Continuing Cardiology Education最新文献

Abdominal aortic aneurysm (AAA) is a frequent cause of death. Management of AAA includes different strategies: open surgery repair, endovascular repair and, for small AAA, medical therapy and careful follow-up. Endovascular repair is a valid alternative to surgical repair, especially in patients whit high procedural risk.

Pulmonary hypertension is a fatal disease of multiple etiologies that is estimated to affect over 100 million people worldwide. The disease is defined hemodynamically as a mean pulmonary artery pressure ≥ 25 mmHg at rest. Despite important advances in our understanding of the pathobiology of this disease and improvements in patient management, outcomes are still poor and no curative treatments are currently available. The complex nature of this disease requires detailed clinical evaluation for accurate diagnosis and treatment. Recent advances in clinical recognition, classification, and understanding of the underlying pathological processes in pulmonary hypertension have led to improved diagnostic testing and therapeutic options for patients. A hallmark of pulmonary hypertension is an increased pulmonary vascular resistance which leads to progressive elevations in pulmonary artery pressure, resulting in compensatory right ventricular hypertrophy and, ultimately, heart failure. Clinically, these pulmonary vascular changes initially present as nonspecific symptoms, including unexplained dyspnea on exertion, fatigue, chest pain, and syncope. Signs of right ventricular dysfunction are also frequently present. Common pathogenic features of pulmonary hypertension include sustained pulmonary vasoconstriction, vascular remodeling of the small pulmonary arteries, in situ thrombosis, and increased vascular wall stiffness, resulting in increased pulmonary arterial pressure due to increased pulmonary vascular resistance. Despite improvements in clinical classification and understanding of the underlying pathogenic mechanisms of pulmonary hypertension, current therapies are limited to supportive care and targeting pulmonary vasoconstriction. There remains a need to identify novel therapeutic targets in this disease. This review provides a succinct overview of the clinical classification and pathophysiology of PH that can be used as a reference by physicians and physician-scientists.

Myocardial perfusion imaging with single-photon emission computed tomography (SPECT) is an important and widely used non-invasive imaging test for the diagnosis and semiquantification of myocardial ischemia. SPECT data, acquired after a stress test and at rest on a gamma camera, shows left ventricular tracer uptake during stress and at rest. The tracer distributions are proportionate to the relative, regional coronary-flow distributions, respectively. A stress-induced perfusion defect reflects myocardial ischemia, while a permanent defect, unchanged from stress to rest, indicates myocardial infarction. By ECG-gating global and regional left ventricular function can also be assessed. The three most important indications for SPECT in the setting of interventional cardiology include (1) the diagnosis of coronary artery disease in intermediate-risk patients, (2) the assessment of ischemia in patients with prior successful revascularization and recurrence of symptoms, and (3) the diagnosis of acute coronary syndrome in the emergency department. The amount of ischemia is related to the outcome of patients undergoing revascularization. It was observed that patients with an ischemic area of <10% of the left ventricle demonstrated by SPECT benefit from staying on optimal medical therapy, whereas patients with more ischemia on SPECT benefit from revascularization. Guidelines and appropriate use criteria for the indications of SPECT in relation to interventional cardiology have been published by the European Society and American College of Cardiology.

The number of patients with pulmonary arterial hypertension related to congenital heart disease (PAH-CHD) seen in specialist centers continues to increase. The extreme end of the spectrum, namely Eisenmenger's syndrome, is further compromised with chronic cyanosis and multiorgan disease, In this review we present the current knowledge on definition, prevalence, pathophysiology, classification, diagnosis, and treatment of this entity that has great impact on CHD patients’ life.

Pulmonary hypertension (PH) is a disorder with sometimes a challenging diagnosis, which can be made only by right heart catheterization. The role of echocardiography in the work-up of these patients is manifold. Its main contribution is in the assessment of the presence of PH in the setting of a clinical suspicion and thus it serves as a gatekeeper to avoid unnecessary invasive catheterizations. In this regard, estimation of pulmonary artery pressure is a central but not the only component that should be pursued, since there are many other additional echocardiographic features that can help the clinician to estimate the probability of the presence of PH more accurately and to fully assess its pathophysiological consequences. In addition, echocardiography can offer invaluable insight into right ventricular size and function, which is the cardiac chamber that is mainly affected by the disease and finally, it can provide important clues about the cause of PH and mainly help identify patients with pulmonary venous hypertension, in which treatment is entirely different from patients with precapillary hypertension. This review summarizes the echocardiographic findings commonly observed in patients with PH and focuses on important features that allow the clinician to exploit the full potential of this modality when assessing these patients.

Very late stent thrombosis (VLST) represents a rare, but potentially lethal complication, in the era of percutaneous coronary intervention. Its etiology, pathogenesis, and predictive factors have not yet been established due to its relatively low prevalence and multifactorial nature. In this review article, after presenting the current definitions on stent thrombosis, we focus on the contemporary data on VLST, for both bare-metal stents and drug-eluting stents. Possible pathophysiological mechanisms and predictive factors are also illustrated, with data drawn from several multicenter studies. Factors such as younger patients, smokers at the time of initial DES implantation, STEMI or the presence of thrombus at the time of initial DES implantation, overlapping stents, seem to represent independent predictors of VLST. Finally, there is a special reference on cases of VLST, studied with optical coherence tomography (OCT). OCT managed to identify the cause of VLST in over 97% of the cases in these studies, whereas some of the most common mechanisms of VLST in these patients were stent malapposition, neoatherosclerosis rupture, uncovered struts, and stent underexpansion.

Heart failure (HF) is the common sequela of many cardiovascular diseases. Although device-based treatments and pharmacotherapies have improved patient survival, current standard therapies are far from optimal, and do not address the molecular mechanisms underlying HF pathogenesis. In the last decade, cardiac gene therapy has emerged as an innovative experimental therapeutic strategy for the treatment of advanced HF. Increasing insights into the molecular pathophysiology and improvements in gene targeting approaches provide novel therapeutic modalities. In this review we focus on the recent developments in cardiac gene therapy strategies targeting advanced HF. We emphasize ongoing clinical trials, and discuss the limitations and future evolution of the field.