Left ventricular mechanics in patients with hematological malignancies before initiation of chemo- and radiotherapy.

Objective We sought to investigate left ventricular (LV) structure, function and mechanics in the patients with leukemia and lymphoma before initiation of chemotherapy, as well as the relationship between hematological malignancies and reduced LV longitudinal strain. Methods This retrospective investigation included 71 patients with leukemia and lymphoma before chemotherapy and 36 healthy controls. All participants underwent echocardiographic examination before initiation of chemotherapy and radiotherapy.

Right heart masses in a patient with endometrial stromal sarcoma.

We present the case of a 61-year-old woman with a large tumoral infiltration extending from the pelvis throughout the inferior vena cava inferior to the right atrium, protruding into the right ventricle and right ventricular outflow tract. She had been treated 10 years before for low-grade endometrial stromal sarcoma by hysterectomy and adnexectomy followed by hormone- and radio-therapy. Due to cancer recurrence, she underwent peritonectomy, appendectomy, and resection of terminal ileum.

Phasic Left Atrial Function in Cancer Patients Before Initiation of Anti-Cancer Therapy.

We aimed to explore left atrial (LA) remodeling in the patients with solid cancer before initiation of chemo- or radiotherapy. This retrospective investigation included 92 chemo- and radiotherapy-naive cancer patients and 40 age- and gender-matched controls with a similar cardiovascular risk profile as the cancer group. All participants underwent comprehensive echocardiographic examination before the start of chemo- or radiotherapy.

Right ventricular function and mechanics in chemotherapy- and radiotherapy-naïve cancer patients.

The present research evaluated right ventricular (RV) structure, function and mechanics in the cancer patients before initiation of chemo- or radiotherapy, and the association between cancer and decreased RV longitudinal strain. This retrospective investigation included 101 chemo- and radiotherapy-naïve patients with solid cancer and 38 age- and gender-matched controls with similar cardiovascular risk profile. Echocardiographic examination and strain evaluation was performed in all participants.

Clinical genetics and outcome of left ventricular non-compaction cardiomyopathy.

Aims: In this study, we aimed to clinically and genetically characterize LVNC patients and investigate the prevalence of variants in known and novel LVNC disease genes.

Introduction: Left ventricular non-compaction cardiomyopathy (LVNC) is an increasingly recognized cause of heart failure, arrhythmia, thromboembolism, and sudden cardiac death. We sought here to dissect its genetic causes, phenotypic presentation and outcome.

Right ventricular strain in heart failure: Clinical perspective.

The number of studies demonstrating the importance of right ventricular remodelling in a wide range of cardiovascular diseases has increased in the past two decades. Speckle-tracking imaging provides new variables that give comprehensive information about right ventricular function and mechanics. In this review, we summarize current knowledge of right ventricular mechanics in heart failure with reduced ejection fraction and preserved ejection fraction.

Normal values and clinical relevance of left atrial myocardial function analysed by speckle-tracking echocardiography: multicentre study.

Aims: The aim of this multicentre study was to determine the normal range and the clinical relevance of the myocardial function of the left atrium (LA) analysed by 2D speckle-tracking echocardiography (2DSTE).

Methods And Results: We analysed 329 healthy adult subjects prospectively included in 10 centres and a validation group of 377 patients with left ventricular diastolic dysfunction (LVDD). LA myocardial function was analysed by LA strain rate peak during LA contraction (LA-SRa) and LA strain peak during LA relaxation (LA-Strain).

Beyond the sarcomere: CSRP3 mutations cause hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a frequent genetic cardiac disease and the most common cause of sudden cardiac death in young individuals. Most of the currently known HCM disease genes encode sarcomeric proteins. Previous studies have shown an association between CSRP3 missense mutations and either dilated cardiomyopathy (DCM) or HCM, but all these studies were unable to provide comprehensive genetic evidence for a causative role of CSRP3 mutations.

Noncompaction of the ventricular myocardium is associated with a de novo mutation in the beta-myosin heavy chain gene.

Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin. NVM results presumably from a congenital developmental error and has been traced back to single point mutations in various genes. The objective of this study was to determine the underlying genetic defect in a large German family suffering from NVM.

Recurrent in-stent restenosis is not associated with the angiotensin-converting enzyme D/I, angiotensinogen Thr174Met and Met235Thr, and the angiotensin-II receptor 1 A1166C polymorphism.

Although great progress has been made in reducing renarrowing of the lumen after stenting of coronary arteries, a considerable number of patients develop recurrent in-stent stenosis. Several studies suggest that neointimal proliferation is the crucial pathophysiological process underlying restenosis after stenting. The renin-angiotensin-aldosterone system (RAS) has been implicated in the development of neointimal hyperplasia.

[Familial dilated cardiomyopathy].

Dilated cardiomyopathy (DCM) is the most frequent form of primary myocardial diseases and the third most common cause of heart failure. Clinically, DCM is characterized by a progressive course of ventricular dilatation and systolic dysfunction. The life expectancy is limited and varies according to the underlying etiology with a median survival time of about 5 years after diagnosis.