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Biomedical subjects

Raffaele Calabrò

Publications and source records attributed to Raffaele Calabrò.

At least 19 recordsLinked to original sources
PubMed2006

Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study.

AIMS: The prevalence of obesity is increasing among children in the developed world. The association of obesity and abnormal cardiac function is still debated. The reported changes may reflect the role of comorbidities that contribute to ventricular dysfunction. Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on myocardial function, excluding the influence of possible comorbidities. We sought to define the preclinical effects of obesity on the cardiovascular system, of healthy children with excess weight who have no other clinically appreciable cause of heart disease, using the more sensitive ultrasonic-derived strain and strain rate (SR) imaging. METHODS AND RESULTS: We studied 300 subjects divided into two groups: (i) obese children (Group O: n=150; age, 12+/-3 years); (ii) healthy lean children comparable for age, sex, and pubertal stage (Referents: n=150; mean age, 12+/-3 years). Systolic (SBP) and diastolic blood pressure (DBP), as well as 24 h-SBP and 24 h-DBP were comparable between groups. Left ventricular (LV) mass/height(2.7) was increased (P<0.0001) in Group O (46+/-12 g/m(2.7)) when compared with Referents (31+/-14 gm(2.7)). Standard echocardiographic indices of global systolic function were similar in the two groups. Intima-media thickness measured at the common carotid artery was not significantly different (P=0.4) in obese children (0.46+/-0.09 mm) when compared with Referents (0.45+/-0.07 mm). Obese children showed regional longitudinal peak systolic myocardial deformation properties (SR=-1.4+/-0.7 s(-1)) lower (P<0.0001) than those of Referents (SR=-2.2+/-0.5) in both left and right ventricle. In multivariable analysis, average peak systolic SR was significantly correlated with homeostasis model assessment of insulin resistance (P<0.01; coefficient, 0.02; SE, 0.011), and insulin serum concentration (P<0.01; coefficient, 0.05; SE, 0.023). Average LV peak systolic strain was significantly correlated with body mass index (P=0.0001; coefficient, 0.06; SE, 0.016), LVM/H(2.7) (P=0.006; coefficient, 0.016; SE, 0.018). CONCLUSIONS: Our study demonstrated that obesity, in absence of hypertension, is associated with significant reduction in systolic myocardial deformation properties already in childhood involving both right and left ventricle. Obesity not only is a risk factor for later cardiovascular disease, but also is associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties.

Blood Pressure↗
PubMed2006

Influence of biventricular pacing on myocardial dispersion of repolarization in dilated cardiomyopathy patients.

AIMS: The aim of our study was to evaluate the effect of cardiac resyncronization therapy on QT dispersion (QTd), JT dispersion (JTd), and transmural dispersion of repolarization (TDR), markers of heterogeneity of ventricular repolarization in a study population with severe heart failure. METHODS AND RESULTS: Fifty patients (43 male, 7 female, age 60.2+/-3.1 years) suffering from congestive heart failure (n=39 NYHA class III; n=11 NYHA class IV) as a result of coronary artery disease (n=19) or of dilated cardiomyopathy (n=31), with sinus rhythm (SR), QRS duration >120 ms (mean QRS duration=156+/-21 ms), an ejection fraction <35%, left ventricular end-diastolic diameter >55 mm, presence of atrioventricular asynchrony, intra- and inter-ventricular asynchrony, underwent permanent biventricular pacemaker implantation. A 12-lead standard electrocardiogram was performed at baseline, during right-, left-, and biventricular pacing (BiVP) and QTd, JTd, and TDR were assessed. BiVP significantly reduced QTd (73.93+/-19.4 ms during BiVP vs. 91+/-6.7 ms in SR, P=0.004), JTd (73.18+/-17.16 ms during BiVP vs. 100.72+/-39.04 at baseline, P=0.003), TDR (93.16+/-15.60 vs. 101.55+/-19.08 at baseline, P<0.004), compared with SR. Right ventricular endocardial pacing and left ventricular epicardial pacing both increased QTd (RVendoP 94+/-51 ms, P<0.03; LVepiP 116+/-71 ms, P<0.02), and TDR (RVendoP 108.13+/-19.94 ms, P<0.002; LVepiP 114.71+/-26.1, P<0.05). There was no effect on JTd during right and left ventricular stimulation. CONCLUSIONS: BiVP causes a statistically significant reduction of ventricular heterogeneity of repolarization and has an electrophysiological anti-arrhythmic influence on the arrhythmogenic substrate of dilated cardiomyopathy.

Analysis of Variance↗
PubMed2006

Complete atrioventricular canal.

Complete atrioventricular canal (CAVC), also referred to as complete atrioventricular septal defect, is characterised by an ostium primum atrial septal defect, a common atrioventricular valve and a variable deficiency of the ventricular septum inflow. CAVC is an uncommon congenital heart disease, accounting for about 3% of cardiac malformations. Atrioventricular canal occurs in two out of every 10,000 live births. Both sexes are equally affected and a striking association with Down syndrome was found. Depending on the morphology of the superior leaflet of the common atrioventricular valve, 3 types of CAVC have been delineated (type A, B and C, according to Rastelli's classification). CAVC results in a significant interatrial and interventricular systemic-to-pulmonary shunt, thus inducing right ventricular pressure and volume overload and pulmonary hypertension. It becomes symptomatic in infancy due to congestive heart failure and failure to thrive. Diagnosis of CAVC might be suspected from electrocardiographic and chest X-ray findings. Echocardiography confirms it and gives anatomical details. Over time, pulmonary hypertension becomes irreversible, thus precluding the surgical therapy. This is the reason why cardiac catheterisation is not mandatory in infants (less than 6 months) but is indicated in older patients if irreversible pulmonary hypertension is suspected. Medical treatment (digitalis, diuretics, vasodilators) plays a role only as a bridge toward surgery, usually performed between the 3rd and 6th month of life.

Diagnosis, Differential↗
PubMed2006

LEOPARD syndrome: clinical diagnosis in the first year of life.

LEOPARD syndrome (LS) is an autosomal dominant syndrome characterized by multiple lentigines and café-au-lait spots, electrocardiographic-conduction abnormalities, ocular hypertelorism/obstructive cardiomyopathy, pulmonary stenosis, abnormalities of the genitalia in males, retardation of growth, and deafness. LS shares many features with Noonan syndrome (NS), in which lentigines and deafness are usually not present. Molecular studies have shown that LS and NS are allelic disorders, caused by different missense mutations in PTPN11, a gene encoding the protein tyrosine phosphatase SHP-2 located at chromosome 12q22-qter. The clinical diagnosis of LS is generally difficult in the first months of life because the distinctive lentigines are generally not present at birth and develop during childhood. From January 2002 to December 2004, we suspected LS clinically in 10 patients admitted to our genetic counseling services in the first 12 months of life. A PTPN11 gene mutation was detected in 8/10 (80%) patients. In one patient without a PTPN11 mutation a subsequent clinical diagnosis of neurofibromatosis type 1 (NF1) was made, following the evaluation of the mother, who had previously undiagnosed classic NF1. The age of LS patients with PTPN11 mutation ranged between 1 and 11 months (mean age +/- SD 7.5 +/- 3.96 months). Review of the clinical characteristics of patients with LS confirmed by molecular study during the first year of life demonstrates that the diagnosis of LS in the first months of age can be clinically suspected in patients presenting with three main features, that is, characteristic facial features (100%), hypertrophic cardiomyopathy (HCM) (87%), and cafe-au-lait spots (75%). Characteristic facial features can be mild or severe, and consist of hypertelorism, downslanting palpebral fissures, ptosis, and dysmorphic ears. The clinical suspicion of LS may be confirmed by molecular screening for PTPN11 mutations. An early diagnosis of the disease is useful for the prospective care of associated medical problems and for precise genetic counseling.

DNA Mutational Analysis↗
PubMed2006

"Steal" collaterals: an echocardiographic diagnostic marker for anomalous origin of the left main coronary artery from the pulmonary artery in the adult.

Anomalous origin of the left main coronary artery from the pulmonary artery, also known as Bland-White-Garland syndrome, is a rare malformation. Few patients survive past childhood without surgical repair, and up to 90% die suddenly at a mean age of 35 years. We describe a case of a 60-year-old patient with anomalous origin of the left main coronary artery from the pulmonary artery in which 2-dimensional and color flow Doppler visualization of the intercoronary (so-called "steal") collaterals was the first marker that alerted the examiner to the possibility of this diagnosis, subsequently guided step-by-step the echocardiographic approach.

Collateral Circulation↗
PubMed2006

A rare complication of atrial septal occluders: diagnosis by transthoracic echocardiography.

Atrial septal defect transcatheter occlusion techniques have become a reliable alternative to surgical procedures. Possible complications can derive from unfavorable anatomy of the defect and over-dimensioning of the device. We describe the first case ever reported of anterior mitral leaflet perforation caused by an atrial septal occluder. The diagnosis was performed by conventional echocardiography and 3 dimensions helped for a more accurate anatomic definition. Device removal, atrial septal defect closure, and repair of the mitral tear were then successfully performed.

Adult↗
PubMed2006

Myocardial systolic activation delay in patients with left bundle branch block and either normal or impaired left ventricular function.

AIM OF THE STUDY: to evaluate determinants of myocardial activation delay of both left (LV) and right (RV) ventricle in patients with left bundle branch block (LBBB) and either normal or impaired LV ejection fraction (EF). METHODS: From an initial cohort of patients with LBBB, 42 patients with dilated cardiomyopathy (group A) and 33 with normal global LV systolic function (group B), all comparable in age and sex, underwent standard Doppler echo, pulsed Doppler myocardial imaging (DMI), and coronary angiography. Using DMI, the following regional parameters were evaluated in five different basal myocardial segments (LV anterior, inferior, septal, lateral walls-RV lateral wall): systolic (Sm), early- and late-diastolic (Em and Am) peak velocities. As index of myocardial systolic activation was calculated: precontraction time (PCTm) (from the beginning of Q-wave of ECG to the onset of Sm). Intraventricular systolic dyssynchrony was analyzed by difference of PCTm in different LV myocardial segments. Interventricular activation delay was calculated by the difference of PCTm between the most delayed LV segment and RV lateral wall. RESULTS: Patients of group A showed increased heart rate (HR), QRS duration and LV end-diastolic diameter, and reduced LV EF. By DMI, patients of group A showed reduced myocardial peak velocities and a significant intraventricular delay in activation of LV lateral wall, with increased regional PCTm (P < 0.001). In addition, patients with dilated cardiomyopathy showed a more pronounced interventricular dyssynchrony, even after adjustment for HR and QRS duration. By receiver operating characteristic (ROC) curve analysis, a cut-off value of 55 msec of interventricular delay showed 86% sensitivity and 92% specificity in identifying patients with impaired EF. In the overall population, by use of stepwise forward multivariate linear regression analyses, LV end-diastolic diameter (beta coefficient = 0.52; P < 0.001) and LV EF (beta coefficient =-0.58; P < 0.0001) were the only independent determinants of interventricular activation delay. CONCLUSIONS: Pulsed DMI is an effective noninvasive technique for assessing the severity of regional delay in activation of LV walls in patients with LBBB. The impairment of interventricular systolic sychronicity is strongly related to LV dilatation and to the degree of global systolic dysfunction. Therefore, patients with dilated cardiomyopathy suitable for cardiac resynchronization therapy may be better selected.

Bundle-Branch Block↗
PubMed2006

The usefulness of Doppler myocardial imaging in the study of the athlete's heart and in the differential diagnosis between physiological and pathological ventricular hypertrophy.

Athlete's heart is a cardiac adaptation to long-term, intensive training, which includes changes as increased ventricular cavity diameters, wall thickness and mass, produced with a degree consistent with sports activities and exercise programs. The Doppler myocardial imaging (DMI) permits characterization of the velocities of each ventricular myocardial segment by placing the sample volume at the center of the cardiac muscle. Even if the standard two-dimensional (2D) echocardiography represents an irreplaceable method in the evaluation of cardiac adaptations to physical exercise, the data currently available suggests the usefulness of DMI in the assessment of the myocardial systolic and diastolic functions of the athlete's heart. In particular, an athlete's left ventricular hypertrophy is characterized by a "supernormal" DMI pattern, with increased myocardial early-diastolic velocity. Therefore, DMI analysis in the trained subject has demonstrated interesting prospective for: (1) the differential diagnosis from pathological, both, left and right ventricular hypertrophy; (2) the prediction of cardiac performance during physical effort; (3) the evaluation of the biventricular interaction; (4) the analysis of the myocardial adaptations to various training protocols; and (5) the early identification of specific genotypes associated with cardiomyopathies. On this ground, a combined use of standard 2D echo and DMI may be taken into account for a valid noninvasive and easy-repeatable evaluation of both physiological and pathological ventricular hypertrophies.

Adaptation, Physiological↗
PubMed2006

Transcatheter closure of complex atrial septal defects: feasibility and mid-term results.

OBJECTIVE: Transcatheter closure of atrial septal defects (ASDs) is currently a reliable alternative to surgery, even though challenging in the case of complex septal anatomy. The aim of this study was to evaluate the feasibility and mid-term results of percutaneous closure of complex ASDs in a tertiary referral centre compared with simple ASD closure. METHODS: Between April 2000 and November 2004, 209 patients were submitted to transcatheter ASD closure; 83 patients (39.7%) presented with a complex defect (large ASDs with a deficient rim or a multifenestrated/aneurysmal septum) and were treated using different devices tailored to the atrial septal anatomy. RESULTS: The transcatheter procedure was successful in 72 patients (86.8%), using a single device in 69 patients and two devices in the remaining three patients. Overall, 71 Amplatzer septal occluders, two multifenestrated Amplatzer septal occluders and two Cardioseal/Starflex devices were used. Procedural and fluoroscopy times were 141 +/- 45 min and 28 +/- 22 min, respectively (P < 0.0001 vs. simple ASD closure for both comparisons). Procedure-related complications were recorded in nine patients (12.5%) (P < 0.01 vs. simple ASD closure). One patient required surgical repair of a femoral arteriovenous fistula and another developed mitral valve dysfunction. Immediate ASD occlusion was recorded in 59.7% of patients, reaching 95.9% at the last follow-up control (P = NS vs. simple ASD closure for both comparisons). CONCLUSIONS: Percutaneous closure of complex ASDs may be considered technically feasible, relatively safe and highly effective, although the procedure is still significantly more demanding than transcatheter closure of simple ASDs.

Adolescent↗
PubMed2006

The athlete's heart and hypertrophic cardiomyopathy: two conditions which may be misdiagnosed and coexistent. Which parameters should be analysed to distinguish one disease from the other?

According to the statements from the International Cardiological Committees on Eligibility for Sports, athletes with a clinical diagnosis of hypertrophic cardiomyopathy (HCM) should be excluded from most competitive sports, with the possible exception of those of low intensity. Clinical distinctions between physiological athlete's heart and pathological conditions such as HCM have critical implications especially for trained athletes. Even if the standard two-dimensional echocardiography represents an irreplaceable method in the evaluation of cardiac adaptations to physical exercise, the data currently available suggest the usefulness of Doppler myocardial imaging (DMI) in the assessment of the myocardial systolic and diastolic function of the athlete's heart. On this ground, the combined use of standard two-dimensional echocardiography and DMI may be taken into account for a valid, non-invasive and easily repeatable evaluation of both physiological and pathological ventricular hypertrophy, and in selecting a subgroup of HCM patients at higher risk of cardiac events. In particular, DMI analysis in the trained individual has demonstrated an interesting opportunity for: (1) the differential diagnosis from pathological left ventricular hypertrophy due to HCM; (2) the prediction of cardiac performance during physical effort; (3) the evaluation of bi-ventricular interaction; (4) the analysis of myocardial adaptations to various training protocols; and (5) the early identification of specific genotypes associated with cardiomyopathies.

Cardiomyopathy, Hypertrophic↗
PubMed2006

Late cure after radiofrequency catheter ablation in a pediatric patient.

A 12-year-old female with the Wolff-Parkinson-White syndrome underwent an electrophysiologic study followed by radiofrequency catheter ablation of the left-lateral accessory pathway. After several unsuccessful attempts, the procedure was stopped because of early recurrence of accessory pathway conduction. Twenty-four hours after the procedure, the patient was found without ventricular pre-excitation pattern on the electrocardiogram. During a 12-month follow-up, the Wolff-Parkinson-White pattern was no longer present. A transesophageal electrophysiologic study showed no further tachycardia induction and the patient is still asymptomatic. This report raises the issue that ablation-induced lesions may evolve considerably during the first few days after ablation, leading to either recurrent accessory pathway conduction or long-lasting complete cure.

Catheter Ablation↗
PubMed2006

Potential clinical perspectives of Doppler myocardial imaging and strain rate imaging during stress echocardiography.

Stress echocardiography has become a common non-invasive test in patients with chest pain and known or suspected coronary artery disease, but, as with exercise electrocardiography, it shows several major limitations. Analysis of gray-scale images based on subjective visual interpretation of wall motion and thickening has considerable variability even among experts. Doppler myocardial imaging and strain rate imaging echocardiography provides additional information in comparison with conventional echocardiography. These techniques provide quantification of regional wall motion at rest and during stress. Quantification of both systolic and diastolic myocardial function by either Doppler myocardial imaging or strain rate imaging mapping during dobutamine stress test has been shown to be a feasible, accurate, non-invasive tool that should be considered to be a sensitive alternative to the present echocardiographic and scintigraphic imaging techniques for stress tests. Time consuming off-line analysis of color images is required in the present state of technology. However, these non-invasive techniques are rapidly evolving and expanding. Further refinements in signal processing and quantitative analysis are likely in the near future.

Blood Flow Velocity↗
PubMed2006

[New antithrombotic drugs in cardiovascular disease].

During the past decades, a great bulk of studies have been undertaken to investigate the pathophysiologic mechanisms responsible for thrombus formation. As a consequence, different therapeutic strategies interfering at different levels of the coagulation process have been developed. Many of these compounds did not achieve full development, but others are presently available for the clinician. The present review paper will focus on these new therapeutic strategies developed in the last 10 years.

Azetidines↗