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Biomedical subjects

Giuseppe Limongelli

Publications and source records attributed to Giuseppe Limongelli.

At least 19 recordsLinked to original sources
PubMed2006

Myocardial infarction in a young athlete with non-obstructive hypertrophic cardiomyopathy and normal coronary arteries.

We describe an acute myocardial infarction in a young athlete with non-obstructive hypertrophic cardiomyopathy (HCM) and normal coronary arteries. A 18 year old athlete came to our attention for dispnoea and chest pain during effort. Echocardiography showed non-obstructive HCM, with restrictive physiology. Cardiac catheterization and coronary angiography showed elevated pulmonary artery pressure and normal coronary arteries. He was discharged on sotalol and diuretics. Nine months later, he was resuscitated from a cardiac arrest during mild effort. The ECG revealed a high rate of atrial fibrillation with significant ST-T changes, and echocardiography an akinesia of interventricular septum. Cardiac enzymes were elevated. The coronary angiogram showed normal coronary arteries. This case is important as a reminder that acute myocardial infarction is not only due to coronary artery disease, and that atrial fibrillation may represent a trigger of serious cardiovascular events in patients with HCM.

Adolescent↗
PubMed2006

Fatal hypertrophic cardiomyopathy and nemaline myopathy associated with ACTA1 K336E mutation.

We report on a 2-year-old male child with both nemaline myopathy and hypertrophic cardiomyopathy (HCM). Sequencing of the ACTA1 gene showed a "de novo" missense heterozygous mutation a>g in exon 7 (Lys336Glu). Two-dimensional electrophoresis showed 28% mutant actin present in his muscle biopsy. Actin was isolated from the muscle biopsy and examined by in vitro motility assay. The sliding speed was 13+/-3% less than normal and the affinity of actin for the Z-line protein alpha-actinin was reduced 10 fold. This is the first report on a hypertrophic cardiomyopathy associated with nemaline myopathy and an ACTA1 mutation.

Actinin↗
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

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

Mutation screening of the PTPN11 gene in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a common inherited cardiac disease and a major cause of sudden death. It is an autosomal dominant disorder predominantly caused by mutations in genes encoding for sarcomeric proteins. Only 50-60% of HCM probands have mutations in known genes suggesting the presence of additional disease genes. Noonan and LEOPARD syndromes are characterised by multiple dysmorphia and cardiac defects with HCM present in approximately 20% of cases. Both syndromes are caused by mutations in the PTPN11 gene which codes for the protein tyrosine phosphatase SHP-2. It is suspected but unproven that the cardiac phenotype may predominate or even be present in isolation. In order to determine possible involvement of this gene in the pathogenesis of HCM, we performed mutation screening of the PTPN11 coding region in 250 selected HCM probands (200 patients without mutations in sarcomeric genes and 50 with identified mutations). No mutations in PTPN11 were identified. Our data suggests that mutations in the PTPN11 gene are not a cause of HCM in the absence of Noonan/LEOPARD syndromes.

Adult↗
PubMed2006

Is sudden cardiac death predictable in LEOPARD syndrome?

We report the sudden cardiac death of a young male presenting with classic clinical features of LEOPARD syndrome, shown to be due to a mutation in the PTPN11 gene, and severe non obstructive hypertrophic cardiomyopathy. We also discuss briefly the usefulness of prophylactic risk stratification in patients with syndromic and non syndromic hypertrophic cardiomyopathy.

Adult↗
PubMed2006

Noninvasive risk stratification prevents sudden death due to paroxysmal atrial fibrillation in hypertrophic cardiomyopathy.

Sudden death is a tragic complication of hypertrophic cardiomyopathy. We report the case of a young patient with hypertrophic cardiomyopathy in whom an episode of atrial fibrillation triggered ventricular fibrillation and cardiac arrest. A 21-year-old man with nonobstructive hypertrophic cardiomyopathy underwent cardioverter-defibrillator implantation for primary prevention of sudden death, after risk stratification with noninvasive strategies. After 6 weeks, during a moderate effort, the patient had a syncopal episode, preceded by palpitations and dizziness, and terminated by the cardioverter-defibrillator. Device interrogation revealed an episode of atrial fibrillation with high ventricular response, spontaneously followed by ventricular tachycardia/fibrillation. Atrial fibrillation is a potential trigger of life-threatening arrhythmias and sudden death in patients with hypertrophic cardiomyopathy. Clinical investigation of risk markers for sudden death should be encouraged to identify high-risk patients who may benefit from a prophylactic therapy with an implantable cardioverter-defibrillator.

Adult↗
PubMed2005

Left ventricular hypertrophy in Caucasian master athletes: Differences with hypertension and hypertrophic cardiomyopathy.

AIM: To study, by conventional echocardiography, left ventricular remodelling and function in master athletes, hypertension and hypertrophic cardiomyopathy. METHODS: We studied 30 master athletes (MA; soccer players; mean age 43.9+/-5.9), 24 subjects with essential hypertension (HYP; 46.6+/-6), 20 patients with hypertrophic cardiomyopathy (HCM; 42.2+/-9) and 30 normal individuals (CG; 43.4+/-5). An integrated M-mode/two-dimensional echocardiographic analysis was performed to determine chambers dimensions, relative wall thickness (RWT) and left ventricular mass (LVM), indexed to height in meters raised to the power of 2.7 (LVM/h(2.7)). Cut-off levels for LVM/h(2.7) and RWT were defined to assess 4 different patterns of LV geometric remodelling. In addition, we measured indexes of global systolic performance and indexes of global diastolic function. RESULTS: LV wall thickness and LV end-diastolic dimensions were higher in MA than controls, but significantly lower than other groups. LVH/h(2.7) was increased in 79% of HYP and in 95% of HCM, but was within the normal limits in MA. LV geometry was normal in 22 out of 30 MA (73%), while the remaining (8 athletes, 27%) showed a concentric remodelling. Systolic function (FS and EF) was normal in MA, but was slightly reduced in HYP and increased in HCM. Analysis of diastolic function showed an abnormal relaxation pattern in all HYP and 95% of HCM, but was normal in all MA. The ratio between peak filling rate and stroke volume (PFR/SV), a relatively independent index of diastolic function, was significantly greater in hypertensive patients with normal LV remodelling compared to those without it (4+/-0.39 vs. 4.91+/-0.19; P = 0.0002). CONCLUSION: MA showed lower values of wall thickness, LV dimensions and LV mass compared with HYP and HCM. Despite an abnormal remodelling, all the athletes showed a normal systolic and diastolic function. The differential diagnosis between MA, HYP and HCM is feasible by accurate, comprehensive standard Doppler echocardiography.

Adult↗
PubMed2005

Early myocardial abnormalities in asymptomatic patients with severe isolated congenital aortic regurgitation: an ultrasound tissue characterization and strain rate study.

BACKGROUND: Aortic valve regurgitation (AR) in the pediatric population has increased in recent years because of the expanded use of new surgical and hemodynamic procedures. Unlike adult patients, few predictors for the need of operation have been proposed in young asymptomatic or mildly symptomatic patients with AR. METHODS: To unmask early abnormalities of left ventricular (LV) function, 59 participants were enrolled: 14 asymptomatic patients (mean age 18 years) with congenital isolated severe AR and normal LV function (LV ejection fraction > 50%); and 45 healthy control subjects with comparable age and body surface area. All the studied population underwent standard echocardiographic examination, integrated backscatter, and strain rate imaging study. RESULTS: Conventional echocardiographic indices of global LV systolic performance for patients with AR were similar to that of control subjects. Compared with control subjects, integrated backscatter analysis demonstrated a significant reduction in cyclic variation in both septal and posterior walls ( P < .05). LV radial and longitudinal deformation properties for patients with AR were significantly reduced ( P < .05) as assessed by peak systolic strain rate. CONCLUSION: Our results demonstrated the ability of integrated backscatter and strain rate imaging to detect early subclinical abnormalities in young patients with severe congenital AR despite the presence of a normal ejection fraction.

Adolescent↗
PubMed2005

Impact of pulmonary regurgitation and age at surgical repair on textural and functional right ventricular myocardial properties in patients with tetralogy of Fallot.

BACKGROUND: The aim of this study was to identify non-invasively the potential impact of pulmonary regurgitation and age at surgical repair on the right ventricular (RV) textural and functional myocardial properties in patients operated on for tetralogy of Fallot (TOF). METHODS: We assessed the average intensity (Int.(1B)) and the cyclic variation (CV(IB)) of the echocardiographic backscatter curve in 30 TOF patients (mean age 16.2 +/- 8.3 years), who had undergone corrective surgery (mean age at repair 3.2 +/- 2.6 years, range 0.2-11 years). They were divided into three age- and body surface area (BSA)-matched subgroups according to the results of the surgical repair: 12 patients had no significant postsurgical sequelae (group I), 12 patients had isolated moderate-severe pulmonary regurgitation (group II), and 6 patients had pulmonary regurgitation associated with significant (> 30 mmHg) RV outflow tract obstruction (group III). In addition, 30 age-, sex- and BSA-matched normal subjects were identified as the control group. RESULTS: In our study population, CV(IB) was lower (7.86 +/- 2.5 vs 10.6 +/- 1.4 dB, p < 0.001) and Int.IB higher (-18.6 +/- 4.1 vs -21 +/- 2.8 dB, p = 0.01) compared to the control group. Comparison between the control group and each subgroup of TOF patients showed: a) comparable values of CV(IB) and Int.(IB) in group I (10.6 +/- 1.4 vs 9.4 +/- 2.3 dB, p = 0.07; and -21 +/- 2.8 vs -21.4 +/- 2.3 dB, p = 0.7, respectively); b) Int.(IB) was significantly different only in group III (-21 +/- 2.8 vs -13.3 +/- 4.6 dB, p < 0.0001), c) CV(IB) was different either in group II or III (10.6 +/- 1.4 vs 7.42 +/- 2, p < 0.001; and 10.6 +/- 1.4 vs 5.56 +/- 1.8, p < 0.001, respectively). In addition, comparison of integrated backscatter indexes among the TOF subgroups revealed significant differences of CV(IB) between group I and II (9.4 +/- 2.4 vs 7.4 +/- 2, p = 0.03) and between group I and III (9.4 +/- 2.4 vs 5.56 +/- 1.8, p = 0.004), and of Int.(IB) between group I and III (-21.4 +/- 2.3 vs -13.3 +/- 4.66, p < 0.001) and between group II and III (-21.4 +/- 2.3 vs -18.6 +/- 2.8, p = 0.006). Group III patients, who had the most significant RV dilation, expressed as the ratio between RV and left ventricular end-diastolic diameter (0.55 +/- 0.8) compared to group II (0.67 +/- 0.11, p = 0.038) and group I (0.55 +/- 0.87, p < 0.001), showed the lowest values of CV(IB) (5.56 +/- 1.8 dB) and the highest values of Int.(IB) (-13.3 +/- 4.6 dB) Finally, in our study population, both the degree of RV dilation and the age at surgical repair significantly correlated with Int.(IB) (r = 0.49 and r = 0.4, p = 0.06 and p = 0.033, respectively) and inversely correlated with CV(IB) (r = -0.55 and r = -0.53, p = 0.002 and p = 0.003, respectively). CONCLUSIONS: In patients operated on for TOF: a) integrated backscatter analysis may identify patients with significant RV myocardial abnormalities related to postsurgical sequelae; b) residual pulmonary regurgitation, particularly if associated with pulmonary stenosis, appears to affect RV myocardial properties; c) an earlier repair of TOF may result in better preservation of myocardial characteristics.

Adolescent↗
PubMed2004

Progressive left ventricular remodeling in patients with hypertrophic cardiomyopathy and severe left ventricular hypertrophy.

OBJECTIVES: The aim of this study was to determine the natural history of patients with hypertrophic cardiomyopathy (HCM) and severe left ventricular hypertrophy (LVH) (i.e., maximal left ventricular wall thickness [MLVWT] >/=30 mm) and whether changes in cardiac morphology influence the course of the disease. BACKGROUND: Severe LVH is common in young and rare among elderly patients with HCM. This has been explained by a high incidence of sudden death. We hypothesized that this age-related difference might be explained by left ventricular wall thinning. METHODS: A total of 106 (age 33 +/- 15 years; 71 males) consecutive patients with severe LVH underwent history taking, examination, electrocardiography, echocardiography, cardiopulmonary exercise testing, and Holter analysis. Survival data were collected at subsequent clinic visits or by communication with patients and their general practioners. In order to assess morphologic and functional changes, 71 (67.0%) patients (mean age 31 +/- 15 years; 47 males) followed at our institution underwent serial (>/=1 year) assessment. RESULTS: Of the 106 patients, the majority (78 [71.6%]) were <40 years of age. During follow-up (92 +/- 50 months [range 1 to 169]), 18 (17.0%) patients died or underwent heart transplantation (13 sudden cardiac deaths, 2 heart failure deaths, 1 heart transplantation, 1 stroke, 1 postoperative death). Five-year survival from sudden death was 90.1% (95% confidence interval [CI] 84.0% to 96.3%), and that from heart failure death or transplantation was 97.7% (95% CI 94.5 to 100). In patients serially evaluated over 85 +/- 51 months, there was an overall reduction in MLVWT of 0.6 mm/year (95% CI 0.31 to 0.81, p = 0.00004). Wall thinning >/=5 mm was observed in 41 patients (57.7%; age 35 +/- 13 years; 28 males). On multivariate analysis, the follow-up duration only predicted wall thinning (0.6 mm/year, 95% CI 0.38 to 0.85, p < 0.00001). CONCLUSIONS: Left ventricular remodeling is common in patients with severe LVH and contributes to the low prevalence of severe LVH seen in middle age and beyond.

Adult↗
PubMed2004

Backscatter evaluation of myocardial functional and textural findings in children with right ventricular pressure and/or volume overload.

Integrated backscatter (IBS) analysis represents a recent echocardiographic technique for evaluating the textural and functional state of the right ventricular (RV) myocardium. We undertook our study to (1) define the potential impact of age or morphometric parameters (height, weight, and body surface area) on RV IBS indexes, and (2) compare RV IBS data among normal subjects and children with different conditions of RV overload. We studied 34 patients (mean age 14.6 +/- 4.7 years) divided into 3 groups: 14 patients with RV volume overload related to moderate to large atrial septal defect (group I); (2) 10 patients with RV pressure overload due to transposition of the great arteries after the Mustard procedure (group II); and (3) 10 patients with RV volume and pressure overload due to pulmonary regurgitation and stenosis after corrective surgery for tetralogy of Fallot (group III). In addition, 20 children with structurally normal hearts were enrolled as the control group. The 4 groups were comparable with regard to age and morphometric parameters. IBS parameters were assessed as the magnitude of cyclic variation, determined as the difference between peak and nadir IBS values and the averaged myocardial IBS intensity. In the control group and group I, IBS parameters did not change significantly with age, height, weight, and body surface area. In contrast, in groups II and III, a significant correlation was found between cyclic variation and age at the study (p = 0.021, r = -0.71, and p = 0.006, r = -0.79, respectively). Furthermore, compared with the control group, cyclic variation and IBS intensity were significantly different only in groups II (p = 0.01 and p = 0.006, respectively) and III (both p <0.0001) but not in group I (p = 0.23 and p = 0.38, respectively). The lowest values of cyclic variation and the highest values of intensity were detected in group III patients. Thus, our data suggest that (1) in normal subjects, there is no correlation between RV IBS indexes and age or any morphometric parameters, and (2) IBS analysis is able to noninvasively detect differences in myocardial functional and textural properties in the presence of different conditions of RV overload.

Adolescent↗
PubMed2004

Familial aggregation of genetically heterogeneous hypertrophic cardiomyopathy: a boy with LEOPARD syndrome due to PTPN11 mutation and his nonsyndromic father lacking PTPN11 mutations.

BACKGROUND: Nonsyndromic hypertrophic cardiomyopathy (HCM) is a primary cardiac disease transmitted as an autosomal dominant trait. Multiple chromosomal loci have been found to be involved in the etiology of this defect. LEOPARD syndrome is a genetic condition characteristically associated with HCM. Additional features of the syndrome include multiple lentigines, facial anomalies, sensorineural deafness, and growth retardation. Mutations in PTPN11, a gene encoding the protein tyrosine phosphatase SHP-2 located at chromosome 12q24, have been identified in patients with LEOPARD syndrome. CASES: We report here on a patient with HCM presenting with classic clinical features of LEOPARD syndrome, whose father also has HCM, but lacks phenotypic anomalies of the syndrome. Molecular analysis searching for PTPN11 mutations was performed in this family. A missense mutation (836A-->G; Tyr279Cys) in exon 7 of PTPN11 gene was identified in the patient with LEOPARD syndrome, whereas no mutation in PTPN11 gene was detected in the father or in additional family members. CONCLUSIONS: Aggregation of syndromic and nonsyndromic HCM in the same family is an unusual pattern of recurrence. Although genetic heterogeneity of LEOPARD and nonsyndromic HCM is not disputed, the existence of peculiar interactions linking genes causing nonsyndromic HCM and HCM in LEOPARD syndrome can be hypothesized. Different genes can work together, and a more severe cardiac phenotype can be due to additive effects. The involvement of familial susceptibility to specific cardiac malformations based on the presence of common predisposing factors can also be considered. Further molecular studies may shed light on these observations.

Adult↗
PubMed2003

Right ventricular myocardial adaptation to different training protocols in top-level athletes.

OBJECTIVE: The aim of this study was to analyze right ventricular (RV) myocardial function in competitive athletes with left ventricular (LV) hypertrophy induced by either endurance or strength training. METHODS: Standard Doppler echo, maximal electrocardiogram (ECG) ergometric test, and pulsed tissue Doppler (TD) of LV mitral annulus and of RV tricuspid annulus were performed in 32 competitive endurance athletes (long-distance swimmers; ATE) and in 26 strength-trained athletes (short-distance swimmers; ATS), all males. By use of TD, the following parameters of myocardial function were assessed: systolic peak velocities (Sm), precontraction time, contraction time, early (Em) and late (Am) diastolic velocities, Em/Am ratio, and relaxation time. RESULTS: The two groups were comparable for age, but ATS at rest exhibited higher heart rate, systolic blood pressure, and body surface area. LV mass index did not significantly differ between the two groups. However, ATS characterized increased wall thickness and relative wall thickness, whereas LV stroke volume and both LV and RV end-diastolic diameters were greater in ATE. All transmitral and transtricuspid Doppler indexes were higher in ATE, with increased E/A ratios. TD analysis demonstrated in ATE higher Em and Em/Am ratio as well as longer relaxation time both at mitral and at tricuspid annulus level. In the overall population, distinct multiple linear regression models evidenced independent positive association between RV peak Em velocity and LV end-diastolic diameter (P < 0.001) as well as independent direct correlation of the same RV peak Em velocity with both LV stroke volume and maximal workload achieved by bicycle ergometer (both P < 0.001). CONCLUSIONS: Right ventricular early diastolic myocardial function is positively influenced by preload increase in athletes, and represents an independent determinant of cardiac performance during physical effort. Therefore, pulsed TD may be taken into account to distinguish different cardiac adaptation to either endurance or strength sport activities, and eventually to quantify RV adaptation degree to long-term training.

Adaptation, Physiological↗