Aspirin challenge/desensitisation before coronary stenting in subjects with history of hypersensitivity. A pragmatic approach.

BACKGROUND: Aspirin hypersensitivity may represent a major problem in patients with ischemic coronary disease who need a stenting procedure. In those patients, clinically unsettled reasonably quick desensitisation procedures are needed. In our study we attempted to select the most suitable procedure on the basis of characteristics and severity of ASA hypersensitivity. METHODS: Thirty patients with a history of mild reactions to anti-inflammatory doses of aspirin (> 325 mg) were considered at low risk and underwent a tolerance test in 5 steps. Thirty-one patients, with a history of severe reactions to anti-platelet doses of aspirin 0 mg) underwent a slow desensitisation in 12 steps, reaching a cumulative dose of 150 mg ASA in 220 minutes. RESULTS: In the first group, 29 patients tolerated the challenge. One developed urticaria, thus underwent challenge/desensitisation and achieved tolerance. In the second group, 3 patients did not tolerate the procedure and had to discontinue. CONCLUSION. Our approach to aspirin hypersensitivity in patients needing coronary stenting, based on a severity stratification, allowed to achieve an effective tolerance to aspirin in the majority of subject in a reasonable short time.

An angiographic evaluation of restenosis rate at a six-month follow-up of patients with ST-elevation myocardial infarction submitted to primary percutaneous coronary intervention.

BACKGROUND: Percutaneous coronary intervention (PCI) is considered to be the optimal type of revascularization in patients with ST-segment elevation myocardial infarction (STEMI). However, the long-term effectiveness of this procedure can be reduced by restenosis. This investigation was aimed at a prospective evaluation, in a group of STEMI patients of "the real world" (not involved in randomised trials), of the angiographic restenosis rate at a 6-month follow-up, and at identifying the relationship between restenosis and the patients' characteristics. MATERIALS AND METHODS: Our study population consisted of 123 patients with STEMI submitted to primary PCI to then undergo stress echocardiography 3 months after PCI and an angiographic evaluation at a 6-month follow-up. RESULTS: a) In real life the restenosis rate is quite high (42.3%); b) no correlation was found between patients' clinical characteristics and restenosis; c) restenosis rate was higher in patients with bare metal stents than in those with drug-eluting stents (55.8% vs. 11.1%; p<0.001); in patients with longer stents (21.6+/-8.62 vs 18.1+/-6.34 mm, p=0.015) and when more than one stent was implanted. Moreover, a consistent number of patients showed restenosis though asymptomatic. CONCLUSIONS: Our data suggest that primary PCI is associated with a high incidence of angiographic restenosis. No correlation was found between patients' clinical characteristics and restenosis. The length and the number of implanted stents seem to be associated with a more probable restenosis at six-month angiographic evaluation. Drug-eluting stent implantation seems to be associated with a lower incidence of restenosis even in STEMI patients.

Use of Impella Recover 2.5 left ventricular assist device in patients with cardiogenic shock or undergoing high-risk percutaneous coronary intervention procedures: experience of a high-volume center.

AIM: Percutaneous coronary interventions are increasingly applied to high-risk patients. The availability of hemodynamic support devices offers a promising option to prevent and treat low-output syndrome in these patients. The aim of this study was to evaluate the feasibility, safety and efficacy of the Impella Recover'' LP 2.5 left ventricular assist device in patients with cardiogenic shock or undergoing high-risk percutaneous coronary interventions. METHODS: Eleven patients presenting cardiogenic shock (N=6) or scheduled for high-risk percutaneous revascularization (N=5) were evaluated. The Impella pump was successfully implanted in all patients, except one. When implanted, the device was correctly positioned in the left ventricle and remained in a stable position. RESULTS: Bleedings occurred in 7 patients (5 of them presented cardiogenic shock), while renal failure and severe thrombocytopenia were observed in 4 and 1 patients respectively, all with cardiogenic shock. During high-risk procedures, the Impella pump succeeded in obtaining hemodynamic stability, while in only two patients with cardiogenic shock the device determined a significant improvement of hemodynamic variables. All elective patients and two patients with cardiogenic shock were discharged from the hospital and were still alive at 30-day follow-up. CONCLUSION: These data, although preliminary due to the limited sample size, demonstrated the feasibility, safety and efficacy of the Impella Recover LP 2.5 during high-risk percutaneous procedures, even though the benefits of prophylactic deployment of such a system have to be further investigated. The use of Impella Recover LP 2.5 in patients with cardiogenic shock is feasible and safe, however it maybe insufficient in reversing an advanced cardiogenic shock which, probably, has to be treated with more powerful left ventricular assist devices.

Venture wire control catheter in percutaneous treatment of complex coronary bifurcation. A case report.

We present a case report of a man with atherosclerotic involvement of a left main trifurcation treated by the Venture wire control catheter. The patient was submitted to primary percutaneous transluminal coronary angioplasty (PTCA) in a primary center for acute occlusion of the left anterior descending artery, then he was transferred to our tertiary center to perform left main trifurcation revascularization that was unsuccessful by traditional approach. In our high volume center (operator >600 PTCA/year) as well, the attempts at crossing the lesion with a number of different guidewires failed because of the extreme angulation of the circumflex artery. At last, a successful attempt was reached using the Venture wire control, a low profile catheter with a tip that can be deflected up to 90 degrees . Once the lesion was crossed and wiring of other branches obtained, crush stenting of the left anterior descending artery and intermediate ramus and T-stent of the circumflex artery were performed with an optimal angiographic result.

Transferring patients for direct coronary angioplasty: a retrospective analysis of 135 unselected patients with acute myocardial infarction.

BACKGROUND: Direct coronary angioplasty (PTCA) represents the most effective treatment for acute myocardial infarction. However, only a minority of patients are initially admitted to hospitals with direct PTCA facilities available 24 hours daily. The safety and benefits of transfer direct PTCA are debated, and we have no data about the early return of patients to the admission hospital. METHODS: We report our experience with transfer direct PTCA in unselected patients with acute myocardial infarction, and the early post-procedural return to the referring hospitals. RESULTS: One hundred and thirty-five unselected patients with acute myocardial infarction were referred to our center for direct PTCA during 1998. The majority of patients (n = 93, 69%, group T) were initially admitted to a primary hospital whereas the rest (n = 42, 31%, group NT) were directly admitted to our hospital. One hundred and thirty-four patients underwent coronary angiography, and direct PTCA was attempted in 126 patients. The median time interval between admission and direct PTCA was higher in group T (60 vs 40 min, p < 0.001). Only 3 patients (3.2%) had severe complications during transfer to our center: 1 patient with cardiogenic shock died, and 2 patients had ventricular fibrillation. The procedural and in-hospital outcomes of both groups were similar. The early post-procedural transfer to the referring hospital was possible in 88% of patients; no complications occurred during the transfer. The incidences of cardiac mortality at 6 months and at long-term follow-up were 3.4 and 5.1% respectively. CONCLUSIONS: In our experience, interhospital transfer for direct PTCA in unselected patients with acute myocardial infarction is feasible and safe. The early return to the admission hospital is safe and does not negatively influence the in-hospital outcome.

Evidence for the existence of a functional cardiac renin-angiotensin system in humans.

BACKGROUND: The presence of mRNA for the essential components of the renin-angiotensin system (RAS) has been found in animal and human hearts. The present study was designed to provide evidence for the existence of a (functional) cardiac RAS. METHODS AND RESULTS: Twenty-four patients with atypical chest pain undergoing coronary angiography for diagnostic purposes were investigated. The cardiac production rate of angiotensins was estimated by measurement of the cardiac extraction of 125I-angiotensin I and 125I-angiotensin II associated with the determination of endogenous angiotensins in aortic and coronary sinus blood in normal, low, or high sodium diets. In a normal sodium diet, angiotensin I and II aorta-coronary sinus gradients were tendentially negative (-1.8 +/- 2.5 and -0.9 +/- 1.7 pg/mL, respectively), and the amounts of angiotensin I and II added by cardiac tissues were 6.5 +/- 3.1 and 2.7 +/- 1.3 pg/mL, respectively. The low sodium diet caused a significant increase in both plasma renin activity (PRA) and angiotensin I concentration in aortic but not in coronary sinus blood, resulting in a more negative aorta-coronary sinus gradient (-9.7 +/- 3.1 pg/mL, P < .01). Angiotensin formation by PRA in blood during transcardiac passage increased (P < .001), whereas angiotensin I formed by cardiac tissues decreased dramatically. Accordingly, in the low sodium diet, 125I-angiotensin II extraction did not change, the cardiac fractional conversion rate of 125I-angiotensin I to 125I-angiotensin II notably decreased (P < .01), and angiotensin II formation by cardiac tissues was undetectable. The high sodium diet caused a decrease in PRA and no changes in cardiac extraction of radiolabeled angiotensins; conversely, angiotensin I formed by cardiac tissues, cardiac Ang I fractional conversion rate, and angiotensin II formed during transcardiac passage significantly (P < .01 for all) increased. CONCLUSIONS: These results provide evidence for the existence of a functional cardiac RAS independent of but related to the circulating RAS.

[The cardiac tissue renin-angiotensin system]. / II sistema renina-angiotensina tessutale cardiaco.

In the last years molecular biological studies proved the presence of mRNA for the various components of the renin-angiotensin system (RAS) in animal and, more recently, in human myocytes. Moreover, higher mRNA levels for the various components of cardiac RAS were demonstrated in different experimental conditions such as myocardial hypertrophy, infarction and heart failure. These experimental evidences suggest the existence of a cardiac RAS, even if up to now direct evidence is lacking of a cardiac functioning RAS autonomous from the plasmatic system.

[The tissue renin-angiotensin systems]. / I sistemi renina-angiotensina tessutali.

Over the past 10 years, our understanding of the renin-angiotensin system has changed greatly, reflecting significant advances in this field. Studies in cell biology, the application of molecular biological techniques, and studies of angiotensin kinetics have provided evidence for the existence in various sites (cardiac, cerebral, renal, vascular and gonadal) of tissue-based renin-angiotensin system that function independently of the plasma renin-angiotensin system. These local systems contribute to the functional activity of their plasma counterpart through the local production of angiotensins I and II; at the same time, they are autonomous autocrine-paracrine systems with their own regulatory mechanisms. This multicentric organization of the renin-angiotensin system has physiologic and pathophysiologic implications. However, it also has important therapeutic consequences, since it follows that inhibition of the plasma renin-angiotensin system alone is probably not sufficient for therapeutic purposes.