Endovascular treatment of primitive persistent trigeminal artery aneurysm associated with middle cerebral artery aneurysm.

We report the case of a primitive trigeminal artery aneurysm associated with an ipsilateral middle cerebral artery aneurysm. A 64-year-old Caucasian woman suffered from a severe acute headache. A head CT scan displayed subarachnoid hemorrhage and subsequent cerebral angiography showed right, wide-necked persistent trigeminal artery and ipsilateral middle cerebral artery aneurysms. The patient underwent embolization of both aneurysms with Guglielmi detachable coils. The association of a PPTA aneurysm and an ipsilateral MCA aneurysm has not been reported in the English literature.

Non-invasive assessment of reperfusion of the infarct-related artery during coronary thrombolysis and its relation with left ventricular function.

We monitored ST segment continuously for at least 3 h after the beginning of lytic treatment in 103 patients undergoing early coronary thrombolysis for acute myocardial infarction in order to ascertain whether this technique, which has been shown to be useful to assess recanalization of the infarct-related artery, is also able to identify the improvement in left ventricular function associated with successful reperfusion. Global left ventricular function (assessed in the 30 degrees right anterior oblique projection with the area/length method) and infarct zone wall motion (studied with the centerline method) were evaluated at least 4 weeks after the event. Reperfusion was thought to be achieved when ST segment elevation dropped > 50% relative to the most abnormal peak documented at any time in the study. Eighty patients (78%) met the criterium for successful reperfusion (group 1), and 23 (22%) did not (group 2). Both groups had similar clinical and angiographic characteristics. All indexes of global left ventricular function were significantly better in group 1 than in group 2 patients (end-diastolic volume: 176 +/- 51 vs. 209 +/- 76 ml, end-systolic volume: 66 +/- 40 vs. 97 +/- 55 ml, ejection fraction: 65 +/- 13 vs. 57 +/- 11%, respectively, all P < 0.02). Also the severity (-1.6 +/- 1.3 vs. -2.6 +/- 1.01 S.D./chord, respectively, P < 0.001) and the extension of hypokinesia in the infarct zone (number of chords with > 2 S.D.: 13 +/- 16 vs. 28 +/- 17, respectively, P < 0.0001) were less in group 1 than in group 2 patients. Furthermore, in reperfused patients, both global left ventricular function and regional wall motion were better in those admitted < 60 min from onset of pain. In conclusion, patients with rapid ( > 50%) decrease of ST segment elevation have smaller infarct size and better global left ventricular function than patients without electrocardiographic signs of reperfusion as assessed by continuous ST segment monitoring. This suggests that this non-invasive technique is a powerful tool able to identify patients most benefiting from thrombolytic therapy.

Prodromal angina limits infarct size. A role for ischemic preconditioning.

BACKGROUND: In the experimental setting, it has been demonstrated that preconditioning myocardium before prolonged occlusion with brief ischemic episodes affords substantial protection to the cells by delaying lethal injury, thereby limiting infarct size. Whether the same occurs in humans remains unknown. METHODS AND RESULTS: This study was undertaken to determine whether new-onset prodromal angina, defined as chest pain episodes limited to the 24 hours before myocardial infarction, is the clinical correlate of the ischemic preconditioning phenomenon. Twenty-five patients with their first anterior myocardial infarction treated with thrombolysis (recombinant tissue plasminogen activator [r-TPA], 100 mg/3 hours) were retrospectively included in the study because they met the following criteria: (1) < 120 minutes from onset of symptoms to reperfusion therapy, (2) < 90 minutes from the beginning of thrombolytic therapy to reperfusion (defined as rapid ST elevation reduction > 50%), (3) a patient infarct-related coronary artery with TIMI 3 flow and complete absence of collateral circulation to the infarct related artery (assessed at 24 +/- 5 days), and (4) the presence of new-onset prodromal angina, ie, typical chest pain episodes occurring at rest within 24 hours or, alternatively, a complete absence of symptoms before onset of infarction. Therefore, on the basis of their clinical status before infarction, the patients were divided into two groups: group 1, 13 patients without prodromal angina, and group 2, 12 patients with prodromal angina. Despite no difference in time to treatment (81 +/- 19 versus 75 +/- 21 minutes in group 1 and group 2, respectively; P = NS) and time to reperfusion (58 +/- 34 versus 46 +/- 24 minutes; P = NS), the peak of CKMB release was markedly lower in group 2 (86.3 +/- 66 versus 192.3 +/- 108.3 IU/L; P < .01). In addition, although both groups were comparable in terms of area at risk (amount of myocardium beyond the infarct-related stenosis; 15.1 +/- 4.6 versus 13.7 +/- 4.6 hypokinetic segments in group 1 and group 2, respectively, P = NS), the final infarct size (11 +/- 7.5 versus 5.6 +/- 4 hypokinetic segments, P < .04) was smaller in group 2. Thus, the limitation of the infarct size was significantly greater in group 2 (69% versus 36%; P < .05), and this represents an additional 33% reduction (95% confidence intervals, 7.1% to 58.9%; P = .01) in the group of patients with prodromal angina. Also, the third index, that is, the ECG, showed a favorable trend toward a lesser number of Q waves and a higher sigma R waves, although the values did not reach statistical significance. CONCLUSIONS: Despite a similar area at risk, patients with new-onset prodromal angina showed a significantly smaller infarct size compared with patients without prodromal symptoms. Since the two groups had similar times to reperfusion and no evidence of collateral circulation to the infarct related artery, the protection afforded by angina in group 2 patients might be explained by the occurrence of ischemic preconditioning.