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38 False activation for primary percutaneous coronary intervention is not a benign phenomenon
  1. U Chaudhry,
  2. C Mavroudis,
  3. R D Rakhit
  1. Cardiology Department, Royal Free Hospital, London, UK

Abstract

Introduction 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.

Aim To review the clinical outcome of patients presenting to our heart attack centre with false activation PPCI.

Method 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.

Results 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<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.

Conclusion 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.

  • False activation
  • Primary percutaneous coronary intervention
  • outcome

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