Which video technology brings the higher cognitive burden and motion sickness in laparoscopic colorectal surgery: 3D, 2D-4 K or 3D-4 K? a propensity score study.

BACKGROUND: Technological development has offered laparoscopic colorectal surgeons new video systems to improve depth perception and perform difficult task in limited space. The aim of this study was to assess the cognitive burden and motion sickness for surgeons during 3D, 2D-4 K or 3D-4 K laparoscopic colorectal procedures and to report post-operative data with the different video systems employed. METHODS: Patients were assigned to either 3D, 2D-4 K or 3D-4 K video and two questionnaires (Simulator Sickness Questionnaire-SSQ- and NASA Task Load Index -TLX) were used during elective laparoscopic colorectal resections (October 2020-August 2022) from two operating surgeons. Short-term results of the operations performed with the three different video systems were also analyzed. RESULTS: A total of 113 consecutive patients were included: 41 (36%) in the 3D Group (A), 46 (41%) in the 3D-4 K Group and 26 (23%) in the 2D-4 K Group (C). Weighted and adjusted regression models showed no significant difference in cognitive load amongst the surgeons in the three groups of video systems when using the NASA-TLX. An increased risk for slight/moderate general discomfort and eyestrain in the 3D-4 K group compared with 2D-4 K group (OR = 3.5; p = 0.0057 and OR = 2.8; p = 0.0096, respectively) was observed. Further, slight/moderate difficulty focusing was lower in both 3D and 3D-4 K groups compared with 2D-4 K group (OR = 0.4; p = 0.0124 and OR = 0.5; p = 0.0341, respectively), and higher in the 3D-4 K group compared with 3D group (OR = 2.6; p = 0.0124). Patient population characteristics, operative time, post-operative staging, complication rate and length of stay were similar in the three groups of patients. CONCLUSIONS: 3D and 3D-4 K systems, when compared with 2D-4 K video technology, have a higher risk for slight/moderate general discomfort and eyestrain, but show lower difficulty focusing. Short post-operative outcomes do not differ, whichever imaging system is used.

[Appropriateness in Cardiology: a statement of the ANMCO Veneto Region]. / L'appropriatezza prescrittiva in Cardiologia: documento dell'ANMCO Regione Veneto.

Inappropriate tests are responsible for longer waiting lists, higher economical costs for the National Health System and major clinical risks due to radiation exposure from prescription abuse of diagnostic testing. Clinical inappropriateness frequently derives from poor knowledge of guidelines, "defensive medicine" approach and/or repeat requests of patients and family members. About one third of non-invasive imaging tests are considered inappropriate.In order to define the most appropriate instruments for the follow-up of the most common cardiovascular diseases with the highest risk of inappropriateness, all the cardiologists of the Veneto Region (Italy), along with the local chapters of the main national cardiology societies and general practitioners have been involved by the Regional Section of the Italian Association of Hospital Cardiologists (ANMCO) in several scientific meetings on the following topics: hypertension, chronic ischemic heart disease, valvular heart disease, heart failure, and atrial fibrillation. This has led to the present document where: (i) the most appropriate clinical and diagnostic strategies are taken into account, and (ii) the most robust scientific evidence is provided for the regulatory commission of the Veneto Region Health Service to identify inappropriateness, prescription unsuitability, and economical sustainability.

Comparison of clinical features of arrhythmogenic right ventricular cardiomyopathy in men versus women.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heart muscle disease characterized by myocardial necrosis followed by fibrous-fatty replacement. The pathologic process constitutes the basis for ventricular arrhythmias due to re-entrant circuits. Even if this genetic disease is transmitted in the majority of cases with autosomal dominant trait, in all reported series ARVC is prevalent in men. In this study we investigate the impact that gender may have on clinical presentation in a large series of patients with ARVC. A total of 171 consecutive patients (mean 29 +/- 12 years, range 13 to 65) affected by ARVC were examined with family and personal history, 12-lead electrocardiogram (ECG), 24-hour ECG, signal-averaged ECG, and echocardiogram. Moreover, electrophysiological study and ventricular angiography were performed in selected cases. In the 171 subjects, 71% were men and 29% women (p = 0.02). No gender differences were found considering the age at the time of diagnosis and of study enrolment and the prevalence of index cases and family members. The genders differed in prevalence of abnormal ECG (69% vs 52%, p = 0.036) and presence of late potentials (60% vs 40%, p = 0.01). Moreover, men had larger right ventricular dimensions and practiced competitive sports more frequently (26% vs 14%, p <0.001). Nonetheless, gender was not associated with a high incidence of life-threatening ventricular arrhythmias or with a poor outcome. In conclusion, our data show that diagnosis of ARVC is less common in female patients, who present a higher prevalence of mild forms. Nonetheless, the degree of electrical instability does not differ significantly between genders in affected subjects. Even if ARVC remains mainly a male disease, gender does not have a role in patients' outcome. The cause of the under-representation of women is not clear, even if potentially important factors such as sexual hormones and physical activity could play a role.

[Screening for asymptomatic left ventricular systolic dysfunction in high-risk patients. Preliminary experience with a program based on the use of ECG and natriuretic peptide]. / Lo screening della disfunzione sistolica ventricolare sinistra asintomatica nei pazienti ad alto rischio cardiovascolare. esperienza pilota di un programma basato sull'utilizzo dell'ECG e dei peptidi natriuretici.

BACKGROUND: Patients with asymptomatic left ventricular systolic dysfunction (ALVSD) have an increased risk of heart failure (HF) and a worse life expectancy. Since valuable therapies may prevent such dismal evolution, screening programs for ALVSD have recently been advocated to detect as early as possible such ominous condition. Echocardiography represents the gold standard for the assessment of ALVSD but its indiscriminate use in screening programs is impractical. Clinical multivariate risk assessment associated with ECG and serum brain natriuretic peptide (BNP) may be a feasible strategy to screen ALVSD. We prospectively sought to investigate the feasibility and effectiveness of a screening program for ALVSD based on ECG and BNP used in a hierarchical sequence in patients at high risk for HF. METHODS: Patients > or =55 years old with > or =2 risk factors for HF or > or =70 years old with > or =1 risk factor for HF entered the study performing sequentially ECG, BNP and echocardiographic evaluation. ALVSD was defined as a left ventricular ejection fraction < or =50%. RESULTS: Thirty-three of 122 enrolled patients (27%) had ALVSD. They were older, presented more frequently a history of chemotherapy exposure, had often bundle branch block and higher BNP levels. No patient without any major abnormalities (atrial fibrillation, left ventricular hypertrophy, STT alterations of ischemic/strain origin, pathologic Q wave, bundle branch block) on ECG (n=31, 24.4%) had ALVSD. Among the 91 patients with abnormal ECG, ALVSD was observed in 33 (36%). The area under the receiver operating characteristic curve to detect ALVSD by BNP was 0.86 (confidence interval 0.79-0.94, p<0.0001) and BNP values of > or =43 pg/ml showed a sensitivity and a specificity of 94% and 57%, respectively. The proposed screening program was able to identify 95% (31/33) of patients with ALVSD saving 53% of echocardiographic examinations with a substantial reduction of the costs to diagnose ALVSD. CONCLUSIONS: Our prospective investigation confirms that ECG and BNP may be useful in detecting ALVSD in high-risk patients. A cost-effective screening program based on such simple and low-cost diagnostic tests might be employed for the prevention of HF in primary and secondary prevention programs in high-risk patients.

Homozygous SCN5A mutation in Brugada syndrome with monomorphic ventricular tachycardia and structural heart abnormalities.

AIMS: To describe a patient showing monomorphic ventricular tachycardia, ECG aspect of Brugada syndrome, and structural heart abnormalities due to a homozygous missense mutation in SCN5A. METHODS AND RESULTS: Thirteen subjects (six males, seven females, mean age 46 +/- 22 years) belonging to the same family underwent physical examination, basal biochemical marker detection, 12-lead ECG, Holter ECG, signal-averaged ECG, echocardiogram and genetic analysis. The proband underwent a stress test together with left and right ventricular angiography and electrophysiological study. Three subjects (the proband, his mother, and one brother) showed on ECG an ST-segment elevation in the right precordial leads with coved type aspect. Moreover, the proband presented a sustained monomorphic ventricular tachycardia (left bundle branch block aspect with superior axis), whereas all other family members were asymptomatic. Imaging techniques documented right ventricular structural abnormalities only in the proband. Mutation screening in SCN5A gene was performed in the proband and in available family members. The proband carries a novel SCN5A mutation, R814Q, in homozygous, whereas the parents and four siblings were heterozygous carriers of the same mutation. CONCLUSION: This study provides the first evidence of a homozygous missense mutation in SCN5A associated with atypical ventricular arrhythmias and right structural abnormalities.

Long-term follow-up of the signal-averaged ECG in arrhythmogenic right ventricular cardiomyopathy: correlation with arrhythmic events and echocardiographic findings.

AIMS: The aims of our study were to evaluate late potential changes during long-term follow-up in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and to correlate these results with echocardiographic findings and sustained ventricular tachycardia (VT) occurrence. METHODS AND RESULTS: We studied 31 patients (22 males and 9 females; mean age 29+/-16) during 8 years of follow-up by signal-averaged ECG (SAECG) and echocardiography. Ten subjects experienced episodes of sustained VT. During follow-up, all the SAECG parameters showed a progressive significant increase in late potentials. In contrast, echocardiographic indices did not show evidence of relevant modifications. Patients with sustained VT were characterized by significantly lower left and right ventricular ejection fractions, longer values of filtered QRS at 25/40/80-250 Hz filters, and longer high-frequency low-amplitude (HFLA) signals at 25-250 Hz at baseline. The analysis of SAECG modification during follow-up indicated that only HFLA signals at 25-250 Hz increased significantly in the sustained VT group. CONCLUSION: We detected a progressive increase in delayed ventricular conduction by SAECG not associated with significant echocardiographic changes. Therefore, the conduction disturbance seems to increase independently from anatomical alterations. The baseline SAECG and echocardiographic parameters, more than their modifications during follow-up, appear to be useful in identifying patients with sustained VT.

Late-onset arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary myocardial pathology usually diagnosed at a young age. Although ARVC is characterized by well-known clinical and instrumental features, the diagnosis in older patients can sometimes be difficult, due to the frequent left ventricular involvement and possible concomitant coronary artery disease. In the present study, we describe two female patients in whom morphological and kinetic abnormalities of the right ventricle, in keeping with the diagnosis of ARVC, appeared when they were aged in their fifties. These two cases indicate that clinical screening should be continued throughout adult life in people who are at risk of ARVC.

Mutations in desmoglein-2 gene are associated with arrhythmogenic right ventricular cardiomyopathy.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy characterized by progressive myocardial atrophy with fibrofatty replacement. The recent identification of causative mutations in plakoglobin, desmoplakin (DSP), and plakophilin-2 (PKP2) genes led to the hypothesis that ARVC is due to desmosomal defects. Therefore, desmoglein-2 (DSG2), the only desmoglein isoform expressed in cardiac myocytes, was screened in subjects with ARVC. METHODS AND RESULTS: In a series of 80 unrelated ARVC probands, 26 carried a mutation in DSP (16%), PKP2 (14%), and transforming growth factor-beta3 (2.5%) genes; the remaining 54 were screened for DSG2 mutations by denaturing high-performance liquid chromatography and direct sequencing. Nine heterozygous DSG2 mutations (5 missense, 2 insertion-deletions, 1 nonsense, and 1 splice site mutation) were detected in 8 probands (10%). All probands fulfilled task force criteria for ARVC. An endomyocardial biopsy was obtained in 5, showing extensive loss of myocytes with fibrofatty tissue replacement. In 3 patients, electron microscopy investigation was performed, showing intercalated disc paleness, decreased desmosome number, and intercellular gap widening. CONCLUSIONS: This is the first investigation demonstrating DSG2 gene mutations in a significant number of ARVC-unrelated probands. Cardiac phenotype is characterized clinically by typical ARVC features with frequent left ventricular involvement and morphologically by fibrofatty myocardial replacement and desmosomal remodeling. The presence of mutations in desmosomal encoding genes in 40% of cases confirms that many forms of ARVC are due to alterations in the desmosome complex.

Pregnancy in women with arrhythmogenic right ventricular cardiomyopathy/dysplasia.

OBJECTIVES: Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a cardiac disease characterised by myocardial necrosis followed by fibro-fatty substitution leading to the onset of ventricular arrhythmias. The aim of the present study was to analyse pregnancy in women affected by this condition. STUDY DESIGN: Six women affected by ARVC/D who underwent a pregnancy were studied with a follow-up programme, consisting of 12-lead ECG, signal-averaged ECG, 24-h ECG and two-dimensional and Doppler echocardiogram performed before the beginning of the pregnancy, at 3rd and 7th month of gestation and after the delivery. RESULTS: All women were on antiarrhythmic therapy during pregnancy; two complained of palpitations in the last 3 months. Delivery was performed at full terms in all, with caesarean section and epidural anaesthesia in four. Mean weight at birth was 3490g. No adverse reactions on the newborns were detected. All patients were advised against breast-feeding. No significant morphological changes were detected. During the period following the delivery (1-6years, mean 2,6years) one subject experienced a sustained ventricular tachycardia. CONCLUSIONS: Pregnancy seems to be well tolerated in patients affected by ARVC/D, but a programmed clinical protocol is mandatory particularly in the last trimester and puerperium, due to increased risk of ventricular arrhythmias.

Clinical profile of four families with arrhythmogenic right ventricular cardiomyopathy caused by dominant desmoplakin mutations.

AIMS: To characterize the clinical profile of patients belonging to families affected with autosomal dominant arrhythmogenic right ventricular cardiomyopathy (ARVC) due to mutations of the gene encoding for the cell-to-cell adhesion protein desmoplakin (DSP). METHODS AND RESULTS: Thirty-eight subjects belonging to four families showing different DSP mutations (three missense and one in the intron-exon splicing region) underwent clinical and genetic investigation, including annual 12-lead ECG, signal averaged ECG, 24 h Holter ECG, and two-dimensional echocardiography. Twenty-six family members (11 males and 15 females) were found to carry a DSP mutation. After a follow-up of 1-24 years, median 6, 14 (54%) fulfilled (mean age at diagnosis 33+/-15 years) and 12 (mean age 43+/-24 years at the last follow-up) did not fulfil the established diagnostic criteria of ARVC, although five of them had some cardiac abnormalities. Clinical presentations were palpitations in six, sudden death (SD) in three, syncope in one, and chest pain with increased myocardial enzymes in two. Abnormal 12-lead ECG findings were present in 15 cases (58%), ventricular arrhythmias in 12 (46%), and late potentials in 11 (42%). Fourteen (54%) had abnormal echocardiographic findings, with left ventricular involvement in seven of them. SD occurred in six subjects and in three it was the first symptom of the disease; moreover, one subject died due to heart failure. The annual disease-related death and SD/aborted SD were 0.028 and 0.023 patient/year, respectively. CONCLUSION: Familial ARVC caused by DSP mutations is characterized by a high occurrence of SD even as first clinical manifestation. Left ventricular involvement is not a rare feature of the disease, which frequently escapes clinical diagnosis by applying the currently available criteria. Genetic screening is mandatory for early identification of asymptomatic carriers and preventive strategies within a family with a genotyped index case.

Three-dimensional electroanatomic voltage mapping increases accuracy of diagnosing arrhythmogenic right ventricular cardiomyopathy/dysplasia.

BACKGROUND: Three-dimensional electroanatomic voltage mapping offers the potential to identify low-voltage areas that correspond to regions of right ventricular (RV) myocardial loss and fibrofatty replacement in patients with arrhythmogenic RV cardiomyopathy/dysplasia (ARVC/D). METHODS AND RESULTS: Thirty-one consecutive patients (22 men and 9 women; mean age, 30.8+/-7 years) who fulfilled the criteria of the Task Force of the European Society of Cardiology and International Society and Federation of Cardiology (ESC/ISFC) for ARVC/D diagnosis after noninvasive clinical evaluation underwent further invasive study including RV electroanatomic voltage mapping and endomyocardial biopsy (EMB) to validate the diagnosis. Multiple RV endocardial, bipolar electrograms (175+/-23) were sampled during sinus rhythm. Twenty patients (group A; 65%) had an abnormal RV electroanatomic voltage mapping showing > or =1 area (mean 2.25+/-0.7) with low-voltage values (bipolar electrogram amplitude <0.5 mV), surrounded by a border zone (0.5 to 1.5 mV) that transitioned into normal myocardium (>1.5 mV). Low-voltage electrograms appeared fractionated with significantly prolonged duration and delayed activation. In 11 patients (group B; 35%), electroanatomic voltage mapping was normal, with preserved electrogram voltage (4.4+/-0.7 mV) and duration (37.2+/-0.9 ms) throughout the RV. Low-voltage areas in patients from group A corresponded to echocardiographic/angiographic RV wall motion abnormalities and were significantly associated with myocyte loss and fibrofatty replacement at EMB (P<0.0001) and familial ARVC/D (P<0.0001). Patients from group B had sporadic disease and histopathological evidence of inflammatory cardiomyopathy (P<0.0001). During the time interval from onset of symptoms to the invasive study, 11 patients (55%) with electroanatomic low-voltage regions received an implantable cardioverter/defibrillator because of life-threatening ventricular arrhythmias, whereas all but 1 patient with a normal voltage map remained stable on antiarrhythmic drug therapy (P=0.02). CONCLUSIONS: Three-dimensional electroanatomic voltage mapping enhanced accuracy for diagnosing ARVC/D (1) by demonstrating low-voltage areas that were associated with fibrofatty myocardial replacement and (2) by identifying a subset of patients who fulfilled ESC/ISFC Task Force diagnostic criteria but showed a preserved electrogram voltage, an inflammatory cardiomyopathy mimicking ARVC/D, and a better arrhythmic outcome.

Arrhythmogenic right ventricular cardiomyopathy type 1 (ARVD1): confirmation of locus assignment and mutation screening of four candidate genes.

Arrhythmogenic right ventricular cardiomyopathy type 1 (ARVD1) is an autosomal dominant disorder characterised by progressive degeneration of right ventricular myocardium, arrhythmias and risk of sudden death. By linkage analysis, we previously mapped the involved gene to chromosome 14q24.3. In the present study we report on linkage analysis of one additional and unrelated family, which enabled to confirm previous locus assignment. Another family is reported, in which genetic and clinical data suggest linkage to the same locus. Direct sequencing of DNA from individuals belonging to established ARVD1 families failed to detect causative mutations in exonic sequences of four genes (POMT2, TGFbeta3, KIAAA1036 and KIAA0759) expressed in the heart and which defects could possibly induce plasma membrane instability or apoptosis, key features of ARVD pathogenesis.

alpha-Adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity.

OBJECTIVE: Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular morbidity and mortality. Epidemiological studies suggest that LVH may be influenced by genetic factors. However, the evidence associating individual genes with left ventricular (LV) mass is inconsistent and contradictory. METHODS: We investigated the association between angiotensin-converting enzyme insertion/deletion, angiotensinogen and alpha-adducin polymorphisms with LV mass and plasma renin activity (PRA) in 162 men with mild, never-treated hypertension who were recruited for the Hypertension and Ambulatory Recording Venetia Study. The effect of each polymorphism on LV mass and PRA was tested in one-way analysis of covariance using LV mass index or PRA as the dependent variable after adjusting for covariates. RESULTS: The alpha-adducin polymorphism was the only individual polymorphism independently associated with LV mass index (F = 7.78, P= 0.006). Patients homozygous for the allele of that polymorphism had a LV mass index (123.4 +/- 10.5 g/m(2) ) significantly higher compared with heterozygotes (90.8 +/- 2.5 g/m(2) , P<0.01) or homozygotes (94.7 +/- 1.7 g/m(2) , P<0.05). These subjects also have significantly lower PRA (F = 4.2, P= 0.017). Albeit uncommon, 40% of homozygotes of the alpha-adducin polymorphism had LVH (odds ratio, 15.1; 95% confidence interval, 3.0-82.1). CONCLUSIONS: The homozygotic state of the allele of alpha-adducin polymorphism is independently associated with increased LV mass and low PRA. These data suggest that genetic considerations may contribute importantly to risk stratification, and perhaps therapeutic interventions targeted at LVH and the renin-angiotensin system in hypertensive patients.