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Endothelial erosion of atherosclerotic plaques is the underlying cause of approximately 30% of acute coronary syndromes (ACS). As the vascular endothelium is profoundly affected by the haemodynamic environment to which it is exposed, we employed computational fluid dynamic (CFD) analysis of the luminal geometry from 17 patients with optical coherence tomography (OCT)-defined plaque erosion, to determine the flow environment permissive for plaque erosion. Our results demonstrate that 15 of the 17 cases analysed occurred on stenotic plaques with median 31% diameter stenosis (interquartile range 28–52%), where all but one of the adherent thrombi located proximal to, or within the region of maximum stenosis. Consequently, all flow metrics related to elevated flow were significantly increased (time averaged wall shear stress, maximum wall shear stress, time averaged wall shear stress gradient) with a reduction in relative residence time, compared to a non-diseased reference segment. We also identified two cases that did not exhibit an elevation of flow, but occurred in a region exposed to elevated oscillatory flow. Our study demonstrates that the majority of OCT-defined erosions occur where the endothelium is exposed to elevated flow, a haemodynamic environment known to evoke a distinctive phenotypic response in endothelial cells. [ABSTRACT FROM AUTHOR]

Postmortem studies reported plaque erosion is frequent in young women. Recent in vivo studies failed to show age and sex differences in the plaque erosion prevalence. The aim of this study was to investigate the prevalence of plaque erosion by age and sex among acute coronary syndromes (ACS) patients. From 1699 ACS patients, 1083 with plaque erosion or rupture were analyzed. Patients were categorized as 5 age groups (≤ 50, 51–60, 61–70, 71–80, ≥ 81 years). Overall prevalence of plaque erosion was similar between males and females (p = 0.831). Males age ≤ 50 had higher (p = 0.018) and age 71–80 had lower (p = 0.006) prevalence of plaque erosion. Females age 61–70 had higher (p = 0.021) and age 71–80 had lower (p = 0.045) prevalence of plaque erosion. In advanced age groups (≥ 71 years), rupture was the dominant etiology in both sexes. In multivariate analysis of males, age ≤ 50 demonstrated a trend to increase (OR 1.418, 95% CI 0.961–2.093, p = 0.078) the erosion risk. Females age ≤ 70 independently increased (OR 2.138, 95% CI 1.249–3.661, p = 0.006) the risk for erosion. The prevalence of plaque erosion was similar between males and females. Plaque erosion risk was increased in the males age ≤ 50 and in the females age ≤ 70 among ACS patients. [ABSTRACT FROM AUTHOR]

Background: Coronary vasomotor dysfunction represents an important mechanism responsible for myocardial ischaemia in patients with non-obstructive coronary artery disease (CAD). The use of invasive provocative tests allows identifying patients with epicardial or microvascular spasm. Of note, clinical characteristics associated with the occurrence of epicardial or microvascular spasm have still not completely clarified. Methods and results: We prospectively enrolled consecutive patients undergoing coronary angiography for suspected myocardial ischaemia/necrosis with evidence of non-obstructive CAD and undergoing intracoronary provocative test for suspected vasomotor dysfunction. Patients with a positive provocative test were enrolled. Clinical, echocardiographic and angiographic characteristics of patients were evaluated according to the pattern of vasomotor dysfunction (epicardial vs. microvascular spasm). We included 120 patients [68 patients with stable angina and 52 patients with myocardial infarction and non-obstructive coronary arteries (MINOCA)]. In particular, 77 (64.2%) patients had a provocative test positive for epicardial spasm and 43 (35.8%) patients for microvascular spasm. Patients with epicardial spasm were more frequently males, smokers, had higher rates of diffuse coronary atherosclerosis at angiography and more frequently presented with MINOCA. On the other hand, patients with microvascular spasm presented more frequently diastolic dysfunction. At multivariate logistic regression analysis male sex, smoking, and diffuse coronary atherosclerosis were independent predictors for the occurrence of epicardial spasm. Conclusions: Our study showed that specific clinical features are associated with different responses to intracoronary provocative test. Epicardial spasm is more frequent in males and in MINOCA patients, whereas microvascular spasm is more frequent in patients with stable angina and is associated with diastolic dysfunction. [ABSTRACT FROM AUTHOR]

Background: Between 10 and 15% of patients admitted for non-ST-segment elevation acute coronary syndrome (NSTE-ACS) show no obstructive coronary artery disease (NO-CAD) at angiography. Coronary microvascular spasm is a possible mechanism of the syndrome, but there are scarce data about coronary microvascular function in these patients. Objectives: To assess coronary microvascular function in patients with NSTE-ACS and NO-CAD. Methods: We studied 30 patients (67 ± 10 years, 19 female) with NSTE-ACS and NO-CAD. Specific causes of NSTE-ACS presentation (e.g., variant angina, takotsubo disease, tachyarrhythmias, etc.) were excluded. Coronary blood flow (CBF) velocity response to IV ergonovine (6 µg/kg up to a maximal dose of 400 µg) was evaluated before discharge by transthoracic Doppler echocardiography. CBF response to IV adenosine (140 μg/kg/min) and cold pressor test (CPT) was also assessed after 1 month. Ten age- and sex-matched patients with non-cardiac chest pain served as controls. Vasoactive tests were repeated after 12 months in 10 NSTE-ACS patients. Results: The ergonovine/basal CBF velocity ratio was 0.79 ± 0.09 and 0.99 ± 0.01 in patients and controls, respectively (p < 0.001). The adenosine/basal CBF velocity ratio was 1.46 ± 0.2 and 3.25 ± 1.2 in patients and controls, respectively (p < 0.001), and the CPT/basal CBF velocity ratio was 1.36 ± 0.2 and 2.43 ± 0.3 in the 2 groups, respectively (p < 0.001). In 10 patients assessed after 12 months, CBF velocity responses to ergonovine, adenosine, and CPT were found to be unchanged. Conclusions: Patients with NSTE-ACS and NO-CAD exhibit a significant coronary dysfunction, which seems to involve both an increased constrictor reactivity, likely mainly involving coronary microcirculation, and a reduced microvascular dilator function, both persisting at 12-month follow-up. [ABSTRACT FROM AUTHOR]

The efficacy of DEB in modifying the high restenosis risk associated with BMS implantation is doubtful. Optical coherence tomography (OCT) may allow precise assessment of neointimal formation after stent implantation. We performed a single-center, prospective, 1:2 randomized trial comparing BMS implantation alone (BMS group) vs. additional DEB (DEB group). DEB patients were further randomized 1:1 to DEB before stenting (pre-DEB group), or after stenting (post-DEB group). Primary endpoint was OCT-assessed neointimal hyperplasia (expressed both as mean in-stent neointimal area and as percentage obstruction of the mean stent area) at 6 months. Secondary endpoints were the percentage of uncovered and malapposed stent struts. Thirty patients were enrolled and randomized to BMS ( n = 10), pre-DEB ( n = 10), post-DEB ( n = 10). At 6-month OCT follow-up, DEB significantly reduced neointimal area compared with BMS: mean neointimal area 2.01 ± 0.89 vs. 3.03 ± 1.07 mm ( p = 0.02), percentage area obstruction 24.56 ± 12.50 vs. 37.51 ± 12.26 % ( p = 0.02). The percentage of uncovered and malapposed stent struts did not differ significantly between BMS and DEB. In the comparison between pre-DEB and post-DEB, no significant difference was observed for both primary and secondary endpoints. In de novo coronary lesions treated with BMS, DEB use could be associated with a mild reduction in neointimal hyperplasia at 6 months; this effect could be unrelated to the timing of DEB dilation (pre- or post-stenting). Clinical Trial Registration Information: . Identifier: NCT01057563. [ABSTRACT FROM AUTHOR]

Plaque rupture (PR) and superimposed thrombosis have been shown as the most frequent underlying substrate in acute coronary syndromes (ACS). Coronary angiography is a luminogram not able to define in vivo features of the culprit plaques. The aim of the study was to use optical coherence tomography (OCT) to investigate the pathology underlying complex (CL) and non-complex angiographic lesions (NCL). We retrospectively enrolled 107 ACS patients admitted to our institution; 83 with non-ST elevation ACS (NSTE-ACS) and 24 with ST-elevation myocardial infarction. Coronary angiography was performed and culprit lesions were classified according to Ambrose criteria into NCL (n = 47) and CL (n = 60). OCT imaging was then performed to better identify plaque morphology; either PR or intact fibrous cap, the presence of superimposed thrombosis, lipid rich plaque, and thin cap fibroatheroma (TCFA). OCT analysis showed that 58 lesions (54.2 %) were classified as PR and 48 lesions (44.9 %) were associated with thrombi. Lipid rich plaques were identified in 62 lesions (57.9 %). PR, intracoronary thrombi, lipid rich plaques and TCFA were more frequent in CL compared with NCL (71.7 vs 31.9 %, 63.3 vs 21.3 %, 71.7 vs 40.4 % and 46.7 vs 21.3 % respectively), but PR with superimposed thrombus may be also detected in NCL. OCT demonstrates PR and thrombosis in the majority of ACS patients presenting with CL. However, one-third of NCL show PR by OCT, suggesting that additional intracoronary imaging by OCT may better identify the underlying mechanism of coronary instability than coronary angiography alone. [ABSTRACT FROM AUTHOR]

This study was performed to analyze the impact of transradial intervention (TRI), performed by long (25-cm) hydrophilic-coated radial introducer sheath (HRS), on radial artery (RA). Both acute damages and chronic intimal modifications, occurring in RA, were assessed using frequency domain-optical coherence tomography (FD-OCT). FD-OCT evaluation of RA was performed in 51 consecutive patients, undergoing TRI by long (25-cm) HRS. FD-OCT was performed from RA ostium to the puncture site. Acute damages such as intimal tears and medial dissections together with chronic intimal modifications, assessed as intimal hyperplasia indexes, were observed and compared between proximal and distal RA segments. Intimal tears were detected in 37 % of patients, especially located in proximal RA segment ( p = 0.09). Medial dissections were imaged in 9.8 % of patients with no significant difference between proximal and distal RA segments. Intimal hyperplasia indexes were higher in distal RA segment, with no significant association with a previous history of TRI. In the setting of TRI, performed by long HRS, intimal tears represented the main RA injury occurring in about one-third of patients, while medial dissections only occurred in a small proportion of patients. Distal RA segment was more prone to intimal thickening, although this phenomenon was not associated with repeated transradial procedures. [ABSTRACT FROM AUTHOR]

Objective: Toevaluatethelong-termeffectsofdrospirenone(DRSP)/ethinylestradiol(EE)alone,metforminalone,andDRSP/ + null EE-metforminonCD4 CD28 Tlymphocytesfrequency,acardiovascularriskmarker,inpatientswithhyperinsulinemic polycysticovarysyndrome(PCOS). Design: Randomizedclinicaltrial. Interventions: Ninetythreepatientswithhyper- insulinemicPCOSwereagematchedandbodymassindexmatchedandrandomizedtoreceivea6monthsdailytreatmentwith DRSP(3mg)/EE(0.03mg),ormetformin(1500mg),orDRSP/EEcombinedwithmetformin. MainOutcomeMeasures: + null CD4 CD28 T-cellfrequencies. Results: TheDRSP/EEandmetformingroupsdidnotshowanysignificantchangeinthe + null + null CD4 CD28 frequencycomparedtothebaseline.Interestingly,astatisticallysignificantdecreaseinCD4 CD28 frequency occurredafter6monthsofDRSP/EE-metformin(median 3-1.5; P <.01).Ofnote,thisstatisticallysignificantassociationwas confirmedafteradjustingforbaselinevaluesinDRSP/EE-metformingroupbyanalysisofcovariance(P <.05). Conclusions: In womenwithhyperinsulinemicPCOS,combinedtherapywithDRSP/EEandmetforminmayreducecardiovascularrisk. [ABSTRACT FROM AUTHOR]

No-reflow after primary percutaneous coronary intervention (pPCI) may be reversible. 40 patients undergoing pPCI were evaluated by assessing either improvement or lack of changes regarding angiographic and electrocardiographic indexes of no-reflow between admission and pre-discharge. Myeloperoxidase (MPO; in nanograms per milliliter), C-reactive protein (CRP; in milligrams per liter), endothelin-1 (ET-1; in nanograms per milliliter), angiopoietin-2 (Ang-2, in picograms per milliliter), and their pre-discharge/basal values variations (Δ) were related to no-reflow evolution. ΔMPO and ΔCRP were greater in patients with sustained no-reflow or lack of ST-segment resolution (STR) as compared with those with reversible no-reflow or lack of STR ( p = 0.033, p = 0.04, p < 0.001, and p = 0.001, respectively), whereas ΔET-1 was similar in the two groups. ΔAng-2 was greater in patients with sustained no-reflow or lack of STR as compared with those with reversible no-reflow or lack of STR ( p = 0.01 and 0.044, respectively). Bigger ΔMPO, ΔCRP (increasing levels), and ΔAng-2 (decreasing levels) are associated with sustained no-reflow, thus they might have a role in no-reflow evolution. [ABSTRACT FROM AUTHOR]

Infarct size (IS) and microvascular obstruction (MO) following ST-elevation myocardial infarction (STEMI) reperfusion may affect left ventricular (LV) remodeling. We evaluated the impact of extent and transmurality of IS and MO in LV remodeling using contrast-enhanced cardiac magnetic resonance imaging (MRI). Thirty-six consecutive patients presenting with a first STEMI and undergoing contrast-enhanced cardiac MRI within 5 days of successful primary percutaneous coronary intervention (PPCI) were enrolled. Gadolinium-enhanced MRI at first passage and in delayed imaging was performed to assess MO and IS. LV remodeling was evaluated by echocardiography at 6-month-follow-up and defined as a percent increase in the LV end-diastolic volume >20%. Thirteen patients (36%) developed LV remodeling. IS and MO extent score was associated with LV remodeling (OR 1.5, 95% CI 1.02-2.38, P = 0.04, and OR 3.1, 95% CI 1.45-6.64, P = 0.003, respectively), along with IS and MO trasmurality (OR 1.4, 95% CI 1.007-2.12, P = 0.046, and OR 3.1, 95% CI 1.24-7.89, P = 0.016, respectively). Importantly, IS and MO extent score combination gave an OR of 3.4 (95% CI 1.4-7.9, P = 0.004) and the combination of IS and MO transmurality increased the OR to 4.8 (95% CI 1.5-15.2, P = 0.007). Finally, when combining simultaneously IS and MO extent score and transmurality the OR reached 5.3 (95% CI 3.34-18.2, P = 0.0008). The evaluation of both IS and MO extent and transmurality by MRI is of prognostic utility in patients undergoing PPCI. Importantly, IS and MO transmurality significantly increases the risk of adverse remodeling and should be routinely assessed in post-STEMI patients. [ABSTRACT FROM AUTHOR]

Previous studies indicate that percutaneous transluminal coronary angioplasty (PTCA) is associated with platelet activation. It is not well-established whether enhanced platelet aggregability after PTCA is prevented by the association of ticlopidine with aspirin. The aim of this study was to evaluate whole blood platelet aggregability before and after elective PTCA in patients with chronic stable angina receiving ticlopidine and aspirin. We studied 16 patients referred for elective PTCA, treated for≥72 hours with oral aspirin and ticlopidine (group 1), and 10 patients referred for diagnostic coronary angiography, treated with oral aspirin alone (group 2). An intravenous bolus of heparin was administered at the start of PTCA. In both groups, platelet aggregability was assessed at baseline and 24 hours after the procedure, using the PFA 100® system. This method measures the time required for flowing whole blood to occlude a collagen and adenosine diphosphate (ADP)–coated ring, shorter times indicating greater aggregability. In both groups, platelet aggregability after the procedure was significantly increased compared with baseline: 104±30 seconds before versus 88±24 seconds at 24 hours in group 1 ( p=0.03) and 84±16 seconds before versus 69±14 seconds at 24 hours in group 2 ( p=0.004). Group 1 patients, compared with group 2, showed a trend toward reduced aggregability at baseline ( p=0.06) and significantly lower aggregability 24 hours after the procedure ( p=0.03). Ticlopidine and aspirin reduce whole-blood platelet aggregability compared with aspirin alone but fail to suppress the increased aggregability that occurs 24 hours after PTCA. [ABSTRACT FROM AUTHOR]