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Myocardial infarction with non-obstructive coronary artery disease (MINOCA) is a heterogeneous clinical condition affecting 5% to 8% of patients presenting with acute myocardial infarction. Initially it was considered a favorable clinical diagnosis, nowadays it is known that MINOCA can significantly affect patient quality of life and portends a guarded prognosis. Therefore, it is of utmost importance to identify the specific pathophysiological mechanism underlying this clinical condition in order to set up a targeted pharmacological and non-pharmacological therapy. Coronary angiography is still a mandatory diagnostic test to rule out obstructive coronary artery disease but has limited capability to identify other potential functional and structural etiologies of MINOCA. The purpose of this review is to provide an overview of the invasive diagnostic work-up of patients with MINOCA, highlighting the diagnostic tools warranted beyond coronary angiography inside the cath lab (intracoronary provocation tests, intracoronary imaging and indexes for the assessment of coronary microvascular dysfunction), and the remaining essential knowledge gaps in this field.

Coronary artery disease (CAD) patients are at high ischemic risk, and new biomarkers reflecting atherosclerotic disease severity and coronary plaque vulnerability are required. The Brain-Derived Neurotrophic Factor (BDNF) affects endothelial and macrophage activation suggesting its involvement in atherosclerotic plaque behavior. To investigate whether plasma BDNF is associated with in vivo coronary plaque features, assessed by optical coherence tomography (OCT), in both acute myocardial infarction (AMI) and stable angina (SA) patients, we enrolled 55 CAD patients (31 SA and 24 AMI), and 21 healthy subjects (HS). BDNF was lower in CAD patients than in HS (p < 0.0001), and it decreased with the presence, clinical acuity and severity of CAD. The greater BDNF levels were associated with OCT features of plaque vulnerability in overall CAD as well as in SA and AMI patients (p < 0.03). Specifically, in SA patients, BDNF correlated positively with macrophages’ infiltration within atherosclerotic plaque (p = 0.01) and inversely with minimal lumen area (p = 0.02). In AMI patients a negative correlation between BDNF and cap thickness was found (p = 0.02). Despite a small study population, our data suggest a relationship between BDNF and coronary plaque vulnerability, showing that vulnerable plaque is positively associated with plasma BDNF levels, regardless of the clinical CAD manifestation.

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Background: Plaque erosion is responsible for 25% to 40% of patients with acute coronary syndromes (ACS). Recent studies suggest that anti-thrombotic therapy without stenting may be an option for this subset of patients. Currently, however, an invasive procedure is required to make a diagnosis of plaque erosion. The aim of this study was to identify clinical or laboratory predictors of plaque erosion in patients with ACS to enable a diagnosis of erosion without additional invasive procedures. Methods and Results: Patients with ACS who underwent optical coherence tomography imaging were selected from 11 institutions in 6 countries. The patients were classified into plaque rupture, plaque erosion, or calcified plaque, and predictors were identified using multivariable logistic modeling. Among 1241 patients with ACS, 477 (38.4%) patients were found to have plaque erosion. Plaque erosion was more frequent in non–ST-segment elevation-ACS than in ST-segment–elevation myocardial infarction (47.9% versus 29.8%, P=0.0002). Multivariable logistic regression models showed 5 independent parameters associated with plaque erosion: age <68 years, anterior ischemia, no diabetes mellitus, hemoglobin >15.0 g/dL, and normal renal function. When all 5 parameters are present in a patient with non–ST-segment elevation-ACS, the probability of plaque erosion increased to 73.1%. Conclusions: Clinical and laboratory parameters associated with plaque erosion are explored in this retrospective registry study. These parameters may be useful to identify the subset of ACS patients with plaque erosion and guide them to conservative management without invasive procedures. The results of this exploratory analysis need to be confirmed in large scale prospective clinical studies. Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT03479723.

Aims Layered plaques represent signs of previous plaque destabilization. A recent study showed that acute coronary syndrome (ACS) patients with layered culprit plaque have more vulnerability at the culprit lesion and systemic inflammation. We aimed to compare the characteristics of non-culprit plaques between patients with or without layered plaque at the culprit lesion. We also evaluated the characteristics of layered non-culprit plaques, irrespective of culprit plaque phenotype. Methods We studied ACS patients who had undergone pre-intervention optical coherence tomography (OCT) imaging. The and results number of non-culprit lesions was evaluated on coronary angiogram and morphological characteristics of plaques were studied by OCT. In 349 patients, 99 (28.4%) had layered culprit plaque. The number of non-culprit plaques in patients with or without layered culprit plaque was similar (3.2 ± 0.8 and 2.8 ± 0.8, P = 0.23). Among 465 non-culprit plaques, 145 from patients with layered culprit plaque showed a higher prevalence of macrophage infiltration (71.0% vs. 60.9%, P = 0.050). When analysed irrespective of culprit plaque phenotype, layered non-culprit plaques showed higher prevalence of lipid (93.3% vs. 86.0%, P = 0.028), thin cap fibroatheroma (29.7% vs. 13.7%, P < 0.001), and macrophage infiltration (82.4% vs. 54.0%, P < 0.001) than non-layered plaques. Plaques with layered phenotype at both culprit and non-culprit lesions had the highest vulnerability. Conclusion In ACS patients, those with layered phenotype at the culprit lesion demonstrated greater macrophage infiltration at the non-culprit sites. Layered plaque at the non-culprit lesions was associated with more features of plaque vulnerability, particularly when the culprit lesion also had a layered pattern.

Background Seasonal variations in acute coronary syndromes (ACS) have been reported, with incidence and mortality peaking in the winter. However, the underlying pathophysiology for these variations remain speculative. Methods and Results Patients with ACS who underwent optical coherence tomography were recruited from 6 countries. The prevalence of the 3 most common pathologies (plaque rupture, plaque erosion, and calcified plaque) were compared between the 4 seasons. In 1113 patients with ACS (885 male; mean age, 65.8±11.6 years), the rates of plaque rupture, plaque erosion, and calcified plaque were 50%, 39%, and 11% in spring; 44%, 43%, and 13% in summer; 49%, 39%, and 12% in autumn; and 57%, 30%, and 13% in winter (P=0.039). After adjusting for age, sex, and other coronary risk factors, winter was significantly associated with increased risk of plaque rupture (odds ratio [OR], 1.652; 95% CI, 1.157-2.359; P=0.006) and decreased risk of plaque erosion (OR, 0.623; 95% CI, 0.429-0.905; P=0.013), compared with summer as a reference. Among patients with rupture, the prevalence of hypertension was significantly higher in winter (P=0.010), whereas no significant difference was observed in the other 2 groups. Conclusions Seasonal variations in the incidence of ACS reflect differences in the underlying pathobiology. The proportion of plaque rupture is highest in winter, whereas that of plaque erosion is highest in summer. A different approach may be needed for the prevention and treatment of ACS depending on the season of its occurrence. Registration URL: https://www.clini​caltr​ials.gov. Unique identifier: NCT03479723.

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Background and aims: Plaque erosion (PE) is responsible for at least one-third of acute coronary syndrome (ACS), and inflammation plays a key role in plaque instability. We assessed the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) at the culprit site in ACS patients with PE, evaluating their clinical and OCT correlates, along with their prognostic value. Methods: ACS patients undergoing OCT imaging and presenting PE as culprit lesion were retrospectively selected. Presence of MØI at culprit site was assessed. The incidence of major adverse cardiac events (MACEs), defined as the composite of cardiac death, recurrent myocardial infarction and target-vessel revascularization (TVR), was assessed [follow-up median (interquartile range, IQR) time 2.5 (2.03–2.58) years]. Results: We included 153 patients [median age (IQR) 64 (53–75) years, 99 (64.7%) males]. Fifty-one (33.3%) patients presented PE with MØI and 102 (66.7%) PE without MØI. Patients having PE with MØI compared with PE patients without MØI had more vulnerable plaque features both at culprit site and at non-culprit segments. MACEs were significantly more frequent in PE with MØI patients compared with PE without MØI [11 (21.6%) vs. 6 (5.9%), p = 0.008], mainly driven by a higher risk of cardiac death and TVR. At multivariable Cox regression, PE with MØI was an independent predictor of MACEs [HR = 2.95, 95% CI (1.09–8.02), p = 0.034]. Conclusions: Our study demonstrates that among ACS patients with PE the presence of MØI at culprit lesion is associated with more vulnerable plaque features, along with a worse prognosis at a long-term follow-up.

OBJECTIVE: Healed plaques, signs of previous plaque destabilization, are frequently found in the coronary arteries. Healed plaques can now be diagnosed in living patients. We investigated the prevalence, angiographic, and optical coherence tomography features of healed plaques in patients with stable angina pectoris. Approach and Results: Patients with stable angina pectoris who had undergone optical coherence tomography imaging were included. Healed plaques were defined as plaques with one or more signal-rich layers of different optical density. Patients were divided into 2 groups based on layered or nonlayered phenotype at the culprit lesion. Among 163 patients, 87 (53.4%) had layered culprit plaque. Patients with layered culprit plaque had more multivessel disease (62.1% versus 44.7%, P=0.027) and more angiographically complex culprit lesions (64.4% versus 35.5%, P<0.001). Layered culprit plaques had higher prevalence of lipid plaque (83.9% versus 64.5%, P=0.004), macrophage infiltration (58.6% versus 35.5%, P=0.003), calcifications (78.2% versus 63.2%, P=0.035), and thrombus (28.7% versus 14.5%, P=0.029). Lipid index (P=0.001) and percent area stenosis (P=0.015) were greater in the layered group. The number of nonculprit plaques, evaluated using coronary angiograms, tended to be greater in patients with layered culprit plaque (4.2±2.5 versus 3.5±2.1, P=0.053). Nonculprit plaques in patients with layered culprit lesion had higher prevalence of layered pattern (P=0.002) and lipid phenotype (P=0.005). Lipid index (P=0.013) and percent area stenosis (P=0.002) were also greater in this group. CONCLUSIONS: In patients with stable angina pectoris, healed culprit plaques are common and have more features of vulnerability and advanced atherosclerosis both at culprit and nonculprit lesions.

Background: Microvascular obstruction (MVO) after primary percutaneous coronary intervention (pPCI) leads to higher incidence of both early and late complications. A number of single nucleotide polymorphisms in 9p21 chromosome have been shown to affect angiogenesis in response to ischaemia. In particular, Rs1333040 with its three genotypic vriants C/C, T/C and T/T might influence the occurrence of MVO after pPCI. Methods: We enrolled ST-elevation myocardial infarction (STEMI) patients undergoing pPCI. The Rs1333040 polymorphism was evaluated by polymerase chain reaction-restriction fragment length polymorphism using restriction endonucleases (Bsml). Two expert operators unaware of the patients' identity performed the angiographic analysis; collaterals were assessed applying Rentrop's classification. Angiographic MVO was defined as a post-pPCI Thrombolysis In Myocardial Infarction (TIMI)<3 or TIMI 3 with myocardial blush grade 0 or 1, whereas electrocardiographic MVO was defined as ST segment resolution Results: Among our 133 STEMI patients (mean age 63 +/- 11 years, men 72%), 35 (26%) and 53 (40%) respectively experienced angiographic or electrocardiographic MVO. Angiographic and electrocardiographic MVO were different among the three variants (p= 0.03 and p=0.02 respectively). In particular, T/T genotype was associated with a higher incidence of both angiographic and electrocardiographic MVO compared with C/C genotype (p=0.04 and p=0.03 respectively). Moreover, Rentrop score <2 detection rate differed among the three genotypes (p=0.03). In particular T/T genotype was associated with a higher incidence of a Rentrop score <2 as compared with C/C genotype (p= 0.02). Conclusion: Rs1333040 polymorphism genetic variants portend different MVO incidence. In particular, T/T genotype is related to angiographic and electrocardiographic MVO and to worse collaterals towards the culprit artery.

Importance: At one end of the coronary artery disease (CAD) spectrum, there are patients with multiple recurrent acute coronary syndromes (rACS), and at the other end there are those with long-standing clinical stability. Predicting the natural history of these patients is challenging because unstable plaques often heal without resulting in ACS. Objective: To assess in vivo the coronary atherosclerotic phenotype as well as the prevalence and characteristics of healed coronary plaques by optical coherence tomography (OCT) imaging in patients at the extremes of the CAD spectrum. Design, Setting, and Participants: This is an observational, single-center cohort study with prospective clinical follow-up. From a total of 823 consecutive patients enrolled in OCT Registry of the Fondazione Policlinico A. Gemelli-IRCCS, Rome, Italy, from March 2009 to February 2016, 105 patients were included in the following groups: (1) patients with rACS, defined as history of at least 3 acute myocardial infarctions (AMIs) or at least 4 ACS with at least 1 AMI; (2) patients with long-standing stable angina pectoris (ls-SAP), defined as a minimum 3-year history of stable angina; and (3) patients with a single unheralded AMI followed by a minimum 3-year period of clinical stability (sAMI). Data were analyzed from January to August 2018. Exposures: Intracoronary OCT imaging of nonculprit coronary segments. Main Outcomes and Measures: Coronary plaque features and the prevalence of healed coronary plaques in nonculprit segments as assessed by intracoronary OCT imaging. Results: Of 105 patients, 85 were men (81.0%); the median (interquartile range) age was 68 (63-75) years. Median (interquartile range) time of clinical stability was 9 (5.0-15.0) years in the ls-SAP group and 8 (4.5-14.5) years in the sAMI group. Patients in the rACS and sAMI groups showed similar prevalence of lipid-rich plaque and thin-cap fibroatheroma, which was significantly higher than in those with ls-SAP (lipid-rich plaqu

Importance: At one end of the coronary artery disease (CAD) spectrum, there are patients with multiple recurrent acute coronary syndromes (rACS), and at the other end there are those with long-standing clinical stability. Predicting the natural history of these patients is challenging because unstable plaques often heal without resulting in ACS. Objective: To assess in vivo the coronary atherosclerotic phenotype as well as the prevalence and characteristics of healed coronary plaques by optical coherence tomography (OCT) imaging in patients at the extremes of the CAD spectrum. Design, Setting, and Participants: This is an observational, single-center cohort study with prospective clinical follow-up. From a total of 823 consecutive patients enrolled in OCT Registry of the Fondazione Policlinico A. Gemelli-IRCCS, Rome, Italy, from March 2009 to February 2016, 105 patients were included in the following groups: (1) patients with rACS, defined as history of at least 3 acute myocardial infarctions (AMIs) or at least 4 ACS with at least 1 AMI; (2) patients with long-standing stable angina pectoris (ls-SAP), defined as a minimum 3-year history of stable angina; and (3) patients with a single unheralded AMI followed by a minimum 3-year period of clinical stability (sAMI). Data were analyzed from January to August 2018. Exposures: Intracoronary OCT imaging of nonculprit coronary segments. Main Outcomes and Measures: Coronary plaque features and the prevalence of healed coronary plaques in nonculprit segments as assessed by intracoronary OCT imaging. Results: Of 105 patients, 85 were men (81.0%); the median (interquartile range) age was 68 (63-75) years. Median (interquartile range) time of clinical stability was 9 (5.0-15.0) years in the ls-SAP group and 8 (4.5-14.5) years in the sAMI group. Patients in the rACS and sAMI groups showed similar prevalence of lipid-rich plaque and thin-cap fibroatheroma, which was significantly higher than in those with ls-SAP (lipid-rich plaqu

Background: The role of endothelial dysfunction in predicting angina recurrence after percutaneous coronary intervention is unknown. Design: We assessed the role of peripheral endothelial dysfunction measured by reactive-hyperaemia peripheral-artery tonometry (RH-PAT) in predicting recurrence of angina after percutaneous coronary intervention. Methods: We enrolled consecutive patients undergoing percutaneous coronary intervention with second-generation drug-eluting stents. RH-PAT was measured at discharge. The endpoint was repeated coronary angiography for angina recurrence and/or evidence of myocardial ischaemia at follow-up. Patients with in-stent restenosis and/or significant de novo stenosis were defined as having angina with obstructed coronary arteries (AOCA); all other patients as having angina with non-obstructed coronary arteries (ANOCA). Results: Among 100 patients (mean age 66.7 ± 10.4 years, 80 (80.0%) male, median follow-up 16 (3–20) months), AOCA occurred in 14 patients (14%), ANOCA in nine patients (9%). Repeated coronary angiography occurred more frequently among patients in the lower RH-PAT index tertile compared with middle and upper tertiles (14 (41.2%) vs. 6 (18.2%) vs. 3 (9.1%), p = 0.006, respectively). ANOCA was more frequent in the lower RH-PAT index tertile compared with middle and upper tertiles. In the multivariate regression analysis, the RH-PAT index only predicted angina recurrence. The receiver operating characteristic curve of the RH-PAT index to predict the angina recurrence demonstrated an area under the curve of 0.79 (95% confidence interval: 0.69–0.89; p < 0.001), with a cut-off value of 1.705, having sensitivity 74% and specificity 70%. Conclusions: Non-invasive assessment of peripheral endothelial dysfunction using RH-PAT might help in the prediction of recurrent angina after percutaneous coronary intervention, thus identifying patients who may need more intense pharmacological treatment and risk factor control.

Functional alterations of epicardial coronary arteries or coronary microcirculation represent a frequent cause of myocardial infarction and non-obstructive coronary arteries (MINOCA). We aimed at assessing the prognostic value of intracoronary provocative tests in patients presenting with MINOCA and in which other causes of MINOCA have been excluded. Methods and results We prospectively evaluated patients with a diagnosis of MINOCA, excluding patients with aetiologies other than suspected coronary vasomotor abnormalities. Immediately after coronary angiography, an invasive provocative test using acetylcholine or ergonovine was performed. The incidence of death from any cause, cardiac death, and recurrence of acute coronary syndrome (ACS) was assessed at follow-up. We also assessed angina status using Seattle Angina Questionnaires (SAQ). We enrolled 80 consecutive patients [mean age 63.0±10.7 years, 40 (50%) male]. Provocative test was positive in 37 (46.2%) patients without any complication. Among patients with a positive test, epicardial spasm was detected in 24 (64.9%) patients and microvascular spasm in 13 (35.1%) patients. After a median follow-up of 36.0 (range 12.0-60.0)months, patients with a positive test had a significantly higher occurrence of death from any cause [12 (32.4%) vs. 2 (4.7%); P= 0.002], cardiac death [7 (18.9%) vs. 0 (0.0%); P= 0.005], and readmission for ACS [10 (27.0%) vs. 3 (7.0%); P= 0.015] as well as a worse angina status as assessed by SAQ [Seattle score: 88.0 (33.0-100.0) vs. 100.0 (44.0-100.0); P = 0.001] when compared with patients with a negative test. Conclusions We demonstrate that in patients presenting with MINOCA and suspected coronary vasomotor abnormalities, a positive provocative test for spasm is safe and identifies a high-risk subset of patients.

Background: Perilipin 2 (PLIN2) is a protein that potentially facilitates atherogenesis in native coronary arteries or arteries with an implanted drug-eluting stent (DES). The aim of the study was to determine PLIN2 protein levels in peripheral monocytes of enrolled subjects and compare them between patients with native coronary artery disease (CAD) and those with an in-stent restenosis (ISR) due to neoatherosclerosis occurring >1 year after DES implantation. Methods: Forty-two patients were prospectively enrolled in the study in 3:1 fashion and underwent coronary catheterization. Both groups were angiographically matched for CAD burden with respect to the number of diseased vessels. Neoatherosclerosis was determined by intracoronary optical coherence tomography (OCT) among patients with ISR. Results: Patients with ISR due to neoatherosclerosis had significantly higher PLIN2 protein levels in peripheral blood monocytes compared to patients with native CAD (342.47 ± 75.63[SE] versus 119.51 ± 20.95, p < 0.001). PLIN2 protein levels did not significantly differ between unstable and stable disease phenotype (125.59 ± 131.02 vs. 146.14 ± 111.87, p = 0.109). Conclusions: In this explorative study, PLIN2 protein levels are significantly increased in patients with neoatherosclerosis, irrespective of clinical presentation, implicating that it might play a pathogenetic role in accelerated atherosclerosis after DES implantation. Further larger clinical studies are warranted to confirm these initial findings.

Aims: Plaque rupture (PR) represents the most common substrate of coronary thrombosis, in at least 50% of cases. Chronic low grade inflammation is a common background for atherosclerosis development; however, increased plaque inflammation may predispose by itself to PR. In the last decade, studies performed by optical coherence tomography (OCT) have allowed to establish the severity of plaque inflammation by assessing macrophage infiltration (MØI). Our retrospective study aimed at assessing the role of plaque inflammation in PR among patients with acute coronary syndrome (ACS) using OCT. Methods and results: We enrolled 56 patients with ACS exhibiting PR at the site of the culprit stenosis identified by OCT. Patients were divided into two cohorts according to the presence of MØI at OCT analysis, defined as signal-rich, distinct, or confluent punctate regions that exceed the intensity of background speckle noise. Serum high-sensitivity C-reactive protein (CRP) was measured on admission by latex-enhanced immunophelometric assay. Thirty-seven (66%) patients had MØI at the site of PR, whereas 19 (34%) patients had no evidence of MØI. Patients with MØI showed a higher rate of CRP values >3 mg/dL as compared with those without MØI (92% vs. 47%, P = 0.004). In contrast, patients without MØI had a higher prevalence of hypertension compared with those with MØI (89% vs. 59%, P = 0.021). Furthermore, the group with MØI exhibited a significantly higher rate of lipid-rich plaques (86% vs. 50%, P = 0.008), a higher rate of multifocal disease (59% vs. 10%, P < 0.001), and an MØI in both culprit and remote lesions (97% vs. 0%, P < 0.001) compared with those without MØI. At multivariate analysis, CRP value >3 mg/dL was the only independent predictor of MØI in the culprit plaque (OR 8.72, 95% CI 1.78-41.67, P= 0.007). Conclusions: In conclusion, PR can be caused by predominant inflammatory or non-inflammatory mechanisms, over a common low-grade chronic inflamm

BACKGROUND: Cytotoxin-associated gene antigen (CagA)-positive strains of Helicobacter pylori have previously been associated with acute coronary syndromes. However, the role of CagA-positive strains of Helicobacter pylori in recurring cardiac events after ST-segment elevation myocardial infarction (STEMI) has not yet been assessed. METHODS: We enrolled 181 consecutive patients (155 men, mean age 64±13 years) presenting with STEMI. In all patients, serum levels of IgG anti-CagA were assessed. Levels of IgG anti-hepatitis A virus were also evaluated in all patients in order to exclude the presence of a bystander activation of the immune system. Finally, a previous history of acute coronary syndrome and the rate of major adverse cardiovascular events as a composite of cardiovascular death, recurring myocardial infarction and target lesion revascularisation within 2 years follow-up were evaluated. RESULTS: Anti-CagA IgG seropositive patients presented more frequently with a previous history of acute coronary syndrome compared with seronegative patients (28.3% vs. 14%, P=0.019). Interestingly, no differences were observed between anti-CagA IgG seropositive and anti-CagA IgG seronegative patients concerning the prevalence of anti-hepatitis A virus IgG seropositivity (20% vs. 21.4%, P=0.48). At 2-year follow-up, 40 patients experienced major adverse cardiovascular events. The major adverse cardiovascular event rate was higher in anti-CagA IgG seropositive compared with seronegative patients (hazard ratio 2.25, 95% confidence interval 1.34-2.95, P=0.013), which was confirmed at Cox multivariate analysis (hazard ratio 2.33, 95% confidence interval 1.30-3.14, P=0.009). CONCLUSIONS: CagA-positive strains of Helicobacter pylori seem to be involved in the pathogenesis of recurring acute coronary syndromes, and seropositivity for anti-CagA IgG predicts prognosis after STEMI, possibly due to the increased risk of recurring cardiac events.

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Aims Microvascular obstruction (MVO) is associated with a worse prognosis in patients with ST-elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (PCI). However, data about incidence, clinical outcome and correlates of MVO in latecomers after STEMI are still lacking. Methods We prospectively enrolled consecutive patients that were latecomers after STEMI (symptoms onset > 12 h) undergoing PCI. We performed an angiographic analysis to assess the occurrence of MVO [defined as TIMI flow grade ≤ 2 or 3 with a myocardial blush grade < 2]. Moreover, we performed a clinical and echocardiographic follow-up to assess the occurrence of major adverse cardiovascular events (MACE), defined as the composite of cardiac death, myocardial infarction and rehospitalization for heart failure, and to evaluate left ventricle remodelling. Results Seventy-eight patients were enrolled [mean age 67.58 ± 11.72 years, 57 (73%) male; mean time of symptom onset 23.14 ± 16.06 h] with a mean follow-up time of 29.7 ± 14.1 months. MVO occurred in 39 (50%) patients. Patients with MVO had a higher rate of MACE [18 (46%) vs. 3 (8%), p < 0.001] and LV remodelling [25 (64%) vs. 6 (15%), p < 0.001] compared with patients without MVO. By multivariable Cox regression MVO and left anterior descending artery were independent predictors of MACE. Conclusions Latecomers after STEMI have a high risk to develop MVO that is related to an adverse prognosis. Appropriate management and follow-up strategies should be implemented in such high-risk patients group.

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Background: Natriuretic peptides are diagnostic/prognostic biomarkers in major cardiovascular diseases. We aimed at assessing the predictive role of N-terminal pro-A-type (NT-proANP) and pro-B-type (NT-proBNP) natriuretic peptides levels toward cardiovascular outcome in both stable and unstable coronary artery disease (CAD) patients after percutaneous coronary intervention (PCI) in a non-primary PCI setting. Methods: A total of 395 patients undergoing PCI with stent implantation for either stable angina (SA) or non ST-elevation acute coronary syndrome (NSTE-ACS) were enrolled. Pre-procedural NT-proANP and NT-proBNP levels were measured. Occurrence of major adverse cardiac events (MACEs), composite of cardiac death, non-fatal myocardial infarction, and clinically driven target lesion revascularization (c-TLR), was the endpoint of the study. Follow up mean time was 48.53 ± 14.69 months. Results: MACEs occurred in forty-four patients (11%) during follow up. Both NT-proANP levels [3170 (2210-4630) vs 2283 (1314-3913) fmol/mL, p = 0.004] and NT-proBNP levels [729 (356-1353) vs 511 (267-1006) fmol/mL, p = 0.04] were significantly higher in patients with MACEs compared to patients without MACEs. Similar results were found when considering hard MACEs (myocardial infarction and cardiac death). NT-proANP levels were significantly higher in patients with c-TLR compared with patients without c-TLR [3705 (2766-5184) vs 2343 (1340-3960) fmol/mL, p = 0.021]. At multivariate analysis, NT-proANP levels were a significant predictor of MACEs (HR 1.09, 95% CI 1.03-1.18, p = 0.04). Kaplan-Meyer curves revealed that patients with elevated NT-proANP levels (>. 2.100 fmol/mL) had a lower MACE free survival (p = 0.003). Conclusions: Both NT-proANP and NT-proBNP levels were higher in CAD patients experiencing MACEs following PCI in a non-primary setting. Notably, only NT-proANP levels significantly affected prognosis after PCI.

BACKGROUND: Cytotoxin-associated gene antigen (CagA)-positive strains of Helicobacter pylori have previously been associated with acute coronary syndromes. However, the role of CagA-positive strains of Helicobacter pylori in recurring cardiac events after ST-segment elevation myocardial infarction (STEMI) has not yet been assessed. METHODS: We enrolled 181 consecutive patients (155 men, mean age 64±13 years) presenting with STEMI. In all patients, serum levels of IgG anti-CagA were assessed. Levels of IgG anti-hepatitis A virus were also evaluated in all patients in order to exclude the presence of a bystander activation of the immune system. Finally, a previous history of acute coronary syndrome and the rate of major adverse cardiovascular events as a composite of cardiovascular death, recurring myocardial infarction and target lesion revascularisation within 2 years follow-up were evaluated. RESULTS: Anti-CagA IgG seropositive patients presented more frequently with a previous history of acute coronary syndrome compared with seronegative patients (28.3% vs. 14%, P=0.019). Interestingly, no differences were observed between anti-CagA IgG seropositive and anti-CagA IgG seronegative patients concerning the prevalence of anti-hepatitis A virus IgG seropositivity (20% vs. 21.4%, P=0.48). At 2-year follow-up, 40 patients experienced major adverse cardiovascular events. The major adverse cardiovascular event rate was higher in anti-CagA IgG seropositive compared with seronegative patients (hazard ratio 2.25, 95% confidence interval 1.34-2.95, P=0.013), which was confirmed at Cox multivariate analysis (hazard ratio 2.33, 95% confidence interval 1.30-3.14, P=0.009). CONCLUSIONS: CagA-positive strains of Helicobacter pylori seem to be involved in the pathogenesis of recurring acute coronary syndromes, and seropositivity for anti-CagA IgG predicts prognosis after STEMI, possibly due to the increased risk of recurring cardiac events.

Aims Fractional flow reserve (FFR)-guided percutaneous coronary intervention (PCI), along with optimal medical therapy, improves clinical outcome by targeting ischemia-inducing stenosis. Yet, plaque progression or stent failure may cause recurring cardiac events. We assessed the potential prognostic role of different inflammatory biomarkers, known to be associated with plaque progression or stent failure, in patients undergoing FFR-guided PCI. Methods We prospectively enrolled 169 stable angina patients with intermediate coronary stenosis at angiography undergoing FFR-guided PCI. PCI was performed if FFR was 0.80 or less, deferred if FFR was more than 0.80. Serum baseline levels of high-sensitivity C-reactive protein (hs-CRP), eosinophil cationic protein (ECP), cystatin-C (Cys-C), and thromboxane A2 (TXA2) were assessed. Rate of major adverse cardiovascular events (MACE), defined as a composite of cardiovascular death, recurrent myocardial infarction, and target vessel revascularization (TVR), was evaluated. Results PCI was performed in 78 patients (46%) (mean age 69 +/- 10 years, men 73%) and deferred in 91 patients (54%) (mean age 64 +/- 11 years, men 53%). Mean clinical follow-up was 31 +/- 11 months. Within the PCI group, patients with MACE (n=14 [18%]) had significantly higher ECP levels than those without (14.4 [9.3-19.5] vs. 4.9 [2.8-10.9] mg/l, P<0.001), and ECP was a significant predictor of MACE (hazard ratio: 1.05, 95% confidence interval [1.01-1.09], P=0.021). Within the deferred group, patients with MACE (n=8 [9%]) had significantly higher CRP levels than those without (15 [6.5-31.9] vs. 1.6 [0.9-2.9] mg/l, P<0.001) and CRP was a significant predictor of MACE (hazard ratio: 1.04, 95% confidence interval [1.01-1.07], P=0.015). Cys-C and TXA2 were not significantly different between the two groups. Conclusion Assessing inflammatory biomarkers allows the identification of patients remaining at residual higher risk of MACE after FFR-guided PCI.

BACKGROUND: Angiographic and electrocardiographic (ECG) indexes of microvascular obstruction (MVO) have been described. We aimed at assessing by cardiac magnetic resonance (CMR) anatomical features underlying concordance between them. METHODS: Forty-one patients were enrolled. Patients presented with neither angiographic nor ECG indexes of MVO (without MVO) (44%), with either angiographic or ECG indexes of MVO (discordant with MVO) (22%) or with both angiographic and ECG indexes of MVO (concordant with MVO) (34%). All patients underwent in-hospital CMR. Echocardiographic data obtained after 6 months were compared with those obtained in hospital. RESULTS: Concordant patients with MVO had larger infarct size, lower myocardial salvage index and higher rate of myocardial haemorrhage (all assessed by CMR) [33% (25-41%), 15% (10-29%) and 88%, respectively] as compared with patients without MVO [12% (9-16%), 66% (52-79%) and 0%; Bonferroni-adjusted P < 0.001, Bonferroni-adjusted P < 0.001 and P < 0.001, respectively], or with discordant ones [25% (21-39%), 35% (20-48%) and 7%; Bonferroni-adjusted P = 0.03, Bonferroni-adjusted P = 0.002 and P = 0.04, respectively]. After 6 months, ejection fraction significantly decreased in concordant patients with MVO (P < 0.001) without significant changes in the other groups. CONCLUSIONS: Concordance of angiographic and ECG indexes of MVO reflects more severe myocardial damage translating into unfavourable left ventricular remodelling.

BACKGROUND: This study evaluated the long-term outcome of patients undergoing emergency coronary artery bypass grafting (eCABG) for cardiogenic shock after acute myocardial infarction. METHODS: Sixty-seven consecutive patients underwent eCABG for cardiogenic shock at 2 European institutions during an 11-year period. Preoperative, intraoperative, postoperative, and long-term follow-up data of all patients were prospectively collected. RESULTS: Hospital survival was 86% (58 of 67), with all deaths due to cardiac causes. At a mean follow-up of 78 ± 48 months (range, 1 to 153 months), 43 of the 58 patients (74%) discharged from the hospital were alive. Causes of death in 9 of the 15 follow-up deaths (60%) were noncardiac. Overall survival rate at the end of follow-up was 64% (43 of 67). Of the 43 survivors, 41 (95%) were in New York Heart Association Functional Classification I to II, ischemia free, had a Karnofsky performance status exceeding 80, and an excellent quality of life as assessed by the Seattle Angina Questionnaire. The use of cardiopulmonary bypass and the internal thoracic artery were associated with significantly better long-term survival. CONCLUSIONS: The long-term survival and quality of life of patients who undergo eCABG for cardiogenic shock after acute myocardial infarction are good, and eCABG should be considered a valuable therapeutic option in this setting. The use of cardiopulmonary bypass and the internal thoracic artery at the time of the operation are strongly advocated.

Fractional flow reserve (FFR)-guided percutaneous coronary intervention (PCI), along with optimal medical therapy, improves clinical outcome by targeting ischemia-inducing stenosis. Yet, plaque progression or stent failure may cause recurring cardiac events. We assessed the potential prognostic role of different inflammatory biomarkers, known to be associated with plaque progression or stent failure, in patients undergoing FFR-guided PCI.

Gonadal function is thought to be involved in existing atherosclerotic plaques stabilization and might affect reperfusion after primary percutaneous coronary intervention (pPCI). We aimed to compare the prevalence of hypotestosteromenia between ST-elevation myocardial infarction (STEMI) and stable angina (SA) patients and between patients with and without microvascular obstruction (MVO).

This study evaluated the long-term outcome of patients undergoing emergency coronary artery bypass grafting (eCABG) for cardiogenic shock after acute myocardial infarction.

Angiographic and electrocardiographic (ECG) indexes of microvascular obstruction (MVO) have been described. We aimed at assessing by cardiac magnetic resonance (CMR) anatomical features underlying concordance between them.

Gonadal function is thought to be involved in existing atherosclerotic plaques stabilization and might affect reperfusion after primary percutaneous coronary intervention (pPCI). We aimed to compare the prevalence of hypotestosteromenia between ST-elevation myocardial infarction (STEMI) and stable angina (SA) patients and between patients with and without microvascular obstruction (MVO).

Guidelines report that the optimal treatment for ST-elevation myocardial infarction (STEMI) is a primary percutaneous coronary intervention (PPCI) when performed timely by trained operators. Yet, the reopening of the infarct-related artery (IRA) is not always followed by myocardial reperfusion. This phenomenon is most commonly called "no-reflow", is caused by microvascular obstruction (MVO) and is associated to a worse outcome. Electrocardiogram (ECG) is crucial for the diagnosis of STEMI, but is also useful for the assessment of MVO. In this review we summarize ECG-derived parameters associated to MVO and their prognostic relevance.

The primary goal in patients with ST-elevation myocardial infarction (STEMI) is the restoration of myocardial tissue-level perfusion. In a variable proportion of patients with STEMI, however, microcirculatory impairment may persist after epicardial coronary artery recanalization. This phenomenon is known as "myocardial no-reflow". Of note, no-reflow is associated with a worse prognosis both at short- and long-term follow-up. Depending on the population under study and the diagnostic technique used for its detection, the incidence of no-reflow ranges from 5 to 50%. No-reflow can be directly assessed in the cath-lab in several ways, including angiographic Thrombolysis in Myocardial Infarction (TIMI) flow grade assessment and more complex angiographic indexes, such as TIMI frame count, TIMI perfusion grade, myocardial blush grade, or by direct invasive assessment of coronary flow. After the cath-lab, both the evaluation of electrocardiographic ST-segment resolution and imaging techniques, as myocardial contrast echocardiography or cardiac magnetic resonance, are able to monitor no-reflow evolution, with imaging playing a crucial role in its quantification. In this article, we review indexes of no-reflow used both in the cath-lab and thereafter.

Coronary aneurysmatic dilatation may be localized to a segment or may involve multiple segments. We herein report a case of a diffuse aneurysmatic dilatation of the right coronary artery.

Laser atherectomy might decrease procedural complications during percutaneous coronary intervention (PCI) of degenerated saphenous vein grafts (SVGs) in case of unstable or thrombotic lesions because of its ability to debulk and vaporize thrombus. We aimed at prospectively evaluating the safety and efficacy of excimer laser coronary angioplasty (ELCA) as a primary treatment strategy in consecutively unstable patients undergoing PCI of degenerated SVG lesions. Seventy-one consecutive patients with non-ST elevation acute coronary syndrome (mean age 69 ± 10 years, 66 men [89%]) undergoing PCI of degenerated SVG were enrolled in a prospective case-control registry, using 2 different distal protection devices (DPDs; FilterWire EZ [Boston Scientific, Natick, Massachusetts; n = 24] and SpiderRX [Ev3, Plymouth, Minnesota; n = 23]) or ELCA (n = 24). Primary end points of the study were incidence of angiographic microvascular obstruction (Thrombolysis In Myocardial Infarction flow grade of <3 or Thrombolysis In Myocardial Infraction flow grade of 3 with myocardial blush grade 1 to 2) and incidence of type IVa myocardial infarction. Angiographic microvascular obstruction incidence tended to be less in ELCA-treated patients compared with DPD-treated patients (3 [13%] vs 15 [32%], p = 0.09). Type IVa myocardial infarction incidence was more in DPD-treated patients compared with ELCA-treated patients (23 [49%] vs 5 [21%], p = 0.04). In conclusion, in patients with non-ST elevation acute coronary syndrome undergoing PCI of degenerated SVG, ELCA compared with DPD, is associated with a trend for better myocardial reperfusion and a lesser incidence of periprocedural necrosis. Controlled randomized trials are warranted to confirm these early observations.

Persistent oxidative stress may play a key role in microvascular obstruction (MVO). We aimed at assessing the role of platelet gp91phox (NOX2), the catalytic subunit of NADPH oxidase in MVO.

BACKGROUND: A diffuse pattern of in-stent restenosis (ISR) has been shown to have a worse prognosis when compared to a focal pattern. It is still unknown whether baseline C-reactive protein (CRP) levels predict ISR pattern. METHODS: Our database was searched retrospectively for patients presenting with ISR after m-TOR inhibitor drug-eluting stent (DES) implantation from January 2007 to December 2009. Angiographic restenosis patterns were evaluated according to the simplified Mehran classification and patients were allocated either to the diffuse or focal pattern group. Predictors of restenosis pattern were assessed among clinical, angiographic, procedural and laboratory data, including baseline high-sensitivity CRP, recorded at the time of the first percutaneous intervention. RESULTS: 72 patients (age, 65 ± 9 years; male sex, 64%) found to have ISR after DES implantation were enrolled. 34 patients presented with a focal pattern, whereas 38 patients presented with a diffuse pattern. At multivariate analysis, CRP levels were the only independent predictor of a diffuse ISR pattern [odds ratio, 2.5; 95% confidence interval, 1.4-4.3; p = 0.001)]. Rising CRP tertiles were associated with an increased rate of diffuse pattern (13% versus 26% versus 61%; p for trend = 0.0001). CONCLUSION: Baseline CRP serum levels are associated with a diffuse ISR pattern after m-TOR inhibitor DES implantation. These findings suggest that baseline inflammatory reactivity may contribute to aggressive restenosis occurring despite drug elution.