Increased prevalence of psoriasis in patients with coronary artery disease: results from a case-control study.

BACKGROUND: The incidence of myocardial events has been reported to be increased in patients with psoriasis. OBJECTIVES: To investigate whether psoriasis is an independent risk factor for coronary artery disease (CAD). METHODS: We compared the prevalence of psoriasis between case patients with a diagnosis of CAD based on coronary angiography findings and control patients with no CAD referred to the emergency surgery department for an acute noncardiovascular condition. Case and control patients were examined for the presence of psoriasis by two dermatologists. The prevalence of psoriasis was compared among patients with CAD according to CAD severity. Five-hundred cases and 500 age- and sex-matched controls were included. RESULTS: Using matched univariate analysis, the prevalence of psoriasis was about twofold higher in CAD case patients than in control patients [8·0% vs. 3·4%, odds ratio (OR) 2·64; 95% confidence interval (CI) 1·42-4·88]. Using unconditional multivariate analysis, the association of psoriasis with CAD appeared to be borderline significant (OR 1·84; 95% CI 0·99-3·40). Psoriasis in patients with CAD was significantly associated with three-vessel involvement relative to one-or two-vessel involvement (13·1% vs. 6·1%; OR 3·07; 95% CI 1·50-6·25). CONCLUSIONS: The prevalence of psoriasis is twofold higher in patients with CAD than in control patients without CAD. It is associated with a more severe coronary artery involvement.

Multimodal imaging in the diagnosis of isolated left ventricular noncompaction.

Left ventricular noncompaction (LNVC), first described in 1984, is a rare congenital cardiomyopathy that is thought to be caused by arrest of normal embryogenesis of the endocardium and the myocardium, and characterized by multiple prominent trabeculations with deep intertrabecular recesses. LVNC can be associated with other congenital cardiac abnormalities such as atrial septal defect and ventricular septal defect, but it can occur in isolation. The clinical manifestations of the disease are variable, ranging from no symptoms to signs of heart failure, systemic emboli, and ventricular arrhythmias. The diagnosis is established by two dimensional echocardiography or magnetic resonance imaging. We report the case of a 44-year-old man with LVNC and discuss the role of multimodal imaging in the diagnosis and assessment of the disease.

MR delayed enhancement imaging findings in suspected acute myocarditis.

The purpose of the study was to prospectively assess the clinical impact of routinely performed delayed enhancement imaging in suspected acute myocarditis. A two-centre prospective study was performed in patients with suspected acute myocarditis. The protocol included horizontal long axis, vertical long axis and short axis ciné MR and delayed enhancement imaging after Gd-DTPA infusion (0.2 mmol/kg). Sixty consecutive patients were enrolled (aged 49.4 +/- 17.8 years). MRI demonstrated delayed enhancement sparing the subendocardicardial layer in 51.6% of patients, concordant with the diagnosis of acute myocarditis; 16.7% of patients exhibited delayed enhancement involving the subendocardial layer with irregular margins, concordant with the diagnosis of acute myocardial infarction; 31.7% of patients had delayed enhancement imaging that was considered normal. Routine imaging to identify delayed enhancement provided crucial information in suspected acute myocarditis by reinforcing the diagnosis in 51.6% of patients and correcting a misdiagnosed acute myocardial infarction in 16.7% of patients.

[SAMHD1 acts at stalled replication forks to prevent interferon induction]. / SAMHD1 agit sur les fourches de réplication bloquées pour empêcher l'induction d'interféron.

DNA replication is an extremely complex process, involving thousands of replication forks progressing along chromosomes. These forks are frequently slowed down or stopped by various obstacles, such as secondary DNA structures, chromatin-acting proteins or a lack of nucleotides. This slowing down, known as replicative stress, plays a central role in tumour development. Complex processes, which are not yet fully understood, are set up to respond to this stress. Certain nucleases, such as MRE11 and DNA2, degrade the neo-replicated DNA at the level of blocked forks, allowing the replication to restart. The interferon pathway is a defense mechanism against pathogens that detects the presence of foreign nucleic acids in the cytoplasm and activates the innate immune response. DNA fragments resulting from genomic DNA metabolism (repair, retrotransposition) can diffuse into the cytoplasm and activate this pathway. A pathological manifestation of this process is the Aicardi-Goutières syndrome, a rare disease characterized by chronic inflammation leading to neurodegenerative and developmental problems. In this encephalopathy, it has been suggested that DNA replication may generate cytosolic DNA fragments, but the mechanisms involved have not been characterized. SAMHD1 is frequently mutated in the Aicardi-Goutières syndrome as well as in some cancers, but its role in the etiology of these diseases was largely unknown. We show that cytosolic DNA accumulates in SAMHD1-deficient cells, particularly in the presence of replicative stress, activating the interferon response. SAMHD1 is important for DNA replication under normal conditions and for the processing of stopped forks, independent of its dNTPase activity. In addition, SAMHD1 stimulates the exonuclease activity of MRE11 in vitro. When SAMHD1 is absent, degradation of neosynthesized DNA is inhibited, which prevents activation of the replication checkpoint and leads to failure to restart the replication forks. Resection of the replication forks is performed by an alternative mechanism which releases DNA fragments into the cytosol, activating the interferon response. The results obtained show, for the first time, a direct link between the response to replication stress and the production of interferons. These results have important implications for our understanding of the Aicardi-Goutières syndrome and cancers related to SAMHD1. For example, we have shown that MRE11 and RECQ1 are responsible for the production of DNA fragments that trigger the inflammatory response in cells deficient for SAMHD1. We can therefore imagine that blocking the activity of these enzymes could decrease the production of DNA fragments and, ultimately, the activation of innate immunity in these cells. In addition, the interferon pathway plays an essential role in the therapeutic efficacy of irradiation and certain chemotherapeutic agents such as oxaliplatin. Modulating this response could therefore be of much wider interest in anti-tumour therapy.

La réplication de l'ADN est un processus extrêmement complexe, impliquant des milliers de fourches de réplication progressant le long des chromosomes. Ces fourches sont fréquemment ralenties ou arrêtées par différents obstacles, tels que des structures secondaires de l'ADN, des protéines agissant sur la chromatine ou encore un manque de nucléotides. Ce ralentissement, qualifié de stress réplicatif, joue un rôle central dans le développement tumoral. Des processus complexes, qui ne sont pas encore totalement connus, sont mis en place pour répondre à ce stress. Certaines nucléases, comme MRE11 et DNA2, dégradent l'ADN néorépliqué au niveau des fourches bloquées, ce qui permet le redémarrage des réplisomes. La voie interféron est un mécanisme de défense contre les agents pathogènes qui détecte la présence d'acides nucléiques étrangers dans le cytoplasme et active la réponse immunitaire innée. Des fragments d'ADN issus du métabolisme de l'ADN génomique (réparation, rétrotransposition) peuvent diffuser dans le cytoplasme et activer cette voie. Une manifestation pathologique de ce processus est le syndrome d'Aicardi-Goutières, une maladie rare caractérisée par une inflammation chronique générant des problèmes neurodégénératifs et développementaux. Dans le cadre de cette encéphalopathie, il a été suggéré que la réplication de l'ADN pouvait générer des fragments d'ADN cytosoliques, mais les mécanismes impliqués n'avaient pas été caractérisés. SAMHD1 est fréquemment muté dans le syndrome d'Aicardi-Goutières ainsi que dans certains cancers, mais son rôle dans l'étiologie de ces maladies était jusqu'à présent largement inconnu. Nous montrons que de l'ADN cytosolique s'accumule dans les cellules déficientes pour SAMHD1, particulièrement en présence de stress réplicatif, activant la réponse interféron. Par ailleurs, SAMHD1 est important pour la réplication de l'ADN en conditions normales et pour le processing des fourches arrêtées, indépendamment de son activité dNTPase. De plus, SAMHD1 stimule l'activité exonucléase de MRE11 in vitro. Lorsque SAMHD1 est absent, la dégradation de l'ADN néosynthétisé est inhibée, ce qui empêche l'activation du checkpoint de réplication et entraine un défaut de redémarrage des fourches de réplication. De plus, la résection des fourches de réplication est réalisée par un mécanisme alternatif qui libère des fragments d'ADN dans le cytosol, activant la réponse interféron. Les résultats obtenus montrent, pour la première fois, un lien direct entre la réponse au stress réplicatif et la production d'interférons. Ces résultats ont des conséquences importantes dans notre compréhension du syndrome d'Aicardi Goutières et des cancers liés à SAMHD1. Par exemple, nous avons démontré que MRE11 et RECQ1 sont responsables de la production des fragments d'ADN qui déclenchent la réponse inflammatoire dans les cellules déficientes pour SAMHD1. Nous pouvons donc imaginer que bloquer l'activité de ces enzymes pourrait diminuer la production des fragments d'ADN et, in fine, l'activation de l'immunité innée dans ces cellules. Par ailleurs, la voie interférons joue un rôle essentiel dans l'efficacité thérapeutique de l'irradiation et de certains agents chimiothérapiques comme l'oxaliplatine. Moduler cette réponse pourrait donc avoir un intérêt beaucoup plus large en thérapie anti-tumorale.

XPC is an RNA polymerase II cofactor recruiting ATAC to promoters by interacting with E2F1.

The DNA damage sensor XPC is involved in nucleotide excision repair. Here we show that in the absence of damage, XPC co-localizes with RNA polymerase II (Pol II) and active post-translational histone modifications marks on a subset of class II promoters in human fibroblasts. XPC depletion triggers specific gene down-expression due to a drop in the deposition of histone H3K9 acetylation mark and pre-initiation complex formation. XPC interacts with the histone acetyltransferase KAT2A and specifically triggers the recruitment of the KAT2A-containing ATAC complex to the promoters of down-expressed genes. We show that a strong E2F1 signature characterizes the XPC/KAT2A-bound promoters and that XPC interacts with E2F1 and promotes its binding to its DNA element. Our data reveal that the DNA repair factor XPC is also an RNA polymerase II cofactor recruiting the ATAC coactivator complex to promoters by interacting with the DNA binding transcription factor E2F1.

[Revascularisation of unprotected left main coronary artery disease: an update]. / Revascularisation du tronc commun coronaire gauche non protégé.

Coronary bypass grafting is the reference treatment of unprotected left main coronary disease. Nevertheless, the experience of invasive cardiologists and the introduction of active stents make angioplasty possible in selected cases. Only the results of controlled clinical trials (SYNTAX trial currently under way) will enable physicians to choose the most appropriate method of revascularisation for their patients.

[Aortic bioprosthesis implanted percutaneously: three year follow up]. / Bioprothèse aortique implantée par voie percutanée: suivi à trois ans.

Percutaneous implantation of a bioprosthesis for the treatment of degenerative aortic stenosis ushered in a new era for interventional cardiology, and now represents the best therapeutic option for a growing number of patients for whom surgical aortic replacement would be too risky. This is the case in about a third of symptomatic patients affected. Between 2003 and 2005, we performed initial feasibility studies (I-REVIVE and RECAST) in Rouen, on non-operable patients in a critical state, included for purely compassionate reasons. The valve used was a pericardial bioprosthesis mounted in an expandable balloon stent. The mean age of the patients was 80 years, all had multiple co-morbidity and had been turned down by the cardiac surgeons. In 33 of the 36 included patients, the technique was attempted by the anterograde trans-septal approach (n=27, success rate 80%) or by the retrograde arterial route (n=7, success rate 57%). Echocardiography following implantation revealed a final aortic surface area of 1.70 cm2 and a transvalvular gradient of 9 mmHg. A significant paravalvular aortic leak was noted in 5 cases. There were 6 deaths by 1 month, related to the procedure, and 10 deaths by 6 months, from non-cardiac causes and not related to the procedure. There was no occurrence of coronary occlusion, secondary displacement or dysfunction of the prosthesis. In December 2006, 8 patients reached 2 years of follow up, and two others reached 3 years, symptom free and still with an unchanged valvular function. Significant technological improvements have made the technique simpler, quicker and safer, with very much improved short and long term results. The new trans-apical approach is under evaluation with some promising initial results. More than 280 patients have been implanted to date. Other implantable prostheses are under evaluation. This therapeutic modality looks likely to develop rapidly, and in the near future it should offer a new and optimal solution for all high surgical risk or non-operable patients.

[Balloon aortic valvuloplasty in the adult. Immediate results and in-hospital complications in the latest series of 141 consecutive patients at the University Hospital of Rouen (2002-2005)]. / Valvuloplastie aortique par ballonnet chez l'adulte. Résultats immédiats et complications intrahospitalières dans la dernière série de 141 patients consécutifs au CHU de Rouen (2002-2005).

UNLABELLED: With the aging population, elderly patients with degenerative, severely calcified, and symptomatic aortic stenosis are becoming a frequent problem in medical decision making, particularly because many are declined for surgical valve replacement. For these patients, balloon aortic dilatation could be a palliative treatment. PATIENTS AND METHODS: we analyzed retrospectively our techniques and complications during hospitalization for percutaneous aortic balloon dilatation in 141 consecutive patients (45% women, mean age 83 +/- 10 y) from January 2002 to April 2005. The Parsonnet's score was 41 +/- 8 and the Euroscore was 10 +/- 2. We excluded the patients enrolled for percutaneous aortic valve implantation. This technique was performed under local anesthesia, from retrograde or antegrade approach. Rapid pacing stimulation (220/bpm) with a pacing-lead placed in the right ventricle was performed during balloon inflation. RESULTS: the aortic valve area was increased from 0.59 +/- 0.19 to 1.02 +/- 0.34 cm2 (p < 0.001) and the transvalvular mean gradient decreased from 49.3 +/- 21.2 to 22.2 +/- 11.8 mmHg (p < 0.001). Six patients (4%) died (3 during aortic valve dilatation) and 9 patients (6%) had non fatal complications: 2 transitory strokes, 8 non surgical vascular complications and 5 episodes of atrio-ventricular complete block (these complication were non exclusive). The patients were discharged at 5, 6 +/- 3 days. CONCLUSION: In the hands of skilled operators, aortic percutaneous balloon dilatation has become a simple technique, associated with a low risk of complications despite a very ill patient population. This technique remains a good option for a number of patients before the onset of percutaneous aortic valve implantation.

[Intra-stent restenosis following implantation of a bare endoprosthesis]. / Resténose intra-stent après implantalion d'une endoprothèse nue.

The aim of this retrospective study was to evaluate the immediate and long-term results of various treatments for patients with a primary lesion of intra-stent restenosis (ISR). The study included 214 patients (233 endoprostheses, site of a primary ISR), with an average age of 61+/-11 years. These patients had received one of the following treatments: balloon angioplasty alone (101 patients), implantation of a second endoprosthesis (32 patients), medical treatment (65 patients), or revascularisation surgery with aorto-coronary bypass (16 patients). After retrospective analysis of the initial data, clinical follow-up was studied for all patients, and severe cardiac events were recorded. The immediate treatment of the ISR with angioplasty or bypass had an initial success rate of 100%. At the end of follow up (26+/-1.8 months) for the series as a whole, 9 patients (4.1%) had died, 7 (3.2%) had suffered a myocardial infarction, and 22 (10.3%) had had to undergo a secondary revascularisation procedure. 111 (52%) patients had angiographic follow up. A second ISR was noted in 43 cases (39%). The type of treatment provided was not a predictive factor for the occurrence of a severe cardiac event. In conclusion, whatever treatment of ISR is used, the immediate result is satisfactory. The rate of severe cardiac events is acceptable and in 10.3% of cases necessitates a secondary revascularisation procedure within 2 years. The very promising recent development of new active endoprostheses could alter the management of coronary patients in the years to come.

[Immediate results and clinical follow-up of patients treated with drug eluting stents implantation in routine clinical practice]. / Résultats immédiats et suivi clinique des patients traités par implantation de stents actifs en pratique courante.

Multiple recent randomized studies have demonstrated the superiority of drug eluting stents (DES) compared to bare stents for reduction of restenosis rates after angioplasty. We sought to study if the results obtained in these studies with highly selected patients could be translated to patients treated in routine clinical practice. To this end, we retrospectively reviewed hospital charts of 134 consecutive patients treated in our center with 202 DES implantation between November 2002 and January 2004. Thirty nine % of patients had diabetes and 59% had multivessel disease. Coronary lesions were often complex (type B2: 24%, type C: 35%). Mean percent diameter stenosis was 68 +/- 13% with a reference artery diameter of 2.62 +/- 0.5 mm. One patient (0.75%) died in-hospital from cardiogenic shock. At a mean follow-up of 12 +/- 2.6 months, 7 patients (5.3%) died, including 2 extracardiac deaths. Recurrent chest pain occurred in 16 patients (12%), with only 3 (2.3%) in-stent restenosis. Major adverse cardiac event rate was 8.2%. This study confirms that in a non-selected population, the rate of subsequent revascularization after DES implantation is very low. It can be hoped that the indications of implantations will progressively spread with a lowered cost of these DES.

Catheter ablation of typical atrial flutter: a randomized comparison of 2 methods for determining complete bidirectional isthmus block.

BACKGROUND: Complete bidirectional isthmus conduction block (CBIB) was initially assessed by sequential detailed activation mapping at both sides of the ablation line during proximal coronary sinus and anteroinferior right atrium pacing. Mapping only the ablation line ("on-site" atrial potential analysis) was recently reported as a means of CBIB identification. The study was designed to compare these 2 techniques prospectively regarding the diagnosis of CBIB. METHODS AND RESULTS: In 76 consecutive patients (mean age, 63.4+/-10.5 years), typical atrial flutter ablation was performed using either the activation mapping technique (group I) or on-site atrial potential analysis (group II). Criteria for CBIB using on-site atrial potential analysis was the recording of parallel, widely spaced double atrial potentials along the ablation line. The CBIB criterion was retrospectively searched using the alternative technique at the end of the procedure. In successful patients, the mean radiofrequency delivery duration was longer in group II (845+/-776 versus 534+/-363 s; P:=0.03). On-site, clear-cut, widely spaced double atrial potentials and activation mapping suggesting CBIB were concomitantly observed in only 47 patients (54%), and ambiguous/atypical double potentials were recorded in 31 patients (39%). CONCLUSIONS: Although feasible, the on-site atrial potential analysis seemed to be inferior to the classic activation mapping technique, mainly because of the ambiguity of electrogram interpretation along the ablation line. However, when combined with the activation mapping technique, it provided additional information regarding isthmus conduction properties in some cases. Therefore, optimally, both methods should be used concomitantly.

Tissue Doppler imaging differentiates transmural from nontransmural acute myocardial infarction after reperfusion therapy.

BACKGROUND: The evaluation of transmural extent of necrosis after acute myocardial infarction remains a major problem in clinical practice. We sought to determine whether color M-mode tissue Doppler imaging (TDI) could differentiate transmural from nontransmural myocardial infarction. METHODS AND RESULTS: Twenty-one anesthetized open-chest dogs underwent 90 or 120 minutes of left anterior descending coronary artery occlusion followed by 180 minutes of reperfusion. The transmural extension of infarct was measured by triphenyltetrazolium chloride (TTC) staining. Segment shortening in the endocardium and epicardium of the anterior and posterior walls was assessed by sonomicrometry. Regional myocardial blood flow was measured by radioactive microspheres. TDI was obtained from an epicardial short-axis view. We calculated systolic and diastolic velocities within the endocardium and epicardium of myocardial walls and the subsequent myocardial velocity gradient (MVG). TTC staining could identify 2 groups according to the transmural extent of necrosis: 15 dogs had a nontransmural (NT) necrosis (42+/-3% of wall thickness), and 6 dogs developed a transmural (T) infarct (81+/-4% of wall thickness). In both groups, ischemia resulted in a significant and similar reduction in endocardial and epicardial velocities, with a resulting low systolic MVG in the anterior wall (0.10+/-0.07 in NT and 0.10+/-0.08 s(-1) in T). At 60 minutes of reperfusion, systolic MVG failed to change significantly in the transmural group (-0.20+/-0.09 s(-1)). In contrast, it increased significantly after reflow in the NT group compared with ischemic values (-0.99+/-0.20 versus 0.10+/-0.07 s(-1), P:<0.05). CONCLUSIONS: TDI can differentiate transmural from nontransmural myocardial infarction early after reperfusion.

Assessment of nonuniformity of transmural myocardial velocities by color-coded tissue Doppler imaging: characterization of normal, ischemic, and stunned myocardium.

BACKGROUND: Transmural myocardial contractile performance is nonuniform across the different layers of the left ventricular wall. We evaluated the accuracy of color M-mode tissue Doppler imaging (TDI) to assess the transmural distribution of myocardial velocities and to quantify the severity of dysfunction induced by acute ischemia and reperfusion in the inner and outer myocardial layers. METHODS AND RESULTS: Thirteen open-chest dogs underwent 15 minutes of left anterior descending coronary artery occlusion followed by 120 minutes of reperfusion. M-mode TDI was obtained from an epicardial short-axis view. Systolic velocities were calculated within endocardium and epicardium of the anterior and posterior walls. Regional myocardial blood flow was assessed by radioactive microspheres. Segment shortening was measured by sonomicrometry in endocardium and epicardium of both the anterior and posterior walls. At baseline, endocardial velocities were higher than epicardial velocities, resulting in an inner/outer myocardial velocity gradient. Ischemia caused a significant and comparable reduction in endocardial and epicardial systolic velocities in the anterior wall with the disappearance of the velocity gradient. Systolic velocities significantly correlated with segment shortening in both endocardium and epicardium during ischemia and reperfusion. In the first minutes after reflow, endocardial velocities showed a greater improvement than epicardial velocities, and the velocity gradient resumed although to a limited extent, indicative of stunning. CONCLUSIONS: TDI is an accurate method to assess the nonuniformity of transmural velocities and may be a promising new tool for quantifying ischemia-induced regional myocardial dysfunction.

Stent placement compared with balloon angioplasty for small coronary arteries: in-hospital and 6-month clinical and angiographic results.

BACKGROUND: Stenting has been demonstrated to be superior to balloon angioplasty in de novo focal lesions located in large native vessels. However, in small vessels, the benefit of stenting remains questionable. METHODS AND RESULTS: A total of 381 symptomatic patients with de novo focal lesion located on a small coronary segment vessel (<3 mm) were randomly assigned to either stent implantation (192 patients; 197 lesions) or standard balloon angioplasty (189 patients; 198 lesions). The primary end point was the angiographic restenosis rate at 6 months, as determined by quantitative coronary angiography. On intention-to-treat analysis, angiographic success rate and major adverse cardiac events were comparable: 97.9% and 4.6% versus 93.9% and 5.8% in the stent group and the balloon group, respectively. After the procedure, a larger acute gain was achieved with stent placement (1.35+/-0.45 versus 0.94+/-0.47 mm, P=0.0001), resulting in a larger minimal lumen diameter (2.06+/-0.42 versus 1.70+/-0.46 mm, P=0.0001). At follow-up (obtained in 91% of patients), angiographic restenosis rate was 21% in the stent group versus 47% in the balloon group (P=0.0001), a risk reduction of 55%. Repeat target lesion revascularization was less frequent in the stent group (13% versus 25%, P=0.0006). CONCLUSIONS: Elective stent placement in small coronary arteries with focal de novo lesions is safe and associated with a marked reduction in restenosis rate and subsequent target lesion revascularization rate at 6 months.

Balloon angioplasty for the treatment of coronary in-stent restenosis: immediate results and 6-month angiographic recurrent restenosis rate.

OBJECTIVES: The purpose of this prospective study was to evaluate the immediate results and the 6-month angiographic recurrent restenosis rate after balloon angioplasty for in-stent restenosis. BACKGROUND: Despite excellent immediate and mid-term results, 20% to 30% of patients with coronary stent implantation will present an angiographic restenosis and may require additional treatment. The optimal treatment for in-stent restenosis is still unclear. METHODS: Quantitative coronary angiography (QCA) analyses were performed before and after stent implantation, before and after balloon angioplasty for in-stent restenosis and on a 6-month systematic coronary angiogram to assess the recurrent angiographic restenosis rate. RESULTS: Balloon angioplasty was performed in 52 patients presenting in-stent restenosis. In-stent restenosis was either diffuse (> or =10 mm) inside the stent (71%) or focal (29%). Mean stent length was 16+/-7 mm. Balloon diameter of 2.98+/-0.37 mm and maximal inflation pressure of 10+/-3 atm were used for balloon angioplasty. Angiographic success rate was 100% without any complication. Acute gain was lower after balloon angioplasty for in-stent restenosis than after stent implantation: 1.19+/-0.60 mm vs. 1.75+/-0.68 mm (p=0.0002). At 6-month follow-up, 60% of patients were asymptomatic and no patient died. Eighteen patients (35%) had repeat target vessel revascularization. Angiographic restenosis rate was 54%. Recurrent restenosis rate was higher when in-stent restenosis was diffuse: 63% vs. 31% when focal, p=0.046. CONCLUSIONS: Although balloon angioplasty for in-stent restenosis can be safely and successfully performed, it leads to less immediate stenosis improvement than at time of stent implantation and carries a high recurrent angiographic restenosis rate at 6 months, in particular in diffuse in-stent restenosis lesions.

Catheter ablation of atrioatrial conduction as a cure for atrial arrhythmia after orthotopic heart transplantation.

OBJECTIVES: We present three patients in whom atrial arrhythmia was treated by ablation of electrical conduction across a surgical suture line. BACKGROUND: Conduction across the suture line separating the donor and native right atria has recently been described after orthotopic heart transplantation. METHODS: Mapping and pacing of both grafted and recipient right atrium was performed to assess the relation between both atria and its relevance to clinical arrhythmia, prior to successful radiofrequency at the site of electrical communication. RESULTS: In cases 1 and 3, atrioatrial conduction was bidirectional. In both, two types of P waves were observed during sinus rhythm. In case 2, conduction from the recipient to the grafted atrium yielded a very particular surface ECG pattern of atrial extrasystole. The block being unidirectional, the recipient atrial sinus rhythm was not perturbed and behaved like an atrial parasystole. Ablation was performed during sinus rhythm in case 1, recipient right atrial pacing in case 2 and grafted right atrial pacing in case 3 at the site with the shortest conduction time to the other tissue. At the successful ablation site multiple component potentials were recorded. Respectively, 1, 4 and 2 radiofrequency pulses were followed by total atrioatrial conduction interruption. No tachycardia could be induced at the end of the procedure and late follow-up was event free. CONCLUSIONS: The existence of arrhythmogenic atrioatrial conduction should be taken into account when evaluating atrial arrhythmias in the transplanted heart because it is potentially curable by radiofrequency catheter ablation.

Percutaneous transluminal balloon valvuloplasty of adult aortic stenosis: report of 92 cases.

Percutaneous transluminal balloon valvuloplasty was attempted in 92 adult patients with severe calcific aortic stenosis. The mean age was 75 +/- 11 years (range 38 to 91) and 35 patients were more than 80 years old. Most of the patients were severely disabled; 66 were in New York Heart Association functional class III or IV, 27 had syncopal attacks and 21 had severe angina pectoris. Because of unacceptably high surgical risk or contraindication to thoracic surgery, 42 patients could not be considered for valve replacement. Other patients either were in a category of high operative risk or refused the surgical intervention. Valvuloplasty was performed by way of the femoral route (82 patients) or the brachial route (10 patients). Catheters of size 15, 18 and 20 mm were successively placed across the aortic valve and three inflations were usually done with each of them, lasting 80 seconds on average, until a decrease in peak to peak systolic pressure gradient to 40 mm Hg or less was attained, a result considered satisfactory. The inflated balloons were not totally occlusive in most cases and clinical tolerance of inflation was good. Valvuloplasty resulted in a reduction of mean systolic gradient from 75 +/- 26 to 30 +/- 13 mm Hg (p less than 0.001); the final gradient was less than 40 mm Hg in 78 patients. Mean calculated aortic valve area increased from 0.49 +/- 0.17 to 0.93 +/- 0.36 cm2 (p less than 0.001). Immediately after the procedure, ejection fraction increased from 48 +/- 16 to 51 +/- 16% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Angioscopic evaluation of rotational atherectomy followed by additional balloon angioplasty versus balloon angioplasty alone in coronary artery disease: a prospective, randomized study.

OBJECTIVES: This study sought to compare, by angioscopy, the morphologic changes induced by rotational atherectomy, followed by additional angioplasty, with those observed after balloon angioplasty alone. BACKGROUND: Rotational atherectomy and balloon angioplasty act by different mechanisms, which could explain the difference in morphologic changes induced by these two techniques. METHODS: The study group included 50 patients with 50 lesions who were randomly assigned to undergo rotational atherectomy (n = 24) or balloon angioplasty (n = 26). Rotational atherectomy with a single burr (approximately equal to 70% of coronary diameter) was systematically followed by additional balloon angioplasty. Angioscopy was performed immediately after the procedure. Abnormal angioscopic findings were 1) flaps, graded from 1 to 3 (1 = intimal flap; 2 = flap protruding into < 50% of the lumen; 3 = flap protruding into > or = 50% of the lumen); 2) thrombi, graded from 1 to 3 (1 = flat deposits; 2 = protruding but nonocclusive thrombus; 3 = occlusive thrombus); 3) subintimal hemorrhage; 4) longitudinal dissection. The two groups were comparable for clinical and angiographic baseline data. RESULTS: On angioscopy, flaps were observed less frequently after rotational atherectomy followed by additional balloon angioplasty (8 [33%] of 24 lesions) than after balloon angioplasty alone (14 [54%] of 26 lesions, p = 0.08) and were also less severe (grade 1 in 6 lesions, grade 2 in 2 and grade 3 in none vs. grade 1 in 4 lesions, grade 2 in 5 and grade 3 in 5). Longitudinal dissections were also significantly less frequent: one versus six (p = 0.05). There was no difference in the incidence of angioscopic thrombi (p = 0.16) or subintimal hemorrhage (p = 0.15), but the power to detect a significant difference was low for these variables (37% and 26%, respectively). CONCLUSIONS: Rotational atherectomy followed by additional balloon angioplasty leads to fewer angioscopic dissections and a trend toward fewer intimal flaps than balloon angioplasty alone. However, our angioscopic differences did not lead to an outcome difference between the two groups.

Dobutamine stress echocardiography in orthotopic heart transplant recipients. VACOMED Research Group.

OBJECTIVES: This study sought to determine whether dobutamine stress echocardiography could accurately identify coronary artery disease after heart transplantation. BACKGROUND: After heart transplantation, coronary artery disease is related to either diffuse concentric intimal thickening or focal stenosis and may be underdiagnosed by coronary angiography. METHODS: We enrolled 41 patients, a mean (+/- SD) of 40 +/- 20 months after heart transplantation, at the time of their routine control coronary angiogram. Three patients were excluded because of poor echogenicity on the angiogram and one because of ventricular premature beats. Standard echocardiographic views were acquired at baseline and at incremental dobutamine infusion levels (from 5 to a maximal dose of 40 micrograms/kg body weight per min at 3-min intervals). Regional wall motion score was calculated from a 16-segment model, and each segment was graded from 1 (normal) to 4 (dyskinesia). Coronary angiography was performed 24 h after dobutamine stress echocardiography, and angiograms were analyzed in blinded manner. RESULTS: Twenty-three (62%) of 37 patients had normal coronary angiographic findings. Dobutamine stress echocardiography showed abnormalities in only 2 of 23 patients. Fourteen patients (38%) had abnormal angiographic findings, seven of whom had stenoses > 50%. Dobutamine stress echocardiography correctly identified the corresponding hypoperfused segments in these seven patients. More of interest were the other seven patients, of whom three had angiographic nonsignificant stenoses (< 50%), and four had minor diffuse coronary irregularities. Dobutamine stress echocardiography showed hypokinesia in five of these seven patients despite nonsignificant lesions at coronary angiography. The respective overall sensitivity and specificity of dobutamine stress echocardiography were 86% and 91%. At follow-up, 2 of the 37 patients had an acute myocardial infarction. Both had abnormal findings on dobutamine stress echocardiography: One had normal coronary angiographic results, and one had significant coronary lesions. CONCLUSIONS: Dobutamine stress echocardiography is a useful technique for the diagnosis of coronary artery disease after heart transplantation. These preliminary results indicate that dobutamine stress echocardiography may have a predictive value for further ischemic events in heart transplant recipients.

Improved myocardial ischemic response and enhanced collateral circulation with long repetitive coronary occlusion during angioplasty: a prospective study.

OBJECTIVES: The goal of the study was to evaluate the progressive increase in ischemic threshold with multiple sequential transient coronary occlusions and to assess the role of the collateral circulation in adaptation to ischemia. BACKGROUND: It has been observed that the duration of balloon inflations during coronary angioplasty can be gradually prolonged during subsequent dilations with a reduction in patient symptoms and diminished ischemic electrocardiographic (ECG) changes. Although the mechanism has not been fully explained, recruitment of coronary collateral circulation induced by repeated coronary occlusion has been reported. The stimuli for recruitment and the natural history of coronary collateral circulation are not understood. METHODS: Seventeen patients with isolated stenosis of the left anterior descending coronary artery and a normal left ventricle were enrolled. Angioplasty consisted of five successive prolonged inflations. Sequential changes in clinical, intracoronary ECG and left ventricular indexes of myocardial ischemia were examined. Coronary collateral channels were evaluated during balloon inflations by ipsilateral and contralateral injections of contrast medium and hemodynamically by occlusion pressure. RESULTS: An improved tolerance to myocardial ischemia with repetitive coronary occlusions was demonstrated by a significant reduction of angina, ST segment deviation, left ventricular filling pressure and less impairment of ejection fraction. Left ventricular wall motion abnormalities remained unchanged. Collateral angiographic grade did not change in 7 patients and increased in 10. CONCLUSIONS: This study confirms a progressive adaptation of myocardial ischemia to repetitive coronary occlusions and supports the concept that sequential episodes of myocardial ischemia are a stimulating factor for the recruitment of collateral channels in humans. These results also suggest that enhancement of recruitable collateral circulation might be an underlying mechanism of myocardial ischemic preconditioning.