Patient features that increase the likelihood of cardiac syncope are increasing patient age, history of atrial fibrillation or flutter, history of cardiac failure, and history of severe structural heart disease. Some precipitating factors can decrease the likelihood of cardiac syncope, such as syncope in a warm place, during a medical procedure, or after using the toilet. Dyspnoea or chest pain prior to syncope are associated with higher likelihood of cardiac syncope, whereas cold sensitivity, headache, mood change, and abdominal discomfort decrease the likelihood of cardiac syncope. Witnessed cyanosis is associated with higher likelihood of cardiac syncope, whereas inability to remember details prior to the episode and mood changes after the episode are associated with lower likelihood of cardiac syncope. A combination of normal ECG and no history of cardiac disease is associated with a lower likelihood of cardiac syncope. Contrary to popular teaching, the presence or absence of injury does not predict for or against cardiac syncope.
Two clinical scores, Evaluation of Guidelines in SYncope Study (EGSYS) and vasovagal score), assign scores on the basis of a combination of clinical factors and have some predictive value over and above individual patient characteristics. EGSYS uses six patient variables and a score less than three has a likelihood ratio of cardiac syncope of 0.12–0.17. The vasovagal score has only been prospectively evaluated in one study but a cut‐off score of less than –2 has likelihood ratio of over 8 for cardiac syncope and equal to or more than –2 has a likelihood ratio of 0.10, making this score a potentially good discriminator, if results can be duplicated.
Biomarkers are not yet utilised in widespread practice for the evaluation of syncope, but there is some evidence that high‐sensitivity troponin and N‐terminal pro‐B‐type natriuretic peptide may become useful in ruling out cardiac syncope.
Several clinical features have high specificity, but low sensitivity for the diagnosis of seizure. These include head turning during the event, unusual posturing during the event, urinary incontinence, tongue trauma, and the patient having no recall of witnessed unusual behaviours.
Albassam O, Redelmeier R, Shadowitz S, et al. Did This Patient Have Cardiac Syncope? JAMA. 2019;321(24):2448.
https://jamanetwork.com/journals/jama/article‐abstract/2736568
12. Answer: C
This patient's clinical features, unexplained fever, myalgia, sudden appearance of several small, cool, cyanotic and painful areas of the toe, and AKI are consistent with cholesterol embolisation. Cholesterol embolism is caused by showers of cholesterol crystals from an atherosclerotic plaque that occludes small arteries. Embolisation can occur spontaneously or as an iatrogenic complication from an invasive vascular procedure (angiography or vascular surgery) and after anticoagulant therapy as a result of interference with the protective clot over ulcerative atheromatous plaques and thrombolytic therapy may lyse thrombi, including those covering atherosclerotic plaques.
Once in the circulation, cholesterol crystal emboli lodge in small arteries (150–200 um in diameter); which then cause an inflammatory reaction, intimal proliferation, and intravascular fibrosis leading to the narrowing or obliteration of the lumen and ischaemic changes. Peak incidence is usually two to four weeks after a procedure.The true incidence of cholesterol embolisation is difficult to estimate. Retrospective autopsy (incidence 10–27%) or biopsy (incidence 1%) studies may include subclinical cases. The hallmark of the condition is the presence of needle‐shaped empty spaces in histological sections as the lipids are dissolved by the techniques used to prepare the tissue for histological examination (See below).
Patients can be asymptomatic, or they can present with a distinct clinical syndrome, ranging from a cyanotic toe to a multiorgan systemic disease that can mimic other systemic diseases such as vasculitis. The distribution of end‐organ damage depends on the anatomical location of the original atherosclerotic plaques and the extent of organ involvement. Laboratory investigations are non‐specific. Eosinophilia appears to be the most common finding up to 80% of cases.
The presence of a triad of a precipitating event, AKI, and peripheral embolisation strongly suggests the diagnosis. The presence of other complications of atheroembolism, such as gastrointestinal bleeding and neurological involvement, should raise the suspicion level. To confirm diagnosis, a biopsy of the target organs is needed.
There is no effective treatment apart from symptomatic and supportive measures, including dialysis. Anticoagulants should be avoided if possible because they can potentiate the problem. Disagreement exists concerning steroid treatment. Recently, statins have been found to be associated with better renal outcome likely due to statin‐induced plaque stabilisation and regression. Patients with cholesterol embolisation have a poor prognosis with one‐year mortality rate ranging from 64–87%.
Kronzon I, Saric M. Cholesterol Embolization Syndrome. Circulation. 2010;122(6):631–641.
https://www.ncbi.nlm.nih.gov/pubmed/21993354
Scolari F, Ravani P. Atheroembolic renal disease. The Lancet. 2010;375(9726):1650–1660.
https://www.ncbi.nlm.nih.gov/pubmed/20381857
13. Answer: D
Computed tomography coronary angiography (CTCA) is an imaging test that has been shown in meta‐analyses to have excellent sensitivity (98%) and good specificity (88%) for significant coronary artery disease (CAD) with stenosis >50%. Its high negative predictive values (96–100%) suggest CTCA is an excellent test for ruling out significant disease in patients with low‐to‐intermediate pretest probability of CAD. Current data does not support the use of CTCA in asymptomatic patients.
CTCA is not recommended in patients with previous coronary stents as the stents may produce artefact and make the results uninterpretable. Stent diameter <3 mm is thought to be unevaluable. However, very selective cases can be evaluated using CTCA, including large stents and simple left main stents. CTCA is not appropriate for patients with STEMI given the need for invasive coronary angiogram without any delay.
To avoid artefacts which may hamper interpretation of the results, the patient should be in sinus rhythm with a heart rate <65 beats/min, able to hold their breath for 10 seconds, able to tolerate beta blockers and nitrates (nitrates are given to dilate the coronary arteries by most centres), and able to hold their arms above the head during the scan. Previous contrast allergy must be ruled out prior to CTCA. If the patient has significant renal impairment, CTCA may not be the best investigation for CAD due to the risk of contrast nephropathy.
Liew G, Feneley M, Worthley S. Appropriate indications for computed tomography coronary angiography. Medical Journal of Australia. 2012;196(4):246–249.
https://www.mja.com.au/journal/2012/196/4/appropriate‐indications‐computed‐tomography‐coronary‐angiography
14. Answer: B
This patient has evidence of native mitralvalve infective endocarditis (IE) complicated by cerebral emboli. IE is the infection of the endocardial surface of the heart and may involve one or more heart