scholarly journals Does stress echocardiography still have a role in the rapid access chest pain clinic post NICE CG95?

2019 ◽  
Vol 6 (2) ◽  
pp. 17-23 ◽  
Author(s):  
Victoria Pettemerides ◽  
Thomas Turner ◽  
Conor Steele ◽  
Anita Macnab

Introduction The 2016 NICE clinical guideline 95 (CG95) demoted functional imaging to a second-line test following computed tomography coronary angiography (CTCA). Many cardiac CT services in the UK require substantial investment and growth to implement this. Chest pain services like ours are likely to continue to use stress testing for the foreseeable future. We share service evaluation data from our department to show that a negative stress echocardiogram can continue to be used for chest pain assessment. Methods 1815 patients were referred to rapid access chest pain clinic (RACPC) between June 2013 and March 2015. 802 patients had stress echocardiography as the initial investigation. 446 patients had normal resting left ventricular (LV) systolic function and a negative stress echocardiogram. At least 24 months after discharge, a survey was carried out to detect major adverse cardiovascular events (MACE) (cardiac death, myocardial infarction, admission to hospital for heart failure or angina, coronary artery disease at angiography, revascularisation by angioplasty or coronary artery bypass grafting) within 2 years. Results Overall, 351 patients were successfully followed up. The mean Diamond-Forrester (D-F) score and QRISK2 suggested a high pre-test probability (PTP) of coronary artery disease (CAD). There were nine deaths (eight non-cardiac deaths and one cardiac death). MACE occurred in four patients with a mean time of 17.5 months (11.6–23.7 months). The annual event rate was 0.6%. Conclusion A negative stress echocardiogram can reliably reassure patients and clinicians even in high PTP populations with suspected stable angina. It can continue to be used to assess stable chest pain post CG95.

1991 ◽  
Vol 122 (5) ◽  
pp. 1456-1463 ◽  
Author(s):  
Miguel Zabalgoitia ◽  
Dipeshkumar K. Gandhi ◽  
Pierre Abi-Mansour ◽  
Paul R. Yarnold ◽  
Bassam Moushmoush ◽  
...  

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Sheikh Bilal B Khalid ◽  
Javaria Mahmood

Introduction: Cisplatin-based chemotherapeutic regimen (CBCR) is known for increasing risk of venous thromboembolic (TE) disease. We report a unique case of STEMI associated with CBCR which we believe was caused by coronary artery thrombosis. Case description: A 31-yo man with a past history of germ cell tumor presented with chest pain radiating to back and left arm. It started this morning and intensity did not worsen with exertion. He denied any dyspnea, diaphoresis or palpitations. He was non-smoker and non-obese. He denied any family history of premature coronary artery disease. He had undergone unilateral orchiectomy a year ago, and was currently receiving chemotherapy with bleomycin, etoposide and cisplatin; the last dose of his 3 rd cycle was given the day before. EKG showed ST elevation in leads I, aVL, V4 and V5. Troponin I was high to 6.9 ng/ml (ULN 0.045 ng/ml). He received intravenous infusion of thrombolytic. An angiogram done the next day showed moderate mid-LAD disease with residual clot. A CT scan and an echocardiogram later showed left ventricular thrombus (LVT). He was kept on therapeutic enoxaparin along with aspirin. Follow up echocardiogram showed resolution of the thrombus. His chemotherapy was stopped, and he has been kept on active surveillance since then. Discussion: Most cases of CBCR-associated myocardial infarction that have been reported have been seen in the older population with other risk factors for coronary artery disease. Cases where angiographic data was available, coronary artery vasospasm appeared to be the culprit rather than a true plaque rupture. While the presence of LVT raises possibility of thromboembolism to coronaries causing MI, the angiographic findings support accelerated plaque formation to be the cause of infarction. In earlier reports, elevated pre-treatment level of von Willebrand factor has been postulated to have some role in the disease pathogenesis. Other possible mechanisms for pathogenesis include endothelial cell damage, platelet activation, and imbalance between thromboxane-prostacyclin levels. This case emphasizes the need to keep cardiac etiologies of chest pain in the differential when evaluating patients on CBCR as timely intervention is life saving and prevent morbidity.


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