Cardiology in Review最新文献

Drug-coated balloons are a cornerstone of a "leave nothing behind" strategy in percutaneous coronary intervention. While paclitaxel-coated balloons (PCBs) are established, sirolimus-coated balloons (SCBs) represent a newer alternative. This meta-analysis integrates the latest evidence to compare the efficacy and safety of SCBs versus PCBs for coronary artery disease. We conducted a systematic review and meta-analysis following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, prospectively registered with International Prospective Register of Systematic Reviews (CRD420251157954). We searched PubMed, Embase, and Cochrane Central Register of Controlled Trial through September 2025 for randomized controlled trials and observational studies comparing PCB-only with SCB-only percutaneous coronary intervention. The primary clinical outcome was target lesion failure at 12 months. Key angiographic outcomes included in-segment late lumen loss, minimal lumen diameter, and diameter stenosis (DS). Fourteen studies (8 randomized controlled trials and 6 observational) with 6420 patients were included (PCB: n = 2042; SCB: n = 4378). The risk of target lesion failure was comparable between SCBs and PCBs [8.5% vs 9.2%; odds ratio 0.86, 95% (confidence interval) CI 0.71-1.05; P = 0.15], with no differences in its individual components. However, PCBs demonstrated superior angiographic outcomes, with significantly lower late lumen loss [Mean Difference (MD) -0.09 mm, 95% CI -0.15 to -0.01; P = 0.02] and larger minimal lumen diameter (MD 0.08 mm, 95% CI 0.01-0.14; P = 0.02). The reduction in DS with PCBs was not statistically significant (MD -2.11%, 95% CI -4.75 to 0.52; P = 0.12). This angiographic advantage was primarily driven by comparisons with the phospholipid-encapsulated SCB (MagicTouch). SCBs and PCBs demonstrate comparable clinical safety and efficacy at 1-year follow-up. Despite this, PCBs maintain an angiographic advantage, which is significantly influenced by the specific SCB excipient technology.

Hence, this research aims to establish the correlation between cardiac troponin and results in acute ischemic stroke (AIS) patients with heart failure. It examines 367 AIS patients stratified into 2 age groups: 65-74 years and ≥75 years. According to the findings, independent ambulation at admission or discharge signifies less severe strokes National Institutes of Health Stroke Scale. That is, the characteristics that are important for the stroke severity in patients of different ages are different: while the patients aged 75 and older, the important predictors are peripheral vascular disease and increased heart rate, the stroke severity in the younger age is predicted by smoking history and increased serum creatinine. Further, the article examines the value of troponin in a consecutive series of 1145 AIS patients and demonstrates that increased troponin is an independent predictor of in-hospital mortality. Mortality of the troponin-positive patients is significantly high with an odds ratio of 4.28. Moreover, the second trial on 200 AIS patients demonstrated that the cardiac troponin isoforms size is an independent predictor of major adverse cardiac events, odds ratio of 9.76. A study of 151,972 reaffirms the relationship between high troponin levels, increased stroke severity, and worse clinical prognosis. In conclusion, the current work fosters the significance of evaluating cardiac troponin in AIS patients with heart failure for enhanced mortality and adverse cardiovascular events' risk estimation.

A significant number of physicians are unclear of the vast clinical manifestations of dysautonomia and imbalance of the autonomic nervous system, specifically the parasympathetic and sympathetic nervous systems. The major obstacle has been an inability to determine the mechanism of action as well as multisystem dysfunction and a lack of clear-cut testing. Dysautonomia, a pathophysiological malfunction of the sympathetic and parasympathetic nerves in our bodies, can present as altered clinical functions of heart rate (tachycardia/bradycardia), altered breathing patterns, blood pressure (hypertension/hypotension), sweating, digestion, syncope, etc. These symptoms have caused specialists to miss this diagnosis because of relative nonspecificity. Our current analysis of patients demonstrates significant delays in diagnosis, misdiagnosis, and the development of chronic syndromes because of the above. We demonstrate that monitoring of heart rate and blood pressure with changes in position and respiration can be easily and quickly performed without orthostatic stress and can demonstrate the entities of sympathetic withdrawal, cholinergic excessive aspects as well as tachycardia, blood pressure dips with posture, etc. This analysis takes less than an hour without the need for injections or medication, thus more quickly informing the cardiologist/neurologist of the correct diagnosis. We will attempt to demystify these issues so that clinicians and the scientific community will have a better understanding of this entity and consider a diagnosis of dysautonomia earlier in the differential diagnostic process and start treatment approaches sooner.

The coalescence of anthracycline-induced cardiotoxicity and the evolving role of sodium-glucose co-transporter-2 (SGLT-2) inhibitors in oncology and cardiology has prompted a comprehensive review of their mechanisms, clinical implications, and future directions. Anthracyclines, potent chemotherapeutic agents, have been integral in cancer treatment, yet their potential for cardiac harm necessitates careful monitoring and management. We explore the multifactorial nature of anthracycline-induced cardiotoxicity, encompassing diverse patient populations, cumulative doses, and interplay with other treatments. While advancements in imaging and biomarker assessments aid in early detection, the lack of standardized criteria poses challenges. The emergent role of SGLT-2 inhibitors, initially developed for diabetes management, presents a novel avenue for cardioprotection. Beyond glycemic control, these inhibitors exhibit pleiotropic effects, including enhanced diuresis, anti-inflammatory actions, and modulation of energy sources. Consequently, SGLT-2 inhibitors are being investigated for their potential to mitigate cardiotoxic effects, promising an innovative approach in cardio-oncology. Despite these advancements, limitations in data interpretation and patient-specific considerations persist. The future of anthracycline-induced cardiotoxicity research lies in predictive biomarkers, precision medicine, multidisciplinary collaboration, and tailored treatment regimens. By navigating these challenges and harnessing emerging strategies, we aim to optimize cancer treatment efficacy while safeguarding cardiovascular health, ultimately paving the way for a new era of personalized and comprehensive oncologic care.

Titin, an extraordinary protein known for its colossal size and multifaceted roles, is a cornerstone in the structural and functional dynamics of striated muscle tissues, including the heart and skeletal muscles. Its sheer enormity, with a molecular weight exceeding 3000 kDa, is paralleled only by the immense influence it exerts on muscle physiology. This review will delve into the remarkable structural organization of Titin and the genetics of this molecule, including the common mutations resulting in various cardiomyopathies. We will delve deeper into its role in dilated cardiomyopathy, familial restrictive cardiomyopathy, hypertrophic cardiomyopathy, and left ventricular noncompaction cardiomyopathy. This review culminates by discussing the prospects of therapeutic strategies targeting Titin. While these interventions remain primarily theoretical, the possibilities are intriguing. Patients with Titin truncation mutations present unique challenges, but innovative approaches like gene therapy or preemptive treatments with drugs such as angiotensin-converting enzyme inhibitors or beta-blockers offer hope. This multi-pronged approach highlights the significance of understanding Titin's multifaceted role and its potential as a target for future therapeutic interventions.

Rapid deployment/sutureless (RDS) valves have recently emerged as an innovative surgical solution, providing an alternative to traditional methods of surgical aortic valve replacement (SAVR) by eliminating the need for suture placement and tying. This innovation leads to a reduction in aortic crossclamp and cardiopulmonary bypass times, enhancing the efficiency of the procedure. Among the 2 available RDS valves, the Edwards Intuity valve in particular has been demonstrated to be a particularly promising substitute in the field of SAVR. The Intuity valve distinguishes itself from other RDS and conventional valves by yielding superior outcomes, such as a significant reduction in mortality, increase in the longevity of the valve, and a marked decrease in both mean and peak transvalvular pressure gradients. These benefits collectively contribute to its appeal as a favorable new solution. However, further investigation is needed to conclusively determine the long-term outcomes and safety of RDS valves. Nevertheless, the utilization of the Intuity valve presents an exciting solution to the existing limitations of conventional and minimally invasive SAVR, especially for patients afflicted with severe aortic stenosis.

Endocardial fibroelastosis emerged as a challenging clinical phenomenon in the 1940s. It is characterized by an atypical proliferation of fibrous and elastic tissue within the heart and is primarily observed in childhood, occasionally displaying familial inheritance. While the precise cause remains elusive, various factors, including genetic, infectious, metabolic, autoimmune, oncologic, and medication-related influences, appear to play a role in its pathogenesis. The coexistence of endocardial fibroelastosis with multiple cardiac structural abnormalities manifests in symptoms of congestive heart failure and rhythm abnormalities. Despite its challenging diagnosis, various findings from ECG and imaging have proven beneficial in further evaluation of this condition. Finally, the treatment approach to endocardial fibroelastosis became complex due to addressing its concurrent cardiac abnormalities. Strategies for managing and preventing this condition are still under investigation. In this review, we intend to highlight the existing knowledge and illuminate future considerations regarding the etiology, diagnosis, and management of this disease.

Nowadays there is a lot of interest among the general population regarding the ketogenic diet (KD) and its health benefits. Most people following this diet have a reduced intake of carbohydrates which gets replaced by calories coming from fat and protein. Even though KD has shown some limited health benefits, there is no consensus on long-term effects and cardiovascular safety profile, especially the relation of KD to coronary artery disease (CAD). This concern comes predominantly from increased fat intake in KD and other similar diets with decreased carbohydrate intake. One study has shown a link between type 1 diabetes and increased coronary artery calcium scores but, in addition to many other limitations, after adjusting for other cardiovascular risk factors, the association was not significant. Results from a subanalysis of the CARDIA prospective study found that progression of CAD measured by coronary artery calcium was more pronounced in people with low-carbohydrate intake, especially when the compensatory calorie intake was from animal sources as compared to plant-based sources. In addition, other studies have tried to find a link between this type of diet and other traditional cardiovascular risk factors that have been traditionally associated with CAD, especially comparing low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride (TAG) levels without clear clinical significance. Other studies found an association between KD and all-cause mortality, but no association with cardiovascular mortality. Lastly, there is an association between animal-based KD and all-cause mortality in patients who have already suffered a myocardial infarction. These findings are modified when accounting for saturated fat intake, which may give us an insight into possible mechanisms to explain these differences.

Contrast-induced nephropathy (CIN) is a significant complication in patients undergoing coronary angiography, and its development is associated with increased morbidity and mortality. Left ventricular end-diastolic pressure (LVEDP) provides one index of left heart filling status. An elevated LVEDP can reflect volume overload or abnormal diastolic function and indicates a cardiac disorder. Data on the association between an elevated LVEDP and CIN are limited and have had conflicting results. We systematically searched the databases PubMed, Embase, and Scopus for full-text articles from database inception to May 2022. Studies were included if they evaluated the association between a high LVEDP and the incidence of CIN in patients undergoing coronary angiography. The study was registered in the PROSPERO CRD42022334070. A second search in PubMed identified randomized controlled trials using LVEDP to guide fluid administration during coronary procedures. Four studies were identified that used LVEDP to classify patients into groups to determine the association between the level and the development of CIN. In these studies, 240 patients of 2441 patients (9.8%) developed CIN. One study found no association between LVEDP levels and the development of CIN. Two studies found an increased frequency of CIN in patients with elevated levels using 2 cutoff points for LVEDP, ≥20 mm Hg and >30 mm Hg. One study found that lower LVEDP levels (5-14 mm Hg) were associated with the development of CIN. Three randomized control trials used LVDEP levels to manage fluid administration in patients undergoing coronary procedures; only one study found that the use of these levels to guide fluid administration resulted in better outcomes. In patients undergoing coronary angiography, an elevated LVEDP was not consistently associated with increased risk of CIN, and using LVEDP levels to guide fluid administration during these procedures did not always improve outcomes in comparison to other protocols. The use of LVEDP levels can help classify patients with cardiac disorders but does not necessarily provide an adequate description of the hemodynamic patterns in these patients to predict or prevent CIN in patients undergoing angiography.

Postcardiac injury syndrome (PCIS) serves as a comprehensive term encompassing a spectrum of conditions, namely postpericardiotomy syndrome, postmyocardial infarction (MI) related pericarditis (Dressler syndrome), and post-traumatic pericarditis stemming from procedures like percutaneous coronary intervention or cardiac implantable electronic device placement. These conditions collectively give rise to PCIS, triggered by cardiac injury affecting pericardial or pleural mesothelial cells, leading to subsequent inflammation syndromes spanning from uncomplicated pericarditis to substantial pleural effusion. A thorough literature search conducted on MEDLINE/PubMed utilizing search terms including "postacute cardiac injury syndrome," "postcardiac injury syndrome," "postcardiotomy syndrome," "postpericardiotomy syndrome," and "post-MI pericarditis" was instrumental in collating pertinent studies. To encapsulate the amassed evidence, relevant full-text materials were meticulously selected and amalgamated narratively. The pathophysiology of PCIS is proposed to manifest through an autoimmune-mediated process, particularly in predisposed individuals. This process involves the development of anti-actin and antimyosin antibodies after a cascade of cardiac injuries in diverse forms. Treatment strategies aimed at preventing recurrent PCIS episodes have shown efficacy, with colchicine and nonsteroidal anti-inflammatory drugs, including ibuprofen, demonstrating positive outcomes. Conversely, corticosteroids have exhibited no discernible benefit concerning prognosis or recurrence rates for this ailment. In summary, PCIS serves as a unifying term encompassing a spectrum of cardiac injury-related syndromes. A comprehensive review of relevant literature underscores the autoimmune-mediated pathophysiology in susceptible individuals. The therapeutic landscape involves the proficient use of colchicine and Nonsteroidal anti-inflammatory drugs to deter recurrent PCIS episodes, while corticosteroids do not appear to contribute to improved prognosis or reduced recurrence rates. This nuanced understanding contributes to an enhanced comprehension of PCIS and its multifaceted clinical manifestations, potentially refining its diagnosis and management.