Intracoronary optical coherence tomography: Clinical and research applications and intravascular imaging software overview.

By providing valuable information about the coronary artery wall and lumen, intravascular imaging may aid in optimizing interventional procedure results and thereby could improve clinical outcomes following percutaneous coronary intervention (PCI). Intravascular optical coherence tomography (OCT) is a light-based technology with a tissue penetration of approximately 1 to 3 mm and provides near histological resolution. It has emerged as a technological breakthrough in intravascular imaging with multiple clinical and research applications. OCT provides detailed visualization of the vessel following PCI and provides accurate assessment of post-procedural stent performance including detection of edge dissection, stent struts apposition, tissue prolapse, and healing parameters. Additionally, it can provide accurate characterization of plaque morphology and provides key information to optimize post-procedural outcomes. This manuscript aims to review the current clinical and research applications of intracoronary OCT and summarize the analytic OCT imaging software packages currently available. © 2017 Wiley Periodicals, Inc.

Early Experience with the HeartMate Percutaneous Heart Pump from the SHIELD II Trial.

The HeartMate Percutaneous Heart Pump (PHP) is a novel circulatory support catheter delivering a self-expanding 24 French impeller across the aortic valve. The SHIELD II trial compares outcomes among heart failure patients undergoing high-risk percutaneous coronary intervention (HR-PCI) with the PHP versus Impella systems. The trial was halted in 2017 due to device malfunctions. We aimed to describe procedural, hemodynamic, and clinical outcomes among HR-PCI patients treated with PHP as part of the SHIELD II trial roll-in phase. Procedural, hemodynamic, and 90 day outcomes were assessed among patients undergoing HR-PCI with a left ventricular ejection fraction ≤35% and last patent coronary conduit, unprotected left main disease, or significant three vessel disease. The primary endpoint was the 90 day composite of cardiovascular death, myocardial infarction, stroke, repeat revascularization, major bleeding, new/worsening aortic regurgitation, and severe hypotension. Among 75 roll-in phase patients, PHP support duration was 101 ± 53 minutes with 2.5 ± 1.4 coronary lesions treated per patient. Compared with predevice values, the PHP system increased cardiac power and mean arterial pressure. Maximum recorded device flows were 0.4-6.2 L/minute with 26% (n = 19/73) and 9.6% (n = 7/73) of patients achieving peak flows above 3.5 or 5.0 L/minute, respectively. Five PHP device malfunction events (6.7%) were observed. At 90 days, the composite endpoint occurred in 24.3% (18/74) of patients. Early PHP experience demonstrated successful device performance in the majority of enrolled patients; however, unexpected malfunctions led to device revision. Completion of the SHIELD II trial will be required to confirm the safety and efficacy of this iteration of the PHP system in HR-PCI.

Inhibition of MCP-1/CCR2 signaling does not inhibit intimal proliferation in a mouse aortic transplant model.

BACKGROUND: Transplant arteriopathy is the leading cause of long term morbidity and mortality following heart transplantation. Animal models have demonstrated that monocyte chemoattractant protein (MCP)-1 is induced early after transplant in cardiac and aortic allografts. We have previously reported that deficiency of MCP-1 or its receptor, CC chemokine receptor 2 (CCR2), is associated with a reduction in intimal proliferation in a mouse femoral artery injury model. Using knockout mice, we have now examined the role of MCP-1 and CCR2 in the development of the intimal proliferation of transplant arteriopathy. METHODS: C57Bl/6 CCR2 and MCP-1 wild-type and knockout mice were used in the studies and aortic transplants were performed between Balb/c mice and C57Bl/6 mice. Aortas from recipient animals were harvested 8 weeks after transplant. RESULTS: Unlike arterial injury, in an aortic transplant model inhibition of MCP-1/CCR2 signaling did not result in reduced intimal proliferation. CONCLUSIONS: Despite a pathology that appears similar, the inflammatory mediators that regulate transplant arteriopathy differ from those regulating intimal proliferation secondary to wire injury. Our results suggest that targeting MCP-1/CCR2 signaling is not sufficient to block transplant arteriopathy across a complete MHC-mismatch barrier.

Contemporary Sex-Based Differences by Age in Presenting Characteristics, Use of an Early Invasive Strategy, and Inhospital Mortality in Patients With Non-ST-Segment-Elevation Myocardial Infarction in the United States.

BACKGROUND: Prior studies have reported higher inhospital mortality in women versus men with non-ST-segment-elevation myocardial infarction. Whether this is because of worse baseline risk profile compared with men or sex-based disparities in treatment is not completely understood. METHODS AND RESULTS: We queried the 2003 to 2014 National Inpatient Sample databases to identify all hospitalizations in patients aged ≥18 years with the principal diagnosis of non-ST-segment-elevation myocardial infarction. Complex samples multivariable logistic regression models were used to examine sex differences in use of an early invasive strategy and inhospital mortality. Of 4 765 739 patients with non-ST-segment-elevation myocardial infarction, 2 026 285 (42.5%) were women. Women were on average 6 years older than men and had a higher comorbidity burden. Women were less likely to be treated with an early invasive strategy (29.4% versus 39.2%; adjusted odds ratio, 0.92; 95% confidence interval, 0.91-0.94). Women had higher crude inhospital mortality than men (4.7% versus 3.9%; unadjusted odds ratio, 1.22; 95% confidence interval, 1.20-1.25). After adjustment for age (adjusted odds ratio, 0.96; 95% confidence interval, 0.94-0.98) and additionally for comorbidities, other demographics, and hospital characteristics, women had 10% lower odds of inhospital mortality (adjusted odds ratio, 0.90; 95% confidence interval, 0.89-0.92). Further adjustment for differences in the use of an early invasive strategy did not change the association between female sex and lower risk-adjusted inhospital mortality. CONCLUSIONS: Although women were less likely to be treated with an early invasive strategy compared with men, the lower use of an early invasive strategy was not responsible for the higher crude inhospital mortality in women, which could be entirely explained by older age and higher comorbidity burden.

Hybrid Coronary Revascularization has Improved Short-term Outcomes but Worse Mid-term Reintervention Rates Compared to CABG: A Propensity Matched Analysis.

OBJECTIVE: We evaluated short-term outcomes and mid-term survival and reintervention of hybrid coronary revascularization versus conventional coronary artery bypass grafting using a propensity score matched cohort. METHODS: We conducted a retrospective review of patients undergoing surgery for multivessel coronary artery disease from 2007 to 2015 at a single institution. Patients were propensity matched 1:1 to receiving hybrid coronary revascularization or conventional bypass grafting by multivariate logistic regression on preoperative characteristics. Short-term outcomes were compared. Freedom from reintervention and death were assessed by Kaplan-Meier analysis, log-rank test, and Cox proportional hazards regression. RESULTS: Propensity score matching selected 91 patients per group from 91 hybrid and 2601 conventionally revascularized patients. Hybrid revascularization occurred with surgery first in 56 (62%), percutaneous intervention first in 32 (35%), and simultaneously in 3 (3%) patients. Median intervals between interventions were 3 and 36 days for surgery first and percutaneous intervention first, respectively. Preoperative characteristics were similar. Patients undergoing hybrid revascularization had shorter postoperative length of stay (median = 4 vs 5 days, P < 0.001), less postoperative transfusion (13.2% vs 34.1%, P = 0.001), and respiratory failure (0% vs 6.6%, P = 0.03). They were more likely to be discharged home (93.4% vs 71.4%, P < 0.001), with no difference in 30-day mortality (P = 0.99), readmission (P = 0.23), or mid-term survival (P = 0.79). Hybrid revascularization was associated with earlier reintervention (P = 0.02). Hazard ratios for reintervention and patient mortality of hybrid coronary revascularization versus conventional revascularization were 3.60 (95% confidence interval = 1.16-11.20) and 1.17 (95% confidence interval = 0.37-3.72), respectively. CONCLUSIONS: Despite having favorable short-term outcomes and similar survival, hybrid coronary revascularization may be associated with earlier reintervention compared with conventional techniques.

Association of Chronic Kidney Disease With In-Hospital Outcomes of Transcatheter Aortic Valve Replacement.

OBJECTIVES: This study sought to determine the association of chronic kidney disease (CKD) with in-hospital outcomes of transcatheter aortic valve replacement (TAVR). BACKGROUND: CKD is a known independent risk factor for worse outcomes after surgical aortic valve replacement (SAVR). However, data on outcomes of patients with CKD undergoing TAVR are limited, especially in those on chronic dialysis. METHODS: The authors used data from the 2012 to 2014 National Inpatient Sample database to identify all patients ≥18 years of age who underwent TAVR. International Classification of Diseases-Ninth Revision-Clinical Modification codes were used to identify patients with no CKD, CKD (without chronic dialysis), or end-stage renal disease (ESRD) on long-term dialysis. Multivariable logistic regression models were constructed using generalized estimating equations to examine in-hospital outcomes. RESULTS: Of 41,025 patients undergoing TAVR from 2012 to 2014, 25,585 (62.4%) had no CKD, 13,750 (33.5%) had CKD, and 1,690 (4.1%) had ESRD. Compared with patients with no CKD, in-hospital mortality was significantly higher in patients with CKD or ESRD (3.8% vs. 4.5% vs. 8.3%; adjusted odds ratio [no CKD as reference]: 1.39 [95% confidence interval: 1.24 to 1.55] for CKD and 2.58 [95% confidence interval: 2.09 to 3.13] for ESRD). Patients with CKD or ESRD had a higher incidence of major adverse cardiovascular events (composite of death, myocardial infarction, or stroke), net adverse cardiovascular events (composite of major adverse cardiovascular events, major bleeding, or vascular complications), and pacemaker implantation compared with patients without CKD. Acute kidney injury (AKI) and AKI requiring dialysis were associated with several-fold higher risk-adjusted in-hospital mortality in patients in the no CKD and CKD groups. Moreover, the incidence of AKI and AKI requiring dialysis did not decline during the study period. CONCLUSIONS: Patients with CKD or ESRD have worse in-hospital outcomes after TAVR. AKI is associated with higher in-hospital mortality in patients undergoing TAVR and the incidence of AKI has not declined over the years.

Culprit-lesion only versus complete multivessel percutaneous intervention in ST-elevation myocardial infarction: A systematic review and meta-analysis of randomized trials.

BACKGROUND: ST-segment elevation myocardial infarction (STEMI) in patients with concomitant multivessel (MV) coronary artery disease (CAD) is associated with poor outcomes. Percutaneous coronary intervention (PCI) of the culprit-lesion only (CLO) as compared with a MV PCI approach to revascularization remains uncertain. Our objective is to gain a better understanding of the efficacy and safety of CLO as compared with MV PCI in patients with STEMI by conducting an updated meta-analysis. METHODS: A comprehensive search of PubMed, CENTRAL, EMBASE, The Cochrane Central Register, the ClinicalTrials.gov Website, and Google Scholar databases of randomized controlled trials (RCTs) was performed. RESULTS: Seven RCTs were included, enrolling a total of 2006 patients. We found that there was a significant reduction in major adverse cardiovascular events (MACE) (OR, 0.62; 95% CI, 0.43-0.90), cardiovascular mortality (OR, 0.46; 95% CI, 0.27-0.80), and repeat revascularization (RRV) (OR, 0.39; 95% CI, 0.30-0.51) favoring MV over the CLO approach for patients undergoing primary PCI. The number needed to treat in order to prevent one CV mortality, RRV, or MACE event is 47, 11, and 16 patients, respectively. No differences were observed between MV vs. CLO PCI for subsequent myocardial infarction (OR, 0.74; 95% CI, 0.40-1.39), all-cause mortality (OR, 0.78; 95% CI, 0.53-1.15), non-cardiovascular mortality (OR, 1.35; 95% CI, 0.74-2.48), all-bleeding events (OR, 0.82; 95% CI, 0.40-1.65), contrast-induced nephropathy (OR, 0.72; 95% CI, 0.33-1.54), and stroke (OR, 1.28; 95% CI, 0.47-3.46). CONCLUSIONS: MV PCI significantly reduces the rate of MACE, CV mortality, and RRV without significant harm as compared to CLO PCI.

Mice deficient in tissue factor demonstrate attenuated intimal hyperplasia in response to vascular injury and decreased smooth muscle cell migration.

Tissue factor (TF) is the primary initiator of the coagulation cascade and is thought to play a key role in the generation of arterial thrombosis. Recent studies have suggested that TF mediates inflammatory processes in the arterial wall and may be an important regulator of intimal hyperplasia. We have employed genetically engineered mice (mTF(-/-) /hTF(+)) with markedly diminished TF activity ( approximately 1% normal levels) o examine the role of TF in mediating the response to arterial injury. mTF(-/-)/hTF(+) displayed a marked reduction in intimal hyperplasia (46% decrease in intimal area, 60% decrease in intimal/medial ratio) in response to femoral artery injury when compared to wild type controls. The decreased intimal hyperplasia seen in low TF mice was noted in a model of vascular injury not associated with significant thrombosis, suggesting that it may be mediated by non-procoagulant properties of TF. Smooth muscle cells from mTF(-/-)/hTF(+) mice grew normally in response to serum, but exhibited a marked defect in cell migration in a modified Boyden chamber assay. In contrast, there was no difference in platelet derived growth factor- induced migration, suggesting that the effect of TF on smooth muscle cell migration is agonist dependent. These data suggest that TF may mediate intimal hyperplasia by regulating smooth muscle cell migration.

Immunologic factors in transplant arteriopathy: insight from animal models.

Transplant arteriopathy is the leading cause of long-term morbidity and mortality following heart transplantation. The pathologic hallmark of this disease is intimal proliferation. Animal models have demonstrated that immunologic factors, including cytokines, cellular adhesion molecules and inflammatory cells, play a significant role in the development of this arteriopathy. One goal of future studies will be to translate findings in animal models into effective treatments in humans.

Comparison of provisional 1-stent and 2-stent strategies in diabetic patients with true bifurcation lesions: the EES bifurcation study.

BACKGROUND: Percutaneous coronary intervention (PCI) of true bifurcation lesions (Medina classification 1, 1, 1; 1, 0, 1; or 0, 1, 1) is challenging and may involve either a 1-stent strategy with provisional side branch stenting, or a 2-stent strategy. Diabetes mellitus is associated with greater atherosclerotic burden and higher incidence of bifurcation lesions, and unfavorable outcomes after PCI. It is unknown whether use of newer everolimus-eluting stent (EES) implantation impacts relative outcomes of 1-stent and 2-stent strategies in patients with diabetes. METHODS: We performed a retrospective analysis of consecutive patients with diabetes mellitus and complex true bifurcation lesions (side branch diameter >2.0 mm) who underwent PCI with EES between February 2010 and December 2011. We grouped subjects based on initial treatment to a 1-stent (n = 81) or 2-stent (n = 54) strategy, and compared baseline characteristics, quantitative coronary angiography, and 1-year major adverse cardiovascular event (MACE) rates, defined as death, myocardial infarction, target lesion revascularization (TLR), or target vessel revascularization (TVR). RESULTS: Baseline characteristics were well matched. A 2-stent strategy was associated with larger side-branch reference vessel diameter at baseline and post PCI. In-hospital events included 1 periprocedural myocardial infarction in each group and no deaths. At 1 year, there was no significant difference between 1-stent and 2-stent strategies in TVR rates (6.2% vs 3.7%; P=.53), TLR (both 3.7%; P>.99), or MACE (7.4% vs 3.7%; P=.37). CONCLUSION: In this series of diabetic patients undergoing complex bifurcation PCI using EES implantation, there was no difference between 1-stent and 2-stent strategies with respect to ischemic events at 1 year.

CXCR4 modulates contractility in adult cardiac myocytes.

The inflammatory response is critical to the development and progression of heart failure. Chemokines and their receptors are a distinct class of inflammatory modulators that may play a role in mediating myocardial dysfunction in heart failure. Levels of the chemokine CXCL12, also known as stromal cell-derived factor (SDF), and its receptor, CXCR4, are elevated in patients with heart failure, and we undertook this study to determine whether this chemokine system can directly affect cardiac function in the absence of leukocytes. Murine papillary muscles and adult rat cardiac myocytes treated with CXCL12, the only identified ligand of CXCR4, demonstrate blunted inotropic responses to physiologic concentrations of calcium. The negative inotropic effects on cardiac myocytes are accompanied by a proportional diminution of calcium transients. The effects are abrogated by AMD3100, a specific CXCR4 inhibitor. Overexpression of the receptor through adenoviral infection with a CXCR4 construct accentuates the negative inotropic effects of CXCL12 on cardiac myocytes during calcium stimulation. CXCR4 activation also attenuates beta-adrenergic-mediated increases in calcium mobilization and fractional shortening in cardiac myocytes. In electrophysiologic studies, CXCL12 decreases forskolin- and isoproterenol-induced voltage-gated L-type calcium channel activation. These studies demonstrate that activation of CXCR4 results in a direct negative inotropic modulation of cardiac myocyte function. The specific mechanism of action involves alterations of calcium channel activity on the membrane. The presence of functional CXCR4 on cardiac myocytes introduces a new target for treating cardiac dysfunction.