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Introduction: We aimed to assess the impact of left atrial appendage closure (LAAC) on the incidence of cardiac mortality, stroke, bleeding and quality of life (QOL) in a standardized single center registry. Methods: At our institution LAAC using the Watchman device has been recommended since 2010 in all patients (pt) with atrial fibrillation (AF) and bleeding events under oral anticoagulation therapy (OAC). Postprocedural antithrombotic therapy included aspirin for life, OAC or low molecular weight heparins (LMWH) for 45 days, followed by clopidogrel up to 6 months after LAAC. In pt with absolute contraindications against OAC, clopidogrel was started after LAAC and given for 6 months without OAC/LMWH. An ambulatory examination with transesophageal echo at 45 days and a standardized clinical follow-up (f/u) at 1 year including QOL assessment using a modified 17-questions AFEQT™ questionnaire were routinely performed. Results: Ninety consecutive pt (52 males) aged between 53 - 90 years (74.3 ± 7, median 75) underwent LAAC between 2010 and 2013. The CHA2DS2VASc score ranged between 2 - 6 (4.1 ± 1.1, median 4) and the HAS-BLED score between 2 - 8 (4.4 ± 1.6, median 4). Confirmed history of stroke was present in 11 pt, of whom 9 had a non-chicken wing morphology of the appendage (p < 0.01). Procedural success was obtained in 89 of 90 pt, while 3 pt needed 2 occluders to fully close the LAA. Clinical f/u data and the modified AFEQT™ questionnaire, which was completed by 49 pt are shown in Tables 1 and 2. Conclusions: In AF pt with high stroke and bleeding risk LAAC effectively reduced both bleeding complications and ischemic stroke and also significantly improved quality of life at 1-year follow-up.

Background— Intracoronary Doppler guidewires can be used for real-time detection and quantification of microembolism during percutaneous coronary interventions (PCIs). We investigated whether the frequency of Doppler-detected microembolism is related to the incidence of myonecrosis during elective PCI. Methods and Results— The study population included 52 consecutive patients (aged 64±10 years; 36 men, 16 women) with coronary artery disease who underwent elective PCI of a single-vessel stenosis. Using intracoronary Doppler ultrasound, we compared the frequency of microembolism during PCI in 22 patients with periprocedural non–ST-segment elevation myocardial infarctions (pNSTEMI) and 30 patients without pNSTEMI. The 2 groups were comparable with regard to their clinical and procedural characteristics. In the group with pNSTEMI, the total number of coronary microemboli after PCI (27±10 versus 16±8, P P =NS), they were higher in the group with pNSTEMI after PCI (12.6±10.4 versus 6.1±5.1 mg/L, P r =0.565, P r =−0.506, P r =0.499, P Conclusions— Patients with pNSTEMI had a significantly higher frequency of coronary microembolization during PCI, and their systemic inflammatory response and microvascular impairment after PCI were more pronounced. Intracoronary Doppler ultrasound provides evidence that pNSTEMI in patients undergoing elective PCI is caused by microembolization during the procedure.

Background— The clinical impact of late incomplete stent apposition (ISA) for drug-eluting stents is unknown. We sought to prospectively investigate the incidence and extent of ISA after the procedure and at 6-month follow-up of paclitaxel-eluting stents in comparison with bare metal stents (BMS) and survey the clinical significance of ISA over a period of 12 months. Methods and Results— TAXUS II was a randomized, double-blind study with 536 patients in 2 consecutive cohorts comparing slow-release (SR; 131 patients) and moderate-release (MR; 135 patients) paclitaxel-eluting stents with BMS (270 patients). This intravascular ultrasound (IVUS) substudy included patients who underwent serial IVUS examination after the procedure and at 6 months (BMS, 240 patients; SR, 113; MR, 116). The qualitative and quantitative analyses of ISA were performed by an independent, blinded core laboratory. More than half of the instances of ISA observed after the procedure resolved at 6 months in all groups. No difference in the incidence of late-acquired ISA was observed among the 3 groups (BMS, 5.4%; SR, 8.0%; MR, 9.5%; P =0.306), with a similar ISA volume (BMS, 11.4 mm 3 ; SR, 21.7 mm 3 ; MR, 8.5 mm 3 ; P =0.18). Late-acquired ISA was the result of an increase of vessel area without change in plaque behind the stent. Predictive factors of late-acquired ISA were lesion length, unstable angina, and absence of diabetes. No stent thrombosis occurred in the patients diagnosed with ISA over a period of 12 months. Conclusions— The incidence and extent of late-acquired ISA are comparable in paclitaxel-eluting stents and BMS. ISA is a pure IVUS finding without clinical repercussions.

Background — Coronary steal can occur in collateral-dependent myocardium during pharmacologically induced vasodilation. This study assessed coronary steal invasively in chronic total coronary occlusions (TCOs). Methods and Results — In 35 consecutive patients with a percutaneous transluminal coronary angioplasty of a TCO (duration >4 weeks), coronary flow velocity (APV) by a Doppler wire and distal pressure (P D ) by a pressure wire were assessed in the collateral-dependent vascular bed before dilatation. Indexes of peripheral resistance (R P ) and for the collateral pathway, including the donor artery segment (R CP ), were calculated. Changes of these parameters were assessed during intravenous adenosine (140 μg · kg −1 · min −1 ). Adenosine caused a decrease of APV, ie, coronary steal, in 13 patients (37%; group S), an increase in 11 patients (group R), and no change in 11 patients (group N). Angiographic analysis of collateral pathways showed no difference between the groups, except that in group S all collateral connections were continuously visible but no large collaterals (>0.5 mm) were found. In group N, collaterals were least developed. The increase of APV in group R was associated with a decrease of R P , whereas R CP remained unchanged. In contrast, group S showed no change in R P but a significant increase of R CP , indicating an increased resistance of the donor segment. Conclusions — Coronary steal is observed in about one third of TCOs and is associated with specific hemodynamic changes of R P and R CP . Steal occurred only with well-developed angiographically visible collaterals but not with very large collaterals.

Background Evidence is arising that calcium antagonists in idiopathic dilated cardiomyopathy (IDC) may have beneficial effects on virus-induced cardiopathology, alcohol toxicity, microcirculatory disorders, and impaired calcium cycling, all possibly involved in the pathogenesis of the disease. Thus, the effect of adjunct diltiazem (60 to 90 mg TID) on standard treatment was investigated. Methods and Results The Diltiazem in Dilated Cardiomyopathy (DiDi) trial was a randomized, double-blind, placebo-controlled, multicenter trial of 186 patients (92 receiving diltiazem, 94 receiving placebo) with IDC diagnosed by coronary angiography, catheterization of the left side of the heart, and a left ventricular ejection fraction of P =.444). After 24 months, only diltiazem significantly increased cardiac index at rest ( P =.01) and under a workload ( P =.02), systolic and diastolic pressures ( P =.003 and P =.004), stroke volume index ( P =.003), and stroke work index ( P =.000) and decreased both pulmonary artery pressure under workload ( P =.007) and heart rate ( P =.001). Diltiazem also increased exercise capacity ( P =.002) and subjective well-being ( P =.01). Adverse reactions were minor and evenly distributed in both groups, except for an increase in the PQ interval in the diltiazem group. Conclusions In patients with IDC, the adjunct therapy of diltiazem improves cardiac function, exercise capacity, and subjective status without deleterious effects on transplant listing–free survival.

Aim of this study was to evaluate the ability of different echocardiographic modalities to detect myocardial ischemia due to non-critical coronary stenosis, compared to the fractional flow reserve (FFR) as gold standard. Material and Methods: We investigated 22 consecutive patients presenting with stable angina, negative exercise tests and coronary 1-vessel disease with 50–75% diameter stenosis. TDE/SRI was performed at baseline and at peak hyperemia during 0.14 mg/kg/min adenosine infusion simultaneously with intracoronary FFR measurements. Angioplasty was carried out if FFR < 0.75, repeating TDE/SRI during first balloon inflation. Visual wall motion score, peak systolic values for myocardial velocity (Vs), strain rate (SRs), strain (Ss) and peak overall strain (Smax) were determined in the region of interest. Postsystolic shortening (PSS), accepted as typical marker of acute myocardial ischemia, was defined as (Smax-Ss)/Smax > 0.3, with reduced Ss < 15%. Results: Pathologic FFR < 0.75 was found in 11 patients (Table 1 ), who underwent angioplasty. Myocardial contractility reflected by SRs increased during hyperemia only in the patient group with FFR > 0.75 and decreased markedly during balloon inflation. Hyperemic SRs variation correlated with FFR (r = 0.5, p = 0.018) and predicted significantly pathologic FFR with an area under ROC curve of 0.86 (p Conclusion: Functional assessment of moderate-to-severe coronary stenosis remains a diagnostic challenge. PSS occurrence cannot serve as a reliable noninvasive alternative to FFR. However, the blunted hyperemic variation of systolic strain rate was able to predict a pathologic FFR, even in this small group of patients. Therefore, TDE/SRI emerges as a promising tool to enhance the diagnostic accuracy of adenosine stress echocardiography. Table 1

Background— Collaterals can maintain myocardial function or preserve viability in chronic total coronary occlusions (CTOs). It is unknown whether and to what extent collaterals regress after successful recanalization of a CTO. Methods and Results— In 103 patients with successful recanalization of a CTO collateral function was assessed by intracoronary Doppler and pressure recordings before and after recanalization, and again after 5.0±1.3 months. Doppler (CFI) and pressure-derived collateral function indexes (CPI) and collateral (R Coll ) and peripheral resistance indexes (R P ) were calculated. In 10 patients with reocclusion, all without myocardial infarction during follow-up, collateral function had reached a similar level as before the first recanalization. In the other 93 patients with or without restenosis, collateral function was attenuated during follow-up. CPI had decreased by 23% immediately after recanalization ( P P Coll increased immediately after recanalization by 82% ( P P P increased only by 22% after recanalization ( P P 0.30, presumably sufficient to prevent ischemia during acute occlusion. Conclusions— Collateral function regresses during long-term follow-up, especially in collaterals with a small diameter. In the majority of patients, collaterals are not readily recruitable in the case of acute occlusion. However, collaterals have the potential to recover in the case of chronic reocclusion.

Background— The evaluation of new therapeutic modalities to induce collateral growth in coronary artery disease require improved methods of angiographic characterization of collaterals, which should be validated by quantitative assessment of collateral function. Methods and Results— In 100 patients with total chronic occlusion of a major coronary artery (duration >2 weeks) collaterals were assessed angiographically by the Rentrop grading, by their anatomic location, and by a new grading of collateral connections (CC grade 0: no continuous connection, CC1: threadlike continuous connection, CC2: side branch–like connection). The interobserver variability was 10%. Collateral function was assessed by Doppler flow (average peak velocity) and pressure recordings distal to the occlusion before recanalization. A collateral resistance index (R Coll ) was calculated. Recruitable collateral flow was measured during a final balloon inflation >30 minutes after the baseline measurement. The comparison of the anatomic location, the Rentrop, and the collateral connection grade showed only for the latter an independent and significant relation with R Coll . CC2 collaterals preserved regional left ventricular function better than did CC1 collaterals and provided a higher collateral flow reserve during adenosine infusion. CC0 collaterals were predominantly observed in recent occlusions of 2 to 4 weeks’ duration, with the highest R Coll . During balloon reocclusion, recruitable collateral function was best preserved with CC2 and least with CC0. Conclusions— The angiographic grading of collateral connections in total chronic occlusions could differentiate collaterals according to their functional capacity to preserve regional left ventricular function and was closely associated with invasively determined parameters of collateral hemodynamics.

Background — Observational studies in selected patients have shown remarkably low restenosis rates after ultrasound-guided stent implantation. However, it is unknown whether this implantation strategy improves long-term angiographic and clinical outcome in routine clinical practice. Methods and Results — A total of 550 patients with a symptomatic coronary lesion or silent ischemia were randomly assigned to either ultrasound-guided or angiography-guided implantation of ≤2 tubular stents. The primary end points were angiographic dichotomous restenosis rate, minimal lumen diameter, and percent diameter stenosis after 6 months as determined by quantitative coronary angiography. Secondary end points were the occurrence rates of major adverse cardiac events (death, myocardial infarction, coronary bypass surgery, and repeat percutaneous intervention) after 6 and 12 months of follow-up. At 6 months, repeat angiography revealed no significant differences between the groups with ultrasound- or angiography-guided stent implantation with respect to dichotomous restenosis rate (24.5% versus 22.8%, P =0.68), minimal lumen diameter (1.95±0.72 mm versus 1.91±0.68 mm, P =0.52), and percent diameter stenosis (34.8±20.6% versus 36.8±19.6%, P =0.29), respectively. At 12 months, neither major adverse cardiac events (relative risk, 1.07; 95% CI 0.75 to 1.52; P =0.71) nor repeat percutaneous interventions (relative risk 1.04; 95% CI 0.64 to 1.67; P =0.87) were reduced in the ultrasound-guided group. Conclusions — This study does not support the routine use of ultrasound guidance for coronary stenting. Angiography-guided optimization of tubular stents can be performed with comparable angiographic and clinical long-term results.

Background — Microvascular dysfunction is defined as reduced coronary flow reserve in the absence of an epicardial stenosis. This study determined its prevalence and relation to regional myocardial function in chronic total coronary occlusions (TCO). Methods and Results — After recanalization and stenting of a TCO (duration, >4 weeks) in 42 patients, coronary flow velocity reserve (CFVR) was measured by intracoronary Doppler. In a subset of 27 patients, intracoronary pressure was recorded to obtain the fractional flow reserve (FFR). In 21 patients, the CFVR was reassessed after 24 hours. CFVR was r =0.03). A low CFVR was associated with a higher baseline average peak velocity (35.6±16.6 versus 22.4±11.5 cm/s; P =0.006). Doppler parameters did not change within 24 hours. Regional dysfunction had no influence on CFVR. Patients with diabetes and/or hypertension had a lower CFVR than those without this comorbidity (1.86±0.69 versus 2.36±0.45; P Conclusions — Microvascular dysfunction was observed in 55% of TCOs, independent of the impairment of regional myocardial function. Dysfunction was observed more often in patients with diabetes and hypertension. Neither CFVR or FFR alone is appropriate for assessing angioplasty results in patients with a TCO; CFVR should be combined with FFR to differentiate microvascular dysfunction from residual coronary stenosis or diffuse disease.

Background —Coronary collaterals are essential to maintain myocardial function in chronic total coronary occlusions (TCOs). The aim of the present study was to assess the collateral circulation in TCOs before coronary angioplasty and to determine the recruitable collateral perfusion after recanalization by use of intracoronary Doppler flow velocimetry. Methods and Results —In 21 patients with TCOs (duration >4 weeks), Doppler recordings of basal collateral flow were obtained before the first balloon inflation. Angioplasty was performed with stent implantation in all lesions. At the end of the procedure, recruitable collateral flow was measured during a repeat balloon inflation. The collateral flow index (CFI) was calculated from the velocity integral during the occlusion/velocity integral of antegrade flow. In 17 of 21 patients, angiography was repeated after 24 hours, and CFI was reassessed. Average peak velocity of collateral flow was 10.9±5.6 cm/s with a predominantly systolic flow (diastolic/systolic velocity ratio 1.5). After recanalization, the average peak velocity of recruitable collateral flow dropped by >50% to 4.7±2.5 cm/s. CFI fell from 0.48±0.25 to 0.21±0.16 ( P P Conclusions —Collateral circulation in TCO provided 50% of antegrade coronary flow. A considerable fraction of collateral flow was immediately lost after recanalization, indicating that TCO may not remain protected from future ischemic events by a well-developed collateral function.

Background In cardiac arrest, use of percutaneous cardiopulmonary bypass support (PCPS) may lead to left ventricular loading, with deleterious effects on the myocardium, and is often accompanied by an increase in pulmonary artery pressure. The present study was designed to assess the potential of artificially induced pulmonary valve incompetency to retrogradely decompress the left ventricle during PCPS in ventricular fibrillation. Methods and Results Studies were performed using a standardized experimental animal model in sheep (n=12; body weight, 77 to 112 kg). When PCPS was used during fibrillation, an increase in left ventricular pressure (from 21.4±5.0 mm Hg after 1 minute to 28.4±9.5 mm Hg after 10 minutes of fibrillation) was observed in all animals, with a simultaneous increase in pulmonary artery pressure in 6 animals from 15.5± 3.8 to 24.3±5.4 mm Hg (group A). In these animals, artificial pulmonary valve incompetency, which was induced by a special “pulmonary valve spreading catheter,” led to effective decompression of both the pulmonary circulation (decrease in pulmonary artery pressure from 24.3 to 11.3 mm Hg) and the left ventricle (decrease in left ventricular pressure from 30.5 to 17.7 mm Hg). We simultaneously measured a decrease in the myocardial release of lactate (increase in arterial coronary-venous difference in lactate content from −0.01 to 0.14 mmol/L), demonstrating the myocardial protective effect of the procedure. In contrast, in 6 animals without an increase in pulmonary artery pressure during PCPS (group B), artificial pulmonary valve incompetency did not reduce left ventricular loading, which was probably because of competent mitral valves in these animals. Conclusions In case of increasing pulmonary artery pressure during PCPS in cardiac arrest, artificial pulmonary valve incompetency might be a useful tool for effective pulmonary and retrograde left ventricular decompression.

There is clinical evidence that human dilated cardiomyopathy is related to microcirculatory disorders. We used an experimental preparation of the disease that consisted of a study of the microcirculation of 45 cardiomyopathic Syrian and 18 control hamsters with timed plasma staining. To investigate dynamic vascular disorders a double injection technique was used that permitted demonstration of all permanently and temporarily perfused capillaries in the same animal. The results showed a total capillary density of 3423 +/- 470 capillaries/mm2 in the cardiomyopathic hamster during the premyocytolic phase (30 days of age) and that of 3289 +/- 506 capillaries/mm2 during the myocytolytic phase (44 days). These values were not significantly different from those in the control group (3349 +/- 473 capillaries/mm2 at 30 days and 3383 +/- 556 capillaries/mm2 at 44 days). However, tissue areas with extended coronary transit times were detected only in the cardiomyopathic hamsters. These areas were of the same individual and cumulative size at 30 days (diameter approximately 200 micron, 4% of the tissue) as the myocytolytic zones at 44 days. In cardiomyopathic hamsters verapamil and hydralazine prevented both hypoperfusion and myocytolysis. The results favor the view that microcirculatory disorders generate tissue damage in the cardiomyopathic hamster and that these disorders can be prevented through treatment with the calcium antagonist verapamil or with the vasodilator hydralazine.