Complications after Transfemoral Transcatheter Aortic Valve Replacement with a Balloon-Expandable Prosthesis: The Importance of Preventative Measures and Contingency Planning.

Transcatheter aortic valve replacement (TAVR) with balloon-expandable Edwards-SAPIEN valve was superior to standard therapy in inoperable patients and noninferior to surgical aortic valve replacement in high surgical-risk, but operable patients, with severe symptomatic aortic stenosis in the randomized controlled PARTNER trial. Since the first case of TAVR with a balloon-expandable valve in 2002, several groups have reported their experience with balloon-expandable valves with high-procedural success. In the United States, the balloon-expandable Edwards-SAPIEN valve is the only transcatheter heart valve approved by the FDA for commercial use. Moreover, this is only in high-risk inoperable patients. Despite increasing experience with the TAVR procedure, it can be associated with complications, which can be technically challenging, even for an experienced operator. Complications associated with TAVR include vascular complications, valve malpositioning, regurgitation, embolization, coronary compromise, conduction abnormalities, stroke/transient ischemic attack, acute kidney injury, cardiac tamponade, and hemodynamic collapse. A thorough understanding of the procedure is essential for pre-emptive planning for procedural complications and early identification and management of complications are necessary for procedural success. We hereby review our experience of transfemoral TAVR with balloon-expandable valves, offer practical tips to maximize the likelihood of procedural success, describe pre-emptive strategies to prevent peri-procedural complications and bailout measures to manage them, should they occur. © 2018 Wiley Periodicals, Inc.

Intrinsic cardiac origin of human cardiosphere-derived cells.

AIMS: Cardiosphere-derived cells (CDCs) are in clinical development as a regenerative cell product which can be expanded ex vivo from patient cardiac biopsies. Cardiosphere-derived cells are clonogenic, exhibit multilineage differentiation, and exert functional benefits in preclinical models of heart failure. The origin of CDCs remains unclear: are these cells endogenous to the heart, or do they arise from cells that populate the heart via blood-borne seeding? METHODS AND RESULTS: Right ventricular endomyocardial biopsies were obtained from cardiac transplant recipients (n = 10, age 57 ± 15 years), and CDCs expanded from each biopsy. Donor-recipient mismatches were used to probe the origin of CDCs in three complementary ways. First, DNA analysis of short-tandem nucleotide repeats (STRs) was performed on genomic DNA from donor and recipient, then compared with the STR pattern of CDCs. Second, in two cases where the donor was male and the recipient female, CDCs were examined for the presence of X and Y chromosomes by fluorescence in situ hybridization. Finally, in two cases, quantitative PCR (qPCR) was performed for individual-specific polymorphisms of a major histocompatability locus to quantify the contribution of recipient cells to CDCs. In no case was recipient DNA detectable in the CDCs by STR analysis. In the two cases in which a female patient had received a male heart, all CDCs examined had an X and Y chromosome, similarly indicating exclusively donor origin. Likewise, qPCR on CDCs did not detect any recipient DNA. CONCLUSION: Cardiosphere-derived cells are of endogenous cardiac origin, with no detectable contribution from extra-cardiac seeding.

Comparison of long-term outcomes of drug-eluting stents and bare metal stents for saphenous vein graft stenosis.

OBJECTIVE: Our aim was to compare the long-term outcomes between drug-eluting stents and bare-metal stents for saphenous vein graft stenosis. BACKGROUND: The ideal type of stent to treat saphenous vein graft stenosis has not been clearly established. Short-term randomized controlled trial results comparing drug-eluting stents with bare-metal stents for saphenous vein graft stenosis are conflicting, intermediate-term retrospective studies and meta-analyses at two years suggest no difference in outcomes, and there are no long term follow-up studies. The need for long term follow-up data has become emerged with concern over late stent thrombosis. METHODS: 246 saphenous vein graft patients undergoing stenting from August 2002-December 2008 were studied. Overall survival and event-free survival were compared by Kaplan-Meier method. Hazard ratios (HR) were calculated by Cox-proportional hazards models. RESULTS: We treated 133 patients with DES (median follow-up four years) and 113 patients with BMS (median follow-up four years) for SVG stenosis. Overall survival (77.0% ± 3.9% vs. 70.6% ± 4.6%, log-rank P = 0.60) and MACE-free survival (57.5% ± 4.6% vs. 56.8% ± 4.9, log-rank P = 0.70) were not significantly different between the DES and BMS groups. Although BMS was associated with increased risk of target lesion revascularization (TLR) (freedom from TLR 85.2% ± 3.5% vs. 90.0% ± 3.0%, HR 2.07, 95% CI 0.97-4.42, log-rank P = 0.05), there was no significant difference in the freedom from myocardial infarction (86.7% ± 3.3% vs. 88.7% ± 3.2%, log-rank P = 0.39) or target vessel revascularization (77.1% ± 4.2% vs. 76.1% ± 4.2%, log-rank P = 0.33) between the two groups. CONCLUSIONS: Although mortality is not statistically different between DES and BMS for SVG stenosis, BMS is associated with increased risk of revascularization, thus suggesting the superiority of DES over BMS in the long term.

The inflammation hypothesis and its potential relevance to statin therapy.

Inflammatory cytokines have a central role in atherogenesis and plaque rupture. These mediators, including tumor necrosis factor, interleukins, and matrix metalloproteinases and transforming growth factor-beta are also prominent in other chronic progressive diseases characterized by cell apoptosis and tissue fibrosis. This review extends the inflammation hypothesis to critical analysis of studies to bearing on the role of inflammation in chronic conditions that commonly accompany coronary disease. Because statins inhibit the expression of inflammatory mediators, the review then analyzes the laboratory and clinical data that may justify trials of statins in nonatherosclerotic disease. In conclusion, despite far different clinical presentations, chronic progressive diseases characterized by apoptosis and fibrosis have persistence of inflammatory cytokines as a final common pathway, and thus may benefit from the pleiotropic effects of statin therapy.

Clinical Impact of Diabetes Mellitus on Outcomes After Transcatheter Aortic Valve Replacement: Insights From the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry.

BACKGROUND: Diabetes mellitus (DM) adversely affects morbidity and mortality for cardiovascular diseases and procedures. Data evaluating the outcomes of transcatheter aortic valve replacement (TAVR) in diabetic patients are limited by small sample size and contradictory results. We aimed to establish the magnitude of risk and the incremental influence of insulin dependency by examining short- and long-term adverse outcomes according to DM status and therapy in the world's largest TAVR registry. METHODS AND RESULTS: We analyzed data from the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry. In-hospital mortality, 30-day mortality, and 1-year mortality after TAVR in patients with and without DM were evaluated using multivariate modeling. Among 47 643 patients treated with TAVR from November 2011 through September 2015 at 394 US hospitals, there were 17 849 (37.5%) patients with DM. Overall, 6600 of the diabetic patients were insulin treated (IT). Thirty-day mortality was 5.0% in patients with DM (6.1% in IT DM and 4.4% in non-IT DM; P<0.001) versus 5.9% in patients without DM (P<0.001). Overall, 1-year mortality was 21.8% in patients with DM (24.8% in IT DM and 20.1% in non-IT DM; P<0.001) versus 21.2% in patients without DM (P=0.274). In a multivariable model, DM was associated with increased 1-year mortality (hazard ratio, 1.30; 95% confidence interval, 1.13-1.49; P<0.001). Subgroup multivariable analysis showed stronger mortality association in IT diabetics (hazard ratio, 1.57; 95% confidence interval, 1.28-1.91; P<0.001) than in non-IT diabetics (hazard ratio, 1.17; 95% confidence interval, 1.00-1.38; P=0.052). CONCLUSIONS: Our data establish the magnitude of short- and long-term risk conferred by DM and the incremental risk conferred by insulin dependency in the performance of TAVR. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01737528.

Increasing high-density lipoprotein cholesterol in dyslipidemia by cholesteryl ester transfer protein inhibition: an update for clinicians.

Reduced HDL cholesterol may be a risk factor comparable in importance to increased LDL cholesterol. Interventions that raise HDL are antiatherosclerotic, presumably through acceleration of reverse cholesterol transport and by antioxidant and antiinflammatory effects. In the hypercholesterolemic rabbit, HDL levels can be increased by >50% by inhibition of cholesteryl ester transfer protein (CETP), a molecule that plays a central role in HDL metabolism. This HDL-raising effect is antiatherosclerotic in moderately severe hyperlipidemia but appears to be ineffective in the presence of severe hypertriglyceridemia. In humans, mutations resulting in CETP inhibition have been associated with both reduced and increased risk of atherosclerosis. Proposed explanations for these apparently disparate observations are that the antiatherosclerotic effect of CETP inhibition varies with either the metabolic milieu or the degree of CETP inhibition. We now have pharmacological inhibitors of CETP that are capable of increasing HDL by as much as 50% to 100% in humans. The importance of this development is that reduced HDL is a risk factor independent of LDL and that these new agents alter HDL by a magnitude comparable to that of statins on LDL. Clinical trials, now beginning, will need to identify the patient subsets in which CETP inhibition may be more or less effective.

Emerging strategies for increasing high-density lipoprotein.

High-density lipoprotein cholesterol is a potent and independent epidemiologic risk factor and is a proved antiatherosclerotic agent in animal models of atherosclerosis, acting through the principal mechanisms of accelerating cholesterol efflux and inhibiting oxidation and inflammation. Lifestyle modification increases serum levels by 5% to 15%, whereas niacin, the drug most widely used to increase high-density lipoprotein cholesterol, increases it by 25% to 35% at the highest doses. This review examines the potent methods of increasing high-density lipoprotein and/or enhancing reverse cholesterol transport, including cholesterol ester transfer protein inhibitors, apolipoprotein A-I Milano, D4F, the dual peroxisome proliferator-activated receptor agonists, and rimonabant, that are now in clinical trials. In conclusion, these new agents, used alone or in combination with existing therapies, carry the potential to markedly reduce the incidence of new coronary disease and cardiac events in this decade.

Intravenous mesenchymal stem cell therapy early after reperfused acute myocardial infarction improves left ventricular function and alters electrophysiologic properties.

UNLABELLED: Direct intramyocardial injection of mesenchymal stem cells (MSCs) improves left ventricular ejection fraction (LVEF) and may increase ventricular arrhythmia in hearts with myocardial infarction (MI). We hypothesized that intravenous MSCs given early after acute MI would engraft in injured myocardium, improve LV function, and result in pro-arrhythmic electrical remodeling. We created an apical infarction in swine by balloon occlusion/reperfusion, administered diI-labeled allogeneic bone marrow derived MSCs intravenously 30 min post-reperfusion and measured LVEF and wall thickness at baseline, 1 month, and 3 months. Epicardial effective refractory periods (ERPs) were determined before sacrifice. At 3 months, treated pigs [n=7] had significantly higher LVEF than controls [n=8] (49+/-2% vs. 44+/-3%, P=0.015) and significantly less wall thickening of non-infarcted myocardium. ERPs were significantly shorter than controls at all pacing cycle lengths (P

Administration of cells with thermosensitive hydrogel enhances the functional recovery in ischemic rat heart.

The lack of cell retention clearly represents a potentially serious limitation for therapeutic efficacy of stem cells. To enhance the efficacy, we developed a novel hydrogel that is thermosensitive and biodegradable and possesses desirable stiffness in a solid form. Immediately after induction of myocardial infarction of male rat, cardiac outgrowth cells embedded in hydrogel (HG) or saline (CO) were injected directly into the peri-infarct area. Left ventricular ejection fraction, cell retention rate, and a spectrum of biochemical markers were measured to evaluate the effect of the treatment. Left ventricular ejection fraction was significantly higher in the cell-injected groups (HG and CO) than in the control group at 1 week after treatment. This functional benefit was continued only in the HG group, accompanied with more retained cells. Furthermore, the expression of insulin-like growth factor-1 was significantly higher in the HG group with less progression of cell apoptosis.

Comparison of effectiveness of hand-carried ultrasound to bedside cardiovascular physical examination.

This study compared the accuracy of cardiovascular diagnoses by medical students operating a small hand-carried ultrasound (HCU) device with that of board-certified cardiologists using standard physical examinations. Sixty-one patients (38% women; mean age 70 +/- 19 years) with clinically significant cardiac disease had HCU studies performed by 1 of 2 medical students with 18 hours of training in cardiac ultrasound and physical examinations by 1 of 5 cardiologists. Diagnostic accuracy was determined by standard echocardiography. Two-hundred thirty-nine abnormal findings were detected by standard echocardiography. The students correctly identified 75% (180 of 239) of the pathologies, whereas cardiologists found 49% (116 of 239) (p <0.001). The students' diagnostic specificity of 87% was also greater than cardiologists' specificity of 76% (p <0.001). For nonvalvular pathologies (115 findings), students' sensitivity was 61%, compared with 47% for cardiologists (p = 0.040). There were 124 clinically significant valvular lesions (111 regurgitations, 13 stenoses). Students' and cardiologists' sensitivities for recognizing lesions that cause a systolic murmur were 93% and 62% (p <0.001), respectively. Students' sensitivity for diagnosing lesions that produce a diastolic murmur was 75%; cardiologists recognized 16% of these lesions (p <0.001). The diagnostic accuracy of medical students using an HCU device after brief echocardiographic training to detect valvular disease, left ventricular dysfunction, enlargement, and hypertrophy was superior to that of experienced cardiologists performing cardiac physical examinations.

Intramyocardial injection of allogenic bone marrow-derived mesenchymal stem cells without immunosuppression preserves cardiac function in a porcine model of myocardial infarction.

BACKGROUND: We investigated the efficacy of directly injected allogenic bone marrow-derived mesenchymal stem cells in improving left ventricular function in a porcine model of myocardial infarction. METHODS: Left ventricular infarction was created in 16 adult Yorkshire pigs by coil embolization and thrombotic occlusion distal to the second diagonal artery. One month after myocardial infarction was induced, the animals were randomized to either direct injection of allogenic mesenchymal stem cells or sham treatment (culture medium). Allogenic bromodeoxyuridine-labeled mesenchymal stem cells (2 +/- 0.1 x 10(8)) were directly injected into the infarct and peri-infarct areas during an open chest procedure. No immunosuppressive therapy was used. The left ventricular function was measured using serial biplane left ventricular angiography at baseline, 30, 60, and 90 days before sacrifice. Mesenchymal stem cells were localized using bromodeoxyuridine, and differentiation of mesenchymal stem cells was assessed by confocal microscopic colocalization of bromodeoxyuridine with immunofluorescent antibodies specific for cardiomyocytes (troponin I and MF-20) and endothelial cells (von Willebrand factor). RESULTS: Mesenchymal stem cells labeled with bromodeoxyuridine engrafted the peri-infarct zone and colocalized with both cardiomyocyte-specific and endothelial cell-specific immunofluorescence. No intramyocardial bromodeoxyuridine was observed in sham-treated animals. At the time of the mesenchymal stem cell injection 30 days after myocardial infarction, the left ventricular ejection fraction (LVEF) was 58% +/- 3% in mesenchymal stem cell-treated pigs and 56% +/- 2% in sham-treated pigs (P = NS). LVEF deteriorated progressively thereafter in untreated pigs (8.5% and 10.5% decline at 60 days and 90 days after myocardial infarction, respectively), but was preserved in mesenchymal stem cell-treated pigs (2.1% increase and -2.0% decline at 60 and 90 days post-MI respectively) (P < .05). CONCLUSIONS: Direct intramyocardial injection of mesenchymal stem cells results in successful intramyocardial engraftment and differentiation into cardiomyocytes and endothelial cells and preserves left ventricular function after myocardial infarction in pigs.

Persistence of inflammatory cytokines cause a spectrum of chronic progressive diseases: implications for therapy.

Chronic progressive disease (CPD) are the Western world's major cause of mortality (National Center for Health Statistics. Vol. 52. National vital 176 statistics reports. Deaths: final data for 2001; 2003, p. 3). Most chronic diseases present with symptoms and signs specific for the dysfunctional organ. Nonetheless, substantial commonalities are identifiable at the tissue and cellular level. These include a striking increase in inflammatory cytokines in both the tissue and the serum, accompanied by tissue destruction, apoptosis and tissue fibrosis. Individual inflammatory cytokines possess the capacity to induce these tissue effects in vitro and in vivo. Further, an elevation in systemic levels of cytokines and CRP predict an increase risk at all stages of these diseases. Therapies that inhibit the stimuli, the mediators or the responses to persistent inflammation appear to have an inhibitory effect on progression of specific diseases. We hypothesize that a unifying paradigm for CPD can be constructed based on these observations. Destabilizing stimuli activate the normal protective homeostatic inflammatory response in tissue. As the stimulus is eliminated and tissue heals, the inflammatory response recedes, re-establishing homeostasis. If inflammatory cytokines persist, however, both cell apoptosis and tissue fibrosis can be induced. Two aspects of evolution provide a potential mechanistic basis for this hypothesis. We may speculate that Darwinian selection favored early development of a system that channeled a broad spectrum of external and internal challenges through a generic response system. Thus, the mediators that respond to noxious stimuli became universal throughout organisms and species. Because these genetic responses were part of the DNA programming of all cells prior to differentiation, the tissue response to inflammation is also both uniform in nature, and narrow in scope. Subsequent cell differentiation resulted in vast differences in tissue function, so that organ dysfunction appears with the myriad symptoms and signs we recognize as individual diseases. Interference with inflammatory cytokines, e.g., with HMG Coa reductase inhibitors, inhibits a spectrum of chronic progressive diseases, independent of any LDL lowering effect.

Prevention of plaque rupture: a new paradigm of therapy.

Acute coronary syndromes--unstable angina, myocardial infarction, and sudden cardiac death--are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstable plaque is not necessarily obstructive, it may cause no symptoms before rupture. The cellular processes that lead to the characteristic histologic features of unstable plaque have recently been identified. This new understanding of the cell biology of plaque instability suggests new therapeutic strategies: passivation of the endothelium, reduction of low-density lipoprotein (LDL) in the vessel wall by decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidation, inhibition of inflammatory cytokine expression, and inhibition of thrombus formation. Although the morbidity and mortality resulting from acute coronary disease have been reduced by more than 50% over the past 30 years, it is reasonable to anticipate further reductions of similar magnitude in the decade ahead.

Transfemoral access assessment for transcatheter aortic valve replacement: evidence-based application of computed tomography over invasive angiography.

BACKGROUND: Although computed tomography (CT) is commonly used for iliofemoral evaluation for transfemoral transcatheter aortic valve replacement, many centers worldwide use invasive angiography alone for this purpose. No study to date has evaluated the value of CT over angiography for the prediction of vascular complications. In addition, no data exist for the value of noncontrast CT. METHODS AND RESULTS: Of the 588 transcatheter aortic valve replacement patients, we reviewed 496 consecutive transfemoral cases. Vessel diameters were measured by CT or angiography. Sheath-related complication (SRC) was defined as an iliofemoral arterial injury not including a cannulation site. Receiver operating characteristic models were generated using sheath-to-iliofemoral artery ratios as a variable and SRC as an end point. In patients undergoing both contrast CT and angiography (n=283; 35 SRCs), contrast CT showed a greater predictive value than angiography by area under the curve P<0.001): 0.87 (95% confidence interval: 0.82-0.91) versus 0.72 (95% confidence interval: 0.66-0.77). In patients undergoing both noncontrast CT and angiography (n=103; 17 SRCs), there was no difference between noncontrast CT and angiography: 0.79 (95% confidence interval: 0.70-0.86) versus 0.73 (95% confidence interval: 0.63-0.81). Three-dimensional assessments of calcification and tortuosity provided limited additional value for SRC prediction. CONCLUSIONS: Contrast CT has a greater predictive value for post-transcatheter aortic valve replacement vascular complications than angiography. Because these complications increase mortality, an accurate assessment of the vasculature is a critical component of proper access selection.

Angiographic changes in saphenous vein grafts are predictors of clinical outcomes.

BACKGROUND: Previous studies have suggested that angiographic evidence of disease progression in coronary arteries increases the risk of subsequent coronary clinical events. This study ascertained whether patients enrolled in the Post Coronary Artery Bypass Graft Clinical Trial (POST CABG) who had substantial progression of atherosclerosis in >or=1 saphenous vein grafts (on the basis of assessment of baseline and follow-up angiograms obtained 4-5 years after study entry), but who had not reported clinical symptoms before follow-up angiography, were at a higher risk of subsequent events than patients who did not have substantial progression of atherosclerosis (decrease >or=0.6 mm in lumen diameter at site of greatest change from baseline). METHODS: All 1351 patients enrolled in the trial underwent baseline angiography; only the 961 patients who had follow-up angiography and no coronary events before the follow-up study were included in this analysis. The clinical center staff contacted patients to ascertain the events that had occurred after follow-up angiography (approximately 3.4 years later). RESULTS: Sixty-nine patients had died; 870 patients or relatives were interviewed, and 22 patients could not be contacted. Univariable estimates of relative risk associated with substantial progression ranged from 2.2 (P <.001) for cardiovascular death or nonfatal myocardial infarction to 3.3 (P <.001) for revascularization. Multivariable and univariable estimates of risk were similar. CONCLUSIONS: The findings provide evidence that patients who had substantial progression of atherosclerosis in vein grafts are at an increased risk for subsequent coronary events and suggest that angiographic changes in vein grafts are appropriate surrogate measures for clinical outcomes.

Common ancestors: chronic progressive diseases have the same pathogenesis.

In multiple organ systems, chronic progressive disease is characterized at the tissue level by increase in inflammatory cytokines, cell apoptosis and progressive fibrosis, suggesting a possible commonality of pathogenesis. This speculation is supported by the observation that elevated systemic levels of cytokines and/or CRP predict the appearance of disease, progression of disease, and disease complications. Some therapeutic interventions that reduce the expression of inflammatory cytokines, such as HMG Co-A reductase inhibitors, slow the progression of a number of chronic diseases, independent of their effect on cholesterol level. Taken together, these data suggest a unifying hypothesis for many chronic progressive diseases. Diverse noxious stimuli activate a normal protective inflammatory response. This response typically defervesces with elimination of the stimulus, reestablishing homeostasis. When homeostasis is not restored, that is, the inflammatory response persists, cell apoptosis and tissue fibrosis can result. The universality of this tissue response derives from the fact that all cells derive from the same blastocyst. Since cell differentiation results in different tissue functions, however, the clinical manifestations of disease are also vastly different, obscuring the underlying disease process. The relevance of this insight is that it provides a potential framework for testing old and new therapies which might inhibit a diverse set of clinical conditions at several levels of the disease process.

A novel regimen of alternate day clopidogrel would provide a cost-effective strategy to prevent very late stent thrombosis.

BACKGROUND/OBJECTIVES: ACC/AHA/SCAI recommendations include dual anti-platelet therapy (aspirin and clopidogrel) for 12 months after drug-eluting stent percutaneous coronary intervention (DES PCI). Numerous case reports have emerged of "very late stent thrombosis" (VLST) (>1 year post-DES-PCI) even 1-5 years after DES-PCI manifesting with myocardial infarction and death when clopidogrel therapy was interrupted or stopped. HYPOTHESIS: We hypothesize that a novel regimen of alternate day clopidogrel would provide a cost-effective strategy to prevent VLST taking into account the known facts about clopidogrel pharmacodynamics, stent endothelialization and stent thrombosis. We hypothesized that the degree of anti-platelet effect required to prevent VLST decreases with time as the stent endothelializes-that is the "therapeutic threshold" required to prevent VLST decreases with time. The anti-platelet effect of clopidogrel lasts for 5-7 days. Typically, stent thrombosis on interruption of clopidogrel (with bare metal stents within first 30 days) occurs after 3-4 days signifying recovery of enough platelet function to produce stent thrombosis--recovery of platelet inhibition beyond the therapeutic threshold. Since the therapeutic threshold required to prevent VLST in DES after 1 year is much lower, this degree of platelet inhibition can be conceivably achieved with just administering clopidogrel on alternate days. EMPIRICAL DATA: We studied efficacy and safety of regimen of daily aspirin 81 mg and alternate-day clopidogrel 75 mg beyond 12 months after PCI with DES for prevention of VLST by following 347 patients for occurrence of death, myocardial infarction (MI), VLST, target vessel revascularization (TVR) and bleeding. There were no occurrence of major bleeding, VLST events or death. CONCLUSIONS: Long term dual anti-platelet therapy with aspirin 81 mg daily and clopidogrel 75 mg every other day beyond 12 months after PCI with DES may be a safe and efficacious cost-saving strategy to prevent VLST.

Predictive accuracy of SYNTAX score for predicting long-term outcomes of unprotected left main coronary artery revascularization.

The American College of Cardiology/American Heart Association recently updated recommendations for percutaneous coronary intervention (PCI) of unprotected left main coronary artery (ULMCA) disease from class III to II(b) according to the results of the SYNergy between percutaneous coronary intervention with TAXus and cardiac surgery (SYNTAX) trial. The SYNTAX score is an angiographic tool using solely the coronary anatomy. We studied the effect of co-morbidities (Parsonnet's score) on the ability of the SYNTAX score to predict long-term outcomes in patients with ULMCA disease treated by revascularization. A total of 328 patients underwent revascularization of ULMCA from April 2003 to February 2007. Of the 328 patients, 120 underwent PCI (median follow-up 973 days) and 208 underwent coronary artery bypass grafting (CABG) (median follow-up 1,298 days). The ability of the SYNTAX score to predict outcomes was assessed using the Cox proportional hazards model. The outcomes between the PCI and CABG groups were compared by propensity analysis. The median SYNTAX score was 26 in the PCI and 28 in the CABG group (p = 0.5). In the PCI group, greater quartiles were associated with worse survival (62.1% at SYNTAX score of ≥36 vs 82.4% at SYNTAX score of <36, p = 0.03) and all-cause mortality, myocardial infarction, cerebrovascular events, and target vessel revascularization-free (MACCE) survival (47.7%, SYNTAX score ≥20 vs 76.6%, SYNTAX score <20, p = 0.02). Using the Parsonnet score as a covariate, the SYNTAX score continued to be an independent predictor of MACCE and demonstrated a trend toward predicting mortality in the PCI group. In contrast, the SYNTAX score did not predict the outcomes for the CABG group. No difference was found in mortality between the PCI and CABG groups for ULMCA disease, regardless of coronary complexity; although greater SYNTAX scores were associated with increased MACCE rates with PCI compared to CABG. Both the coronary anatomy (SYNTAX score) and co-morbidities (Parsonnet's score) predicted long-term outcomes for PCI of ULMCA disease. In contrast, the SYNTAX score did not predict the outcomes after CABG. In conclusion, the ideal scoring system to guide an appropriate revascularization decision for ULMCA disease should take into account both the coronary anatomy and the co-morbidities.