1,720,976 research outputs found
Safety of non-vitamin K antagonist oral anticoagulants: concerns in patients with atrial fibrillation and glomerular hyperfiltration?
No full textPrediction of post percutaneous coronary intervention myocardial ischaemia
No full textFollowing revascularisation the majority of patients obtain symptom relief and improved quality of life. However, myocardial ischaemia may recur or persist in a significant patient subset. Symptom recurrence is usually attributed to inaccurate evaluation of epicardial stenosis, incomplete revascularisation or stent failure and disease progression. However, technological advances with modern imaging and/or physiological evaluation of epicardial plaques have not solved this issue. Conversely, recent clinical studies have shown that abnormal coronary vasomotion and increased myocardial resistance are frequent determinants of post-percutaneous coronary intervention (PCI) myocardial ischaemia. Strategies to enhance prediction of post-PCI angina include proper selection of patients undergoing revascularisation, construction of clinical prediction models, and further invasive evaluation at the time of coronary angiography in those with high likelihood
Pharmacological Agents Targeting Myocardial Metabolism for the Management of Chronic Stable Angina : an Update
No full textDespite continuous advances in myocardial revascularization procedures and intracoronary devices, patients with ischemic heart disease (IHD) still experience worse prognosis and poor quality of life (QoL). Indeed, chronic stable angina (CSA) is a common disease with a large burden on healthcare costs. Traditionally, CSA is interpreted as episodes of reversible myocardial ischemia related to the presence of stable coronary artery plaque causing myocardial demand/supply mismatch when myocardial oxygen consumption increases. Accordingly, revascularization procedures are performed with the aim to remove the flow limiting stenosis, whereas traditional medical therapy (hemodynamic agents) aims at reducing myocardial oxygen demands. However, although effective, none of these treatment strategies or their combination is either able to confer symptomatic relief in all patients, nor to reduce mortality. Failure to significantly improve QoL and prognosis may be attributed at least in part to this “restrictive” understanding of IHD. Despite for many years myocardial metabolic derangement has been overlooked, recently it has gained increased attention with the development of new pharmacological agents (metabolic modulators) able to influence myocardial substrate selection and utilization thus improving cardiac efficiency. Shifting cardiac metabolism from free fatty acids (FA) towards glucose is a promising approach for the treatment of patients with stable angina, independently of the underling disease (macrovascular and/or microvascular disease). In this sense cardiac metabolic modulators open the way to a “revolutionary” understanding of ischemic heart disease and its common clinical manifestations, where myocardial ischemia is no longer considered as the mere oxygen and metabolites demand/supply unbalance, but as an energetic disorder. Keeping in mind such an alternative approach to the disease, development of new pharmacological agents directed toward multiple metabolic targets is mandatory
Long-Term Follow-Up of Elective Chronic Total Coronary Occlusion Angioplasty Analysis From the U.K. Central Cardiac Audit Database
No full textTrimetazidine
No full textCoronary revascularization is not a suitable option for all patients with chronic stable angina (CSA) and, even when such a strategy is adopted, in conjunction with optimal medical therapy (OMT) as suggested by international guidelines, not all of them succeed to be symptom free. Importantly, this subset represents an increasing population, being widespread among diabetics and elderly. Irrespective of the mechanism responsible for myocardial ischemia, it has been shown that when ischemia develops it promotes substantial changes at the level of myocardial metabolism and reduces cardiac efficiency. Indeed, an increase in fatty acids (FFAs) oxidation and a decrease in glucose oxidation are both observed during myocardial ischemia, along with intracellular proton (H+) accumulation and enhanced oxygen consumption (O2). In this scenario, therapeutic interventions that promote glucose utilization may improve cardiac efficiency and angina symptoms. This metabolic shift can be achieved by inhibiting fatty acid oxidation, stimulating glucose oxidation, or both. Anti-angina drugs exist that induce a cardiac metabolic shift from FFA oxidation toward glucose consumption, which, in turn, results in increased ATP generation per unit of O2 consumption. Trimetazidine, a partial inhibitor of fatty acid oxidation, is a ‘metabolic'’ anti-angina drug that can improve symptoms in patients with chronic stable angina. This agent can be safely added to conventional therapy i.e., β-blockers (BBs), calcium channel blockers (CCBs), and nitrates. The safety and clinical benefits of trimetazidine have been known since the early 1980s. Unfortunately, however, a relatively small group of European centres have access to this therapy
Appropriateness of use criteria in echocardiography: an Italian experience
No full textAIM: Appropriateness of use criteria (AUC) for transthoracic echocardiography (TTE) provide a simple and practical approach to avoid unneeded testing. METHODS: We collected and analyzed consecutive requests and corresponding reports for TTE in an Italian University Hospital. RESULTS: 500 echocardiographic request and related reports were collected. The mean age was 56 years old with 305 (61%) males. 19% of patients had TTE due to shortness of breath. Inappropriate indications account about 11% of the overall population. 30% of all studies were evaluated as normal 54% as major TTE findings and 16% showed minor TTE findings. CONCLUSION: Application of AUC would improve money expenditure. Understand if our country is going into the right direction is mandatory
Therapy against ischemic injury
No full textThe advent of reperfusion therapy constituted a historical change for the management of myocardial infarction (MI) patients. However, shortly after, experimental models recognized an intrinsic damage, related to reperfusion itself, which was termed as ischemiareperfusion injury (IRI). Clinical studies attribute IRI a significant burden of morbidity and mortality observed in patients undergoing successful epicardial reperfusion. Several mechanisms have been identified and, as many strategies, have been investigated to address the phenomenon. In this review we will discuss the current evidence for IRI, pharmacological and non-pharmacological preventive strategies adopted both in experimental models and in clinical practice. Finally, we will try to provide a critical appraisal to the lack of consistent benefit observed in translational medicine
Microvascular function/dysfunction downstream a coronary stenosis
No full textFor decades coronary macrovascular atherosclerosis has been considered the principal manifestation of coronary heart disease, with most of our effort dedicated to identifying and removal of coronary stenosis. However, growing body of literature indicates that coronary microcirculation also contributes substantially to the pathophysiology of cardiovascular disease. An understanding of mechanisms regulating microvascular function is of critical importance in understanding its role in disease, especially because these regulatory mechanisms vary substantially across species, vascular bed and due to comorbidities. Indeed, the most obvious consequence of coronary stenosis is that it may limit blood supply to the dependent myocardium to the point of causing ischaemia during exercise or even at rest. However, this flow limiting effect is not only due to the passive hydraulic effect of a narrowed conduit, but also to active responses in the coronary microcirculation triggered by the presence of an epicardial stenosis. To understand this problem it is important to review the inter-related mechanisms that regulate flow to the left ventricular wall and modulate transmural distribution of flow. These regulatory mechanisms operate hierarchically and are heterogeneously distributed along the coronary vascular tree. It is also important to discuss the effect of myocardial performance in modulating both blood flow demands and coronary resistance. Some of the interactions between coronary stenosis and microcirculation are transient, like those documented in acute coronary syndromes or during percutaneous interventions. However, microcirculatory remodeling may be triggered by a chronic coronary stenosis, leading to a sustained impairment of blood supply even after successful removal of the epicardial stenosis. A deeper understanding of these phenomena may explain paradoxical findings in patients undergoing coronary revascularization, particularly when functional tests are used in their assessment. These aspects are discussed in detail in this review
Pharmacological approaches to coronary microvascular dysfunction
No full textIn recent decades coronary microvascular dysfunction has been increasingly identified as a relevant contributor to several cardiovascular conditions. Indeed, coronary microvascular abnormalities have been recognized in patients suffering acute myocardial infarction, chronic stable angina and cardiomyopathies, and also in patients with hypertension, obesity and diabetes. In this review, we will examine pathophysiological information needed to understand pharmacological approaches to coronary microvascular dysfunction in these different clinical contexts. Well-established drugs and new pharmacological agents, including those for which only preclinical data are available, will be covered in detail. (C) 2014 Published by Elsevier Inc
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