CASZ1 loss-of-function mutation contributes to familial dilated cardiomyopathy.

BACKGROUND: The zinc finger transcription factor CASZ1 plays a key role in cardiac development and postnatal adaptation, and in mice, deletion of the CASZ1 gene leads to dilated cardiomyopathy (DCM). However, in humans whether genetically defective CASZ1 contributes to DCM remains unclear. METHODS: The coding exons and splicing junction sites of the CASZ1 gene were sequenced in 138 unrelated patients with idiopathic DCM. The available family members of the index patient harboring an identified CASZ1 mutation and 200 unrelated, ethnically matched healthy individuals used as controls were genotyped for CASZ1. The functional characteristics of the mutant CASZ1 were analyzed in contrast to its wild-type counterpart using a luciferase reporter assay system. RESULTS: A novel heterozygous CASZ1 mutation, p.K351X, was identified in an index patient with DCM. Genetic analysis of the mutation carrier's family showed that the mutation co-segregated with DCM, which was transmitted in an autosomal dominant pattern with complete penetrance. The nonsense mutation, which was absent in 400 referential chromosomes, altered the amino acid that was highly conserved evolutionarily. Biological investigations revealed that the mutant CASZ1 had no transcriptional activity. CONCLUSIONS: The current study reveals CASZ1 as a new gene responsible for human DCM, which provides novel mechanistic insight and potential therapeutic target for CASZ1-associated DCM, implying potential implications in improved prophylactic and therapeutic strategies for DCM, the most common type of primary myocardial disease.

TBX5 loss-of-function mutation contributes to familial dilated cardiomyopathy.

The cardiac T-box transcription factor TBX5 is crucial for proper cardiovascular development, and mutations in TBX5 have been associated with various congenital heart diseases and arrhythmias in humans. However, whether mutated TBX5 contributes to dilated cardiomyopathy (DCM) remains unclear. In this study, the coding exons and flanking introns of the TBX5 gene were sequenced in 190 unrelated patients with idiopathic DCM. The available family members of the index patient carrying an identified mutation and 200 unrelated ethnically matched healthy individuals used as controls were genotyped for TBX5. The functional characteristics of the mutant TBX5 were explored in contrast to its wild-type counterpart by using a dual-luciferase reporter assay system. As a result, a novel heterozygous TBX5 mutation, p.S154A, was identified in a family with DCM inherited in an autosomal dominant pattern, which co-segregated with DCM in the family with complete penetrance. The missense mutation was absent in 400 control chromosomes and the altered amino acid was completely conserved evolutionarily across various species. Functional assays revealed that the mutant TBX5 had significantly decreased transcriptional activity. Furthermore, the mutation markedly diminished the synergistic activation of TBX5 with NKX2-5 or GATA4, other two transcription factors causatively linked to DCM. This study firstly associates TBX5 loss-of-function mutation with enhanced susceptibility to DCM, providing novel insight into the molecular mechanisms of DCM, and suggesting the potential implications in the development of new treatment strategies for this common form of myocardial disorder.

A Novel TBX1 Loss-of-Function Mutation Associated with Congenital Heart Disease.

Congenital heart disease (CHD) is the most prevalent type of birth defect in humans and is the leading non-infectious cause of infant death worldwide. There is a growing body of evidence demonstrating that genetic defects play an important role in the pathogenesis of CHD. However, CHD is a genetically heterogeneous disease and the genetic basis underpinning CHD in an overwhelming majority of patients remains unclear. In this study, the coding exons and splice junction sites of the TBX1 gene, which encodes a T-box homeodomain transcription factor essential for proper cardiovascular morphogenesis, were sequenced in 230 unrelated children with CHD. The available family members of the index patient carrying an identified mutation and 200 unrelated ethnically matched healthy individuals used as controls were subsequently genotyped for TBX1. The functional effect of the TBX1 mutation was predicted by online program MutationTaster and characterized by using a dual-luciferase reporter assay system. As a result, a novel heterozygous TBX1 mutation, p.Q277X, was identified in an index patient with double outlet right ventricle (DORV) and ventricular septal defect (VSD). Genetic analysis of the proband's available relatives showed that the mutation co-segregated with CHD transmitted in an autosomal dominant pattern with complete penetrance. The nonsense mutation, which was absent in 400 control chromosomes, altered the amino acid that was completely conserved evolutionarily across species and was predicted to be disease-causing by MutationTaster. Biochemical analysis revealed that Q277X-mutant TBX1 lost transcriptional activating function when compared with its wild-type counterpart. This study firstly associates TBX1 loss-of-function mutation with enhanced susceptibility to DORV and VSD in humans, which provides novel insight into the molecular mechanism underlying CHD and suggests potential implications for the development of new preventive and therapeutic strategies for CHD.

T-Cell Mineralocorticoid Receptor Deficiency Attenuates Pathologic Ventricular Remodelling After Myocardial Infarction.

BACKGROUND: Mineralocorticoid receptor (MR) antagonists have been widely used to treat heart failure (HF). Studies have shown that MR in T cells plays important roles in hypertension and myocardial hypertrophy. However, the function of T-cell MR in myocardial infarction (MI) has not been elucidated. METHODS: In this study, we used T-cell MR knockout (TMRKO) mouse to investigate the effects of T-cell MR deficiency on MI and to explore the underlying mechanisms. Echocardiography and tissue staining were used to assess cardiac function, fibrosis, and myocardial apoptosis after MI. Flow cytometry and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect immune cell infiltration and inflammation. RESULTS: T-cell MR deficiency significantly improved cardiac function, promoted myocardial repair, and inhibited myocardial apoptosis, fibrosis, and inflammation after MI. Luminex assays revealed that TMRKO mice had significantly lower levels of interferon-gamma (IFN-γ) and interleukin-6 (IL-6) in serum and infarcted myocardium than littermate control mice. In cultured splenic T cells, MR deficiency suppressed IL-6 expression, whereas MR overexpression enhanced IL-6 expression. Chromatin immunoprecipitation (ChIP) assay demonstrated that MR bound to the MR response element on the promoter of IL-6 gene. Finally, T-cell MR deficiency significantly suppressed accumulation of macrophages in infarcted myocardium and differentiation of proinflammatory macrophages, thereby alleviating the consequences of MI. CONCLUSIONS: T-cell MR deficiency improved pathologic ventricular remodelling after MI, likely through inhibition of accumulation and differentiation of proinflammatory macrophages. At the molecular level, MR may work through IFN-γ and IL-6 in T cells to exert functions in MI.

Prevalence and spectrum of NKX2.5 mutations in patients with congenital atrial septal defect and atrioventricular block.

Congenital atrial septal defect (ASD) and progressive atriventricular block (AVB) are the two most common phenotypes linked to NK2 homeobox 5 (NKX2.5) mutations in animals and humans. However, the prevalence and spectrum of NKX2.5 mutation in patients with ASD and AVB remain to be elucidated. In the present study, the coding exons and flanking introns of the NKX2.5 gene, which encodes a homeobox­containing transcription factor essential for development of the heart, were sequenced in a cohort of 62 unrelated patients with ASD and AVB, and subsequently in a mutation carrier's available family members. As controls, 300 unrelated, ethnically­matched healthy individuals were recruited, who were also genotyped for NKX2.5. The functional consequence of the mutant NKX2.5 was evaluated in contrast to its wild­type counterpart using a dual­luciferase reporter assay system. As a result, a novel heterozygous NKX2.5 mutation, p.Q181X, was identified in an index patient with ASD and AVB, with a prevalence of ~1.61%. Genetic analysis of the proband's pedigree revealed that the mutation co­segregated with ASD and AVB with complete penetrance. The nonsense mutation, which eliminated partial homeobox and the carboxyl terminus, was absent in the 600 control chromosomes. Functional evaluation showed that the NKX2.5 mutant had no transcriptional activity. Furthermore, the mutation disrupted the synergistic activation between NKX2.5 and GATA binding protein 4, another cardiac core transcription factor associated with ASD. The results of the present study expand the spectrum of NKX2.5 mutations linked to ASD and AVB, and indicated that NKX2.5 loss­of­function mutations are an uncommon cause of ASD and AVB in humans.

TBX5 loss-of-function mutation contributes to atrial fibrillation and atypical Holt-Oram syndrome.

Previous genome-wide association studies have demonstrated that single nucleotide polymorphisms in T­box (TBX)5 are associated with increased susceptibility to atrial fibrillation (AF), and a recent study has causally linked a TBX5 mutation to atypical Holt-Oram syndrome and paroxysmal AF. However, the prevalence and spectrum of TBX5 mutations in patients with AF remain to be elucidated. In the present study, a cohort of 190 unrelated patients with idiopathic AF were prospectively recruited, with 400 unrelated healthy individuals recruited as controls. The coding exons and flanking introns of the TBX5 gene were sequenced in the participants. The functional characteristics of the mutant TBX5 were delineated in contrast with its wild­type counterpart using a dual­luciferase reporter assay system. As a result, a novel heterozygous TBX5 mutation, p.P132S, was identified in an index patient with AF, with a mutational prevalence of ~0.53%. Genetic analysis of the proband's family showed that the mutation co­segregated with AF, and was transmitted in an autosomal dominant pattern. The missense mutation was absent in the 800 control chromosomes, and the altered amino acid was completely evolutionarily conserved across species. Functional analyses revealed that the mutant TBX5 had significantly reduced transcriptional activity. Furthermore, the mutation markedly decreased the synergistic activation between TBX5 and NK2 homeobox 5, another transcription factor which has been causatively linked to AF. The present study was the first, to the best of our knowledge, to report on the association between a TBX5 loss­of­function mutation and increased susceptibility to AF. These results provide novel insight into the molecular mechanism underpinning AF, and have potential implications in the development of novel prophylactic and therapeutic strategies for AF, the most common form of sustained cardiac arrhythmia.

A HAND2 Loss-of-Function Mutation Causes Familial Ventricular Septal Defect and Pulmonary Stenosis.

Congenital heart disease (CHD) is the most common developmental abnormality, and is the leading noninfectious cause of mortality in neonates. Increasing evidence demonstrates that genetic defects play an important role in the pathogenesis of CHD. However, CHD exhibits substantial heterogeneity, and the genetic determinants for CHD remain unknown in the overwhelming majority of cases. In the current study, the coding exons and flanking introns of the HAND2 gene, which encodes a basic helix-loop-helix transcription factor essential for normal cardiovascular development, were sequenced in 192 unrelated patients with CHD, and a novel heterozygous mutation, p.S65I, was identified in a patient with congenital ventricular septal defect (VSD). Genetic analysis of the index patient's pedigree revealed that the mutation was present in all seven affected family members available, but absent in the 13 unaffected family members examined. Besides, in addition to VSD, five of the proband's close relatives also had pulmonary stenosis (PS), and the proband's son also had double outlet right ventricle (DORV). The missense mutation, which altered an evolutionarily conserved amino acid, was absent in 300 unrelated, ethnically matched healthy individuals. Biological analyses using a dual-luciferase reporter assay system showed that the mutant HAND2 was associated with significantly diminished transcriptional activity. Furthermore, the mutation abolished the synergistic activation between HAND2 and GATA4, as well as NKX2.5-two other cardiac core transcriptional factors that have been causally linked to CHD. These findings indicate that HAND2 loss-of-function mutation contributes to human CHD, perhaps via its interaction with GATA4 and NKX2.5.

Comparison of combination therapy of high-dose oral N-acetylcysteine and intravenous sodium bicarbonate hydration with individual therapies in the reduction of Contrast-induced Nephropathy during Cardiac Catheterisation and Percutaneous Coronary Intervention (CONTRAST): A multi-centre, randomised, controlled trial.

INTRODUCTION: N-acetylcysteine (NAC) and sodium bicarbonate (SOB) therapies may prevent contrast-induced nephropathy (CIN). However, the efficacy of using combination over individual therapies was not established, and there was no large randomised study comparing abbreviated SOB therapy with conventional sustained saline pre-hydration with oral NAC. METHODS: In a multi-centre, open-label, randomised, controlled trial (NCT00497328), we prospectively enrolled 548 patients with at least moderate renal impairment undergoing cardiac catheterisation with or without percutaneous coronary intervention. Patients were randomly assigned to 3 groups: 1) NAC: 154 mEq/L sustained sodium chloride regime (1 mL/kg/h 12 h before, during and 6h after the procedure) with oral NAC at 1.2g bid for 3 days (n=185); 2) SOB: 154 mEq/L abbreviated SOB regime at 3 mL/kg/h 1h before the procedure, and 1 mL/kg/h during and 6h after the procedure (n=182); and 3) COM: combination of abbreviated SOB regime and oral NAC (n=181). The primary end point was incidence of CIN. The secondary end points were rise in serum creatinine, hospitalisation duration, haemodialysis, morbidity and mortality within 30 days. RESULTS: The 3 groups had similar baseline characteristics: age 68 ± 10 years, 76% male, 48% diabetic and baseline glomerular filtration rate (GFR) 47.7 ± 13.0 mL/min. There were 41 (8.8%) patients with GFR<30. The CIN incidences were NAC 6.5%, SOB 12.8% and COM 10.6%. The COM regimen was not superior to either the NAC (relative risk (RR)=1.61, 95% confidence interval (CI): 0.76 to 3.45, p=0.225) or SOB (RR=0.83, 95% CI: 0.44 to 1.56, p=0.593) regimens. The CIN incidence was lower in the NAC group than the SOB group (adjusted odds ratio (OR)=0.40, 95% CI: 0.17 to 0.92; p=0.032). Multivariate analysis showed contrast volume (OR=1.99, 95% CI: 1.33 to 2.96, p<0.001 per 100mL), female (OR=2.47, 95% CI: 1.22 to 5.00, p=0.012) and diabetes (OR=2.03, 95% CI: 1.03 to 3.99, p=0.041) were independent risk predictors. There were no differences in the secondary outcomes among the 3 groups. CONCLUSION: The combination regimen was not superior to individual regimens in preventing CIN in patients with baseline renal impairment. There was a trend suggesting that the 12-hour sustained sodium chloride pre-hydration regimen was more protective than the 1-hour abbreviated SOB regimen.

[Effect of Zhenju Jiangya Tablet on the endothelial function of hyperlipidemic rabbits].

OBJECTIVE: To study the effect of Zhenju Jiangya Tablet (ZJ) on the injured endothelial cells and endothelium-dependent relaxation function of hyperlipidemia rabbits. METHODS: Male New Zealand rabbits were randomized into four groups: control group, hyperlipidemia group, ZJ group and sivastatin group. The endothelium-dependent relaxation function was evaluated by APV using intravascular Doppler, and the morphology of endothelial cells was detected by light microscopy and electron microscopy, and nitric oxide synthase was evaluated. RESULTS: ZJ reduced the lesions of hyperlipidemia vessels, and the APV after Ach injection of each group was (1.14+/-0.26), (1.74+/-0.59), (1.22+/-0.37) and (1.17+/-0.41) respectively. The eNOS of each group was (4.21+/-0.37), (1.43+/-0.88), (3.95+/-0.67) and (4.08+/-0.46) nmol x min(-1) x g(-1) respectively. CONCLUSION: ZJ can improve the abnormality of endothelial cells and endothelium-dependent relaxation function of hyperlipidemia.

Traditional chinese medicine tongxinluo improves cardiac function of rats with dilated cardiomyopathy.

The study aimed at testing the hypothesis that tongxinluo capsule might exert its cardioprotective effect by preventing ventricular remodeling and improving coronary microvascular function in a rat model of doxorubicin-induced dilated cardiomyopathy (DCM). Rats that survived DCM induction were randomly divided into three groups to be given 1.5 g·kg(-1)·day(-1) (TXL-H, n = 9) or 0.15 g·kg(-1)·day(-1) (TXL-L, n = 10) of tongxinluo, or normal saline at the same volume (DCM-C, n = 10) intragastrically. Age matched normal rats treated with normal saline were used as normal controls (NOR-C, n = 9). After four weeks of treatment, the DCM-C, TXL-H, and TXL-L groups exhibited significant cardiac dysfunction, left ventricular remodeling, and coronary microvascular dysfunction, compared with the NOR-C rats. However, myocardial functional parameters were significantly improved and microvascular density (MVD) increased in the TXL-H group compared with the DCM-C group (all P < 0.01). Left ventricular remodeling was prevented. There were close linear relationships between CVF and LVEF (r = -0.683, P < 0.05), MVD and LVEF (r = 0.895, P < 0.05), and MVD and CVF (r = -0.798, P < 0.05). It was indicated that high-dose tongxinluo effectively improved cardiac function in rat model of DCM.

A novel NKX2.5 loss-of-function mutation associated with congenital bicuspid aortic valve.

Bicuspid aortic valve (BAV) is the most common form of congenital cardiovascular defect in humans and is associated with substantial morbidity and mortality. Emerging evidence demonstrates that genetic risk factors play an important role in the pathogenesis of BAV. However, BAV is a genetically heterogenous disorder, and the genetic defects underpinning BAV in most patients remain to be identified. In the present study, the coding exons and flanking introns of the NKX2.5 gene, which encodes a homeodomain-containing transcription factor essential for the normal development of the aortic valve, were sequenced in 142 unrelated patients with BAV. The available relatives of the mutation carrier and 200 unrelated healthy subjects used as controls were also genotyped for NKX2.5. The functional characteristics of the mutation were delineated by using a dual-luciferase reporter assay system. As a result, a novel heterozygous NKX2.5 mutation, p.K192X, was identified in a family with BAV transmitted in an autosomal dominant pattern. The nonsense mutation was absent in 400 control chromosomes. Functional analyses revealed that the mutant NKX2.5 had no transcriptional activity compared with its wild-type counterpart. Furthermore, the mutation abolished the synergistic transcriptional activation between NKX2.5 and GATA5, another transcription factor crucial for the aortic valvular morphogenesis. In conclusion, this study is the first to link an NKX2.5 loss-of-function mutation to enhanced susceptibility to human BAV, providing novel insight into the molecular mechanism of BAV and suggesting potential implications for genetic counseling and clinical care of families presenting with BAV.

Clinical characteristics associated with high on-treatment platelet reactivity of patients undergoing PCI after a 300†mg loading dose of clopidogrel, measured by thrombelastography.

BACKGROUND: Dual antiplatelet therapy with clopidogrel and aspirin is the standard of care for patients undergoing percutaneous coronary intervention (PCI). OBJECTIVE: To determine the clinical characteristics associated with high on-treatment platelet reactivity (HPR) of patients undergoing PCI after a 300 mg loading dose of clopidogrel, measured by thrombelastography (TEG). METHODS AND RESULTS: 394 consecutive patients were enrolled in this prospective observational study. All had been receiving aspirin 100 mg/day for more than 7 days, but were clopidogrel naïve. A 300 mg loading dose of clopidogrel was given more than 12 h before the procedure. The cut-off point for HPR was defined as ≥70% adenosine-5-diphosphate-induced aggregation. The prevalence of HPR was 21% as measured by TEG. More women than men (41.7% vs 27.1%, p=0.01) were found in the HPR group. Raised glycosylated haemoglobin (HbA1c) was more prevalent in the HPR group than in the group with normal on-treatment platelet reactivity (NPR) (45.2% vs 30.0%, p=0.009). Patients with HPR had a higher level of total plasma cholesterol (4.8±1.5 mmol/l vs 4.3±1.1 mmol/l, p=0.002) and low-density lipoprotein cholesterol (2.8±1.1 mmol/l vs 2.5±0.9 mmol/l, p=0.022) than those with NPR. Multivariable logistic regression analysis showed that female gender (OR=3.175, 95% CI 1.428 to 7.059, p=0.005) and raised HbA1c (OR=1.911, 95% CI 1.066 to 3.428, p=0.03) independently predicted the occurrence of HPR. CONCLUSIONS: Despite pretreatment with aspirin and a 300 mg loading dose of clopidogrel, 21% patients undergoing PCI exhibited HPR measured by TEG. A raised level of HbA1c and female gender independently predicted the findings.

Safety and effectiveness of drug-eluting stents in Chinese patients with coronary artery disease with off- and on-label indications: results from a single-centre registry.

BACKGROUND: Off-label use of drug-eluting stents (DES) is more common than on-label use and may be associated with a persistently higher rate of adverse angiographic and clinical outcomes. OBJECTIVE: To evaluate the safety and effectiveness of unrestricted use of DES in everyday practice in a Chinese population. METHODS: Between January 2004 and May 2009, we retrospectively enrolled 1209 consecutive patients who received DES in our single centre. 84.7% of patients were treated with sirolimus-eluting stents (SES) and 15.3% of patients were treated with paclitaxel-eluting stents (PES). RESULTS: 59.0% of patients (n=713) were treated for off-label indications, with a significantly higher proportion of patients with previous coronary artery bypass grafting (CABG) (6.2% vs 0.6%, p<0.001). There were no differences in coronary risk factors. During 6-66 months' follow-up, the rate of repeat target vessel revascularisation (TVR) was significantly higher in the off-label group (14.6% vs 9.7%, p=0.011). The risk of death and myocardial infarction were not statistically different with off-label from standard use. Multivariate logistic regression showed that the independent predictors of TVR were stent type (SES vs PES, HR=0.567, 95% CI 0.395 to 0.813), previous CABG (HR=2.393, 95% CI 1.440 to 3.977), the treatment of chronic total occlusion (HR=2.786, 95% CI 1.731 to 4.484) and the treatment of left main lesion (HR=1.854, 95% CI 1.022 to 3.363). CONCLUSIONS: In our local unselected cohort of Chinese people, off-label use of DES was safe in comparison with on-label use and associated with an excellent procedural success rate, but higher TVR.

Toxic epidermal necrolysis after percutaneous coronary intervention: which drug is the culprit?

Toxic epidermal necrolysis (TEN) is a serious, usually drug-induced, dermatosis characterized by extensive erythema, necrosis, bullous detachment of the epidermis, constitutional symptoms, and visceral involvement. We report a 62-year-old man who was diagnosed TEN after percutaneous coronary intervention (PCI). After consulting with a cardiologist, all pre-hospital medication was discontinued except clopidogrel. With supportive care, the patient recovered.

Eighteen-month clinical safety and efficacy outcomes of sirolimus-, paclitaxel- and zotarolimus-drug eluting stents in diabetic patients undergoing percutaneous coronary intervention for complex coronary artery stenosis.

INTRODUCTION: This was a single centre registry study on clinical efficacy and safety of drug-eluting stent (DES) in diabetic patients undergoing percutaneous coronary intervention (PCI) for complex coronary lesions. MATERIALS AND METHODS: A total of 288 diabetic patients who underwent elective PCI between September 2003 and June 2006 in our centre were enrolled and followed-up for 18 months. Among them, 79 (27.4%) patients received sirolimus-eluting stent (SES), 138 (47.9%) paclitaxel-eluting stent (PES) and 71 (24.7%) zotarolimus-eluting stent (ZES). The endpoints were major adverse cardiac events (MACE) and stent thrombosis rates. RESULTS: Baseline demographics were comparable among the 3 DES groups (median age was 60 years; 69% men). Complex lesions (defined as ACC/AHA type C stenosis) accounted for 55.6% of the total lesions: SES (50.6%), PES (65.2%) and ZES (43.7%), P = 0.005. At 18 months follow-up, the composite endpoint of MACE was found in 12.7% in SES group, 8.7% in the PES group, 12.7% in ZES group and (P = 0.55). Stent thrombosis (ST) occurred in 1 patient (1.3%) in the SES group, 2 patients (1.4%) in PES group and 1 patient (1.4%) in ZES group, respectively (P = 1.00). CONCLUSION: The use of DES for elective PCI in diabetic patients was associated with favourable intermediate-term clinical outcomes with no significant differences in efficacy among the 3 groups. Stent thrombosis had low event occurrence rate.

A novel drug-eluting stent using bioabsorbable polymer technology: two-year follow-up of the CURAMI registry.

BACKGROUND: There are safety concerns on drug-eluting stents (DESs) using durable polymer. The long-term outcome of next generation DESs using bioabsorbable polymer technology remains unknown. METHODS: From March to June, 2005, a novel sirolimus-eluting (170 microg/cm2), bioabsorbable polymer (PLA and PLGA, eroded over 45 days) coated stent was implanted for treatment of acute myocardial infarction (AMI) in 49 patients (male 86%, age 55+10 years, diabetes 31%). All culprits were de novo lesions in the native coronary artery. On discharge, aspirin and clopidogrel for 3 months followed by life-long aspirin were prescribed. Angiographic follow-up was performed at 8 months. Clinical follow-up was performed at 4, 9 and 24 months. RESULTS: Angiographic success rate was 100%. In-hospital adverse events consisted of 1 death (2%). All except one patient (due to aspirin allergy) were compliant to the 3 months dual antiplatelet therapy, and there was no adverse event during this period. One patient developed re-infarction in another coronary territory at 6 months. Twenty-seven patients (56%) underwent 8-month angiographic follow-up (Table 3). At 24 months, 6 patients had 7 major adverse cardiac events (12.2%, 1 death, 2 re-infarctions and 4 target lesion revascularizations). There were no incidences of subacute or late stent thrombosis. CONCLUSIONS: The Cura stent, using bioabsorbable polymer technology, appears to be safe at 2 years follow-up. Although the angiographic follow-up parameters were unfavorable, this report paves the way for further studies on DES using bioabsorbable polymer technology.