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Aims To evaluate the clinical impact of early administration of glycoprotein IIb/IIIa agents (IIb/IIIa agents) in the context of a dedicated hub and spoke network allowing very prompt pharmacological/mechanical interventions. Methods and results Using a prospective database, we conducted a cohort study of ST-elevation myocardial infarction (STEMI) patients ( n = 1124) undergoing primary percutaneous coronary interventions (PPCIs) and IIb/IIIa agents administration (period, 2003–2006). Comparisons were planned between patients receiving early IIb/IIIa agents administration (in hub/spoke centre emergency departments or during ambulance transfer; early group, n = 380) or delayed administration (in the catheterization laboratory; late group, n = 744). The primary outcome measure was long-term overall mortality/re-infarction. Baseline characteristics of the two groups were largely comparable. Angiographically, early group patients more often achieved pre-PPCI TIMI Grade 2–3 and TIMI Grade 3 flow. Clinically, the early administration group experienced lower 2-year risk of unadjusted mortality/re-infarction (17 vs. 23%; P = 0.01). After adjustment for potential confounders, early administration was associated with favourable outcome in the overall population (HR = 0.71, P = 0.03) and in high-risk subgroups (TIMI risk index >25, HR = 0.64, P = 0.02; Killip class >1, HR = 0.54, P = 0.01). Conclusion In patients treated by PPCI within a STEMI network setting, early administration of IIb/IIIa agents may provide long-term clinical benefits. Notably, these results appeared magnified in high-risk patients.

Aims We aimed to quantify the release of biomarkers of myocardial damage in relation to direct intramyocardial injections of genes and stem cells in patients with severe coronary artery disease. Methods and results We studied 71 patients with ‘no-option’ coronary artery disease. Patients had, via the percutaneous transluminal route, a total of 11 ± 1 (mean ± SD) intramyocardial injections of vascular endothelial growth factor genes ( n = 56) or mesenchymal stromal cells ( n = 15). Injections were guided to an ischaemic area by electromechanical mapping, using the NOGA™/Myostar™ catheter system. Plasma CKMB (upper normal laboratory limit = 5 µg/L) was 2 µg/L (2–3) at baseline; increased to 6 (5–9) after 8 h ( P < 0.0001) and normalized to 4 (3–5) after 24 h. A total of eight patients (17%), receiving a volume of 0.3 mL per injection, had CKMB rises exceeding three times the upper limit, whereas no patient in the group receiving 0.2 mL had a more than two-fold CKMB increase. No patient developed new ECG changes. There were no clinically ventricular arrhythmias and no death. Conclusion NOGA mapping followed by direct intramyocardial injections of stem cells or genes lead to measurable release of cardiac biomarkers compared with NOGA mapping alone. The increase in biomarkers was related to the injected volume.

Aims To evaluate the predictive value of high sensitivity (hs) C-reactive protein levels on long-term survival in patients with ST-elevation myocardial infarction (STEMI) treated with primary PCI. Methods and results We conducted a retrospective analysis of 758 STEMI patients (from January 2003 to December 2005), with STEMI onset < 12 h and hs-C-reactive protein determination on admission. Patients were classified into four groups [I (hs-C-reactive protein < 0.48 mg/dL), II (hs-C-reactive protein ≥ 0.48 to < 1.2 mg/dL), III (hs-C-reactive protein ≥ 1.2 to < 3.1 mg/dL), IV (hs-C-reactive protein ≥ 3.1 mg/dL)] according to quartiles of hs-C-reactive protein serum level. The IV quartile hs-C-reactive protein group had a higher incidence of in-hospital mortality and cumulative adverse events. At a mean follow-up of 724 ± 376 days (range 0–1393), the IV quartile hs-C-reactive protein group showed lower estimated survival, lower estimated myocardial infarction-free survival and lower estimated event-free survival. At multivariable analysis hs-C-reactive protein appeared to be an independent predictor of long-term mortality (HR: 1.04, 95% CI: 1.01–1.07, P = 0.003), long-term mortality and re-infarction (HR: 1.03, 95% CI: 1.01–1.06, P = 0.008) and adverse events (HR: 1.03, 95% CI: 1.01–1.05, P = 0.03). Conclusion Evaluation of hs-C-reactive protein on admission in STEMI patients undergoing primary PCI allows reliable risk stratification of these patients.

Aims Treatment delay is a powerful predictor of survival in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI). We investigated effectiveness of pre-hospital diagnosis of STEMI with direct referral to PCI, alongside more conventional referral strategies. Methods and results From January 2003 to December 2004, 658 STEMI patients were referred for primary PCI at our intervention laboratory. Three predefined referral routes were compared: (1) for patients within 90 min drive of the PCI centre, pre-hospital diagnosis and direct transportation ( n =166), (2) diagnosis at the interventional hospital emergency department ( n =316), (3) diagnosis at local hospitals before transportation ( n =176). Pre-hospital diagnosis was associated with more than 45 min reduction in treatment delay ( P =0.001). No significant difference in in-hospital mortality was apparent in the overall study population. In the cardiogenic shock subgroup ( n =80), pre-hospital diagnosis was associated with a two-thirds reduction in in-hospital mortality ( P =0.019); mortality was only 6.2% in shock patients who underwent PCI in

To test the hypothesis that mutations in the vascular endothelial growth factor (VEGF) gene are associated with plasma concentration of VEGF and subsequently the ability to influence coronary collateral arteries in patients with coronary heart disease (CHD).Blood samples from patients with chronic ischemic heart disease (n=53) and acute coronary syndrome (n=61) were analysed. Coronary collaterals were scored from diagnostic biplane coronary angiograms.The plasma concentration of VEGF was increased in patients with acute compared to chronic CHD (p=0.01). The genotype frequencies differed significantly from Hardy-Weinberg equilibrium in three of 15 examined loci. Four new mutations in addition to the already described were identified. The VEGF haplotype did not seem to predict plasma VEGF concentration (p=0.5). There was an association between the genotype in locus VEGF-1154 and coronary collateral size (p=0.03) and a significant association between the VEGF plasma concentration and the collateral size (p=0.03).VEGF plasma concentration seems related to coronary collateral function in patients with CHD. The results did not support the hypothesis that polymorphisms in the untranslated region of the VEGF gene were associated with the concentration of circulating VEGF. Increased understanding of VEGF in the regulation of myocardial collateral flow may lead to new therapies in CHD.

We investigated the impact of ambulance-based prehospital triage on treatment delay and all-cause mortality (in hospital and long term) in patients with ST-elevation myocardial infarction (STEMI) complicated by cardiogenic shock referred for primary percutaneous coronary intervention in a prospectively collected registry. During the study period (January 2003 to December 2005), a total of 121 patients was referred for primary percutaneous coronary intervention at our intervention laboratory through 2 main triage groups: (1) after prehospital, ambulance-telemedicine-based triage (42 patients) and (2) by more conventional routes (79 patients) represented by the institutional S. Orsola-Malpighi hospital emergency department triage (44 patients) and spoke hospital triage (35 patients). Total ischemic time was shorter in the prehospital triage (142 minutes, range 106 to 187, vs 212 minutes, range 150 to 366, p = 0.003). Patients with prehospital triage showed a lower rate (29% vs 54%, p = 0.01) of severely depressed (

Tako-tsubo syndrome is a clinical entity of transient left ventricular apical ballooning, frequently precipitated by a stressful event. The syndrome can be complicated by left ventricular outflow tract (LVOT) obstruction and can be recurrent. Herewe describe a case of a 64 years old female who had two episodes of tako-tsubo syndrome characterized by a similar stressful event and similar clinical and instrumental characteristics. Apical ballooning syndrome (or Tako-tsubo cardiomyopathy) is a clinical entity characterized by acute but rapidly reversible left ventricular (LV) systolic dysfunction. Recurrence of Tako-stubo syndrome is not frequent as well as LVOT obstruction, mitral regurgitation and shock. We describe a case of recurrent tako-tsubo cardiomyopathy with recurrence of LVOT obstruction and mitral regurgitation and complicated by cardiogenic shock. A 64 years old female with hypertension and chronic obstructive pulmonary disease (COPD) was admitted to the hospital in June 2005 with an acute recurrent chest pain. The patient was on cortisone from 24 h before because of an asthma exacerbation and she reported having also vomit and fright. The clinical symptom started in the morning but she had the first medical contact only in the evening. At the admission in intensive care unit (ICU) the patients was asymptomatic, the electrocardiogram (ECG) showed a 1.5 mm ST elevation from V3 to V6, DI, DII and aVL. Systolic blood pressure was 90 mm Hg, and an echocardiography exam showed an apical ballooning of the left ventricle with moderate mitral regurgitation secondary to left ventricular outflow tract (LVOT) obstruction (Fig. 1). Promptly, glycoprotein inhibitors and heparine were started and coronary angiography was performed the day after. Ventriculography confirmed the apical ballooning and normal coronary artery. Left ventricular ejection fraction (LVEF) was 35% (Fig. 2). The peak of plasma MB-creatinine kinase and of troponin I was 28.5 ng/mL and 6.9 ng/mL respectively. The systolic pressure remained stable at 90 mm Hg for four days with gradually recover until 110 mm Hg. The patient had no signs of congestive heart failure and was discharged after six days. Complete normalization of LVEF was documented at the follow-up. In December 2009 the woman was admitted in hospital for an exacerbation of her COPD. She was treated for eight days with cortisone, ipratropium, salmeterol and antibiotics with a good clinical response. During her stay she presented chest pain and the ECG showed a 2.5 mm STelevation fromV3 to V6, DI and aVL. The coronary angiography showed no obstructive coronary lesions and an apical ballooning aspect at the ventriculogram (Fig. 3). In ICU the patient developed a cardiogenic shock (initial systolic blood pressure of 90 mm Hg with rapid deterioration until 60 mm Hg). An urgent echocardiogram showed the apical ballooning with the concomitance of LVOT obstruction, systolic anterior motion of mitral valve and severe mitral regurgitation (Figs. 3 and 4). Peak dynamic intraventricular pressure gradient detected by echocardiography was 80 mm Hg. The LVEF was 25%. Urgently an intra-aortic balloon pump (IABP) was placed and then she was treated with low-dose beta-blockers until restoration of good pressure and initial recovery of LVEF. After a period of seven days the IABP was removed: the LVEF was 35% and the peak dynamic pressure gradient was lower (12 mm Hg). The peak of plasma MB-creatinine kinase and troponin T was 18.07 μg/L and 0.55 μg/L respectively. She was discharged after other eight days with a good pressure, no sign of congestive heart failure, a LVEF of 48% and absence of sign of LVOT obstruction and mitral regurgitation. Normalization of LVEF was after documented. Tako-tsubo syndrome, which is also called stress cardiomyopathy or transient left ventricular apical ballooning syndrome, is a clinical entity frequently precipitated by a stressful event. Initially, the syndrome was described in Japanese and afterwards an increasing number of cases has been reported also in Caucasian [1,2]. The main features are the absence of coronary atherosclerosis disease and the reversibility of left ventricular dysfunction. Recurrence of Tako-tsubo syndrome is not frequent. The yearly recurrence rate is 2.9% over the first few years, subsequently decreasing to 1.3% per year [3,4]. The syndrome can be also complicated by LVOT obstruction as previously described [5]. The report described is a rare case of recurrent Tako-Tsubo syndrome with recurrence of similar clinical and instrumental signs. In both episodes the main common findings were hypotension and an echocardiographic aspect of LVOT obstruction, systolic anterior motion and secondary mitral regurgitation. The recurrent episode was much more severe with a cardiogenic shock requiring the IABP positioning. Furthermore the patients experienced in both cases the same physical stressful event.