38 False activation for primary percutaneous coronary intervention is not a benign phenomenon

Abstract

<h3>Introduction</h3> Primary percutaneous coronary angioplasty (PPCI) is the preferred reperfusion strategy following an acute ST elevation myocardial infarction (STEMI). Since 2005 24/7 primary PCI has been the first line treatment for an acute STEMI in our centre. 93% of patients are direct access admissions by London Ambulance but a significant proportion (up to 20%) do not fulfil the diagnostic criteria for STEMI and are termed “false activations”. Data on the outcome of this cohort of patients is limited. <h3>Aim</h3> To review the clinical outcome of patients presenting to our heart attack centre with false activation PPCI. <h3>Method</h3> From January 2008 until October 2010, we identified 209 false PPCI activations defined as patients with incomplete diagnostic criteria for acute STEMI: absence of chest pain and/or typical ECG features (ST elevation or new LBBB). Data was collected via a “false activation” database together with retrospective review of case records. <h3>Results</h3> Complete data was available in 165 cases. 71% were male and 29% were female (mean age 67). The mean length of stay was 4 days (range 1–33). 71% presented with chest pains and 29% had no chest pains, but presented with breathlessness, palpitations or syncope. The ECG abnormality was non-specific ST-T changes in 22%, LBBB in 19%, left ventricular hypertrophy in 15%, fixed ST elevation or Q waves in 14%, early repolarisation changes in 10%, RBBB in 8% and other ECG abnormalities in 12%. The final diagnosis was non-ST elevation acute coronary syndrome (NSTEACS) in 19%, sepsis in 19% and congestive heart failure (CHF) in 15%. Stable angina was observed in 8% and syncope in 7%. Musculoskeletal or non-cardiac chest pains were noted in 8% and 7% of the patients respectively. 2% of the patients had pulmonary embolism and in 5%, a gastric cause for presentation was diagnosed. 14% had other cardiac problems, including arrhythmia, dilated cardiomyopathy, hypertension, pericarditis, pericardial effusion and late presentation STEMI. 15% had other diagnoses. The mean follow-up period was 18.7 months, during which 21.5% of false PPCI activation admissions died (n=45). 25% (n=11) died during the index admission and 33% (n=15) died within 30 days of admission. The overall 30-day mortality for false activations was 7.2%, which is higher than the overall PPCI mortality of 6.0% (including cardiogenic shock) (p=0.008) and 3.3% (excluding shock) (p&lt;0.0001) in our centre. 49% of deaths were cardiac (NSTEACS and CHF), 29% sepsis and 22% other causes. The mean age for this cohort was 83. <h3>Conclusion</h3> Patients presenting with false PPCI activation have a high observed mortality. This is probably due to significant associated comorbidities, including occult cardiac disease. Thus, false PPCI activation is not a benign phenomenon and masks underlying significant disease. Robust pathways are required to minimise delay in further investigations and a need for risk stratification for a significant proportion who present with NSTEACS.