SUMMARYIn patients with acute chest pain the prime need, usually, is to diagnose and treat myocardial infarction or ischaemia. When a cardiac origin for the pain has been excluded, patients are commonly discharged without either a diagnosis or a plan for follow-up. We studied a group of such patients to see how far causation was pursued and how their mortality compared with that of patients with a proven cardiac cause for their symptoms. The study population was 250 patients admitted over five weeks with chest pain suspected of being cardiac in origin. Initial assessment included an electrocardiogram and measurement of troponin T. If neither of these indicated a cardiac event, the patient was deemed to have 'atypical' chest pain and the cause, where defined, was recorded. Outcomes at one year were determined by questionnaire and by assessment of medical notes.Of the 250 patients, 142 had cardiac pain (mean age 79 years, 58% male) and 108 atypical chest pain (mean age 60 years, 55% male). Of those with atypical pain, 40 were discharged without a diagnosis; in the remaining 68 the pain was thought to be musculoskeletal (25), cardiac (21), gastrointestinal (12) or respiratory (10) in origin. 41 patients were given a follow-up appointment on discharge. At one year, data were available on 103 (96%) patients.The mortality rate was 2.9% (3 patients) compared with 18.3% in those with an original cardiac event. Half of the patients with atypical pain had undergone further investigations and 14% had been readmitted. The yield of investigative procedures was generally low (20%) but at the end of the year only 27 patients remained undiagnosed.Patients with atypical chest pain form a substantial proportion of emergency admissions. The symptoms often persist or recur. The commonest causation is musculoskeletal, but a sizeable minority remain undiagnosed even after follow-up.

In patients with acute chest pain the prime need, usually, is to diagnose and treat myocardial infarction or ischaemia. When a cardiac origin for the pain has been excluded, patients are commonly discharged without either a diagnosis or a plan for follow-up. We studied a group of such patients to see how far causation was pursued and how their mortality compared with that of patients with a proven cardiac cause for their symptoms. The study population was 250 patients admitted over five weeks with chest pain suspected of being cardiac in origin. Initial assessment included an electrocardiogram and measurement of troponin T. If neither of these indicated a cardiac event, the patient was deemed to have 'atypical' chest pain and the cause, where defined, was recorded. Outcomes at one year were determined by questionnaire and by assessment of medical notes. Of the 250 patients, 142 had cardiac pain (mean age 79 years, 58% male) and 108 atypical chest pain (mean age 60 years, 55% male). Of those with atypical pain, 40 were discharged without a diagnosis; in the remaining 68 the pain was thought to be musculoskeletal (25), cardiac (21), gastrointestinal (12) or respiratory (10) in origin. 41 patients were given a follow-up appointment on discharge. At one year, data were available on 103 (96%) patients. The mortality rate was 2.9% (3 patients) compared with 18.3% in those with an original cardiac event. Half of the patients with atypical pain had undergone further investigations and 14% had been readmitted. The yield of investigative procedures was generally low (20%) but at the end of the year only 27 patients remained undiagnosed. Patients with atypical chest pain form a substantial proportion of emergency admissions. The symptoms often persist or recur. The commonest causation is musculoskeletal, but a sizeable minority remain undiagnosed even after follow-up.

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We describe a cohort of patients with a high rate of mid-term failure following Kinemax Plus total knee replacement inserted between 1998 and 2001. This implant has been recorded as having a survival rate of 96% at ten years. However, in our series the survival rate was 75% at nine years. This was also significantly lower than that of subsequent consecutive series of PFC Sigma knee replacements performed by the same surgeon. No differences were found in the clinical and radiological parameters between the two groups. At revision the most striking finding was polyethylene wear. An independent analysis of the polyethylene components was therefore undertaken. Scanning electron microscopy revealed type 2 fusion defects in the ultra-high molecular weight polyethylene (UHMWPE), which indicated incomplete boundary fusion. Other abnormalities consistent with weak UHMWPE particle interface strength were present in both the explanted inserts and in unused inserts from the same period. We consider that these type 2 fusion defects are the cause of the early failure of the Kinemax implants. This may represent a manufacturing defect resulting in a form of programmed polyethylene failure.