Cardiology in Review最新文献

Hypopituitarism is a rare condition that presents significant diagnostic challenges, particularly in elderly patients (over 65 years of age). It often manifests with a range of symptoms affecting multiple organ systems, with cardiovascular involvement being uncommon. As a result, the underlying diagnosis may be easily overlooked. Physicians must maintain a high level of awareness about hypopituitarism to establish an accurate diagnosis and initiate appropriate treatment. This study reviews recent advances in understanding the cardiovascular manifestations of hypopituitarism.

Postprocedural anticoagulation (PPAC) after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) can mitigate thrombotic events. However, current clinical guidelines do not recommend PPAC after PCI considering the scarce evidence supporting its use. A comprehensive literature search of electronic databases was conducted to identify studies comparing PPAC to no anticoagulation (AC) after PCI for AMI. Using the inverse-variance random-effects model, we pooled risk ratios (RRs) with 95% confidence intervals (CIs), with P < 0.05 considered statistically significant. Seven studies with a total of 47,981 patients (32,010: PPAC and 15,971: no AC) were included in the final analysis. PPAC administration demonstrated no significant difference in 30-day all-cause mortality [RR, 0.73 (95% CI, 0.47-1.16); P = 0.19], 30-day cardiovascular mortality [RR, 0.76 (95% CI, 0.45-1.30); P = 0.32], 30-day myocardial infarction [RR, 0.68 (95% CI, 0.41-1.12); P = 0.13], 30-day stroke [RR, 0.89 (95% CI, 0.47-1.67); P = 0.71], 30-day target vessel revascularization [RR, 0.74 (95% CI, 0.37-1.47); P = 0.39], 30-day stent thrombosis [RR, 1.08 (95% CI, 0.75-1.57); P = 0.67], and 30-day bleeding [RR, 1.25 (95% CI, 0.83-1.88); P = 0.29] compared with no AC. This meta-analysis concludes that there are no benefits of routine PPAC after PCI in AMI. The decision to prolong anticoagulant use post-PCI depends on risk versus benefits, which vary from case to case. Future large-scale multicentric randomized trials are warranted to corroborate the results of this meta-analysis.

Endosaccular flow disruption has emerged as a transformative approach for treating wide-neck intracranial aneurysms, which are characterized by neck diameters exceeding 4 millimeters or dome-to-neck ratios below 2. This review examines the technical specifications and clinical outcomes of major endosaccular devices, including the Woven EndoBridge (WEB) device, the Artisse embolization device, the Medina embolization device, the neck bridging device for bifurcation aneurysms, the polycarbonate urethane membrane-assisted device, the Galaxy saccular endovascular aneurysm lattice, and the Contour Neurovascular System. Analysis of pivotal trials reveals varying degrees of efficacy and safety across platforms. The WEB device demonstrated complete occlusion rates of 51.7% to 56.1% at 1 year, with adequate occlusion reaching 84.6% in the WEB Intrasaccular Therapy Study trial and sustained improvement in 76.8% of cases at 5 years. The Artisse system showed initial promise but concerning declines in adequate occlusion from 66.7% at 6 months to 57.1% at 36 months. More recent innovations such as the Galaxy SEAL device achieved complete occlusion in 76.9% of cases in preliminary studies in 1 year. Thromboembolic complications occurred in 12.9% to 17.7% of cases across devices though procedure-related mortality remained below 2%. While the WEB device has established a robust safety and efficacy profile through long-term follow-up data, newer technologies demonstrate promising early results but require extended surveillance. Current challenges focus on optimizing device sizing, improving delivery systems, and enhancing material properties to maximize occlusion rates while minimizing complications. The evolution of these technologies continues to expand treatment options for complex aneurysms previously challenging to address through conventional endovascular or surgical approaches.

Right ventricular myocardial infarction (RVMI) is a significant and distinct form of acute myocardial infarction associated with considerable morbidity and mortality. It occurs most commonly due to proximal right coronary artery obstruction, often in conjunction with inferior myocardial infarction. RVMI poses unique diagnostic and therapeutic challenges due to the anatomical and functional differences between the right and left ventricles. Key clinical manifestations include symptoms of right-sided heart failure, such as hypotension, jugular venous distention, and peripheral edema. The pathophysiology of RVMI involves impaired right ventricular (RV) function, decreased cardiac output, and poor hemodynamic stability, often leading to cardiogenic shock. Diagnostic tools, including 12-lead electrocardiography, echocardiography, cardiac magnetic resonance imaging, and coronary angiography, play crucial roles in detecting RVMI and determining its severity. Treatment strategies focus on early revascularization through primary percutaneous coronary intervention or thrombolysis, maintaining adequate RV preload, and managing arrhythmias and hemodynamic instability. In severe cases, mechanical circulatory support, such as intra-aortic balloon pumps and extracorporeal membrane oxygenation, may be required. Despite advancements in imaging and therapeutic approaches, RVMI remains a complex condition that demands timely and specialized management to improve patient outcomes. Further research is needed to refine diagnostic and treatment strategies and to reduce the high mortality rates associated with this condition.

The invention of the string galvanometer by Willem Einthoven in 1901 ushered in a new era of clinical investigation. Previous instruments were capable only of rudimentary measurements that were of limited utility. Advances in physiology and engineering allowed Einthoven to construct a device that was uniquely capable of recording the minute electrical currents of the heart. Early string galvanometers were massive, immovable machines. Over time, the apparatus became smaller and portable, allowing examinations at the bedside. In the decades that followed, clinicians used the now ubiquitous instrument to evaluate cardiac arrhythmias, coronary artery disease, and conduction abnormalities. The remainder of the century saw the evolution of the contemporary 12-lead electrocardiogram, with standards established regarding technique and nomenclature. Awarded the Nobel Prize in 1924 for "his discovery of the mechanism of the electrocardiogram," Einthoven's legacy endures in modern clinical medicine.

Moyamoya disease (MMD) is a vascular disorder characterized by steno-occlusive alterations in cerebral arteries, often resulting in ischemic or hemorrhagic events predominantly affecting the female population and more common in Asian populations. Despite its predominantly neurological manifestations, recent research suggests a potential association between MMD and cardiovascular diseases (CVDs). MMD involves various genetic and environmental factors, with mutations in the RNF213 gene being strongly implicated in disease susceptibility, with histopathological findings revealing intimal lesions and smooth muscle proliferation, contributing to vascular occlusion as well as dysregulation of circulating endothelial and smooth muscle progenitor cells further complicating MMD's pathogenesis. However, the exact nature of the relationship between MMD and CVD remains incompletely understood, and emerging evidence suggests a potential interplay between these pathologies. In this study, we discuss the potential link between MMD and CVD, exploring genetic factors, pathophysiological mechanisms, and studies highlighting cardiac manifestations in MMD patients.

Coronary artery calcification is an impediment to percutaneous coronary interventions by obstructing the device pathway or stent deployment. To facilitate percutaneous coronary intervention in such complex lesions, high-pressure balloon dilations, atherectomy procedures, and specialty balloons are used but they all come with considerable limitations and periprocedural complications like dissection and perforation. To surpass these disadvantages, intravascular lithotripsy was introduced which acts by delivering high-pressure pulsatile sonic waves circumferentially thereby destroying the calcium deposits. It is a safe and effective treatment modality in treating severe coronary artery calcification and facilitating stent delivery with minimal complications.

Heart failure (HF) poses a significant medical challenge, affecting millions of adults in the United States. High-output heart failure (HOHF) is a distinct subtype characterized by elevated cardiac output exceeding 8 L/min or a cardiac index >4 L/min/m². Patients with HOHF often present similarly to those with heart failure with reduced ejection fraction and heart failure with preserved ejection fraction. However, the underlying pathophysiology differs; triggered by a progressive decline in systemic vascular resistance, the ensuing elevation of cardiac output eventually leads to left ventricular remodeling and HF. Failure to differentiate HOHF from other variant forms of HF has implications for management, particularly relating to the use of vasodilator medications with potentially deleterious consequences, ensuing from the unrestrained adoption of societal guideline-directed medical therapy recommendations. Despite its clinical importance, HOHF remains under-examined in literature, with limited recognition and understanding among clinicians. This review aims to provide a comprehensive analysis of knowledge surrounding HOHF, exploring its definition, etiopathology, and underlying pathophysiological mechanisms. Recognizing the challenges in diagnosing HOHF, we propose a novel diagnostic algorithm tailored to address the subtleties of this often-misdiagnosed variant of HF.

Obstructive sleep apnea (OSA), a highly prevalent and serious disorder with significant complications, causes considerable daytime and nighttime symptoms as well as long-term consequences and is yet an underdiagnosed and inadequately treated condition. Patients with OSA undergo frequent awakenings during the sleep cycle and find it impossible to get restorative sleep. Individuals are extremely fatigued, sleepy, and irritable throughout the day. Reduced exercise performance and physical activity contribute to a decrease in energy metabolism and weight gain. Those in this population may experience decreased motivation, which could result in depressive symptoms. The abrupt drops in oxygen levels during the sleep cycle result in profound spikes in blood pressure and strain the cardiovascular system. Given its close tie with major cardiovascular risk factors, OSA is linked with various cardiovascular diseases, including coronary artery disease, cardiac arrhythmia, poorly controlled blood pressure, heart failure, and stroke. Continuous positive airway pressure is an effective and tried-trusted approach for symptom relief and improving quality of life. Despite its benefits, patients struggle with compliance and often go untreated because of physical discomfort and perceived inconvenience of using these machines. One other explanation for this could be the lack of awareness, comprehensive data, and extensive research on its effects on long-term cardiovascular and metabolic complications caused by OSA. The current standard treatment for OSA, using adequate positive airway pressure, greatly reduces cardiovascular morbidity. Nevertheless, patients with cardiovascular disorders continue to be highly susceptible to OSA and its detrimental clinical consequences, even with effective therapy available. In summary, continuous positive airway pressure has an indirect potential to affect cardiovascular outcomes, but further studies should be done to address issues with patient compliance and adherence.

The vascular endothelium and its endothelial glycocalyx contribute to the protection of the endothelial cells from exposure to high levels of sodium and help these structures maintain normal function by regulating vascular permeability due to its buffering effect. The endothelial glycocalyx has negative surface charges that bind sodium and limit sodium entry into cells and the interstitial space. High sodium levels can disrupt this barrier and allow the movement of sodium into cells and extravascular fluid. This can generate reactive oxygen species that inhibit nitric oxide production. This leads to vasospasm and increases intravascular pressures. Overtime vascular remodeling occurs, and this changes the anatomy of blood vessels, their intrinsic stiffness, and their response to vasodilators and results in hypertension. Patients with increased salt sensitivity are potentially at more risk for this sequence of events. Studies on the degradation of the glycocalyx provide insight into the pathogenesis of clinical disorders with vascular involvement, but there is limited information available in the context of higher concentrations of sodium. Data on higher intake of sodium and the imbalance between nitric oxide and reactive oxygen species have been obtained in experimental studies and provide insights into possible outcomes in humans. The current western diet with sodium intake above recommended levels has led to the assessment of sodium sensitivity, which has been used in different populations and could become a practical tool to evaluate patients. This would potentially allow more focused recommendations regarding salt intake. This review will consider the structure of the vascular endothelium, its components, the effect of sodium on it, and the use of the salt blood test mini.