Treatment of impending paradoxical embolism with systemic thrombolysis and cerebral embolic protection: a case report.

Background: Impending paradoxical embolism is a rare and life-threatening occurrence and evidence guiding its optimal management is lacking.

Case Presentation: A 73-year-old man presenting with ST-elevation myocardial infarction was diagnosed with impending paradoxical embolism, as a large thrombus was visualized entrapped in a patent foramen ovale. We performed systemic thrombolysis after deployment of a cerebral protection device, which resulted in complete dissolution of the thrombus without major thromboembolic events.

Mitochondrial cardiomyopathies: pathogenesis, diagnosis, and treatment.

Mitochondrial cardiomyopathies are a heterogeneous group of disorders caused by dysfunction of mitochondrial energy production due to genetic mutations affecting mitochondrial or nuclear DNA. Mitochondrial cardiomyopathies can include a wide range of cardiac manifestations and are frequently associated with other multisystemic symptoms, including skeletal myopathy, neurological deficits, and metabolic disturbances. Advances in genetic testing have improved diagnostic accuracy, but early identification remains challenging due to the variable clinical presentation and clinical overlap with other cardiomyopathies.

Mechano-energetic uncoupling in heart failure.

Heart failure (HF) is a major global and life-threatening disease. Despite advances in therapies, the prevalence of HF is increasing owing to an ageing population and the pervasive pandemic of obesity and metabolic disorders, which have transformed the pathophysiology of HF. Changes in cardiac energy metabolism and the related energy deficit crucially contribute to the severity and type of HF.

Epigenetic mechanisms underlying the beneficial effects of cardiac rehabilitation. An overview from the working groups of "cellular and molecular biology of the heart" and "cardiac rehabilitation and cardiovascular prevention" of the Italian Society of Cardiology (SIC).

The benefits of cardiac rehabilitation (CR) have been demonstrated in patients after myocardial infarction (MI), and in patients with chronic heart failure (HF). The core components of the CR program include improvement in exercise tolerance and optimization of coronary risk factors (i.e.

Update on preclinical models of cancer therapy-related cardiac dysfunction: Challenges and perspectives. A scientific statement of the Heart Failure Association (HFA) of the ESC, the ESC Council of Cardio-Oncology, and the ESC Working Group on Cellular Biology of the Heart.

New anticancer therapies with potential cardiovascular side effects are continuously being introduced into clinical practice, with new and often unexpected toxicities becoming apparent only after clinical introduction. These unknown toxicities should be identified and understood beforehand to better prepare patients and physicians, enabling the implementation of effective treatments. Therefore, there is a crucial need for appropriate preclinical models to understand the biological basis of their cardiotoxicity.

[The evolving landscape of hypertrophic cardiomyopathy management: a review of the updated AHA/ACC/multisociety guidelines].

Therapeutic options for the treatment of hypertrophic obstructive cardiomyopathy have recently expanded with the introduction of myosin inhibitors, mavacamten and aficamten, which demonstrated a remarkable effect on functional capacity and symptoms of patients with left ventricular outflow tract obstruction. In recent years, there has also been a change in the approach to physical exercise in patients with hypertrophic cardiomyopathy, which now also includes the possibility of participating in high-intensity and competitive sports for selected patients with a low-risk profile. In this review, we explore the main innovations of the American College of Cardiology/American Heart Association guidelines on hypertrophic cardiomyopathy, we highlight the differences with the guidelines on the management of cardiomyopathies of the European Society of Cardiology, and we highlight some important unresolved issues in the management of the disease.

Mitochondrial calcium signaling and redox homeostasis in cardiac health and disease.

The energy demand of cardiomyocytes changes continuously in response to variations in cardiac workload. Cardiac excitation-contraction coupling is fueled primarily by adenosine triphosphate (ATP) production by oxidative phosphorylation in mitochondria. The rate of mitochondrial oxidative metabolism is matched to the rate of ATP consumption in the cytosol by the parallel activation of oxidative phosphorylation by calcium (Ca) and adenosine diphosphate (ADP).

ErbB2-NOTCH1 axis controls autophagy in cardiac cells.

Although the epidermal growth factor receptor 2 (ErbB2) and Notch1 signaling pathways have both significant roles in regulating cardiac biology, their interplay in the heart remains poorly investigated. Here, we present evidence of a crosstalk between ErbB2 and Notch1 in cardiac cells, with effects on autophagy and proliferation. Overexpression of ErbB2 in H9c2 cardiomyoblasts induced Notch1 activation in a post-transcriptional, p38-dependent manner, while ErbB2 inhibition with the specific inhibitor, lapatinib, reduced Notch1 activation.

Mitochondrial calcium in cardiac ischemia/reperfusion injury and cardioprotection.

Mitochondrial calcium (Ca) signals play a central role in cardiac homeostasis and disease. In the healthy heart, mitochondrial Ca levels modulate the rate of oxidative metabolism to match the rate of adenosine triphosphate consumption in the cytosol. During ischemia/reperfusion (I/R) injury, pathologically high levels of Ca in the mitochondrial matrix trigger the opening of the mitochondrial permeability transition pore, which releases solutes and small proteins from the matrix, causing mitochondrial swelling and ultimately leading to cell death.

Mitophagy modulation for the treatment of cardiovascular diseases.

Background: Defects of mitophagy, the selective form of autophagy for mitochondria, are commonly observed in several cardiovascular diseases and represent the main cause of mitochondrial dysfunction. For this reason, mitophagy has emerged as a novel and potential therapeutic target.

Methods: In this review, we discuss current evidence about the biological significance of mitophagy in relevant preclinical models of cardiac and vascular diseases, such as heart failure, ischemia/reperfusion injury, metabolic cardiomyopathy and atherosclerosis.

Association of inflammatory markers with incident heart failure or cancer in the HUNT3 and Health ABC population studies.

Aims: To investigate the relationship between chronic low-grade inflammation, as measured by high-sensitivity C-reactive protein (hsCRP) levels, and incident heart failure (HF) or cancer.

Methods And Results: We assessed the relationship between baseline hsCRP concentrations and subsequent HF or cancer in two community-based cohorts, the Trøndelag Health Study (HUNT3) and the Health, Aging and Body Composition (ABC) study. In the latter, the analysis was replicated with interleukin (IL)-1, IL-6, or tumour necrosis factor (TNF)-α instead of hsCRP.

Ischaemic heart disease in patients with cancer.

Cardiologists are encountering a growing number of cancer patients with ischaemic heart disease (IHD). Several factors account for the interrelationship between these two conditions, in addition to improving survival rates in the cancer population. Established cardiovascular (CV) risk factors, such as hypercholesterolaemia and obesity, predispose to both IHD and cancer, through specific mechanisms and via low-grade, systemic inflammation.

Real-world candidacy to mavacamten in a contemporary hypertrophic obstructive cardiomyopathy population.

Aims: In the EXPLORER-HCM trial, mavacamten reduced left ventricular outflow tract obstruction (LVOTO) and improved functional capacity of symptomatic hypertrophic obstructive cardiomyopathy (HOCM) patients. We sought to define the potential use of mavacamten by comparing real-world HOCM patients with those enrolled in EXPLORER-HCM and assessing their eligibility to treatment.

Methods And Results: We collected information on HOCM patients followed up at 25 Italian HCM outpatient clinics and with significant LVOTO (i.

Activation of the integrated stress response rewires cardiac metabolism in Barth syndrome.

Barth Syndrome (BTHS) is an inherited cardiomyopathy caused by defects in the mitochondrial transacylase TAFAZZIN (Taz), required for the synthesis of the phospholipid cardiolipin. BTHS is characterized by heart failure, increased propensity for arrhythmias and a blunted inotropic reserve. Defects in Ca-induced Krebs cycle activation contribute to these functional defects, but despite oxidation of pyridine nucleotides, no oxidative stress developed in the heart.

Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.

The present review summarizes the beneficial and detrimental roles of reactive oxygen species in myocardial ischemia/reperfusion injury and cardioprotection. In the first part, the continued need for cardioprotection beyond that by rapid reperfusion of acute myocardial infarction is emphasized. Then, pathomechanisms of myocardial ischemia/reperfusion to the myocardium and the coronary circulation and the different modes of cell death in myocardial infarction are characterized.

An arrhythmogenic metabolite in atrial fibrillation.

Background: Long-chain acyl-carnitines (ACs) are potential arrhythmogenic metabolites. Their role in atrial fibrillation (AF) remains incompletely understood. Using a systems medicine approach, we assessed the contribution of C18:1AC to AF by analysing its in vitro effects on cardiac electrophysiology and metabolism, and translated our findings into the human setting.

Diagnostic yield and predictive value on left ventricular remodelling of genetic testing in dilated cardiomyopathy.

Aims: We assessed the diagnostic yield of genetic testing and the relationship of left ventricular (LV) reverse remodelling (LVRR) with the presence of DNA pathogenic (P) or likely pathogenic (LP) variants in patients with dilated cardiomyopathy (DCM).

Methods And Results: From 680 outpatients followed at the Heart Failure Outpatient Clinic of our institution, we selected subjects with a diagnosis of DCM as defined by LV ejection fraction (LVEF) ≤40% and LV dilatation not explained by coronary artery disease or other causes. All patients were offered genetic investigation of 42 disease-associated DCM genes with next-generation sequencing.

Cardiac Involvement in Mitochondrial Disorders.

Purpose Of Review: We review pathophysiology and clinical features of mitochondrial disorders manifesting with cardiomyopathy.

Recent Findings: Mechanistic studies have shed light into the underpinnings of mitochondrial disorders, providing novel insights into mitochondrial physiology and identifying new therapeutic targets. Mitochondrial disorders are a group of rare genetic diseases that are caused by mutations in mitochondrial DNA (mtDNA) or in nuclear genes that are essential to mitochondrial function.