ABSTRACT
Left cardiac sympathetic denervation (LCSD) has emerged as an alternative therapy for individuals diagnosed with long QT syndrome (LQTS), a genetic disorder characterized by abnormal electrical activity in the heart and sudden cardiac death (SCD). This review examines the history and rationale behind LCSD in LQTS treatment, as well as the procedure, its efficacy, and indications along with the adverse effects that may be associated with it. LQTS presents with prolonged QT intervals on an electrocardiogram and can manifest as seizures, fainting, and SCD. Beta-blockers are the primary treatment for LQTS but some patients do not respond well to these medications or experience side effects. Additionally, implantable cardioverter-defibrillators (ICDs) are not always effective in preventing arrhythmias and can lead to complications. LCSD might offer an alternative approach by disrupting sympathetic activity in the heart. In humans, LCSD reduces the release of norepinephrine, normalizes the QT interval, and decreases the likelihood of life-threatening heart rhythms. The procedure does not impair heart rate or cardiac function due to the compensatory effects of the right cardiac sympathetic nerves. The surgical procedure for LCSD involves the removal of the lower half of the stellate ganglion and thoracic ganglia. Complete denervation is essential for optimal outcomes, while incomplete procedures are considered unacceptable. Traditional and minimally invasive approaches, such as video-assisted thoracic surgery (VATS), are available, with VATS offering shorter hospital stays and fewer complications. In conclusion, LCSD provides a viable treatment option for individuals with LQTS who do not respond well to beta-blockers or require additional protection beyond medication or ICDs. Further research and clinical experience are needed to enhance its acceptance and implementation in routine practice.
ABSTRACT
Hypertension (HTN) is a global health concern due to its increasing prevalence and association with life-threatening complications. An intriguing area of investigation in HTN research is the relationship between HTN and hyperuricemia. In light of this, we conducted a review to summarize the relevant studies exploring the link between elevated serum uric acid (sUA) concentration and new-onset HTN. Through a comprehensive search of PubMed Central, MEDLINE, and PubMed databases, we identified 20 studies that met our inclusion criteria. The research encompassed various study designs, including cohort studies, cross-sectional studies, reviews, and clinical trials. Pathologically, the elevated sUA levels activate the renin-angiotensin system and also cause the formation of urate crystals, triggering inflammation in the kidneys. Additionally, direct effects on the endothelium contribute to inflammation, oxidative stress, nitric oxide depletion, and smooth muscle cell proliferation, ultimately leading to atherosclerosis. These diverse mechanisms collectively play a role in the pathogenesis of HTN. Interestingly, lowering sUA has been shown to reverse early-stage HTN dependent on uric acid. However, this effect is not observed in the uric acid-independent second stage of HTN. Various studies have demonstrated an independent and dose-dependent association between sUA levels and the prevalence of HTN across different populations and genders. The review highlights the potential role of uric acid-lowering drugs, like allopurinol, in the prevention and early-stage management of HTN. However, there is scarce research on the efficacy of other uric acid-lowering agents and combination therapies. We believe our review provides compelling evidence of the association between elevated sUA concentration and new-onset HTN. Identifying and managing hyperuricemia can provide a preventive approach to reducing the burden of HTN and its associated complications.
ABSTRACT
Asthma is a common pathology worldwide that occurs due to chronic inflammation of the respiratory airways. Persistent pulmonary inflammation leads to low-grade systemic inflammation, influencing blood vessels and triggering coronary artery disease (CAD) events. This review's objectives include discussing the susceptible population for CAD, the mechanism underlying CAD creation in asthma patients, the characteristics of asthma, and the influence of anti-asthmatic medications on CAD development. Adult-onset asthma is strongly linked to CAD and stroke. Future research may shed light on these disparities. Atherosclerosis and asthma are linked through both intrinsic and extrinsic pathways, with inflammation being the intrinsic pathway and hypoxia and tachyarrhythmia being the extrinsic pathways. The most probable mechanisms for increased coronary vasospastic angina (CVsA) incidence in asthmatic patients are vascular smooth muscle cell hypercontraction and endothelial dysfunction. Studies have shown a dose-response relationship between asthma control and myocardial infarction (MI) risk, with uncontrolled asthma at the highest risk. Impairment of ventilatory function is a distinct risk factor for lethal MI and cardiovascular death (CVD). The use of beta-2-agonists and chronic oral glucocorticoid therapy in severe asthmatics has been linked to increasing the risk for CAD. However, some studies have shown that the risk of MI among patients with active asthma is not related to the use of asthma medications. Further research is needed to determine the involvement of adult asthma features and their treatments in the development of CAD.
