1,721,146 research outputs found

    Overview of Management of Myocardial Ischemia: a Mechanistic-Based Approach

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    Pharmacologic treatment of myocardial ischemia in patients with chronic stable angina (CSA) is mainly based on heart rate lowering drugs and vasodilator agents. Other drugs are available, however, that act by some peculiar mechanism (ranolazine, trimetazidine) and may add potential anti-ischemic and anti-anginal effects to standard therapeutic mechanisms. While anti-ischemic agents are crucial for controlling angina symptoms and improving quality of life, whether myocardial ischemia portends an ominous prognosis and its suppression improves clinical outcome in CSA patients remain debated issues

    Effect of spinal cord stimulation in patients with refractory angina: evidence from observational studies

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    To review the evidence in observational studies of the effect of spinal cord stimulation (SCS) in patients with refractory angina pectoris (RAP) due to obstructive coronary artery disease. The effect of SCS in patients with refractory microvascular angina (MVA) also was assessed

    New light on a forgotten disease: vasospastic angina

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    Six decades ago Prinzmetal et al. (1) described a particular form of angina that occurred at rest, in the absence of any increase of myocardial oxygen demand, and was associated with ST-segment elevation on electrocardiography rather than with the usual ST-segment depression observed during effort angina. The investigators suggested that this variant form of angina was caused by a primary reduction of coronary blood flow consequent to an increased tonus of stenotic coronary arteries (1). Some years later, coronary angiographic studies showed that variant angina was indeed caused by coronary artery spasm (CAS) (2). Accordingly, it is now often referred as vasospastic angina (VSA). CAS is defined as a sudden, intense, reversible vasoconstriction of a coronary artery branch resulting in subtotal or total occlusion. It can occur in stenotic or angiographically normal coronary segments, can be focal or diffuse, and can involve 1 or multiple epicardial coronary arteries. VSA occurs frequently at night or in the early morning, but in some patients it prevails in the afternoon. Angina episodes may be sporadic or present in clusters and may spontaneously subside and then recur after a variable period of time. Triggers of CAS also differ among patients, with exercise, for example, inducing CAS in about 25% of patients with VSA. Importantly, CAS can cause life-threatening arrhythmias and sudden death, and prolonged CAS is a cause of acute myocardial infarction (3). Accordingly, a prompt diagnosis is mandatory to prevent these serious complications; yet, the diagnosis of VSA is often missed for months after symptom onset (4). Of note, progress in this area has been limited, for 2 main reasons. First, the prevalence of VSA is low (1% to 1.5% of admissions for angina in Caucasian populations) (4), thus making the enrollment of large numbers of patients difficult. Second, calcium-channel blockers (CCBs) prevent CAS in the majority of patients, thus limiting the need for new forms of treatment. Yet, 10% to 20% of patients with VSA are refractory or develop poorly tolerated side effects to CCBs. Thus, elucidating the mechanisms of CAS might be important, as it might lead to development of new forms of treatment. -------------------------------------------------------------------------------

    Primary percutaneous coronary intervention without on-site cardiac surgery backup in unselected patients with ST-segment-elevation myocardial infarction: the Rivoli ST-segment elevation myocardial infarction (RISTEMI) registry

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    Primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy for patients with ST-segment-elevation myocardial infarction (STEMI), but some concerns remain about its safety and efficacy in centers without on-site cardiac surgery (OCS)
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