Our technique for transradial coronary angiography and interventions.

The transradial approach for coronary angiography was introduced twenty years ago. Since then, considerable advancements have been made in this technique that proved to be effective in many interventional procedures and in several, even high-risk patient subsets (acute coronary syndromes, elderly, fully anticoagulated and obese patients). The main advantage of transradial approach over transfemoral approach is represented by the striking reduction in the rate of access-related vascular complications and bleedings. In recent years, bleeding prevention has become an issue of paramount importance, since recent large trials and registries clearly showed that bleedings are associated with major adverse events at follow up. Nevertheless, the prevalence of transradial approach for coronary procedures worldwide is still quite low and nowadays, in the United States, the favourite strategy for bleeding prevention is mostly based on the adoption of new antithrombotic drugs (such as bivalirudin and fondaparinux) rather than on the selection of an alternative, safer vascular access route. In this review we deal with several clinical and technical issues about transradial approach, including: 1) patient selection; 2) cath lab set-up, access technique and dedicated hardware; 3) reaching the coronary ostia: how to deal with anomalous anatomy; 4) selection and manipulation of catheters; 5) haemostasis and post-procedural issues.

Thrombus aspiration during primary angioplasty for cardiogenic shock.

We sought to assess the clinical efficacy of thrombus aspiration during primary percutaneous coronary interventions (PCI) in patients presenting with ST-elevation myocardial infarction (STEMI) complicated by cardiogenic shock (CS). We retrospectively selected 44 patients with CS out of a population of 842 STEMI patients treated with primary PCI at our Hospital between March 2003 and October 2007. Twenty-six patients died during hospital stay (59.1%, Group 1), whereas the remaining 18 were discharged (40.9%, Group 2). Post-procedural ST-segment resolution was greater (68.0%+/-35.6 vs. 43.0%+/-35.0; p=0.06) and in-hospital mortality was significantly lower (21.4% vs 76.6%; p<0.01) in patients treated by TA as compared to patients undergoing standard PCI. At multivariate logistic regression analysis, TA was the only variable independently associated with survival.

MicroRNAs and ischemic heart disease: towards a better comprehension of pathogenesis, new diagnostic tools and new therapeutic targets.

MicroRNAs are key, recently discovered, regulators of gene expression. They are involved in many physiological cellular pathways so it is not surprising that an altered microRNA expression pattern can be involved in the pathogenesis of many disease states. The possibility to manipulate microRNAs to obtain a therapeutical effect is very attractive since they represent specific targets in a particular cellular pathway and because it is quite easy to synthesize short oligonucleotides with the ability to interfere with microRNA mechanism of action. The main problem for microRNA-based therapy is represented by delivery. In the last two years many studies have underlined the involvement of microRNAs in many aspects of ischemic heart disease, the leading cause of morbidity and mortality in the Western World. MiR-29 is involved in fibrotic reaction after myocardial infarction while miR-21 may exert a fundamental role in post-angioplasty restenosis. MiR-208 is involved in the shift toward a fetal gene expression pattern in contractile proteins in heart failure. MiR-1 influences susceptibility to cardiac arrhythmias after myocardial infarction. This review will focus on microRNAs involvement in multiple aspects of ischemic heart disease and on their promising novel therapeutic applications including some recent patents.

Drug-eluting stents in a patient with favism: is the aspirin administration safe?

We describe the case of a 64-year-old patient with glucose-6-phosphate dehydrogenase deficiency who was referred to our hospital because of an acute inferior myocardial infarction.Given the possible risk of acute haemolytic anaemia, aspirin was not given in the acute phase, and the patient was successfully treated by balloon angioplasty of the right coronary artery.After functional and genetic testing showing the presence of the Mediterranean mutation, known to be a class II variant, the patient received oral daily aspirin (100 mg) under strict monitoring in order to promptly detect any sign of haemolysis. After 4 days, a complex percutaneous coronary intervention with an implantation of two drug-eluting stents was successfully performed on the left coronary artery. After 3 months, the patient is free from adverse events.Glucose-6-phosphate dehydrogenase deficiency is commonly considered a contraindication to aspirin intake; however, this case shows that aspirin at low, antiplatelet dosage is well tolerated and should not be denied to patients with ischaemic heart disease and complex coronary anatomy.

Management of multivessel coronary disease after ST elevation myocardial infarction treated by primary angioplasty.

BACKGROUND: Optimal treatment strategy of patients with ST elevation myocardial infarction (STEMI) and multivessel coronary artery disease (CAD) undergoing primary angioplasty is still unclear. Percutaneous coronary intervention (PCI) of non-culprit vessels simultaneously or soon after primary angioplasty is feasible and safe, but available data failed to consistently show a benefit in long-term clinical outcomes. METHODS: We retrospectively compared in-hospital and long-term outcomes for patients with STEMI and multivessel CAD treated by primary angioplasty with (Group 1, n=64) or without (Group 2, n=46) early, staged PCI of other angiographically significant coronary lesions. In-hospital major adverse cardiovascular events (MACE) were defined as a composite of death, periprocedural myocardial infarction after staged, elective PCI, stroke, stent thrombosis, major bleeding, and vascular complications. MACE at follow-up were defined as a composite of death, stroke, stent thrombosis, any coronary revascularization, and re-hospitalization for acute coronary syndrome. RESULTS: Group 1 patients underwent staged PCI 5.9 +/- 3.5 days after primary angioplasty. The mean length of follow-up was 13 months (392 +/- 236 days). The incidence of in-hospital MACE was 20.3% in Group 1 and 10.8% in Group 2 (P=0.186); the incidence of out of hospital MACE was 9.3% in Group 1 and 23.9% in Group 2 (P=0.037). In Group 1 in-hospital MACE were driven by periprocedural myocardial infarction after the elective procedure, which occurred in 15.6% of patients. CONCLUSIONS: Our data show that multivessel, staged PCI in STEMI patients is associated with a low incidence of adverse events at follow-up but with a higher incidence of in-hospital MACE, mainly driven by periprocedural myocardial infarction during the elective procedure.

Very late thrombosis of a drug-eluting stent deployed during primary angioplasty for ST-elevation myocardial infarction.

Drug-eluting stents, despite being very effective in reducing restenosis after percutaneous coronary interventions, are associated with a low but definite risk of late thrombotic occlusion with adverse clinical events. To date, the incidence and overall risk of late thrombosis of drug-eluting stents after primary percutaneous coronary interventions for ST-elevation myocardial infarction are not well defined because of the relative paucity of evidence-based data. We report the case of an angiographically confirmed paclitaxel-eluting stent thrombosis, occurring 20 months after successful primary percutaneous coronary intervention in a 41-year-old woman. To the best of our knowledge, this is the most delayed case of paclitaxel-eluting stent thrombosis described so far.

Inflammation as a possible link between coronary and carotid plaque instability.

BACKGROUND: Multiple complex stenoses, plaque fissures, and widespread coronary inflammation are common in acute coronary syndromes. A systemic cause of atherosclerotic plaque instability is also suggested by studies of ischemic cerebrovascular disease. We investigated the association between coronary and carotid plaque instability and the potential common causal role of inflammation. METHODS AND RESULTS: The ultrasound characteristics of carotid plaques were evaluated retrospectively in patients scheduled for coronary bypass surgery, 181 with unstable and 92 with stable angina, and prospectively in a similar group of patients, 67 with unstable and 25 with stable angina, in whom serum C-reactive protein levels were also measured. The prevalence of carotid plaques was similar in the retrospective and prospective studies and >64% in both unstable and stable coronary patients. The prevalence of complex, presumably unstable carotid plaques was 23.2% in unstable versus 3.2% in stable patients (P<0.001) in the retrospective study and 41.8% versus 8.0% (P=0.002) in the prospective study. C-reactive protein levels were higher in patients with complex (7.55 mg/L) than in those with simple (3.94 mg/L; P<0.05) plaques or without plaques (2.45 mg/L; P<0.05). On multivariate analysis, unstable angina and C-reactive protein levels >3 mg/L were independently associated with complex carotid plaques (OR, 6.09; 95% CI, 1.01 to 33.72; P=0.039, and OR, 5.80; 95% CI, 1.55 to 21.69; P=0.009, respectively). CONCLUSIONS: In unstable angina, plaque instability may not be confined to coronary arteries, and inflammation may be the common link with carotid plaque instability. These observations may have relevant implications for understanding the mechanisms of acute widespread atherothrombotic plaque inflammation.