Alessandro Santo Bortone

Endovascular Treatment of Thoracic Aortic Disease Four Years of Experience

Background—The aim of this retrospective study is to investigate efficacy and middle-term results of the stent graft treatment for diseases of descending thoracic aorta. Methods and Results—From March 1999 to October 2003, 132 patients (113 male and 19 female, mean age 62±14 years) were enrolled. They were divided into 4 groups: aneurysms (43, group A), post-traumatic lesions (24, group B), and complicated type B dissections (43, group C). Twenty-two further patients, with chronic type B dissection and not suitable for endovascular or surgical or hybrid techniques because of multiple entry tears without difference between the true and false lumen and poor clinical conditions, were obliged to receive medical management only (group D). All patients underwent computed tomography (CT) scan and angiography as preoperative assessment. An optimal deployment with exclusion of the aneurysm and/or closure of the entry tear in dissection was achieved in 96.4% (106/110) of the patients that were discharged in good conditions within 6 days. No spinal cord injuries were observed. The follow-up (average 20.82±10.01 months, range 1 to 55 months), performed with serial chest CT scans, was 100% complete. No stent graft-related complications were detected, although only in 1 case, an asymptomatic rupture of the Excluder connecting bar was found with a perforation of the fabric and an intra-aortic exposition of the bar itself. In 2 patients with chronic dissection an asymptomatic type II endoleak was detected. A total of 4 hospital deaths resulted in an overall operative mortality of 3.9%. Seven patients (6.3%) died during the follow-up 5 of them for other diseases (4.5%). However, a 40.9% mortality was observed within the obliged medical treatment group. Conclusions—Endovascular treatment of thoracic aortic diseases, even in the acute phase, may represent a valid option with a low mortality rate. Moreover, the efficacy is proved in the middle-term whereas the long-term follow-up is still pending.

Endovascular stent-graft treatment for diseases of the descending thoracic aorta

OBJECTIVE Assessment of endovascular stent-graft treatment for diseases of the descending thoracic aorta as a valid and effective alternative to surgery. METHODS From March 1999 to August 2000, a total of 16 patients underwent deployment of endovascular stent-grafts in the descending thoracic aorta. Patients were divided into three groups according to the type of lesion. Group A (n=8) included five patients with atherosclerotic aneurysm and three with chronic post-traumatic pseudoaneurysm. Patients with acute post-traumatic pseudoaneurysm (n=3) and type B aortic dissection (n=5) were included in Groups B and C, respectively. All patients underwent 5-mm chest spiral angio-computerized tomography (CT) scan and angiography as preoperative assessment. The deployed stent-graft systems were Talent-Medtronic and Excluder-Gore. RESULTS A total of 20 stent-grafts were placed. Two patients required deployment of two grafts, while three grafts were juxtaposed in a third patient in order to treat larger lesions. There was no mortality related to the procedure, although one patient (6.2%) died because of multiorgan failure 24h post-operatively. The placement of the graft was successful in all cases except one affected with type B dissection and characterized by a very large intimal flap, which was eventually fenestrated by graft guidewire. Therefore, an optimal sealing of the grafts was achieved in 15 patients. However, in one patient the descending aorta had to be surgically replaced because of the calcified pseudoaneurysm still compressing the trachea and left bronchus. Two patients required a left carotid-subclavian by-pass in order to achieve a sufficient neck for the proximal placement of the graft. No spinal cord injuries were observed. At the follow-up, performed with chest spiral angio-CT scan within 72 h and scheduled at 6 and 12 months and once a year, no stent-graft related complications have been detected. CONCLUSIONS Endoluminal stent-graft treatment may represent a valid option in well-selected cases of descending thoracic aorta diseases. A longer follow-up in a larger series of patients is desirable to confirm these initial positive results.

Impact of coronary artery disease in elderly patients undergoing transcatheter aortic valve implantation: insight from the Italian CoreValve Registry.

BACKGROUND Coronary artery disease (CAD) commonly coexists with degenerative aortic stenosis. The impact of CAD in patients undergoing transcatheter aortic valve implantation (TAVI) raises concerns due to the lack of comprehensive and consistent data on this topic. We sought to evaluate the impact of CAD on clinical outcomes in patients undergoing TAVI. METHODS Consecutive patients(N=663) who underwent TAVI with the 18-French CoreValve ReValving System (CRS) (Medtronic Inc, MN USA) from June 2007 through December 2009 at 14 institutions across Italy were included in this prospective web-based registry. Four patients were excluded from the analysis due to failure to successfully release the prosthesis inside the native aortic valve. Previous percutaneous or surgical myocardial revascularizations were used to identify the existence of concomitant CAD (N=251; 38%). The primary endpoint was the incidence of Major Adverse Cerebrovascular and Cardiac Events (MACCE) and all-cause death in CAD and no-CAD groups. RESULTS Patients with CAD were no more likely to develop MACCE within 12-months of the procedure than those who did not (CAD group vs no-CAD group, 15.7% vs 18.3%; adjusted hazard ratio [HR] 0.76; 95% confidence interval [CI] 0.42 to 1.36; p=0.353). The 12-month mortality was 14.5% and 15.9% in CAD group and no-CAD group, respectively (adjusted HR 0.74; 95% CI 0.40 to 1.36; p=0.331). CONCLUSIONS Coexisting CAD does not impact procedural outcomes and mid-term incidence of MACCE and survival in elderly patients undergoing TAVI with CRS prosthesis.

Functional and structural abnormalities in patients with dilated cardiomyopathy

Passive diastolic properties of the left ventricle were determined in 10 control subjects and 12 patients with dilated cardiomyopathy. Simultaneous left ventricular angiography and high fidelity pressure measurements were performed in all patients. Left ventricular chamber stiffness was calculated from left ventricular pressure-volume and myocardial stiffness from left ventricular stress-strain relations with use of a viscoelastic model. Patients with dilated cardiomyopathy were classified into two groups according to the diastolic constant of myocardial stiffness (beta). Group 1 consisted of seven patients with a normal constant of myocardial stiffness less than or equal to 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a beta greater than 9.6. Structural abnormalities (percent interstitial fibrosis, fibrous content) in patients with dilated cardiomyopathy were assessed by morphometry from right ventricular endomyocardial biopsies. Heart rate was similar in the three groups. Left ventricular end-diastolic pressure was significantly greater in patients with cardiomyopathy (18 mm Hg in group 1 and 22 mm Hg in group 2) than in the control patients (10 mm Hg). Left ventricular ejection fraction was significantly lower in groups 1 (37%) and 2 (36%) than in the control patients (66%). Left ventricular muscle mass index was significantly increased in both groups with cardiomyopathy. The constant of chamber stiffness (beta*) was slightly although not significantly greater in groups 1 and 2 (0.58 and 0.58, respectively) than in the control group (0.35). The constant of myocardial stiffness beta was normal in group 1 (7.0; control group 6.9, p = NS) but was significantly increased in group 2 (23.5). Interstitial fibrosis was 19% in group 1 and 43% (p less than 0.001) in group 2 (normal less than or equal to 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (beta) and interstitial fibrosis (IF) (r = 0.95; p less than 0.001) and beta and fibrous content divided by end-diastolic volume index (r = 0.93; p less than 0.001). It is concluded that myocardial stiffness can be normal in patients with dilated cardiomyopathy despite severely depressed systolic function. Structural alterations of the myocardium with increased amounts of fibrous tissues are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. The constant of myocardial stiffness (beta) helps to identify patients with severe structural alterations (group 2), representing possibly a more advanced stage of the disease.

Hemostasis Alterations in Patients With Acute Aortic Dissection

BACKGROUND Surgery for acute aortic dissection (AAD) is frequently complicated by excessive postoperative bleeding and blood product transfusion. Blood flow through the nonendothelialized false lumen is a potential trigger for the activation of the hemostatic system; however, the physiopathology of the aortic dissection induced coagulopathy has never been precisely studied. The aim of the present study is the evaluation of the coagulation and fibrinolytic systems and platelet activation in patients undergoing surgery for AAD. METHODS Eighteen patients undergoing emergent surgery for Stanford type A AAD were enrolled in the study. The activation of the coagulation and fibrinolytic systems and platelet activation were evaluated at 6 different time points before, during, and after the operation, measuring prothrombin fragment 1.2 (F1.2), plasmin-antiplasmin complex, and platelet factor 4, respectively. RESULTS All measured biomarkers were increased before, during, and after the operations indicating a systemic activation of coagulation, fibrinolysis, and platelets. These changes were pronounced even preoperatively (T0), and soon after the beginning of cardiopulmonary bypass (T1) when the influence of hypothermia and prolonged cardiopulmonary bypass time were not yet involved. Time from symptom onset to intervention inversely correlated with preoperative F1.2 (r=-0.75; p=0.002) and plasmin-antiplasmin levels (r=-0.57; p=0.034). CONCLUSIONS Blood flow through the false lumen is a powerful activator of the hemostatic system even before the operation. This remarkable activation may influence postoperative outcome of AAD patients.

Inflammatory response and angiogenesis after percutaneous transmyocardial laser revascularization.

BACKGROUND The aim of our study was to investigate the inflammatory response immediately after percutaneous transmyocardial laser revascularization (PTMR) along with the underlying mechanism of angiogenesis. METHODS Patients with angina pectoris underwent coronary angiography and were divided into two groups. Group A (n = 10) included patients with obstructed vessels who received PTMR, whereas group B (n = 5) comprised patients who had normal coronary arteries. Blood levels of neutrophils, procalcitonin, troponin-I, myoglobin, and creatine kinase (CK) mass were evaluated in each patient before angiography and monitored up to 48 hours after the procedure. Six patients were injected with 99mTc-leukoscan approximately 60 to 90 minutes after PTMR. During the 240 to 300 minutes after the radionuclide administration, single photon emission tomography (SPET) was performed and compared with conventional 99mTc-sestamibi-SPET. RESULTS A significant increase in blood levels of neutrophils and procalcitonin was observed in group A only (p < 0.005). A slight but significant increase of troponin-I was evident in the same group (p < 0.05), and a distinct myocardial uptake of 99mTc-Leukoscan-SPET was observed in each patient along homologous regions treated by PTMR. CONCLUSIONS The increased amount of neutrophils (both circulating and inside the treated myocardial areas) along with the raised levels of procalcitonin were the immediate reactions to PTMR. This systemic and intramyocardial inflammatory response is the underlying mechanism that gives rise to angiogenesis.

Implantable Cardioverter-Defibrillators for Primary Prevention in Patients With Ischemic or Nonischemic Cardiomyopathy: A Systematic Review and Meta-analysis

Sudden death accounts for approximately half the deaths in patients with left ventricular systolic dysfunction. Life-threatening ventricular arrhythmias are the cause of most sudden deaths. Randomized clinical trials have shown that the implantable cardioverter-defibrillator (ICD) is the most effective current therapy to prevent sudden death by terminating ventricular arrhythmias. Moreover, ICD versus no ICD placement has been shown to improve survival among patients with heart failure and reduced ejection fraction (HeFrEF), with or without nonsustained ventricular tachycardia or symptoms (1). As a result, contemporary European and American guidelines assign a class I recommendation for prophylactic ICD therapy in patients with HeFrEF (24). The benefits of ICD therapy are most pronounced in the secondary prevention of life-threatening arrhythmias among high-risk patients with ischemic heart disease and ventricular dysfunction, although implantation is not recommended soon after acute myocardial infarction or in patients with an expected survival of less than 1 year (5). For primary prevention, the main indications for an ICD are related to the prevention of fatal outcomes in patients at increased risk for life-threatening ventricular tachycardia or ventricular fibrillation. In this setting, controversy recently was sparked by the findings of a clinical study questioning the benefits of ICDs and emphasizing the medical improvements in heart failure management (6). In light of this uncertainty, we aimed to systematically address, through a meta-analysis of randomized trials, the effect of ICD therapy versus conventional care for primary prevention of death of various causes in patients with ischemic or nonischemic cardiomyopathy. Methods The present meta-analysis was performed according to established methods recommended by the Cochrane guidelines and in compliance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analyses) statement (7, 8). The protocol, although not registered, was developed on 20 September 2016, with final amendments on 31 March 2017. Originally, we aimed to assess both primary and secondary prevention settings; the current article, however, focuses only on primary prevention. Data Sources and Searches MEDLINE, Cochrane Central Register of Controlled Trials, Google Scholar, and EMBASE databases, as well as the Web sites www.tctmd.com, www.europcr.com, www.clinicaltrials.gov, www.clinicaltrialresults.org, and www.acc.org, were searched, without language restriction, from 1 April 1976 to 31 March 2017. Key words were nonischemic cardiomyopathy, ischemic cardiomyopathy, implantable cardioverter-defibrillator, implantable defibrillator, randomized controlled trials, clinical trials, mortality, death, sudden death, survival, and prevention. (For search strategies, see Supplement Table 1.) Search sources also included previous systematic reviews and abstracts as well as presentations from major cardiovascular medicine meetings. Supplement. Supplement Tables, Figures, and References to Excluded Studies Two authors (M. Koodziejczak and M. Kowalewski) independently assessed titles and abstracts identified by searches, as well as citations mentioned in any relevant systematic reviews or meta-analyses identified in the searches. Citations determined to be potentially eligible by either reviewer were selected for full-text review; both reviewers then independently assessed the full text for eligibility. Study Selection Inclusion criteria were any randomized controlled trial in humans comparing ICD therapy with conventional care (defined as control, contemporary medical therapy, antiarrhythmic medical therapy, or placebo in addition to medical care) and reporting mortality outcomes in the primary prevention setting. No restrictions based on language, follow-up, or study size were applied. Nonrandomized and single-group studies were excluded, as were studies that had a randomized design but compared ICDs with other devices or electrophysiologic procedures. Data Extraction and Quality Assessment Data were abstracted on prespecified forms by 2 independent investigators not involved in any of the retrieved studies. Hazard ratios (HRs) with 95% CIs were abstracted for all available mortality outcomes. When only other summary statistics were available, HRs were calculated according to the method of Parmar and colleagues (7). In SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial), patients with ischemic or nonischemic disease were randomly assigned to receive an ICD, amiodarone, or placebo in a 1:1:1 fashion; trial data on all-cause mortality were presented (and extracted) by disease mechanism. Two investigators not involved in any trial (M. Koodziejczak and E.P.N.) independently assessed the risk of bias for each study according to the Cochrane Collaboration guidelines (treatment sequence generation; concealment of treatment allocation; blinding of participants, personnel, and outcome assessors; adequate assessment of incomplete outcome data; selective outcome reporting; other potential sources of bias) (7). Disagreements regarding extraction or risk-of-bias assessments were resolved by discussion with a third investigator (F.A.). Data Synthesis and Analyses We stratified our synthesis and analyses on the basis of the underlying cause of cardiomyopathy, nonischemic or ischemic, and pooled data for mortality outcomes. For the 3-group SCD-HeFT, we considered amiodarone and placebo as conventional care in the main analyses; we also performed a separate all-cause mortality analysis comparing ICD therapy with amiodarone (antiarrhythmic medical therapy). We used time-to-event outcomes reported for the randomly assigned groups (intention-to-treat principle). We used HRs to summarize time-to-event outcomes, because they account for time as well as the number of events (7). Heterogeneity was assessed by using the Cochran Q test (9). Statistical heterogeneity was summarized by the I 2 statistic, which quantifies the percentage of variation in study results caused by heterogeneity rather than chance (9). Pooled HRs were calculated by using the KnappHartung small-sample estimator method (10). Potential publication bias was examined by constructing a funnel plot in which the SE of the log HR was plotted against the HR of the selected outcomes. Prespecified sensitivity analyses were performed for all-cause mortality in subgroups based on age (<65 years and 65 years), sex, ventricular function (ejection fraction <25% and 25%), heart failure (New York Heart Association [NYHA] class I to II and class III to IV), diabetes mellitus, time after myocardial infarction (<18 months and 18 months), and baseline QRS length (<120 ms and 120 ms). Because event rates for subgroup analyses were provided in only 1 study (DANISH [Danish Study to Assess the Efficacy of ICDs in Patients with Non-ischemic Systolic Heart Failure on Mortality]), exact summary event rates were not calculated; individual study-subgroup data were summarized by using HRs and their respective 95% CIs whenever applicable, by using the random-effects model. Further sensitivity analyses including and excluding studies with early ICD placement after myocardial infarction or coronary bypass surgery were conducted. R, version 3.2.3 (R Foundation), and Comprehensive Meta-analysis software, version 2 (Biostat), were used for statistical computations and graphics. Role of the Funding Source This review received no funding or other support (such as supply of data). No external organizations or patients were involved in defining questions, developing the protocol, carrying out the review, interpreting the data, or deciding to submit the review for publication. Results Study Selection and Patient Population The PRISMA flow chart showing the publication screening process, the search strategies, and a list of excluded studies with reasons for exclusion are provided in Supplement Figure 1 and Supplement Tables 1 and 2. Of 2340 potentially relevant articles, 639 were excluded on the basis of title content and 1656 were excluded after abstract or full-text review. Of the remaining 45 trials, 11 studies, involving 8716 patients, met eligibility criteria (6, 1120). Four trials enrolled 1781 patients with nonischemic cardiomyopathy (6, 1113), 6 trials enrolled 4414 patients with ischemic cardiomyopathy (1520), and 1 trial included 2521 patients with both types of cardiomyopathy (14). Characteristics of the trials and participants are detailed in the Appendix Table and Supplement Table 3. Most of the included studies compared ICD therapy with conventional care; however, 1 study compared ICD therapy specifically with amiodarone (13), and 1 had a 3-group design comparing ICDs, amiodarone, and placebo (14). Mean follow-up was 3.2 years (range, 1.7 to 5.6 years). The earliest trial was published in 1996, but most of the studies were done in the first decade of the 21st century; only 1 study was published in 2016. All trials were funded, at least in part, by industry. Appendix Table. Characteristics of Included Trials: Design, Follow-up, and Timing of Intervention After Diagnosis or Surgery Mean ventricular ejection fraction of trial participants was 26.20%. Most patients had moderately symptomatic heart failure (NYHA class II or III). Only 2 studies included patients with class IV heart failure, who made up 1.0% and 4.6% of the total patient population, respectively (6, 17). Almost half the study population had a history of hypertension, and one third had diabetes mellitus. The lowest burden of comorbid conditions was in DANISH (31.2% and 18.9% had hypertension and diabetes, respectively). Patients included in the studies received several pharmacotherapies: 67.35% received -blockers, 80.12% angiotensin-converting enzyme inhibitors, 62.65% digoxin, and 68.40% diuretics (Supplement Table 4). Pharmacotherapy, however, varied across trials, with -blockers administered

Improved equipment for abdominal fetal electrocardiogram recording: description and clinical evaluation

Reliable computer-based equipment for transabdominal or indirect recording of fetal electrocardiogram (FECG) is described. The proposed equipment allows a real-time displaying of the signals (fetal + maternal ECG) without averaging procedures and it does not require the employment of a shielded room; moreover, it is user-friendly to medical personnel. An elementary form of semi-automatic computation of the fetal heart rate (FHR) was also implemented. The equipment simultaneously acquires three signals from seven electrodes, six placed on the maternal abdomen following the three space axes, and one placed on the left leg as a indifferent electrode. The signals are magnified and analogically filtered before undergoing digital finite impulse response (FIR) filter. Then the signals are displayed on the screen of a personal computer (PC). The PC also provides the possibility of storing the acquired signals for further analysis of elaborations. The quality of the recordings allows the analysis of both the rapid and slow electrical phenomena of the fetal heart, and it is not significantly influenced by the occurrence at the same time of uterine contractions. The performance of this method was assessed in 140 pregnant women with gestation periods of 29-42 weeks. In 131 cases (93.6%) the fetal QRS complex was detected and the FHR was obtained. A reliable evaluation of P and QRS waves and of ST interval, in spite of the interference of the maternal complexes, was possible in 102 cases (72.8%).

A “strange cough”: 3D-echocardiography for diagnosis of late tricuspid valve endocarditis in a former drug addict with septic pulmonary emboli

Tricuspid valve endocarditis (TVE) is not an uncommon finding in intravenous drug addicts [1]. TVE with pulmonary septic embolization, however, is a less common finding [2]. Even more rare is the diagnosis of TVE mainly led by pulmonary signs. We report the case of a 40-year-old man, a former intravenous drug addict, referred to our institution for recurrent episodes of cough and fever mimicking episodes of pneumonitis since a couple of months. The patient was affected by chronic hepatitis C, without history of heart disease. At previous hospitalization, chest radiograph showed 2 parenchyma nodules within left lung (basal and apical). A pneumonitis was therefore hypothesized and the patient was administrated with levofloxacin and ceftriaxone for 2 weeks, without any symptom relief. At present hospitalization, chest X-ray confirmed the presence of a single nodule in the basal segment of the left lung. Physical examination, however, was unremarkable. Rest ECG showed sinus rhythm at 78 bpm without significant ST anomalies (Fig. 1). Systolic blood pressure was 120/80 mm Hg. Troponin was 0.03 ng/ml and N-terminal pro-brain natriuretic peptide 20.6 pg/ml, while C-reactive

A Striking Coronary Artery Pattern in a Grown-Up Congenital Heart Disease Patient

Left ventricular noncompaction (LVNC) is a myocardial disorder probably due to the arrest of normal embryogenesis of the left ventricle. It could be isolated or associated with other extracardiac and cardiac abnormalities, including coronary artery anomalies. Despite the continuous improvement of imaging resolution quality, this cardiomyopathy still remains frequently misdiagnosed, especially if associated with other heart diseases. We report a case of LVNC association with both malposition of the great arteries and a very original coronary artery pattern.