October 2020 Br J Cardiol 2020;27(4) doi: 10.5837/bjc.2020.031
Nathalie Esser, Sakeneh Zraika
The renin–angiotensin system (RAS) has been at the forefront of research aimed at mitigating the infectivity and mortality associated with the coronavirus disease 2019 (COVID-19) pandemic. This stems from the observation that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen that causes COVID-19, utilises angiotensin-converting enzyme 2 (ACE2) as its receptor to invade host cells. Since emergence of COVID-19, conflicting guidance has been published on the use of medications that may increase ACE2 levels. Specifically, initial reports suggested that ACE inhibitors and angiotensin II type 1 receptor blockers (ARBs) may result in increased virulence of COVID-19 due to elevated ACE2. Thus, discontinuation of these RAS blockers was advised. However, the data on ACE2 expression with use of RAS blockers in humans without COVID-19 are not clear, and for humans with COVID-19 are not yet available. Moreover, discontinuation of these medications may be deleterious in some patients for whom they are prescribed to treat heart failure, hypertension and ischaemic heart disease. For this reason, professional organisations, including the American College of Cardiology, American Heart Association, Heart Failure Society of America and the European Society of Cardiology, have issued statements advising against discontinuation of any RAS-related treatments in patients during the COVID-19 crisis.
October 2020 Br J Cardiol 2020;27(4) doi: 10.5837/bjc.2020.032
Paula Finnegan, John Jefferies, Ronan Margey, Barry Hennigan
We provide the details of three cases utilising intravascular lithotripsy, a novel approach to percutaneous coronary intervention (PCI).
October 2020 Br J Cardiol 2020;27(4) doi: 10.5837/bjc.2020.033
Telal Mudawi, Darar Al-Khdair, Muath Al-Anbaei, Asmaa Ali, Ahmed Amin, Dalia Besada, Waleed Alenezi
The benefit of percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI) is undisputed. Clinical trials like DANAMI-2 (DANish Acute Myocardial Infarction 2),1-3 PRAGUE-2 (Primary Angioplasty in AMI Patients from General Community Hospitals Transported to PTCA Units vs Emergency Thrombolysis),4,5 STAT (Stenting Versus Thrombolysis in Acute Myocardial Infarction),6 AIR PAMI (Air Primary Angioplasty in Myocardial Infarction),7 Stent Versus Thrombolysis for Occluded Coronary Arteries in Patients With Acute Myocardial Infarction (STOPAMI)-1,8 and STOPAMI-29 have demonstrated better outcomes with primary PCI over fibrinolysis. Other clinical trials10-14 have demonstrated superiority of PCI over sole medical therapy for non-ST elevation myocardial infarction (NSTEMI) and unstable angina.
In contrast, there is ambiguity surrounding the benefit of elective PCI in stable coronary disease. The available evidence suggests no prognostic advantage over optimum medical therapy but deeper data scrutiny indicates that this remains uncertain. COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation),15 BARI 2D (Bypass Angioplasty Revascularization Investigation 2 Diabetes),16 and ISCHEMIA (Initial Invasive or Conservative Strategy for Stable Coronary Disease)17 are the main trials that examined this issue, all concluding against the prognostic usefulness of elective PCI. We argue that those studies contained inherent flaws that impacted on their results, thereby rendering their final conclusions unreliable. We suggest an alternative design for a new trial so the question can be answered decisively, once and for all.
October 2020 Br J Cardiol 2020;27(4) doi: 10.5837/bjc.2020.034
Iain T Parsons, Michael Hickman, Mark Ingram, Edward W Leatham
The utility of computed tomography (CT) coronary angiography (CTCA) is underpinned by its excellent sensitivity and negative-predictive value for coronary artery disease (CAD), although it lacks specificity. Invasive coronary angiography (ICA) and invasive fractional flow reserve (FFR), are gold-standard investigations for coronary artery disease, however, they are resource intensive and associated with a small risk of serious complications. FFR-CT has been shown to have comparable performance to FFR measurements and has the potential to reduce unnecessary ICAs. The aim of this study is to briefly review FFR-CT, as an investigational modality for stable angina, and to share ‘real-world’ UK data, in consecutive patients, following the initial adoption of FFR-CT in our district general hospital in 2016.
A retrospective analysis was performed of a previously published consecutive series of 157 patients referred for CTCA by our group in a single, non-interventional, district general hospital. Our multi-disciplinary team (MDT) recorded the likely definitive outcome following CTCA, namely intervention or optimised medical management. FFR-CT analysis was performed on 24 consecutive patients where the MDT recommendation was for ICA. The CTCA + MDT findings, FFR-CT and ICA ± FFR were correlated along with the definitive outcome.
In comparing CTCA + MDT, FFR-CT and definitive outcome, in terms of whether a percutaneous coronary intervention was performed, FFR-CT was significantly correlated with definitive outcome (r=0.471, p=0.036) as opposed to CTCA + MDT (r=0.378, p=0.07). In five cases (21%, 5/24), FFR-CT could have altered the management plan by reclassification of coronary stenosis. FFR-CT of 60 coronary artery vessels (83%, 60/72) (mean FFR-CT ratio 0.82 ± 0.10) compared well with FFR performed on 18 coronary vessels (mean 0.80 ± 0.11) (r=0.758, p=0.0013).
In conclusion, FFR-CT potentially adds value to MDT outcome of CTCA, increasing the specificity and predictive accuracy of CTCA. FFR-CT may be best utilised to investigate CTCAs where there is potentially prognostically significant moderate disease or severe disease to maximise cost-effectiveness. These data could be used by other NHS trusts to best incorporate FFR-CT into their diagnostic pathways for the investigation of stable chest pain.
September 2020 Br J Cardiol 2020;27:77–8 doi: 10.5837/bjc.2020.025
Luke Pickup, Jonathan P Law, Jonathan N Townend, Charles J Ferro
“Alone we can do so little, together we can do so much.” Helen Keller
The links between kidney disease and cardiovascular disease have been reported as far back as 1827 with Richard Bright describing the changes in the left ventricle associated with kidney disease, and subsequently, Frederick Akbar Mahomed reporting increased arterial stiffness in patients with Bright’s disease.1 Over the last two to three decades it has become increasingly apparent that kidney disease is the most important predictor of outcomes in all cardiology diseases and that cardiovascular disease is the leading cause of death in patients with chronic kidney disease.2 In 2008, a systematic approach to the bi-directional interactions of heart and kidney diseases, or cardiorenal syndromes (table 1), was proposed.3 Cardiorenal syndromes can be broadly defined as disorders of the heart and kidney whereby acute or chronic dysfunction in one organ can induce acute or chronic dysfunction in the other.4 This was followed by increasing efforts to develop strategies to manage patients with combined heart and kidney dysfunction, as demonstrated by an increasing number of publications on cardiorenal syndromes.5
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