Advanced age alone appears to be a risk factor for increased susceptibility to cardiac arrhythmias. We previously observed in the aged rat heart that sinus rhythm ventricular activation is delayed and characterized by abnormal epicardial patterns although conduction velocity is normal. While these findings relate to an advanced stage of aging, it is not yet known when and how ventricular electrical impairment originates and which is the underlying substrate. To address these points, we performed continuous telemetry ECG recordings in freely moving rats over a six-month period to monitor ECG waveform changes, heart rate variability and the incidence of cardiac arrhythmias. At the end of the study, we performed in-vivo multiple lead epicardial recordings and histopathology of cardiac tissue. We found that the duration of ECG waves and intervals gradually increased and heart rate variability gradually decreased with age. Moreover, the incidence of cardiac arrhythmias gradually increased, with atrial arrhythmias exceeding ventricular arrhythmias. Epicardial multiple lead recordings confirmed abnormalities in ventricular activation patterns, likely attributable to distal conducting system dysfunctions. Microscopic analysis of aged heart specimens revealed multifocal connective tissue deposition and perinuclear myocytolysis in the atria. Our results demonstrate that aging gradually modifies the terminal part of the specialized cardiac conducting system, creating a substrate for increased arrhythmogenesis. These findings may open new therapeutic options in the management of cardiac arrhythmias in the elderly population.
The inadequate long-term efficacy of anti-arrhythmic therapy has been one of the main reasons for the development of non-pharmacological interventions for patients with atrial fibrillation such as catheter and surgical ablation. This has greatly increased interest in the functional morphology and electrophysiological properties of the atria and related anatomical structures. This article is the second of a two-part review that aims to provide anatomical and functional details concerning some of the principal anatomical sites commonly targeted by ablative procedures for treating atrial fibrillation, and covers pulmonary veins, ganglionated plexi, caval veins, and the ligament of Marshall. It also provides some general information about site-specific ablation procedures.
Experimental and clinical evidence suggests that the natural history of atrial fibrillation is characterised by increased structural remodelling, which may play a pivotal role in maintaining the arrhythmia and clinically favours progression from paroxysmal to persistent atrial fibrillation. In this setting, anti-arrhythmic therapy gradually becomes inefficient, and this limitation has led to the introduction of new non-pharmacological interventions such as surgical or catheter ablation. At the same time, interest in the functional morphology and electrophysiological properties of the atria and their related anatomical structures has greatly increased. This article is the first of a two-part review whose main purpose is to describe the anatomical and functional details of some of the principal anatomical locations that are commonly targeted by ablative procedures to treat this supraventricular arrhythmia. In particular, this manuscript has dealt with the atrial structures (atrial myocardium and coronary sinus). General information on ablation procedures has also been provided.
Atrial fibrillation (AF) in mitral regurgitation (MR) is a complex disease where multiple factors may induce left-atrial structural remodeling (SR). We explored the differential SR of the left-atrial posterior wall (LAPW) of patients affected by MR with or without persistent AF, and the expression of key proteins involved in its pathogenesis.
The fact that some atrial and ventricular disorders (e.g., atrial fibrillation and heart failure) have a structural basis and cause atrial myocardial remodeling has led to increasing attention being paid to the atrial chambers. Furthermore, the rapid development of mapping and ablative procedures as a means of diagnosing and treating supraventricular arrhythmias has generated considerable interest in atrial gross anatomy, histology and ultrastructure. The aim of this article is to provide a comprehensive overview of the structure of the left and right atria (at macroscopic, histological and ultrastructural level) in relation to their function. In addition to analyzing normal atria, we also discuss functional anatomy in the case of atrial fibrillation and heart failure.
Carbon monoxide (CO) intoxication is the most common cause of accidental poisoning in developed countries and, although most published data relate to its neurological manifestations, it often leads to cardiac damage. Myocardial hypoxia due to the formation of carboxyhemoglobin is not enough to explain such damage fully as a major role is played by the direct effect of CO on the heart as a result of the reversible inhibition of mitochondrial respiration and oxidative stress. Cardiac damage secondary to CO poisoning can be detected not only in patients with known ischemic heart disease but also in subjects with undamaged coronary arteries. Given the wide range of cardiovascular manifestations (the entity of which is related to the severity of intoxication), useful information can be obtained by carefully recording the patients medical history, analyzing electrocardiographic alterations, and determining the biochemical markers of cardiac necrosis. Moreover, echocardiographic examination may highlight the extent of the alterations in left ventricular function due to myocardial stunning associated with CO intoxication and evaluate its evolution over time. Clinical studies suggest that all patients admitted to hospital with moderate to severe CO poisoning should routinely undergo ECG and serial evaluation of cardiac markers, and that those with positive signs of myocardial cytonecrosis or preexisting ischemic heart disease should also undergo echocardiography. A finding of myocardial damage in patients with CO poisoning seems to indicate an unfavorable long-term prognosis, although it needs further confirmation.
Minimally invasive atrial fibrillation surgery (MIAFS) has become a well established and increasingly used option for managing patients with stand-alone arrhythmia. Pulmonary veins (PVs) isolation continues to be the cornerstone of ablation strategies. Indeed, in most cases, atrial fibrillation (AF) is triggered in or near the PVs. Nevertheless, ectopic beats initiating AF may occasionally arise from non-PV foci. The knowledge of the anatomy and underlying morphology of PVs and non-PV foci is essential for cardiac surgeons treating AF patients with epicardial minimally invasive procedures. The anatomical structures relevant to the pathogenesis and the epicardial treatment of AF include the PVs, the pericardial space, the pericardial sinuses, the phrenic nerve, the left atrium, the retro-atrial and caval ganglionated plexuses, the ligament of Marshall, the caval veins and the left atrial appendage. In this review, we briefly describe the basic anatomy of these structures and discuss their specific correlations for cardiac surgeons interested in performing MIAFS.
In humans, chronic stressors have long been linked to cardiac morbidity. Altered serotonergic neurotransmission may represent a crucial pathophysiological mechanism mediating stress-induced cardiac disturbances. Here, we evaluated the physiological role of serotonin (5-HT) 1A receptors in the autonomic regulation of cardiac function under acute and chronic stress conditions, using 5-HT(1A) receptor knockout mice (KOs). When exposed to acute stressors, KO mice displayed a higher tachycardic stress response and a larger reduction of vagal modulation of heart rate than wild type counterparts (WTs). During a protocol of chronic psychosocial stress, 6 out of 22 (27%) KOs died from cardiac arrest. Close to death, they displayed a severe bradycardia, a lengthening of cardiac interval (P wave, PQ and QRS) duration, a notched QRS complex and a profound hypothermia. In the same period, the remaining knockouts exhibited higher values of heart rate than WTs during both light and dark phases of the diurnal rhythm. At sacrifice, KO mice showed a larger expression of cardiac muscarinic receptors (M2), whereas they did not differ for gross cardiac anatomy and the amount of myocardial fibrosis compared to WTs. This study demonstrates that chronic genetic loss of 5-HT(1A) receptors is detrimental for cardiovascular health, by intensifying acute, stress-induced heart rate rises and increasing the susceptibility to sudden cardiac death in mice undergoing chronic stress.
Acute myocardial infarction (AMI) is a multifactorial disease with a complex pathogenesis where lifestyle, individual genetic background and environmental risk factors are involved. Altered inflammatory responses are implicated in the pathogenesis of atherosclerosis and a premature AMI of parents is associated with an increased risk of the disease in their offspring (Offs). However, the genetic background of familiarity for AMI is still largely unknown. To understand which genes may predispose to increased risk of cardiovascular disease gene polymorphism of immune regulatory genes, and clinical events from the Offs of parents with an early AMI were investigated. Genetics data from Offs were compared with those obtained from healthy subjects and an independent cohort of patients with clinical sporadic AMI. Rates of clinical events during a 24?years follow up from Offs and from an independent Italian population survey were also evaluated.
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