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A key constraint of the LGE technique is the absence of standardized pulse sequences, compounded by the substantial variations in quantification methodologies.

Heart disease resulting from ischemia stands as a major contributor to global morbidity and mortality. Furthermore, the diagnosis and risk evaluation of those with coronary artery disease (CAD) have traditionally relied on finding the presence and extent of ischemia through physical or pharmacological stress testing, coupled with, or without, imaging methods (e.g.). Stress testing, encompassing stress echocardiography, single-photon emission computed tomography, and stress cardiac magnetic resonance, helps in assessing exercise stress. These methods are highly effective for identifying obstructive coronary artery disease, however, their capacity to accurately detect the absence of significant blockages is insufficient. The introduction of coronary computed tomography angiography, the only non-invasive method for analyzing coronary structure, provided a crucial piece of the diagnostic puzzle for patients with possible or longstanding ischemic heart disease. This review investigates the technical and clinical aspects of coronary computed tomography in the assessment of atherosclerotic burden. It focuses on emerging applications such as assessing the functional impact of CAD with FFRct, stress CT perfusion, and analysis of inflammatory markers on images, providing a comprehensive discussion of the strengths and weaknesses of each approach.

Cardiomyopathy, designated ‘arrhythmogenic,’ now encompasses a spectrum of heart muscle disease, extending from right ventricular (ARVC) to include the left ventricle (LV). Phenotypic diversity exists, featuring either biventricular (BIV) involvement or predominant left ventricular (ALVC) damage. The disease, defined as ‘scarring/arrhythmogenic cardiomyopathy (S/ACM)’, manifests with the specific characteristic of losing ventricular myocardium due to myocyte death, later replacing it with fibrous or fibro-fatty scar tissue. Impairment of systolic ventricular function is a consequence of myocardial scarring, which significantly elevates the risk of potentially lethal ventricular arrhythmias. nutlin-3a inhibitor Genetic and acquired conditions (frequently post-inflammatory) are encompassed within the ‘S/ACM’ rubric and show common, scarring phenotypic traits. Differential considerations include non-scarring heart diseases, potentially causing right ventricular expansion from a left-to-right circulatory shunt, or left ventricular enlargement and dysfunction associated with dilated cardiomyopathy. 2020’s refinement of the Padua criteria for S/ACM diagnosis was a direct result of the accumulating clinical insights into the expanded range of S/ACM phenotypes and the improvements in cardiac magnetic resonance (CMR) imaging techniques. The Padua criteria’s goal was improved S/ACM diagnosis, accomplished via the integration of CMR myocardial tissue characterization data. S/ACM patient risk stratification is generally determined by the amount of arrhythmic episodes and the extent of ventricular impairment, although supplementary ECG or imaging parameters may carry some weight. Medical therapy is critical for treating the complications of ventricular arrhythmias and heart failure. The implantable cardioverter defibrillator (ICD) remains the single demonstrably life-saving therapy, yet significant morbidity arises from device-related complications and inappropriate shocks. Selecting those patients who will benefit most profoundly from ICD therapy remains a significant obstacle in the execution of clinical care.

One-third of all ischemic strokes, which are a leading cause of mortality and disability, are directly linked to cardiac embolism. Cryptogenic strokes represent thirty percent of the total number of strokes. Echocardiography is indispensable in the diagnosis, treatment, and prevention of embolic stroke of unknown origin in this context, given its accessibility, safety, and affordability. Transthoracic and transoesophageal echocardiographic findings have significantly influenced therapeutic interventions, leading to the initiation of anticoagulation, antimicrobial treatment, patent foramen ovale closure, or cardiac tumor removal. Cardioembolic sources frequently involve left atrial appendage thrombi, left ventricular thrombi, vegetations arising from endocarditis, paradoxical emboli through patent foramen ovale, prosthetic device thromboses, and intracardiac tumors. The presence of a cardioembolic source, while suggestive of a possible ischemic stroke risk, does not guarantee it is the definite and singular cause. This review details the significance of echocardiography, examining the main sources of cardiac embolism and their observable echocardiographic patterns.

Dilated cardiomyopathy, a primitive heart muscle condition, displays structural and functional irregularities, without a definitively identified cause. Serving as an ‘umbrella’ term, it encompasses the final common pathway of different pathogenic processes and gene-environment interactions. The correlation between a thorough diagnostic workup, an accurate patient characterization, and the positive prognosis of the patient is undeniable. To ensure comprehensive care, the physician should integrate a multi-pronged strategy, including a careful medical history, physical examination, imaging data, and genetic testing. To determine the cause, a characterization must be carried out, and an appropriate assessment of arrhythmic risk should be undertaken. To account for the disease’s temporal evolution and individual risk modifications, follow-up evaluations must be repeated meticulously. In order to establish a diagnosis and a treatment plan specifically for the individual patient, a thorough characterization, utilizing a personalized medicine approach, is essential.

Even with successful reperfusion of the culprit lesion, individuals who have experienced acute coronary syndrome (ACS) still face a risk of major adverse cardiovascular events (MACE). Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i), when integrated with standard lipid-lowering therapies, have proven effective in reducing low-density lipoprotein cholesterol (LDL-C) levels in large, randomized clinical trials enrolling patients at high risk for cardiovascular events, consistently decreasing major adverse cardiovascular events (MACE). The employment of PCSK9i for a rapid and vigorous LDL-C decrease is strongly justified in ACS patients. Through the PACMAN-AMI trial, investigators examined the hypothesis, finding that the addition of biweekly subcutaneous alirocumab to high-intensity statin therapy in ACS patients, compared to a placebo group, resulted in a significantly greater degree of coronary plaque regression in non-infarct-related arteries following a 52-week period, as evaluated using advanced intra-coronary imaging methods. The observed findings potentially justify early, very intensive LDL-C-lowering strategies in the acute phase of ACS, altering the typical treatment course by providing a mechanistic explanation.

A heterogeneous clinical syndrome, acute heart failure is the primary reason for unplanned hospital admissions in those aged over sixty-five. The clinical presentation of heart failure can be influenced by the patient’s prior medical record, pre-existing heart ailments, and the way fluid collects within the blood vessels. Integration of clinical, echocardiographic, and laboratory data is critical to enabling better clinical decisions and therapeutic choices. A pulmonary artery catheter might be indispensable in achieving a more precise evaluation of patient hemodynamics, thereby enabling appropriate escalation or de-escalation of therapy, particularly when clinical, echocardiographic, and laboratory parameters fail to offer clear insights or right ventricular dysfunction is detected. Furthermore, a pulmonary artery catheter could prove advantageous in treating patients experiencing cardiogenic shock and undergoing mechanical circulatory support. As therapy diminished and circulatory stability was achieved, the implementation of guideline-based medical treatments should be prioritized to minimize the potential for future heart failure hospitalizations and fatalities, emphasizing the management of persistent fluid accumulation.

A substantial portion of the global burden of illness is attributable to heart failure (HF), with significant health care costs primarily stemming from hospitalizations. The remote control of vital signs and health status information can potentially forestall the development of heart failure instability-inducing factors by facilitating the initiation of early therapeutic procedures. A key goal of telemedicine is to replace the reactive intervention strategy, where therapy reacts to symptom deterioration, with a proactive strategy, where therapeutic changes are based on changes in monitored parameters during the pre-disease stage. The principal objective of this study is to investigate the most important results observed from employing telemedicine in HF patients, comprising both those with and without cardiac electronic devices, or those equipped with haemodynamic sensors. This is followed by an assessment of the important issues and beneficial applications.

Inherited Brugada syndrome, a channelopathy, is associated with a heightened risk for sudden cardiac death (SCD), originating from ventricular arrhythmias (VA), accompanied by a more frequent occurrence of supraventricular arrhythmias in contrast to the general population. Implantable cardioverter-defibrillators (ICDs), while recommended for the prevention of sudden cardiac death (SCD), do not guarantee the avoidance of ventricular arrhythmias (VA). This article presents a concise overview of pharmacological treatments for Brugada syndrome, with a particular emphasis on the application of quinidine. The preventative role of quinidine in Brugada syndrome-associated ventricular arrhythmias has been documented by a number of limited investigations, particularly among patients with implantable cardioverter-defibrillators who experience repeated shocks or in asymptomatic patients exhibiting inducible ventricular fibrillation (VF) on electrophysiological study.