ABSTRACT
: Mycotic coronary aneurysm is a rare infective disease of arterial vessel walls. Their development could be linked to the presence of an infective endocarditis or could represent a primary infection at the site of an implanted intracoronary stent. Bacterial agents, particularly Staphylococcus aureus, are the most common etiological agents. Due to an aspecific clinical presentation and examination, diagnosis could be challenging. Multiple imaging techniques (both invasive and noninvasive) are often required to reach the final diagnosis. Prognosis is characterized by high morbidity and mortality rates and, in fact, a tempestive treatment is required, although, to date, scanty data concerning the optimal treatment choice are present in literature.
Subject(s)
Aneurysm, Infected/microbiology , Coronary Aneurysm/microbiology , Prosthesis-Related Infections/microbiology , Aneurysm, Infected/diagnostic imaging , Aneurysm, Infected/mortality , Aneurysm, Infected/therapy , Anti-Bacterial Agents/therapeutic use , Cardiac Surgical Procedures , Coronary Aneurysm/diagnostic imaging , Coronary Aneurysm/mortality , Coronary Aneurysm/therapy , Endocarditis/microbiology , Humans , Percutaneous Coronary Intervention/adverse effects , Percutaneous Coronary Intervention/instrumentation , Predictive Value of Tests , Prosthesis-Related Infections/diagnostic imaging , Prosthesis-Related Infections/mortality , Prosthesis-Related Infections/therapy , Risk Factors , Stents/adverse effects , Treatment OutcomeABSTRACT
BACKGROUND: The recovery of left ventricular function (LVF) after revascularization takes time. alpha-Adrenergic blockade acutely improves coronary blood flow and LVF, whereas the effects of more prolonged alpha-adrenergic blockade on LVF recovery after stenting are unknown. METHODS: In 32 patients (age 58 +/- 12 y) with an 82% +/- 6% stenosis, ejection fraction (EF) and systolic thickening (%Th) were measured by transthoracic echocardiography before and 30 minutes to 2 hours after revascularization. In a double-blinded protocol, either 200 microg/kg urapidil or placebo was given intravenously, and LVF was measured 10 minutes later. Two hours later, oral treatment with 30 mg/d drug or placebo was started, and LVF measured again after 24 hours and 3 months. RESULTS: Before revascularization, EF was 49.4% +/- 8.5% (+/-SD) and 51.3% +/- 8.8% in the urapidil-treated and the placebo groups, respectively. Thirty minutes to 2 hours after coronary stenting, EF was unchanged. After intravenous drug administration, EF increased to 56.5% +/- 9.7%). At 24 hours and 3 months after revascularization, EF became 59.5% +/- 7.9% and 59.6% +/- 8.2% in the urapidil-treated group, respectively, whereas EF in the placebo group did not change (50.4% +/- 5.7% and 49.7% +/- 4.9%, respectively). Revascularization did not acutely improve %Th. Intravenous urapidil improved %Th from 31.4% +/- 17.6% to 44.2% +/- 11.6%, whereas there was no change in the placebo group. At 3 months, %Th was 49.5% +/- 12.9% in the urapidil-treated group and 39.7% +/- 8.9% in the placebo group. CONCLUSIONS: These data suggest that long-term alpha-adrenergic blockade might improve LVF at midterm after coronary revascularization.
Subject(s)
Adrenergic alpha-Antagonists/therapeutic use , Angina Pectoris/therapy , Piperazines/therapeutic use , Stents , Stroke Volume/drug effects , Adrenergic alpha-Antagonists/pharmacology , Adult , Aged , Angina Pectoris/drug therapy , Angina Pectoris/physiopathology , Angioplasty, Balloon, Coronary , Double-Blind Method , Female , Humans , Male , Middle Aged , Myocardial Contraction/drug effects , Piperazines/pharmacology , Ventricular Dysfunction, Left/drug therapyABSTRACT
BACKGROUND: Coronary flow reserve (CFR) is not normalized shortly after coronary stenting. We hypothesized that alpha-adrenergic coronary vasoconstriction acts to limit CFR. METHODS AND RESULTS: We assessed flow velocity by Doppler wires and cross-sectional area by angiography in 46 patients undergoing coronary culprit lesion stenting (81+/-4% stenosis). Hyperemia was induced by adenosine (24 micro g IC or 140 micro g/kg per minute IV) before and after stenting. Finally, either the alpha(1)-antagonist urapidil (10 mg IC) or the alpha(2)-antagonist yohimbine (3 mg IC) was randomly combined with adenosine. In 8 subjects with angiographically normal coronary arteries, CFR was increased from 3.21+/-0.30 to 3.74+/-0.43 by yohimbine and to 4.58+/-0.65 by urapidil, respectively (P=0.0001). Patients were divided according to the cutoff of CFR > or =3.0 (n=18) or <2.5 (n=28). Revascularization per se did not change CFR. However, 15 minutes after stenting, CFR decreased to 2.05+/-0.55 from CFR 3.64+/-0.58, whereas in patients with CFR 2.39+/-0.51, it remained unchanged. Yohimbine improved CFR to 3.26+/-0.42 and to 3.41+/-0.58 in patients with >3.0 and <2.05+/-0.55 baseline CFR, respectively. Urapidil improved CFR to 3.52+/-0.30 and 3.98+/-1.07, respectively. CONCLUSIONS: Urapidil and yohimbine attenuated the CFR impairment occurring after revascularization by increasing both the epicardial vasodilator effect of adenosine and the blood flow velocity, thus suggesting that the adrenergic system plays an important role in limiting the capacity of the coronary circulation to dilate.
