suggesting that carefully guided exercise can be both beneficial and safe in patients with HCM, we ask whether it is time to let the shackles off exercise restriction in HCM.
May 2020 Br J Cardiol 2020;27(2) doi: 10.5837/bjc.2020.012
Kevin Cheng, Ranil de Silva
Refractory angina (RA) is a growing clinical problem. Long-term mortality is better than expected and focus has shifted to improving symptoms, quality of life and psychological morbidity. We established a dedicated multi-disciplinary care pathway for patients with RA and assessed its effect on psychological outcomes, quality of life and polypharmacy. We reviewed electronic health records to capture demographics, changes in medication use, and patient-related outcome measures (Seattle Angina Questionnaire [SAQ] and Hospital Anxiety and Depression Scale) before and after enrolment.
One hundred and ninety patients were referred to our service. Pre- and post-questionnaire data were available in 83 patients. Anxiety and depression scores significantly improved (p<0.05) as well as quality of life and all subcategories of the SAQ (p<0.0001). Patients were most commonly on three or four anti-anginal drugs. In patients with no demonstrable reversible ischaemia, there was a significant reduction in anti-anginal usage (mean reduction of two drugs) after completion of our pathway (p<0.025).
In conclusion, a dedicated multi-disciplinary pathway for RA is associated with improvements in quality of life, mental health and polypharmacy. An ischaemia-driven method to rationalise medication may reduce polypharmacy in patients with RA, particularly in patients with no demonstrable ischaemia.
May 2020 Br J Cardiol 2020;27(2) doi: 10.5837/bjc.2020.013
JJ Coughlan, Max Waters, David Moore, David Mulcahy
“I will give you a new heart and put a new spirit in you; I will remove from you your heart of stone and give you a heart of flesh” – Ezekiel 36:26
May 2020 Br J Cardiol 2020;27(2) doi: 10.5837/bjc.2020.014
Sinead Curran, Waleed Arshad, Arvinder Kurbaan, Han B Xiao
The U-wave on electrocardiogram (ECG) is a small deflection following the T-wave, the sixth wave. It is 25% or less of the preceding T-wave in amplitude.1,2 While the genesis of the U-wave is uncertain, it is said to represent repolarisation of the Purkinje fibres.1,2 Disproportionally large U-waves may indicate underlying cardiac or non-cardiac pathology. A relatively frequent cause for a large U-wave is hypokalaemia. It is observed in patients with bradycardia, ventricular hypertrophy, hypothyroidism, hypocalcaemia, hypomagnesaemia, mitral valve prolapse, hypothermia, increased intracranial pressure, or patients on anti-arrhythmic medicine.2 A negative U-wave, on the other hand, may represent early myocardial ischaemia, specifically in the context of a lesion in the left main or proximal left anterior descending coronary artery.2,3