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Background--Interventional cardiologists are increasingly exposed to radiation-induced diseases like cataract and the stochastic risk of left-sided brain tumors. The RADPAD is a sterile, disposable, lead-free shield placed on the patient with the aim to minimize operator-received scatter radiation. The objective of the trial was to examine the RADPAD's efficacy in a real-world situation. Methods and Results--In the current, double-blind, sham-controlled, all-comer trial, patients undergoing diagnostic catheterization or percutaneous coronary interventions were randomized in a 1:1:1 ratio to a radiation absorbing shield (RADPAD), standard treatment (NOPAD), or a sham shield (SHAMPAD). The sham shield allowed testing for shieldinduced radiation behavior. The primary outcome was the difference in relative exposure of the primary operator between the RADPAD and NOPAD arms and was defined as the ratio between operator's exposure (E in µSv) and patient exposure (dose area product in mGy·cm2), measured per procedure. A total of 766 consecutive coronary procedures were randomized to the use of RADPAD (N=255), NOPAD (N=255), or SHAMPAD (N=256). The use of RADPAD was associated with a 20% reduction in relative operator exposure compared with that of NOPAD (P=0.01) and a 44% relative exposure reduction compared with the use of a SHAMPAD (P<0.001). Use of the SHAMPAD was associated with a 43% higher relative radiation exposure than procedures with NOPAD (P=0.009). Conclusions--In clinical daily practice, the standard use of the RADPAD radiation shield reduced operator radiation exposure compared with procedures with NOPAD or SHAMPAD. This study supports the routine use of RADPAD in the catheterization laboratory. [ABSTRACT FROM AUTHOR]

BACKGROUND--The Navvus pressure sensor-equipped microcatheter allows to measure functional stenosis severity over a work-horse guidewire and is used as a more feasible alternative to regular sensor-equipped wires. However, Navvus is larger in diameter than contemporary sensor-equipped guidewires and may, thereby, influence functional measurements. The present study evaluates the hemodynamic influence of the Navvus microcatheter. METHODS AND RESULTS--In patients with intermediate coronary stenosis, coronary pressure and flow velocity were measured using a dual sensor-equipped guidewire before and after introduction of Navvus. Patients were randomized to microcatheter-first or guidewire-first measurement. The primary end point was the difference in hyperemic stenosis resistance index between measurements before and after introduction of Navvus. Measurements were completed in 28 patients (28 stenoses). Mean hyperemic stenosis resistance was 0.37±0.19 Hg/cm/s for wire-only assessment and 0.48±0.26 Hg/cm/s after Navvus introduction (P<0.001). Bland-Altman analysis documented a mean bias of +0.11 Hg/cm/s (limits of agreement: -0.13 to 0.36), proportional to mean hyperemic stenosis resistance (Spearman ρ =0.61; P=0.001). Passing-Bablok analysis revealed absence of a constant difference but significant proportional difference between the methods. Mean fractional flow reserve was 0.86±0.06 for wire-only assessment and 0.82±0.07 after Navvus introduction (P<0.001). Bland-Altman analysis documented a mean bias of -0.033 (limits of agreement: -0.09 to 0.03), proportional to mean fractional flow reserve (Spearman ρ =0.40; P=0.036). Passing-Bablok analysis revealed significant constant and proportional differences between methods. Similar results were documented for resting indices of stenosis severity. CONCLUSIONS--Introduction of the Navvus microcatheter leads to clinically relevant stenosis severity overestimation in intermediate stenosis. [ABSTRACT FROM AUTHOR]

Background--Aortic valve stenosis (AS) can cause angina despite unobstructed coronary arteries, which may be related to increased compression of the intramural microcirculation, especially at the subendocardium. We assessed coronary wave intensity and phasic flow velocity patterns to unravel changes in cardiac-coronary interaction because of transcatheter aortic valve implantation (TAVI). Methods and Results--Intracoronary pressure and flow velocity were measured at rest and maximal hyperemia in undiseased vessels in 15 patients with AS before and after TAVI and in 12 control patients. Coronary flow reserve, systolic and diastolic velocity time integrals, and the energies of forward (aorta-originating) and backward (microcirculatory-originating) coronary waves were determined. Coronary flow reserve was 2.8±0.2 (mean±SEM) in control and 1.8±0.1 in AS (P<0.005) and was not restored by TAVI. Compared with control, the resting backward expansion wave was 45% higher in AS. The peak of the systolic forward compression wave was delayed in AS, consistent with a delayed peak aortic pressure, which was partially restored after TAVI. The energy of forward waves doubled after TAVI, whereas the backward expansion wave increased by >30%. The increase in forward compression wave with TAVI was related to an increase in systolic velocity time integral. AS or TAVI did not alter diastolic velocity time integral. Conclusions--Reduced coronary forward wave energy and systolic velocity time integral imply a compromised systolic flow velocity with AS that is restored after TAVI, suggesting an acute relief of excess compression in systole that likely benefits subendocardial perfusion. Vasodilation is observed to be a major determinant of backward waves. (Circ Cardiovasc Interv. [ABSTRACT FROM AUTHOR]

Discordance between fractional flow reserve (FFR) and coronary flow velocity reserve (CFVR) may reflect important coronary pathophysiology but usually remains unnoticed in clinical practice. We evaluated the physiological basis and clinical outcome associated with FFR/CFVR discordance.We studied 157 intermediate coronary stenoses in 157 patients, evaluated by FFR and CFVR between April 1997 and September 2006 in which revascularization was deferred. Long-term follow-up was performed to document the occurrence of major adverse cardiac events: cardiac death, myocardial infarction, or target vessel revascularization. Discordance between FFR and CFVR occurred in 31% and 37% of stenoses at the 0.75, and 0.80 FFR cut-off value, respectively, and was characterized by microvascular resistances during basal and hyperemic conditions. Follow-up duration amounted to 11.7 years (Q1-Q3, 9.9-13.3 years). Compared with concordant normal results of FFR and CFVR, a normal FFR with an abnormal CFVR was associated with significantly increased major adverse cardiac events rate throughout 10 years of follow-up, regardless of the FFR cut-off applied. In contrast, an abnormal FFR with a normal CFVR was associated with equivalent clinical outcome compared with concordant normal results: 3 years when FFR <0.75 was depicted abnormal and throughout 10 years of follow-up when FFR 0.80 was depicted abnormal.Discordance of CFVR with FFR originates from the involvement of the coronary microvasculature. Importantly, the risk for major adverse cardiac events associated with FFR/CFVR discordance is mainly attributable to stenoses where CFVR is abnormal. This emphasizes the requirement of intracoronary flow assessment in addition to coronary pressure for optimal risk stratification in stable coronary artery disease. [ABSTRACT FROM AUTHOR]

The prognosis of initial survivors of ST-segment-elevation myocardial infarction (STEMI) is affected by both recurrent myocardial infarction (MI) and severe bleeding. The aim of the current study was to investigate how mortality is affected in time after bleeding and recurrent MI.From January 1, 2003, to July 31, 2008, a total of 2002 patients were treated with primary percutaneous coronary intervention for ST-segment-elevation MI and followed up for the occurrence of recurrent MI and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) severe bleeding. Primary outcome was all-cause mortality within 4 years of follow-up. In a time-dependent, covariate-adjusted Cox regression model, both bleeding and recurrent MI were associated with an increase in mortality shortly after the adverse event: hazard ratio, 14.37 (95% confidence interval [CI], 7.69-26.84) for the first day after recurrent MI and 5.42 (95% CI, 2.88-10.22) for the first day after bleeding. Thereafter the risk of subsequent mortality gradually decreased but remained elevated long after a recurrent MI (hazard ratio, 4.95 [95% CI, 3.27-7.48] between 1 day and 1 year after recurrent MI and hazard ratio, 2.56 [95% CI, 1.56-4.21] beyond 1 year after recurrent MI), but decreased to nonsignificant level beyond 1 month after the bleeding (hazard ratio, 0.56 [95% CI, 0.27-1.14]).The occurrence of both recurrent MI and bleeding in the first year after ST-segment-elevation MI is associated with subsequent mortality. The risk implication of recurrent MI, however, was greater and more sustained over time than that of severe bleeding. [ABSTRACT FROM AUTHOR]

Abnormalities in the coronary microcirculation are increasingly recognized as an elementary component of ischemic heart disease, which can be accurately assessed by coronary flow velocity reserve in reference vessels (refCFVR). We studied the prognostic value of refCFVR for long-term mortality in patients with stable coronary artery disease.We included patients with stable coronary artery disease who underwent intracoronary physiological evaluation of ≥1 coronary lesion of intermediate severity between April 1997 and September 2006. RefCFVR was assessed if a coronary artery with <30% irregularities was present. RefCFVR >2.7 was considered normal. Patients underwent revascularization of all ischemia-causing lesions. Long-term follow-up was performed to document the occurrence of (cardiac) mortality. RefCFVR was determined in 178 patients. Kaplan-Meier estimates of 12-year all-cause mortality were 16.7% when refCFVR >2.7 and 39.6% when refCFVR 2.7 (P<0.001), whereas Kaplan-Meier estimates for cardiac mortality were 7.7% when refCFVR >2.7 and 31.6% when refCFVR 2.7 (P<0.001). After multivariable adjustment, refCFVR 2.7 was associated with a 2.24-fold increase in all-cause mortality hazard (hazard ratio, 2.24; 95% confidence interval, 1.13-4.44; P=0.020) and a 3.32-fold increase in cardiac mortality hazard (hazard ratio, 3.32; 95% confidence interval, 1.27-8.67; P=0.014). Impairment of refCFVR originated from significantly higher baseline flow velocity in the presence of significantly lower reference vessel baseline microvascular resistance (P<0.001), indicating impaired coronary autoregulation as its cause.In patients with stable coronary artery disease, impaired refCFVR, resulting from increased baseline flow velocity indicating impaired coronary autoregulation, is associated with a significant increase in fatal events at long-term follow-up. [ABSTRACT FROM AUTHOR]

Microvascular function is increasingly being recognized as an important marker of risk in coronary artery disease, and may be accurately assessed by intracoronary Doppler flow velocity measurements. In the setting of ST-segment-elevation myocardial infarction there are limited data regarding the prognostic value of microvascular function in both infarct-related and reference coronary arteries for long-term clinical outcome. We sought to determine the prognostic value of microvascular function, as assessed by Doppler flow velocity measurements, for cardiac mortality after primary percutaneous coronary intervention for acute ST-segment-elevation myocardial infarction.Between April 1997 and August 2000, we included 100 consecutive patients with a first anterior wall ST-segment-elevation myocardial infarction. Immediately after primary percutaneous coronary intervention, intracoronary Doppler flow velocity was measured in the infarct-related artery, to determine coronary flow velocity reserve (CFVR), diastolic deceleration time, and the presence of systolic retrograde flow, as well as in a reference vessel to determine reference vessel CFVR. The primary end point was cardiac mortality at 10-year follow-up. Complete follow-up was obtained in 94 patients (94%). At 10-year follow-up, cardiac mortality amounted to 14%. Cardiac mortality amounted to 5% when reference vessel CFVR was normal (≥2.1), in contrast to 31% when abnormal (<2.1; P=0.001). Reference vessel CFVR <2.1 was associated with a 4.09 increase in long-term cardiac mortality hazard after multivariate adjustment for identified predictors for cardiac mortality (hazard ratio, 4.09; 95% confidence interval, 1.18-14.17; P=0.03)Microvascular dysfunction, measured by reference vessel CFVR determined after primary percutaneous coronary intervention for acute anterior wall ST-segment-elevation myocardial infarction is associated with a significantly increased long-term cardiac mortality. [ABSTRACT FROM AUTHOR]

The article presents a study of the incidence, prognostic value and predictors of myocardial infarction during transcatheter aortic valve implantation (TAVI). The study measured the serum creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT) levels before and after TAVI. Results show that myocardial injury can be an independent predictor for 30-day mortality following TAVI.

The article presents a study on the reaction of vascular tissue to acute incomplete stent apposition (ISA) in human coronary arteries. The optical coherence study was conducted among 66 stents which were implanted in 43 patients and were analyzed after implantation. The researchers described the use of neointimal healing trends in reducing ISA which resulted in characteristic morphological patterns. They discussed the delay in the coverage of ISA segments with respect to well-apposed segments.

The article presents a study which investigated whether various measures of ST-segment recovery can be applied to unselected ST-segment-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary investigation (PCI). It mentions that the largest study published strongly associated ST-segment recovery with 90-day death, congestive heart failure and shock. The study concludes that comparing summed procedural and postprocedural ST-segment deviation is the best predictor of one-year mortality when assessed at PCI end.

Supplemental Digital Content is available in the text. Background: Numerous randomized clinical trials have demonstrated the superiority of thin-strut biodegradable polymer second-generation drug-eluting stent to the first-generation drug-eluting stent and the noninferiority to the thin-strut second-generation permanent polymer drug-eluting stent. Data on long-term clinical outcomes with a novel ultrathin drug-eluting stent, to date, are limited. Methods: The DESSOLVE III trial (Multicenter Randomized Study of the MiStent Sirolimus Eluting Absorbable Polymer Stent System for Revascularization of Coronary Arteries; n=1398) is a prospective, multicenter, single-blinded, all-comers, randomized controlled trial (NCT02385279), allocating in a 1:1 ratio to either ultrathin-strut biodegradable polymer MiStent sirolimus-eluting stent or to thin-strut permanent polymer Xience everolimus-eluting stent. The primary end point was device-oriented composite end point, defined as the composite of cardiac death, target vessel myocardial infarction, or clinically indicated target lesion revascularization. The secondary end point was patient-oriented composite end point, defined as the composite of all-cause mortality, any myocardial infarction, or any revascularization. Results: At 3 years, follow-up data were available in 1381 patients (98.8%). The primary end point of device-oriented composite end point occurred in 10.5% for MiStent sirolimus-eluting stent and in 11.5% for Xience everolimus-eluting stent (P =0.55). Rates of cardiac death (3.9% versus 3.8%; P =0.88), target vessel myocardial infarction (3.2% versus 2.5%; P =0.43), and clinically indicated target lesion revascularization (5.2% versus 6.5%; P =0.30) did not differ significantly between the 2 devices. The rate of definite or probable stent thrombosis was infrequent and similar between the 2 arms (1.2% versus 1.5%; P =0.64). The 90-day landmark analysis showed no significant difference in device-oriented composite end point between the 2 groups after polymer degradation of MiStent. The risk of patient-oriented composite end point was comparable between the 2 groups (22.7% versus 22.9%; P =0.34). Conclusions: In the DESSOLVE III trial, early safety and efficacy with MiStent sirolimus-eluting bioabsorbable polymer-coated stent are confirmed at a longer term follow-up when compared with Xience everolimus-eluting permanent polymer-coated stent in a large all-comers population. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02385279. [ABSTRACT FROM AUTHOR]

Objective: In the National Institute for Clinical Excellence (NICE) guidelines, lesions with a reference vessel diameter of less than 3.0 mm or lesions with a length of greater than 15 mm are considered carrying a high risk of restenosis. In contrast, lesions with a reference vessel diameter of at least 3.0 mm or a lesion length of 15 mm or less are considered at low risk of restenosis. We performed a retrospective analysis of consecutive patients undergoing nonurgent percutaneous coronary intervention (PCI) comparing bare metal stent (BMS) with drug-eluting stent (DES) using the NICE guidelines., Methods and Results: Between 2003 and 2007, a total of 3883 patients underwent a nonurgent PCI for a de-novo coronary lesion; 2050 patients were considered to be at low risk and 1833 patients were considered at high risk of restenosis according to the NICE criteria. In the low-risk group, the 1-year composite of cardiac death, myocardial infarction, and target vessel revascularization was 10.5% in the BMS group and 11.1% in the DES group (P=0.85). Target lesion revascularization (TLR) was 5.3% by PCI and 1.6% by coronary artery bypass grafting (CABG) in the BMS group and 4.0 and 3.0% in the DES group (P=0.59 and P=0.24). In the high-risk group, the composite of cardiac death, myocardial infarction, and target vessel revascularization was 12.1 and 11.0% in the BMS and DES groups (P=0.48). TLR was 6.7% by PCI and 1.3% by CABG in the BMS group and 3.9 and 2.8% in the DES group (P=0.01; P=0.02). Definite stent thrombosis (ST) was 0.8% in the BMS-treated patients and 1.7% in the DES-treated patients (P=0.09)., Conclusion: In patients with lesions carrying a low risk of restenosis, no differences were observed between BMS and DES in composite end points, TLR, or ST at 1-year follow-up. In patients with lesions carrying a high risk of restenosis, patients treated with BMS had a significantly higher rate of TLR by PCI, but a significantly lower rate of TLR by CABG compared with patients treated with DES. A nonsignificant lower rate of definite ST was observed in the BMS group compared with the DES group.

Background: Restenosis is the major drawback of percutaneous coronary interventions involving excessive activation and proliferation of vascular smooth muscle cells (SMCs). The nuclear receptor Nurr1 is an early response gene known mainly for its critical role in the development of dopamine neurons. In the present study, we investigated Nurr1 in human and experimental vascular restenosis., Methods and Results: In a prospective cohort of 601 patients undergoing percutaneous coronary intervention, including stent placement, we found a strong association between Nurr1 haplotypes and in-stent restenosis risk. Furthermore, Nurr1 is specifically expressed in human in-stent restenosis and induced in cultured human SMCs in response to serum or tumor necrosis factor-alpha. Lentivirus-mediated gain- and loss-of-function experiments in SMCs demonstrated that overexpression of Nurr1 inhibited proliferation, consistent with increased expression of the key cell-cycle inhibitor p27(Kip1), whereas Nurr1 silencing enhanced SMC growth. The tumor necrosis factor-alpha-induced proinflammatory response of SMCs is inhibited by Nurr1, as reflected by reduced interleukin-1beta, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 expression. Consistent with our in vitro data, endogenous Nurr1 reduced wire injury-induced proliferation and vascular lesion formation in carotid arteries of ApoE(-/-) mice., Conclusions: Nurr1 haplotypes are associated with human restenosis risk, and Nurr1 is expressed in human in-stent restenosis. In SMCs, Nurr1 inhibits proliferation and inflammatory responses, which explains the inhibition of SMC-rich lesion formation in mice. The recently identified small-molecule drugs that enhance the activity of Nurr1 reveal this nuclear receptor as an attractive novel target for (local) intervention in restenosis.

Background: The cyclin-dependent kinase inhibitor p27(kip1) is a key regulator of smooth muscle cell and leukocyte proliferation in vascular disease, including in-stent restenosis. We therefore hypothesized that common genetic variations or single nucleotide polymorphisms in p27(kip1) may serve as a useful tool in risk stratification for in-stent restenosis., Methods and Results: Three single nucleotide polymorphisms concerning the p27(kip1) gene (-838C>A, rs36228499; -79C>T, rs34330; +326G>T, rs2066827) were determined in a cohort of 715 patients undergoing coronary angioplasty and stent placement. We discovered that the p27(kip1)-838C>A single nucleotide polymorphism is associated with clinical in-stent restenosis; the -838AA genotype decreases the risk of target vessel revascularization (hazard ratio, 0.28; 95% confidence interval, 0.10 to 0.77). This finding was replicated in another cohort study of 2309 patients (hazard ratio, 0.61; 95% confidence interval, 0.40 to 0.93). No association was detected between this end point and the p27(kip1)-79C>T and +326G>T single nucleotide polymorphisms. We subsequently studied the functional importance of the -838C>A single nucleotide polymorphism and detected a 20-fold increased basal p27(kip1) transcriptional activity of the -838A allele containing promoter., Conclusions: Patients with the p27(kip1)-838AA genotype have a decreased risk of in-stent restenosis corresponding with enhanced promoter activity of the -838A allele of this cell-cycle inhibitor, which may explain decreased smooth muscle cell proliferation.

Background: Routine thrombus aspiration is frequently used during primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction to prevent distal embolization. Recently, evidence of clinical benefit was published. In 50% of the ST-elevation myocardial infarction patients with an onset of symptoms <12 hours before, thrombi were shown to be >1 day old. This observation illustrates that plaque rupture and coronary occlusion are significantly separated in time. In the present study, we correlate the presence of fresh versus older thrombus with long-term mortality., Methods and Results: Thrombus aspiration was performed in 1315 patients treated with primary percutaneous coronary intervention with 3 devices (Rescue, Export, and Proxis). Aspirated material was fixed in formalin and processed for histopathology. If possible, thrombus age was classified as either fresh only (<1 day) or older (>1 day). We identified fresh thrombus in 552 patients and older thrombus in 372 patients. The cumulative Kaplan-Meier estimate of all-cause mortality at 4 years was significantly higher in patients with older thrombus (16.0%) compared with patients with fresh thrombus (7.4%), with a hazard ratio of 1.82 (95% confidence interval, 1.17 to 2.85; P=0.008). Multivariate analysis identified the presence of older thrombus, in addition to other established predictors, as an independent predictor (hazard ratio, 1.83; 95% confidence interval, 1.14 to 2.93; P=0.01) of long-term mortality., Conclusions: Our study demonstrates that the presence of older thrombus, in addition to other established predictors, is an independent predictor of long-term mortality in patients with ST-elevation myocardial infarction treated with thrombus aspiration during primary percutaneous coronary intervention.

Background: Percutaneous coronary intervention (PCI) in a day-case setting might reduce logistic constraints on hospital resources, but data on safety are limited. We evaluated the safety and feasibility of same-day discharge after PCI., Methods and Results: Eight hundred consecutive patients scheduled for elective PCI by femoral approach were randomized to same-day discharge or overnight hospital stay. Four hours after PCI, patients were triaged as suitable for early discharge or not. Suitable patients were discharged immediately or kept overnight, according to randomization. Patients with an indication for extended hospital stay were not discharged regardless of randomization. Primary end points were death, myocardial infarction, coronary artery bypass graft surgery, repeat PCI, or puncture-related complications occurring within 24 hours after PCI. A total of 403 patients were assigned to same-day discharge, of whom 77 (19%) were identified for extended observation; 397 patients were assigned to overnight stay, of whom 85 (21%) were identified for extended observation. Among all patients, the composite primary end point occurred in 9 (2.2%) same-day discharge patients and in 17 (4.2%) overnight stay patients (risk difference, -0.020; 95% CI, -0.045 to -0.004; P for noninferiority <0.0001). Among patients deemed suitable for early discharge, the composite end point occurred in 1 of 326 (0.3%) same-day discharge patients and 2 of 312 (0.6%) overnight-stay patients (risk difference, -0.003; 95% CI, -0.014 to 0.007; P for noninferiority <0.0001). The last 3 events were related to puncture site., Conclusions: Same-day discharge after elective PCI is feasible and safe in the majority (80%) of patients selected for day-case PCI. Same-day discharge does not lead to additional complications compared with overnight stay.

Background: Primary ventricular fibrillation (VF) accounts for the majority of deaths during the acute phase of myocardial infarction. Identification of patients at risk for primary VF remains very poor., Methods and Results: We performed a case-control study in patients with a first ST-elevation myocardial infarction (STEMI) to identify independent risk factors for primary VF. A total of 330 primary VF survivors (cases) and 372 controls were included; patients with earlier infarcts or signs of structural heart disease were excluded. Baseline characteristics, including age, gender, drug use, and ECG parameters registered well before the index infarction, as well as medical history, were not different. Infarct size and location, culprit coronary artery, and presence of multivessel disease were similar between groups. Analysis of ECGs performed at hospital admission for the index STEMI revealed that cumulative ST deviation was significantly higher among cases (OR per 10-mm ST deviation 1.59, 95% CI 1.25 to 2.02). Analysis of medical histories among parents and siblings showed that the prevalence of cardiovascular disease was similar between cases and controls (73.1% and 73.0%, respectively); however, familial sudden death occurred significantly more frequently among cases than controls (43.1% and 25.1%, respectively; OR 2.72, 95% CI 1.84 to 4.03)., Conclusions: In a population of STEMI patients, the risk of primary VF is determined by cumulative ST deviation and family history of sudden death.

Background: Acute ST-elevation myocardial infarction (STEMI) is caused by sudden occlusive coronary thrombosis, after plaque disruption; however, a considerable time interval between plaque disturbance and the onset of symptoms has been suggested. We therefore studied the age of intracoronary thrombi, aspirated during angioplasty in patients with acute STEMI., Methods and Results: Percutaneous intracoronary thrombectomy during angioplasty was performed in 211 consecutive STEMI patients within 6 hours after onset of anginal symptoms. The aspirated material was histologically screened on thrombus and plaque components, and thrombus age was classified as fresh (<1 day), lytic thrombus (1 to 5 days), and organized thrombus (>5 days). In all patients, intracoronary-derived material was retrieved in the filter of the collection bottle. Thrombus was identified in 199 (95%) of 211 patients. In 12 patients (5%), only plaque components were identified, and in 85 patients (41%), both thrombus and plaque material were aspirated. In 18 (9%) of 199 patients, the thrombus was organized, and in 70 patients (35%), the thrombus showed lytic changes, whereas in 98 (49%), a completely fresh thrombus was found. In 14 (7%) of 199 patients, the thrombus showed combined features of both fresh thrombus and organized thrombus., Conclusions: In at least 50% of patients with acute STEMI, coronary thrombi were days or weeks old. This indicates that sudden coronary occlusion is often preceded by a variable period of plaque instability and thrombus formation, initiated days or weeks before onset of symptoms.

Background: Coronary microvascular resistance during maximal hyperemia is generally assumed to be unaffected by percutaneous coronary interventions (PCIs). We assessed a velocity-based index of hyperemic microvascular resistance (h-MR(v)) by using prototypes of a novel, dual-sensor (Doppler velocity and pressure)-equipped guidewire before and after PCI to test this hypothesis., Methods and Results: Aortic pressure, flow velocity (h-v), and pressure (h-P(d)) distal to 24 coronary lesions were measured simultaneously during maximal hyperemia induced by intracoronary adenosine. Measurements were obtained in the reference vessel before PCI and in the target vessel before and after PCI, stenting, and ultrasound-guided, upsized stenting. h-P(d) increased from 57.9+/-17.0 to 85.5+/-15.6 mm Hg, and h-MR(v) (ie, h-P(d)/h-v) decreased from 2.74+/-1.40 to 1.58+/-0.61 mm Hg x cm(-1) . s after stenting (both P<0.001). The reduction in h-MR(v) accounted for 34% of the decrease in total coronary resistance achieved by PCI. h-MR(v) of the target vessel after PCI was lower than that of the corresponding reference vessel despite a higher h-P(d) in the reference vessel (P<0.01). Post-PCI baseline MR(v) was correlated with baseline P(d) before PCI (P<0.01)., Conclusions: PCI-induced restoration of P(d) resulted in a reduction of h-MR(v) in accordance with the pressure dependence of h-MR(v). The decrease in h-MR(v) to a level below that of the corresponding reference vessel in the immediate post-PCI period and a lowered baseline MR(v) suggest microvascular remodeling induced by long-term exposure to a low-pressure environment.