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Many patients provisionally diagnosed with acute myocardial infarction (AMI) have angiographically unobstructed coronary arteries. Despite other potential causes, patients are often diagnosed as AMI with psychosocial implications and medication burden. The aim of this audit was to review such patients at our centre.All patients investigated for possible AMI with coronary angiography from 2007 until 2011 at Christchurch Hospital, New Zealand, in whom cardiac troponin was elevated (with no other cause found for that elevation) but coronary angiography showed diameter stenosis50% were reviewed. Primary outcome was two-year cardiac death and AMI (by universal definition).Of the 351/6493 (5.4%) who met the inclusion criteria, 180 had normal angiograms and 171 had non-obstructive coronary disease (stenosis0% and50%). By two years there were two cardiac deaths (0.6%) and five AMIs (1.4%). The primary outcome rate was therefore 2.0% (2.2% for those with normal angiograms and 1.8% with non-flow limiting coronary disease, p=1.000).Patients who have presented with AMI symptoms, elevated cardiac troponin, and unobstructed coronary arteries on angiography are at very low risk of cardiac death (0.6%), AMI (1.4%) or either (2.0%) at two-year follow-up.

Background: Bioresorbable Scaffolds (BRS) for the treatment of coronary stenosis involves the use of a temporary polymeric scaffold to maintain normal arterial curvature, allow return of vasomotion and enable positive remodelling without a longterm metallic cage. We aimed to determine short-medium term outcomes of patients undergoing percutaneous coronary intervention (PCI) with BRS. Methods: Consecutive patients undergoing PCI with ABSORB BRS at Christchurch Hospital/St George’s Hospital between 18/08/2011-07/02/2014 were followed for Major Adverse Cardiac Events (MACE death, non-fatal myocardial infarction (MI) and revascularisation). Results: Of 62 patients included: mean age 53.2 years, 83% male, 11.3%diabetic. 25.8%STEMIand19.4%NSTEMI.A total of 85 BRS were deployed in 71 vessels (49% LAD) 83.7% 1vessel and 16.3% 2-vessel. There were 56% type-B and 41% type-C lesions with 2 ostial, 2 in-stent restenosis, and 4 bifurcation lesions. Overlap stenting perfomed in 12 patients (6 = BVS/BVS, 6 = BVS/drug eluting stent (DES)). The median stent/scaffold length for overlap stenting was 46mm (20-88mm). The device/procedural success rates were 100%. During median follow up of 7.5 months (0.530.3months), MACE rate was 3.2% (2 cases with STEMI due to sub-acute scaffold thrombosis: one ostial lesion and one bifurcation lesion). No deaths were reported. Conclusions: BRS implantation appears safe in patients with stable angina and MI. Use of overlapping BRS or DES/ BRS appears feasible in treatment of long lesions.

assays have been developed which can detect much lower levels of troponin. Methods: 441 patients with chest pain suggestive of acutemyocardial infarction (AMI)were recruited between November 2006 and May 2007; all were followed for 2 years. Serial blood samples were analysed to compare Roche high sensitivity troponin T (hsTNT)with latest generation Abbott troponin I (TNI) and Roche TNT for the prediction of MACE, defined as composite of cardiovascular death, myocardial infarction or revascularization. Results: 91 patients (20.6%) experienced MACE at 2 years. ROC curve AUC for baseline hsTNT was 0.71 (0.66–0.75), TNI was 0.66 (0.61–0.71) and TNT was 0.62 (0.56–0.67). hsTNT out-performs TNT (p= 0.001) but there is no statistical difference between hsTNT and TNI or TNI andTNT.Hazard ratios (HR) forMACEwere 11.4 (2.8–46.9) for hsTNT, 2.9 (1.9–4.6) for TNI and 2.5 (1.6–3.8) for TNT. WhenHRareadjusted foranypatient characteristic shown to be independent predictors ofMACE (in this study independent predictors were age, prior history of ischaemic heart disease and index admission diagnosis of AMI), only hsTNTconveyedadditional risk,HR, 5.2 (1.2–23.1,p= 0.03). Conclusions: hsTNT outperforms conventional assays in prediction of MACE as seen by ROC curve analysis and Cox proportional hazards modelling and is the only troponin to add prognostic utility when adjusted for all baseline characteristics.

although it occurs with higher frequency in association with certain congenital cardiovascular anomalies [3]. In 1993 Shirani and Roberts proposed a classification system [4] for solitary coronary ostiums based on the location of the ostium relative to the aortic sinuses and the characteristics of aberrant-coursing arteries. Our patient would be subtype IIC4, at that time a theoretical possibility but yet to be reported. Since then many examples of retroaortic left main coronary artery (LMCA) arising from a common ostium with the RCA in the right sinus of Valsalva have been reported [5–9], although these have been subtype IIB4 where the LMCA bifurcates to the LAD and Cx. In contrast, in our patient the Cx arises from the RCA and hence is subtype IIC4 which to the best of our knowledge has not been reported.

winter hospitalisations (EWH) and whether this applied to all subcategories of CVD. Methods:We obtained CVD data (ICD.9 principal diagnosis code 390-459 and ICD.10 code I00-I99) from the New Zealand Health Information Service, including all deaths (1988–2005) and hospitalisations (1988–2007). We derived EWM and EWH for each subcategory of CVD using the ratio between episodes in the winter months (June, July and August) comparedwith summer (December, January, February). We excluded inter-hospital transfers, readmissionswithin30days,plannedadmissionsanddaypatients. Results:Over this period there were 207,012 deaths and 757,870 hospitalisations coded as CVD (42% and 8.8% of the total deaths and admissions, respectively). Mortality andmorbidityweredominatedbycoronarydisease (56.9% and 39.7%) and stroke (23.4% and 14.6%); heart failure also contributing substantially to admissions (13.8%). All 14 subcategories of CVD with total deaths >100 showed EWM with ratios >1.0, most notable being cardiac infections (1.43), heart failure (1.42) and coronary disease (1.32). Similarly all classes showed EWH, especially heart failure (ratio 1.47) although ratios for other diagnostic categories were smaller. Conclusion: All types of CVD deaths and hospitalisations are markedly higher in winter with greater differences among the sickest patients—those dying and those with heart failure. Further research will help to Results:Maori had a higher CHD incidence and higher case fatality than non-Maori. Maori developed CHD at a younger age (medians 56.5 years for males and 58.8 years for females) than non-Maori (medians 67.5 and 77.5, respectively). The lifetime risk of CHD for Maori (36% for males and 34% for females) was only slightly higher than that for the non-Maori population (35% and 28%, respectively) despite higherMaori CHD incidence. This appears to reflect increased age-specificmortality for non-CHD illnesses as well as CHD. Duration of survival with CHD in Maori (9.2 years) was similar to that of the non-Maori population formales (9.5 years) but longer for females (11.2 vs. 6.2 years), which is most likely related to the earlier age of onset in the Maori population. Conclusions: CHD has a markedly higher impact in Maori and at younger ages than in the wider population identifying areas requiring prioritisation. doi:10.1016/j.hlc.2009.04.051

involved a 6-month observation period. Phase 2 involved strategies to expedite movement of the patient from the emergency department (ED) to the catheterization laboratory (10 months). Phase 3 involved initiation of a “Code MI” centralized paging system (11 months). We recorded door (D), call (C) and balloon (B) times. Results: Phase 1 (n= 33) Phase 2 (n= 65) Phase 3 (n= 71) DB—median 99 90 71** CB—median 82 59* 50** DB within 90min 33% 49% 75% DB 90th percentile 205min 185min 110min CB 90th percentile 109min 85min 74min ∗ p< 0.01 vs. Phase 1. ∗∗ p< 0.001 vs. Phase 1. Of the 169 consecutive patients, 105 presented outside normal operating hours, 30 were in cardiogenic shock (CS) and/or had required prolonged resuscitation prior to reaching the catheterization laboratory and there were 15 deaths at 30 days (15/30 in CS and 0/139 not in CS). The introduction of simple strategies to reduce DB times benefits all patients, particularly those for whom prolonged delays may remove the treatment advantage of PCI. doi:10.1016/j.hlc.2008.05.392