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Background Atrial fibrillation (AF) and coronary artery disease (CAD) may be encountered coincidently in a large portion of patients. However, data on coronary artery calcium burden in such patients are lacking. Thus, we sought to determine the value of cardiac computed tomography (CCT) in patients presenting with new-onset AF associated with an intermediate pretest probability for CAD admitted to a chest pain unit (CPU). Methods Calcium scores (CS) of 73 new-onset, symptomatic AF subjects without typical clinical, electrocardiographic, or laboratory signs of acute coronary syndrome (ACS) admitted to our CPU were analyzed. In addition, results from computed tomography angiography (CTA) were related to coronary angiography findings whenever available. Results Calcium scores of zero were found in 25%. Median Agatston score was 77 (interquartile range: 1–270) with gender- and territory-specific dispersal. CS scores above average were present in about 50%, high (> 400)-to-very high (> 1000) CS scores were found in 22%. Overall percentile ranking showed a relative accordance to the reference percentile distribution. Additional CTA was performed in 47%, revealing stenoses in 12%. Coronary angiography was performed in 22% and resulted in coronary intervention or surgical revascularization in 7%. On univariate analysis, CS > 50th percentile failed to serve as an independent determinant of significant stenosis during catheterization. Conclusions Within a CPU setting, relevant CAD was excluded or confirmed in almost 50%, the latter with a high proportion of coronary angiographies and subsequent coronary interventions, underlining the diagnostic value of CCT in symptomatic, non-ACS, new-onset AF patients when admitted to a CPU.

Background About 10% of patients admitted to a chest pain unit (CPU) exhibit atrial fibrillation (AF). Hypothesis To determine whether calcium scores (CS) are superior over common risk scores for coronary artery disease (CAD) in patients presenting with atypical chest pain, newly diagnosed AF, and intermediate pretest probability for CAD within the CPU. Methods In 73 subjects, CS was related to the following risk scores: Global Registry of Acute Coronary Events (GRACE) score, including a new model of a frequency-normalized approach; Thrombolysis In Myocardial Infarction score; European Society of Cardiology Systematic Coronary Risk Evaluation (SCORE); Framingham risk score; and Prospective Cardiovascular Munster Study score. Revascularization rates during index stay were assessed. Results Median CS was 77 (interquartile range, 1–270), with higher values in men and the left anterior descending artery. Only the modified GRACE (ρ = 0.27; P = 0.02) and the SCORE (ρ = 0.39; P < 0.005) were significantly correlated with CS, whereas the GRACE (τ = 0.21; P = 0.04) and modified GRACE (τ = 0.23; P = 0.02) scores were significantly correlated with percentile groups. Only the CS significantly discriminated between those with and without stenosis (P < 0.01). Conclusions Apart from modified GRACE score, overall correlations between risk scores and calcium burden, as well as revascularization rates during index stay, were low. By contrast, the determination of CS may be used as an additional surrogate marker in risk stratification in AF patients with intermediate pretest likelihood for CAD admitted to a CPU.

Aim To analyse the timing of cardiac troponin (cTn) measurements in high-risk and cTn-positive acute coronary syndromes without persistent ST-segment elevation (NSTE-ACS) in two structurally different German chest pain units (CPUs), contrasting an urban university maximum care and a rural regional primary care facility. Methods All patients encoded as NSTEMI during the year 2013 were retrospectively enrolled in two centres: site (I)—centre of maximum care in an urban university setting and site (II)—centre of primary care in a rural regional care setting. Data acquisition included time intervals from admission to baseline cTn and first and second cTn control as well as type and timing of invasive management. Results The median times (site I vs. site II) from admission to cTn result announcement were 26.5 vs. 33.0 min (p = 0.02) for baseline, 4 vs. 4 h (p = 0.43) for the first and 11.0 vs. 16.5 h (p = 0.03) for the second control. Timely announcement, as recommended by guidelines, was available in 86.9 % at baseline, 59.4 % for the first or 41.1 % for the second cTn control. Rates and timing of invasive management were independent from the time point of positive cTn announcement (p = 0.51 and p = 0.68, respectively). Conclusions German CPUs provide timely identification of cTn-positive patients in a narrow and guideline-adherent time frame using a rapid rule-out protocol. Especially, baseline and early cTn timing was comparable between the urban university maximum care and the rural regional primary care facility without relevant impact on guideline-conforming invasive management, underlining the high standard of care in those highly professional institutions.

The aim of this study was to analyze differences in the timing of invasive management of patients with high-risk acute coronary syndrome without persistent ST-segment elevation (hr-NSTE-ACS) or myocardial infarction without persistent ST-segment elevation (NSTEMI) between on- and off-hours in a German chest pain unit (CPU). We retrospectively enrolled 160 NSTEMI patients in the study, who were admitted to two German CPUs in 2013. Patients presenting on weekdays between 8 a.m. and 6 p.m. were compared with patients presenting during off-hours. Data analysis included time intervals from admission to invasive management (goals: for hr-NSTE-ACS

If myocardial infarction remains silent, only clinical signs of complications may unveil its presence. Life-threatening complications include myocardial rupture, thrombus formation, or arterial embolization. In the presented case, a 76-year-old patient was admitted with left-sided hemiparesis. In duplex sonography, a critical stenosis of the right internal carotid artery was identified and initially but retrospectively incorrectly judged as the potential cause for ischemia. During operative thromboendarterectomy, arterial embolism of the right leg occurred coincidentally, more likely pointing towards a cardioembolic origin. Percutaneous interventions remained unsuccessful and local fibrinolysis was applied. Delayed bedside echocardiography by an experienced cardiologist demonstrated a discontinuity of the normal myocardial texture of the left ventricular apex together with an echodense, partly floating structure merely attached by a thin bridge not completely sealing the myocardial defect, accompanied by pericardial effusion. The patient was immediately transferred to emergency cardiac surgery with extirpation of the thrombus, aortocoronary bypass graft placement, and aneurysmectomy. This didactic case reveals decisive structural shortcomings in patient’s admission and triage processes and underlines, if performed timely and correctly, the value of transthoracic echocardiography as a noninvasive and cost-effective tool allowing immediate decision-making, which, in this case, led to the correct but almost fatally delayed diagnosis.

Implantation of bare metal stents (BMS) induces the release not only of particulate debris, but also of soluble vasoconstrictors which contribute to microvascular impairment. So this study aimed at addressing the potential attenuation of such vasoconstriction using paclitaxel eluting stents (PES). Using a distal protection/aspiration device, coronary arterial blood was retrieved before and during stent [n = 14 BMS, n = 14 PES, n = 3 sirolimus eluting stents (SES)] implantation in patients with saphenous vein aorto-coronary bypass stenosis and analyzed for plasma serotonin and thromboxane B(2) concentrations. The vasoconstriction of rat mesenteric arteries with intact (+E) and denuded (-E) endothelium in response to coronary arterial or aspirate plasma was quantified and normalized to that by potassium chloride (KCl(max) = 100%). Coronary arterial plasma before stent implantation induced a vasoconstriction of 30-43%, which was independent of endothelial integrity. Serotonin-release was 2.2 ± 0.5 μmol/l with BMS and 2.0 ± 0.4 μmol/l with PES, thromboxane B(2)-release was 26 ± 5 pg/ml with BMS and 22 ± 8 pg/ml with PES. BMS- and SES-aspirate plasma induced a vasoconstriction of 68 ± 18% (+E)/93 ± 14% (-E) and 81 ± 17% (+E)/124 ± 14% (-E), respectively. In contrast, PES-aspirate plasma induced only minor vasoconstriction of 8 ± 3% (+E)/12 ± 5% (-E). Addition of paclitaxel to BMS-aspirate plasma attenuated vasoconstriction. PES-aspirate induced microtubular condensation in immunofluorescence microscopy. Results indicate that aspirate from PES implantation attenuates vasoconstriction, possibly secondary to microtubular stabilization. Such acute downstream vascular paralysis could be beneficial in preventing a no-reflow phenomenon in patients undergoing stenting.

Few cases of a left atrial thrombus without mitral valve disease have been reported. We present an unusual case in which a patient presented to the emergency department with syncope and acute cerebral ischemia caused by a ball thrombus originating from the left atrium (LA). An emergency bedside echocardiogram showed the LA ball thrombus intermittently obstructing the mitral orifice and, at times, compromising the left ventricular outflow tract. This thrombus was determined to be the source of cerebral embolization resulting in acute ischemia. Surgical excision of the mass was performed. At operation, the thrombus was found to be tethered to the left atrial appendage. This tethering was not apparent on the echocardiographic images, where the thrombus appeared to be free floating. This case demonstrates the utility of transthoracic echocardiography in establishing the etiology of emergent conditions seemingly unrelated to acute cardiac disease, in this situation a neurologic presentation with syncope and cerebral ischemia.

BACKGROUND: Cardiac marker release after percutaneous coronary interventions (PCI) reflects myocardial necrosis which is usually the result of periprocedural (micro)embolization of atherothrombotic debris and associated with impaired left ventricular function and adverse outcome. METHODS: In this prospective study, we examined 55 patients treated by direct stenting of single de-novo lesions to assess the relationship between plaque composition, as determined by preinterventional intravascular ultrasound (IVUS) with radiofrequency data (IVUS-RF) analysis (so-called Virtual Histology) versus coronary microembolization, as determined by serial measurement of cardiac markers. IVUS was performed with an electronic system and 20-MHz IVUS catheters. Serum creatine kinase (CK) and cardiac troponin I (CTnI) were determined before PCI and after 6, 12, and 24 hours. RESULTS: Plaques had a volume of 99 +/- 63 mm(3) and were composed of fibrous (61 +/- 9%) and fibro-fatty tissue (27 +/- 12%), dense calcium (4 +/- 3%), and necrotic core (NC) (8 +/- 6%). NC volume per se, volume per 10 mm of segment length, and volume % were correlated (r = 0.64, 0.66, and 0.52 respectively; all P < 0.01) with the maximum increase in cardiac markers (CK 55.4 +/- 55.7 U/l; CTnI 0.49 +/- 0.68 ng/ml). Patients in the 4th quartile of NC volume (>10.8 mm(3)) had a particularly high increase in markers (P < 0.001). In contrast, total plaque volume and plaque components other than NC had no relation with cardiac markers (ns). CONCLUSIONS: Patients with large NC in culprit lesions may experience more myocardial injury from peri-interventional microembolization. IVUS-RF assessment before PCI has the potential to identify lesions at particular high risk which may help to tailor PCI.

Because of the clinical benefit of lipid lowering in older patients, we hypothesized that the relation between low-density lipoprotein (LDL) cholesterol serum levels and coronary plaque progression may persist throughout aging. We analyzed serial intravascular ultrasound (IVUS) data of 60 left main stems (18 +/- 9 months apart) and evaluated the relation between LDL cholesterol levels and coronary plaque progression at different ages. The population (n = 60) was divided into 3 groups according to age: tertile 1 (n = 20) was a mean age of 48 +/- 6 years (median 51, range 33 to 55), tertile 2 (n = 20) was a mean age of 58 +/- 2 years (median 59, range 55 to 61), and tertile 3 (n = 20) was a mean age of 66 +/- 6 years (median 65, range 61 to 83). Between groups, there was no significant difference in non-age-related demographics, clinical data, lipid profiles, or medications (e.g., statins). There was a positive linear relation between LDL cholesterol and annual changes in plaque plus media area in all age tertiles, which was statistically significant in tertiles 2 and 3 (r = 0.56, p0.01; r = 0.50, p0.02) and showed a strong trend in tertile 1 (r = 0.41, p = 0.07). The estimated LDL cholesterol thresholds, which, as determined by regression analysis, would correspond to no plaque progression, were 74, 60, and 78 mg/dl, respectively, in tertiles 1, 2, and 3. In conclusion, serial IVUS data in left main coronary arteries suggest that the relation between LDL cholesterol serum levels and plaque progression persists during aging.

OBJECTIVES: We present the remodeling index (RI) versus serial intravascular ultrasound (IVUS) data. BACKGROUND: The RI, derived by comparing lesion external elastic membrane (EEM) cross-sectional area versus the reference at one time point, is used in various IVUS studies as a substitute of true remodeling (change in EEM over time), assuming that it represents true remodeling. METHODS: We studied 46 non-stenotic left main arteries using serial IVUS (follow-up 18 ± 8 months). Plaques were divided into subgroups according to the follow-up RI: follow-up RI >1 (n = 27) versus follow-up RI ≤1 (n = 19). RESULTS: Lesions with a follow-up RI >1 had an increase in lumen despite an increase in plaque because of an increase in EEM. Conversely, lesions with a follow-up RI ≤1 had a reduction in lumen as a result of both a plaque increase and EEM decrease. Overall, the follow-up RI correlated directly with changes in lesion site EEM (baseline-to-follow-up). Although there was no correlation between the follow-up RI and changes in reference EEM area, changes in reference EEM area did correlate directly with changes in lesion EEM area. In nearly 90% of lesions with a follow-up RI >1, there was a previously documented increase in EEM area. Using multivariate linear regression analysis, the follow-up RI was dependent on the baseline RI, the increase in lesion EEM area, and the decrease in reference EEM area. The follow-up RI was not dependent on changes in lesion plaque area. CONCLUSIONS: The vast majority of left main lesions with a remodeling index >1 had evidence of a previous increase in lesion-site EEM area.

Aims: The impact of right bundle branch block (RBBB) and left bundle branch block (LBBB) on myocardial perfusion is not completely understood as data are often blurred by underlying cardiac disease. The present study investigates whether conduction delays per se affect coronary perfusion-an indirect measure of myocardial oxygen demand. Methods and results: Intracoronary Doppler and ultrasound were performed in 8 patients with RBBB, 10 patients with LBBB, and 10 control subjects. All patients had angiographically normal coronary arteries and normal left ventricular function. Baseline (bAPV) and adenosine-induced hyperaemic average flow velocity and coronary flow velocity reserve (CFVR) were measured in left anterior descending arteries. Intravascular ultrasound showed no difference in lumen cross-sectional area and plaque burden between groups. Patients with RBBB and LBBB had higher bAPV values than controls (19.0 ± 4.9, 21.9 ± 5.1, and 14.6 ± 2.4 cm/s, respectively; ANOVA P = 0.003). There was no difference between patients with LBBB and RBBB compared with controls in CFVR (2.8 ± 0.5, 3.0 ± 1.0, and 3.4 ± 0.7, respectively; ANOVA P = 0.21). Conclusion: Bundle branch blocks, in particular LBBB, are associated with an increased coronary flow velocity, which indicates enhanced myocardial oxygen demand on the basis of mechanoenergetic disturbance. This may contribute to the unfavourable outcome of patients with intraventricular conduction delay.

Background— Intravascular ultrasound (IVUS) is increasingly used as an end point in studies aimed at reducing progression or inducing regression of coronary artery disease. However, data linking serial changes by IVUS with clinical outcomes are scarce. Methods and Results— In the absence of a validated risk score for secondary prevention, we compared 3 established risk scores for primary prevention—PROCAM, SCORE, and Framingham—with plaque progression and lumen reduction as assessed with serial IVUS (follow-up, 18±9 months) in atherosclerotic left main coronary arteries of 56 patients with established atherosclerosis. For all 3 algorithms, patients at highest estimated risk of events showed greater plaque progression than patients at lowest risk ( P r =0.41 to 0.60; P P P Conclusions— There was a positive linear relationship between the estimated risk of clinical events derived from all 3 established risk-score algorithms and the extent of plaque progression measured by serial IVUS. This translated into stenosis progression (reduction in lumen dimensions) with increasing clinical risk.

Most intravascular ultrasound (IVUS) studies of arterial remodeling in native coronary arteries reported a remodeling index obtained at a single time point. We analyzed serial IVUS examinations, including the vessel cross-sectional area changes (remodeling behavior), of 60 hemodynamically nonstenotic left main lesions (baseline vs 18.4 +/- 9.4 months follow-up). Lumen reduction resulted from vessel reduction (sometimes despite plaque + media decrease), plaque + media increase (with or without vessel increase), or both. The percent annual changes in lumen area correlated strongly with changes in vessel (r = 0.84), but not with changes in plaque + media area. Plaques were classified as group A lesions, reflecting positive remodeling behavior (vessel changes >0), or group B lesions, reflecting negative (or intermediate) remodeling behavior (vessel changes

The mechanisms of lumen enlargement during stent implantation may be significantly affected by arterial remodeling. To assess effects of lesion remodeling, we performed 3-dimensional intravascular ultrasound (IVUS) analyses in 55 coronary lesions before and after deployment of balloon-expandable stents. Standard quantitative analysis was performed, and arterial remodeling was assessed by the remodeling index (target site divided by mean of proximal and distal reference segment vessel areas), which classified lesions into group A (remodeling index ≤1, negative or intermediate remodeling, n = 40) or group B (remodeling index >1, positive remodeling, n = 15) lesions. Characteristics of the 55 patients and the interventional procedures were similar in the 2 groups. IVUS demonstrated that stenting resulted in increased lumen and vessel dimensions and in a reduced plaque size (p ≤0.001 each) in both group A and group B lesions. The extent of lumen increase inside the stents was almost identical, but resulted from different mechanisms: (1) vessel stretch was greater in group A (p

Axial plaque redistribution is an important mechanism of lumen enlargement after stenting of noncalcified lesions. To assess effects of lesion calcification on mechanisms of coronary stenting, we analyzed 55 lesions with noncircumferential calcification with 3-dimensional intravascular ultrasound (IVUS) (standard qualitative and quantitative analyses) before and after implantation of balloon-expandable stents. Thirty-two plaques (58%) showed arcs of calcium120 degrees of vessel circumference (group A), whereas 23 lesions (42%) contained arcs of calciumor =120 degrees of vessel circumference (group B). In the entire cohort of 55 lesions, as well as groups A and B, which were studied separately, both single-slice IVUS analysis (performed at minimum lumen site before intervention) and mean stented segment IVUS analysis showed an increase in lumen and vessel area and a decrease in plaque area (p0.001). The magnitude of lumen and vessel increase and of plaque decrease was similar in both groups. Group A lesions showed significant plaque extrusion into the distal reference segment that was not observed in group B (increase in plaque area of 1.3 +/- 1.9 vs 0.1 +/- 2.0 mm(2), p0.04). Stenting did not alter plaque area of the proximal reference segment in either group. In addition, there was an increase in vessel area of the distal reference of both groups, indicating that stent-induced vessel expansion observed within the lesion also affected the distal reference. Thus, longitudinal plaque redistribution and vessel expansion contribute to increased lumen dimensions during stenting of lesions with varying amounts of calcium; however, marked plaque extrusion was found only in lesions with a calcium arc of120 degrees.

Atherosclerotic coronary arteries are more calcified in patients with than without chronic kidney disease (CKD). We addressed the potential for coronary microvascular obstruction in patients with and without CKD during stenting for saphenous vein aorto-coronary graft (SVG) stenosis under protection with a distal occlusion/aspiration device. In patients with and without CKD (n = 20/20), SVG plaque composition was analyzed from virtual histology using intravascular ultrasound analysis before stent implantation. There was more dense calcium and more necrotic core in patients with than without CKD (14 ± 3 vs. 3 ± 1 % and 21 ± 3 vs. 12 ± 2 % of plaque volume, respectively). Coronary aspirate was retrieved during stent implantation and divided into particulate debris and plasma. Patients with CKD had more particulate debris and calcium release than patients without CKD. In contrast, the release of serotonin was less in patients with than without CKD (0.4 ± 0.1 vs. 1.2 ± 0.3 μmol/L), whereas that of catecholamines, endothelin, tissue factor, thromboxane, tumor necrosis factor α, and C reactive protein was not significantly different. Confirming the biochemical results, aspirate plasma from patients with CKD induced less vasoconstriction of rat mesenteric arteries than that from patients without CKD (with endothelium (+E), 26 ± 7 %; without endothelium (−E): 28 ± 7 % vs. +E, 68 ± 12 %; −E: 95 ± 16 % of maximum KCl-induced vasoconstriction). Graft atherosclerosis of patients with CKD is more degenerated and releases more particulate debris and calcium, but the aspirate has surprisingly less serotonin and vasoconstrictor potential.

Neointimal hyperplasia is one of the key components of the restenotic process. The aim of this study was to evaluate the efficacy and safety of a microbubble delivery of c-myc antisense peptide in reducing restenosis after coronary stenting in de novo stenosis with intravascular ultrasound. A Multi-Link Zeta bare metal stent was implanted in de novo coronary artery lesions (RD ≥ 2.5- ≤ 4.0 mm; TL ≥ 15- ≤ 30 mm in length). Serial intravascular ultrasound analyses were performed in 25 lesions. A dose of 16mg RESTEN-MPTM (AVI BioPharma supplied by Global Therapeutics LLC) was intravenously administered after stenting and again 24 hours later. In three centres in Germany a total of 50patients (51 lesions) were enrolled, 34 in Essen, 13 in Coburg and 3 in Heidelberg. Before stenting, the minimal lumen diameter (MLD) and length of stenosis were determined. 84% (43/51) of the lesions were either Type B2 or C lesions. At six-month follow-up, angiography was performed. Generally the neointimal proliferation was minor. Major adverse cardiac events (MACE) were 10.0% after 6 months and 21.9% after 12 months. The target lesion revascularization was 15.6%, the target vessel revascularization 18.8% after 12 months. Of the 34 patients studied at six-months in the IVUS sub-study, six patients required target lesion revascularization (TLR). Binary restenosis rate by intravascular ultrasound was 26 ± 4%. Generally the neointima proliferation was minor and open vessel lumen could be demonstrated during follow-up. Microbubble delivery of c-myc antisense seems to be effective in reducing neointimal tissue proliferation without the problem of late stent thrombosis. Neointima proliferation seems to be attenuated but not eliminated. MACE was not increased in this study population.

The interventional implantation of a stent into an atherosclerotic coronary artery is a unique and paradigmatic scenario of plaque rupture in humans. The use of protection devices not only prevents the released plaque particles and the superimposed thrombotic material from being washed and embolized into the coronary microcirculation of the individual patient, but permits also the retrieval and ex vivo analysis of particulate plaque debris and soluble substances. The particulate debris comprises typical cholesterol crystals, foam cells, hyalin material and calcium deposits from the atheroma as well as platelets and coagulation material; soluble substances include vasoconstrictors, such as serotonin and thromboxane, as well as inflammatory mediators, such as TNFα which amplifies vasoconstriction by inducing endothelial dysfunction. The vasoconstriction observed in a bioassay ex vivo correlates to clinical symptoms, angiographic stenosis and plaque burden, as assessed by intravascular ultrasound. The release of TNFα into the aspirate correlates to restenosis. Detailed analysis of the human coronary aspirate may promote a better understanding of the pathophysiology of the vulnerable atherosclerotic plaque and help to better antagonize the microvascular consequences of coronary microembolization, including the no reflow phenomenon. This article is part of a Special Issue entitled "Coronary Blood Flow."

Rationale: Stent implantation into atherosclerotic plaques releases, apart from particulate debris, soluble substances that contribute to impaired microvascular perfusion. Objective: To quantify the release of vasoconstrictors and to determine the efficacy of coronary dilators to attenuate their action. Methods and Results: Using a distal protection/aspiration device, coronary arterial blood was retrieved before and during stenting in 22 patients with severe saphenous vein aorto-coronary bypass stenoses. The release of catecholamines, endothelin, serotonin, thromboxane B 2 , and tumor necrosis factor (TNF)α was measured. The response of rat mesenteric arteries with intact (+E) and denuded (−E) endothelium to aspirate plasma was normalized to that by KCl. Responses to selective receptor blockade, adenosine, nitroprusside, and verapamil against the aspirate-induced constriction were determined. The coronary arterial plasma withdrawn before stenting induced 21±5% and the aspirate plasma after stenting induced 95±8% of maximum KCl-induced vasoconstriction. Serotonin, thromboxane B 2 , and TNFα release into aspirate plasma increased by 1.9±0.2 μmol/L, 25.6±3.1 pg/mL, and 19.7±6.1 pg/mL, respectively, during stenting. The aspirate-induced vasoconstriction was largely antagonized by selective serotonin receptor blockade, with little further antagonism by additional thromboxane receptor blockade. TNFα did not induce constriction per se but potentiated the constriction with serotonin and the thromboxane-analog U-46619 in arteries +E. The concentrations to induce half-maximal vasodilation were comparable for nitroprusside (+E, 3.3×10 −8 ; −E, 1.9×10 −8 mol/L) and verapamil (+E, 8.3×10 −8 ; −E, 7.8×10 −8 mol/L), and the vasoconstriction was eventually eliminated. The vasodilator response to adenosine was dependent on functional endothelium and weaker. Conclusion: Serotonin is the main coronary vasoconstrictor after stenting, and thromboxane and TNFα somewhat potentiate the serotonin response. Nitroprusside and verapamil are more potent than adenosine to attenuate the aspirate plasma-induced vasoconstriction, and they are not dependent on functional endothelium.

Coronary microembolization from the erosion or rupture of a vulnerable atherosclerotic plaque occurs spontaneously in acute coronary syndromes and iatrogenically during percutaneous coronary interventions. Typical consequences of coronary microembolization are microinfarcts with an inflammatory response, contractile dysfunction, and reduced coronary reserve. Apart from transient elevations of creatine kinase and troponin, microemboli can be visualized by intracoronary Doppler and the resulting microinfarcts by late-enhancement nuclear magnetic resonance. Statins, antiplatelet agents, and coronary vasodilators protect against microembolization and microinfarction when started before percutaneous coronary interventions. Distal protection devices can retrieve atherothrombotic debris and prevent its embolization into the microcirculation, but their effect on clinical outcome has been disappointing so far, except for saphenous vein bypass grafts. Devices for aspiration of thrombi and thrombus-derived vasoconstrictor, thrombogenic, and inflammatory substances, however, reduce thrombus burden, improve perfusion, and provide protection in patients with acute myocardial infarction.

Percutaneous transcatheter aortic valve implantation (TAVI) is an evolving interventional therapy for high-risk, non-surgical patients with severe, symptomatic aortic valve stenosis (AS). As a standard procedure, 2D transesophageal echocardiography has been used for the preinterventional assessment of the native valve and measurement of the aortic annulus as well as for intraprocedural guidance. Recently, a new matrix array, transesophageal probe for real-time three-dimensional echocardiography (RT3D-TEE) has been introduced. We applied this new technique to monitor percutaneous aortic valve implantation and described our initial experiences with this method in patients undergoing TAVI. We hypothesized that RT3D-TEE provides improved evaluation of the native aortic valve and annulus dimension due to unlimited scan plane orientation. This new technology should also enable accurate guiding of percutaneous cardiac interventions by providing immediate information on prosthesis position and function in real-time. In our preliminary clinical experience real-time three-dimensional transesophageal echocardiography (RT3D TEE) was demonstrated to provide improved guiding of percutaneous aortic valve replacement by superior spatial visualisation of the cardiac structures and facilitated the detection of procedure-related complications. Due to the advantages of real-time 3D TEE monitoring, this technique might improve the outcome of patients treated with percutaneous aortic valve replacement.

The reduction in plaque volume during stent implantation is associated with the release of particulate debris and plaque-derived soluble substances. We studied the potential release of the proinflammatory cytokine TNF-α into the coronary circulation and whether such release is related to the reduction in plaque volume and, possibly, a predictor for restenosis. In 18 male patients ( n = 24 stents) with severe stenosis in a saphenous vein aortocoronary bypass graft (SVG), we used a distal balloon occlusion-aspiration device during stent implantation. The aspirate TNF-α levels were determined before and after stent implantation and related to the angiographic and intravascular ultrasound-assessed severity of stenosis and restenosis. We found that TNF-α is, indeed, released into the aspirate of stented SVG (9 ± 1 and 28 ± 3 pg/ml before and after stent implantation, respectively, P < 0.0001) and that such release is related to the reduction in plaque volume ( r = 0.88, P < 0.0001) and associated with restenosis after 5 mo ( r = 0.71, P = 0.001). The periprocedural release of plaque-derived TNF-α possibly represents the amount and activity of the atherosclerotic process and might be a predictor for restenosis.

Background An asymptomatic and apparently healthy 64-year-old marathon runner underwent comprehensive cardiovascular risk assessment as part of a prospective study on calcified coronary plaque burden in master marathon runners. His profile suggested a low 10-year cardiovascular risk. Investigations Conventional risk-factor assessment, coronary artery calcium quantification, bicycle stress test, echocardiography, coronary angiography, intravascular ultrasonography, including virtual histology, and intracoronary Doppler ultrasonography. Diagnosis Severe coronary atherosclerosis of the left anterior descending, mid left circumflex, and left main arteries. Management Stenting of the left anterior descending artery, CABG surgery, and intensive risk-factor modification. The patient was also advised against participating in future marathon competitions.

A 54-year-old male patient with known 2-vessel coronary artery disease and stable angina presented for elective percutaneous coronary intervention of a proximal right coronary artery stenosis (Figure 1). Previously, the patient had undergone intervention of mid-left anterior descending coronary artery stenosis by sirolimus-eluting stent implantation. Figure 1. Preinterventional coronary angiogram showing the high-grade stenosis in the proximal segment of the right coronary …

Positive remodeling is more often observed in lesions of patients who have acute coronary syndromes or vulnerable (rupture-prone) plaques. However, there are few data that correlate plaque morphology, composition, and arterial remodeling in vivo. We evaluated coronary plaque characterization of lesions with positive remodeling using intravascular ultrasound (IVUS) radiofrequency data analysis. Seventy-seven nonbifurcation native coronary lesions (in 50 patients) were imaged in vivo using 30-MHz IVUS transducers. Lesions were classified into 4 plaque types, fibrous, fibrofatty, dense calcium, and necrotic core, by using processing of the radiofrequency signal validated in vitro. The remodeling index was calculated as the lesion external elastic membrane area divided by the proximal reference external elastic membrane area. Lesions were divided into 2 groups: positive remodeling (remodeling index >1.0, 26 lesions) and intermediate/negative remodeling (remodeling index

Objectives We sought to identify soluble vasoconstrictor substances that are released during stent implantation into saphenous vein aortocoronary bypass grafts. Background Atherosclerotic saphenous vein aortocoronary bypass grafts are particularly vulnerable to plaque rupture. Protection devices prevent particulate debris from being embolized. Additional soluble vasoconstrictor substances possibly also contribute to impaired microvascular perfusion. Methods Peripheral venous blood (VB) and aspirate (AS) were obtained from 14 patients with a significant stenosis in a saphenous vein graft during stent implantation under protection with a distal balloon occlusion device. In five additional patients, arterial blood (AB) was also taken distal to the stented lesion before intervention. Vasomotor substances in VB, AB, and AS plasma were identified in a bioassay of rat mesenteric arteries with intact (+E) and denuded endothelium (−E). Vasoconstriction was normalized to that induced by potassium chloride depolarization (100%). Results Venous blood, AB, and AS plasma induced maximum vasoconstriction within six minutes. The AS plasma induced a vasoconstriction of 138 ± 13% (−E) and 87 ± 14% (+E); VB, of 70 ± 14% (−E) and 23 ± 4% (+E); and AB plasma obtained before intervention, of 49 ± 9% (−E) and 36 ± 8% (+E). The vasoconstrictor potency of AS plasma in endothelium-denuded vessels was related to the severity of anginal symptoms, angiographic stenosis severity, plaque volume, and plaque burden as determined by intravascular ultrasound. The AS plasma-induced vasoconstriction was largely attenuated by combined serotonin/5-hydroxytryptamine (5-HT)2A/2C- and 5-HT1A/1B-receptor blockade and eliminated by additional thromboxane A2 thromboxane-prostanoid (TP)-receptor blockade. Conclusions Stent implantation releases, apart from and in addition to particulate debris, soluble vasoconstrictor substances that possibly contribute to impaired microvascular perfusion.

The direct determinants of coronary flow are lumen area and blood flow velocity; however, the precise mechanisms that control these factors are not fully understood. The aim of the present study was to assess by which mechanisms lumen area and coronary flow velocity interact with hemodynamic and morphometric factors, thereby influencing coronary flow. Intracoronary Doppler and ultrasound measurements were performed in 28 patients without coronary lumen irregularities. Flow velocity and lumen cross-sectional area were measured in the proximal segments of all three coronary arteries. Global lumen cross-sectional area and global flow were obtained by adding up the values of all three coronary arteries. Left ventricular mass was assessed by echocardiography. Stress-mass-heart rate and pressure-rate products reflecting myocardial oxygen demand were calculated. Global coronary flow increased during adenosine-induced hyperemia from 197 ± 72 to 637 ± 204 ml/min ( P < 0.001). Global coronary flow closely correlated with the stress-mass-heart rate product ( r = 0.62; P < 0.001). Looking at the two constituents of flow separately, global coronary cross-sectional area was closely related to left ventricular muscle mass ( r = 0.61; P < 0.001), whereas mean coronary flow velocity at rest showed a strong linear relation with the pressure-rate product ( r = 0.64; P < 0.001). There was no interaction between cross-sectional area and blood flow velocity in any of the coronary vessels. Coronary lumen size and flow velocity, the two determinants of coronary flow, are principally determined by different physiological factors. Long-term flow adaptation is achieved by an increase in coronary lumen size, whereas short-term myocardial oxygen requirements are met by changes in resting flow velocity.

A 57-year-old man presented with a sudden onset of chest pain, which suggested the possibility of myocardial infarction. Coronary angiography revealed a myocardial bridge in the left anterior descending coronary artery. The myocardial bridge decreased the diameter of the artery substantially during systole (Panel A, with arrow pointing to myocardial bridge). Optical coherence tomography showed no evidence of atherosclerosis but did show vessel patency during diastole (Panel B) and collapse during systole (Panel C). A myocardial bridge is a band of myocardial tissue overlying a segment of epicardial coronary artery. Myocardial bridging is a congenital abnormality that typically occurs in . . .