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Background Insulin resistance (IR), constitutes an important cardiovascular risk factor and can cause ischemic heart disease. It can lead to left ventricular dysfunction with a mechanism independent of ischemic heart disease and it is closely associated with impaired vascular function. The aim of our study was to explore the impact of IR on cardiac and vascular function, in patients with cardiovascular risk factors but angiographically undamaged coronary arteries. Methods We studied 32 patients (62.06 ± 11.19 years) with cardiovascular risk factors. All patients underwent coronary angiography, echocardiography, Doppler ultrasound of carotid arteries and laboratory tests. Exclusion criteria were coronary artery disease detected by coronary angiography, diabetes mellitus, creatinine above 1.5 mg/dl, atrial fibrillation or malignant arrhythmias, left-ventricular hypertrophy, valvular heart disease, ejection fraction below 50%. The presence of insulin resistance was assessed using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Each patient underwent a complete echocardiographic examination including Global Longitudinal Strain assessment and carotid artery ultrasound scan including measurement of arterial stiffness. Results The patients were divided into two groups based on the median value of HOMA-IR, the first group for values < 4.14 and, the second, for values ≥ 4.14. Ejection fraction and diastolic function did not significantly differ between the two groups, whether in patients with higher levels of HOMA-IR (≥ 4.14) we observed a Global Longitudinal Strain (GLS) that was significantly reduced (− 16.50 ± 1.37% vs. − 20.73 ± 1.84%, p = 0.0015) vascular stiffness, measured in the carotid arteries as pulse wave velocity (PWV) (9.70 ± 1.75 m/s vs. 7.40 ± 1.89 m/s, p = 0.00148) that was increased. At multivariate analysis HOMA-IR was an independent predictor of myocardial dysfunction (GLS: coefficient 0.1156, p < 0.0001). Conclusion Insulin resistance is associated with subclinical myocardial and vascular alterations in patients without significant coronary artery disease, measured as a reduction of Global Longitudinal Strain, and increased arterial stiffness. Our results underscore the importance of studying the interaction between ventricular function and vessels, in the perspective of more effective preventive and therapeutic interventions. [ABSTRACT FROM AUTHOR]

Abstract: Non-compaction of the ventricular myocardium (LCVM) is a rare disorder of myocardial morphogenesis usually diagnosed in paediatric age. The diagnosis was echocardiographically made on the basis of a reported spongeous/compacted ratio >2 in one or more segments of the left ventricle during the diastolic period. We aimed to test the diagnostic accuracy of cardiovascular magnetic resonance (CMR) imaging in distinguishing pathological left ventricular non-compaction. Methods: We collected a consecutive series of 8 patients, 5 males and 3 females, with a mean age of 14.9 years with non-compaction of left ventricular myocardium. All patients were admitted in our divisions of cardiology. In all cases the diagnosis was performed by echocardiography. The diagnosis was obtained when the spongeous/compacted ratio was >2 in one or more segments of left ventricle, evaluated in systolic and diastolic period. In the end we completed the diagnosis by scanning with a Signa HD 1.5 T (GE, Milwaukee, USA) the same 8 patients affected by non compaction of ventricular myocardium. In all patients cardiac-gated T1 and T2 black-blood FSE images in short axis and in four-chamber horizontal long axis were obtained. Breath hold cine MR sequences (FIESTA) were performed, covering the whole left ventricle in short-axis plane and in four-chamber view. A segmented inversion-recovery fast gradient echo sequence (IR-FGE) was performed in the short-axis plane of the LV and in four-chamber-view after Gadolinium injection in 8 patients affected by non compaction of left ventricle. At the end of examination the spongeous/compacted ratio >2 was calculated in all involved segments of the left ventricle in diastole. Results: In all cases we demonstrated by echocardiography an involvement of the ventricular apex. In 3 cases the structural alterations involved also lateral wall of left ventricle. Magnetic resonance evaluation showed that involvement demonstrated by the echocardiogram was the same: ventricular apex involved in every patient, lateral wall in 3 and all segments in 2. However the spongeous/compacted ratio was >>2 in all patients, with a mean value of 3,1. Conclusions: Although our data refer to a small population of patients and need further confirmation, they suggest that it seems reasonable increase the cut-off for spongeous/compacted ratio from a value of 2 to 2.5 for non-compaction diagnosis when high-resolution magnetic resonance is used. [Copyright &y& Elsevier]

Abstract: Noncompaction of the ventricular myocardium (LVNC) is a rare congenital cardiomyopathy resulting from an arrest in normal endomyocardial embryogenesis. In 2002 Jenni et al. [Jenni R, Wyss CA, Oechslin EN, Kaufmann PA. Isolated ventricular noncompaction is associated with coronary microcirculatory dysfunction. J Am Coll Cardiol 2002; 39:450-454.] reported a microvascular dysfunction in 12 patients affected by non compaction: areas of restricted myocardial perfusion have been documented by scintigraphy, suggesting a reduction of Coronary flow reserve. McMahon et al reported in a recent article a reduction of TD velocities in children with noncompaction of the left ventricle, compared with normal controls. The authors concluded their work saying that the reduction of lateral mitral Ea velocity helps to predict children with LVNC who are at risk of adverse clinical outcomes including death and need for cardiac transplantation. In a precedent report our group reported a strong correlation between pathological tissue Doppler and reduction of ejection fraction. Recently we scanned with a Signa HD 1.5 T (GE, Milwaukee, USA) 8 patients affected by non compaction. Transmural Gd-enhancement was detected in 5/8 patients (62%). In all patients with late enhancement a reduction of EF has demonstrated. In our opinion the late enhancement can depend on a CFR, and is the determinant of the tissue Doppler alterations. So the TD alteration is associated with EF, and is an indirect index of poor clinical outcome, like EF. [Copyright &y& Elsevier]

Abstract: For neurological disorders we consider every possible affection of the central nervous system or neuro-muscular junction, in the presence of complex syndromes as well, such as Cornelia De Lange syndrome or any other. In our experience the incidence of neurological or neuromuscular envolment in patients affected by noncompaction is low. An incidence of comorbidities higher than 20% is not recorded in any centre, in published experiences. Data of the Vienna group could be likely influenced by selection bias (second level centre) or territorial genetic factors, or could depend on higher sensibility of used diagnostic techniques of neurological disease. But, if it was so, in our opinion, let me assert that patients routinely underwent so sensible and accurate neurological tests only for cognitive purpose, without practical implications. [ABSTRACT FROM AUTHOR]

Abstract: In many reports Finsterer and Stöllberger reported a strong association between non compaction of the left ventricle and neuromuscular disorders. In the same report the authors described a neurological involvement in more than 50%. Recently we published our personal experience, about 21 paediatric patients: only 4 patients (19%) showed a neuromuscular disorder, and only 1 of them showed an increased plasmatic level of CK, and in particular of MM isoform, with a normal level of CK-MB. None presented high levels of troponine. Through the experience of 3 centres we collected 61 patients affected by non compaction that performed a neurological control, and only 14 (21%) were affected by neuromuscular disorders. A correlation between neuromuscular disorders and cardiac non compaction is present, even if, until today, genetic involvement has not been identified clearly. However, in our opinion, an estimated incidence of 50% of neuromuscular disorders in this population of patients could be too exaggerated. About the prognostic value of the CK elevation, it is interesting to consider that an increasing of CK plasmatic level is an expression of muscular disorders and not of cardiac alterations. In our experience only 1 patient in 21 patients (4%) with neuromuscular disorders showed an increasing of CK-MM plasmatic value. [Copyright &y& Elsevier]

Abstract: Takotsubo Cardiomyopathy is characterized by a reversible systolic left ventricular apical ballooning. A new pattern of dyskinesia in the absence of angiographic evidence of coronary artery stenosis has been indicated like a variant of takotsubo cardiomiopathy: mid-ventricular akinesis with preservation of apical and basal contractilities revealed at echocardiograms and ventriculographies. We report the case of a 65 years old patient with this pattern, reverted in 4 weeks. [Copyright &y& Elsevier]

Abstract: In a recent report about noncompaction Nemes et al. reported that systolic left ventricular (LV) dysfunction assessed using the wall motion score during 2D echocardiography in noncompaction is not confined to noncompacted LV segments. These results confirmed some published reports of our group. Recently we analyzed a population of 238 patients affected by noncompaction, and demonstrated that the number of noncompacted segment is uncorrelated with the degree of systolic dysfunction. It is an attractive hypothesis that the systolic dysfunction could be depend on the fibrosis of the left ventricle, itself a consequence of microcirculatory dysfunction, which has been confirmed by reports that describe microvascular dysfunction using myocardial scintigraphy. [Copyright &y& Elsevier]

Objective The aim of this study was to evaluate in patients with cardiac syndrome X (CSX), using validated angiography indices, coronary blood flow and myocardial perfusion of the microcirculation to assess whether there is greater microvascular dysfunction in patients with increase of carotid intima media thickness (C-IMT), compared to those who do not have. Methods Our study was performed on a population 124 patients with CSX that underwent coronary angiography and carotid ultrasound. We divided the sample into two categories: patients with increase of C-IMT and those without increase. We calculated Gibson and Yusuf indices for each patient based on angiographic images, including TIMI Frame Count (TFC), Myocardial Blush Grade (MBG) and Total Myocardial Blush Score (TMBS). Results Our sample compared two groups: patients with increase of C-IMT (n-63) and patients without increase of C-IMT (n-61). We showed that patients with increase C-IMT had a longest TFC of three major coronary arteries (TFC LAD 44.7 ± 12.5; TFC RCA 26.2 ± 6.9; TFC CX 27 ± 5.9), than control group. We found lower MBG on three coronary arteries (MBG LAD 2.5 ± 0.3; MBG RCA 2.3 ± 0.3; MBG CX 2.1 ± 0.32) in patients with increase of C-IMT than control group, with good statistical significance. Conclusion Analysis of microcirculation trough angiography indexes in patients with CSX with increase of C-IMT and without has led to asses that patients with increase of C-IMT population has a greater involvement of microcirculation than patients without. [ABSTRACT FROM AUTHOR]

Abstract: Background: Isolated ventricular noncompaction (IVNC) is characterized by multiple prominent trabeculations and deep intertrabecular recesses. Some reports prove that the chronic heart failure may occur in approximately half of the patients. In this report we investigate the correlation between the number of non compacted segments and entity of systolic dysfunction from the registry and subregistries of the SIEC. Method: To identify the correlation between ventricular dysfunction and number of segments involved in non compaction we evaluated a consecutive series of 238 patients affected by non compaction, from the SIEC (Società Italiana di Ecografia Cardiovascolare) registry. The average age of patients was 41.5 years (range: 1–92 years), 137 were males and 101 females. In 122 cases we found ventricular systolic dysfunctions with an EF average of 34.6%. The number of affected segments by non-compactation and diastolic dysfunction were found to be non-independent predictors of LV systolic dysfunction. Conclusion: From the analyses we carried out, it seems that ventricular dysfunction seems to be completely independent from the segment numbers of non compacted segments. [Copyright &y& Elsevier]

Abstract The great therapeutical success achieved by oncology is counterbalanced by growing evidences of cardiovascular (CV) toxicity due to many antineoplastic treatments. Cardiac adverse events may cause premature discontinuation of effective oncologic treatments or occur as late events undermining the oncologic success. Arterial hypertension is both the most common comorbidity in cancer patients and a frequent adverse effect of anticancer therapies. A pre-existing hypertension is known to increase the risk of other cardiac adverse events due to oncologic treatments, in particular heart failure. Moreover, as a strict association between cancer and CV diseases has emerged over the recent years, various analyses have shown a direct relationship between hypertension and cancer incidence and mortality. Finally, many antineoplastic treatments may cause a rise in blood pressure (BP) values, particularly the novel anti VEGF agents, this possibly compromising efficacy of chemotherapy. Aim of this review is to revise the topic and the many aspects linking arterial hypertension and cancer, and to provide a comprehensive and practical guide of the current treatment approaches. Highlights • Arterial hypertension is the most common comorbidity of cancer patients. • It is significantly associated with both cancer incidence and mortality. • Arterial hypertension is a risk factor for cancer therapy-related heart failure. • Arterial hypertension is a common adverse effect of many anticancer drugs. • Anti-hypertensive therapy prevents from premature discontinuation of cancer therapy. [ABSTRACT FROM AUTHOR]

Cardiotoxicity induced by chemotherapeutic agents and radiotherapy is a growing problem. In recent years, an increasing number of new drugs with targeted action have been designed. These molecules, such as monoclonal antibodies and tyrosine kinase inhibitors, can cause different type of toxicities compared to traditional chemotherapy. However, they can also cause cardiac complications such as heart failure, arterial hypertension, QT interval prolongation and arrhythmias. Currently, a field of intense research is the vascular toxicity induced by new biologic drugs, particularly those which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) and other tyrosine kinases. In this review, we aim at focusing on the problem of vascular toxicity induced by new targeted therapies, chemotherapy and radiotherapy, and describe the main mechanisms and emphasizing the importance of early diagnosis of vascular damage, in order to prevent clinical complications. [ABSTRACT FROM AUTHOR]

Background Cardiac resynchronization therapy (CRT) is a successful strategy for heart failure (HF) patients. The pre-requisite for the response is the evidence of electrical dyssynchrony on the surface electrocardiogram usually as left bundle branch block (LBBB). Non-response to CRT is a significant problem in clinical practice. Patient selection, inadequate delivery and sub-optimal left ventricle lead position may be important causes. Objectives In an effort to improve CRT response multimodality imaging (especially echocardiography, computed tomography and cardiac magnetic resonance) could play a decisive role and extensive literature has been published on the matter. However, we are so far from routinary use in clinical practice. Electrocardiography (with respect to left ventricle capture and QRS narrowing) may represent a simple and low cost approach for early prediction of potential non-responder, with immediate practical implications. Conclusion This brief review covers the current recommendations for CRT in HF patients with particular attention to the potential benefits of multimodality imaging and electrocardiography in improving response rate. [ABSTRACT FROM AUTHOR]

Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprotection. Genes critical for signaling pathways in cardioprotection include protectomiRs (e.g., microRNA 125b*), ZAC1 transcription factor, pro-inflammatory genes such as cycloxygenase (COX)-2 and inducible nitric oxide synthase (iNOS), antioxidant enzymes such as hemoxygenase (HO)-1, extracellular and manganese superoxidase dismutases (ec-SOD and Mg-SOD), heat shock proteins (HSPs), growth factors such as insulin like growth factor (IGF)-1 and hepatocyte growth factor (HGF), antiapoptotic proteins such as Bcl-2 and Bcl-xL, pro-apoptotic proteins such as FasL, Bcl-2, Bax, caspase-3 and p53, and proangiogenic genes such as TGFbeta, sphingosine kinase 1 (SPK1), and PI3K-Akt. By identifying the gene expression profiles of IRI and ischemic conditioning, one may reveal potential gene targets responsible for cardioprotection. In this manuscript, we review the current state of the art of gene therapy in cardioprotection and propose that gene expression analysis facilitates the identification of individual genes associated with cardioprotection. We discuss signaling pathways associated with cardioprotection that can be targeted by gene therapy to achieve cardioprotection. [ABSTRACT FROM AUTHOR]

Abstract: Background: Takotsubo cardiomyopathy is a disorder that has been appreciated only recently. In most of reported cases, this syndrome mimes an acute myocardial infarction. Till this moment no data are available from literature about the treatment in the acute phase of this disease. Aim of the study: In our multicentric experience we have retrospectively looked at the benefits of a treatment with ACE-inhibitors, beta-blockers, Aspirin and calcium channels blockers, started until the early phases of the disease and continued for 30 days, in 36 patients affected by Takotsubo cardiomyopathy. We chose as endpoint of the study the efficacy of the used drug in improving left ventricular myocardial function and the rapidity of the effects of the same drug.bethods: from an international registry about the Takotsubo cardiomiopathy, co-ordinate by our research group, we evaluated the long term efficacy of some drugs, administrated like single treatment in some patients. Results: Obtained data did not show any statistically significant difference in the percentages of improvement in the left ventricle ejection fraction evaluated at the admission to the hospital, before the discharge and after 30 days of treatment between each treated group and the control group of non-treated patients. No significant differences were found in hospitalization times between treated patients and controls. None of our patients experienced during the observation period a relapse of the disease. Conclusions: The results of our survey suggest that a chronic treatment with beta-blockers, ACE-inhibitors, calcium channels blockers and aspirin does not provide any benefit in patients with Takotsubo cardiomyopathy. Thus, it seem to be important an early correct differential diagnosis to avoid any chronic treatment in these patients. [Copyright &y& Elsevier]

Abstract: Background:: Isolated left ventricular noncompaction is the result of incomplete myocardial morphogenesis, leading to persistence of the embryonic myocardium. The condition is recognised by an excessively prominent trabecular meshwork and deep intertrabecular recesses of the left ventricle. Whether these intertrabecular recesses are a favorable substrate for supraventricular arrhythmias is unclear, even if the incidence of chronic heart failure seems to be high. Results:: We evaluated a continuous series of 238 patients affected by noncompaction. In 4 cases the patients reported palpitations and in 4 an episode of syncope. Periodic holter monitoring was performed every 6 months for 4 years. Only 9 patients had documented atrial fibrillation. In no cases we observed supraventricular tachycardia. Conclusions:: Noncompaction alone does not seem to be a risk factor for supraventricular arrhythmias. [Copyright &y& Elsevier]

Abstract: Background: Non-compaction of ventricular myocardium is a rare congenital cardiomyopathy characterized by the presence of an extremely thickened endocardial layer with prominent trabeculations and deep recesses in communication with ventricular chamber and determining the typical spongeous aspect. The diagnosis of non-compaction of ventricular myocardium is possible through the identification of morphological alterations by echocardiographic evaluation. Ebstein''s anomaly is a rare congenital cardiac disease, defined as the significant apical displacement of the part of the tricuspid valve causing significant tricuspid regurgitation and reduction of the functional right ventricle, right atrial and right ventricular dilatation and atrial and ventricular arrhythmias. Case report: We present a case of biventricular non-compaction and Ebstein''s anomaly in a 29-year-old Italian man that was referred for chest pain. Diagnosis of Ebstein''s anomaly was made during a medical control for military service through an echocardiographic evaluation which left the suspicion of myocardium non-compaction. We present the cardiac image of the 2D and 3D eco, RMN, scintigraphy and ventriculaography. [Copyright &y& Elsevier]

Abstract: Background: The prevalence of primary cardiac neoplasms is approximately 0.3% and these masses should be distinguished from many of other primary and secondary processes that can occur in the heart. Further assessment of the left ventricular mass presents important clinical implications. Cardiovascular magnetic resonance was used. Clinical case: An asyntomatic 12-year-old child was referred for cardiovascular magnetic resonance imaging to further assess a left ventricular mass found after an echocardiography, executed for assessment for sport activity. His past medical history was absolutely negative. The patient was in optimal state of health. The EKG showed an aspecific ST elevation. A hamartoma was diagnosed. A surgical approach was performed. After 7 days the patient is in good condition. [Copyright &y& Elsevier]

Abstract: Wolff–Parkinson–White (WPW) is a syndrome characterized by the presence of an accessory pathway that skipping A–V node may lead the electrical stimulus from the atrium directly to the ventricle. Some studies reported the finding of myocardial dyskinesia in the segments precociously activated by the accessory pathway, at echocardiogram and at nuclear cardiac study. Soria et al. reported, in 1985, an increased incidence of dilative cardiomyopathy in patients with WPW. The pathophysiological pathway that leads to ventricular dilation may be due to the increase of end-diastolic pressure secondary to a tachycardia-induced cardiomyopathy. Tachycardia-induced cardiomyopathy is usually secondary to frequent and prolonged tachycardia episodes. In this paper we report the cases of three patients affected by WPW who developed dilative cardiomyopathy during the follow-up. Particularly dyskinetic segments, working such as a functional aneurysm, could induce deep modifications of intraventricular haemodynamics, leading to remodelling and progressive ventricular dilation. This hypothesis could have important empirical consequences because it could imply the necessity of a precocious ablative therapy in this kind of patients. [Copyright &y& Elsevier]

Abstract: The Tissue doppler analysis is a new echocardiographic approach to evaluate the diastolic function. In this report we performed a Tissue doppler analysis in a series of 15 children affected by non-compaction. The bidimensional echo-cardiogram showed a systolic function which was reduced only in 8 patients. Alterations of the diastolic function were founded in 7 patients: in 2 cases, a reduction of the E tissue wave was present in all segments. In 3 patients the diastolic dysfunction was limited to apical and lateral segments. In the last 2 children a reduction of the E wave interested only the apical segments. There was a strong correlation between systolic and diastolic dysfunction: in fact all patients with diastolic dysfunction also presented a severe reduction of the systolic function. [Copyright &y& Elsevier]