Direct stenting in angiographically apparent thrombus-containing lesions.

The data regarding the potential benefits of direct stenting in the setting of angiographically apparent thrombus-containing lesions are scarce. The aim of this study was to evaluate the impact of direct stenting on the angiographic results in the setting of thrombus. We reviewed our institutional interventional database and identified 30 patients who had undergone stenting in the setting of angiographically apparent thrombus-containing lesions (33% unstable angina pectoris, 67% acute myocardial infarction). The majority of patients had a baseline TIMI 2 and 3 flow (80%). Of the 6 patients (20%) who had TIMI 0-1 flow at baseline, four of them achieved a TIMI 2 flow immediately after crossing the lesion with a 0.014 guidewire. Although the remaining 2 patients had TIMI 1 flow, as distal opacification beyond the stenosis was obtained we successfully implanted the stents directly. All stents were successfully implanted without any crossing failure or stent loss. There was no "no re-flow", with a final TIMI 3 flow rate in 93%. In 1 patient with TIMI 2 flow after stenting, TIMI 3 flow was obtained after intracoronary verapamil. In 2 patients (7%, TIMI 2 flow), a final TIMI 3 flow could not be achieved despite intracoronary nitroglycerin and verapamil. There was no stent loss and imprecise stent placement. There were no in-hospital deaths, repeat interventions or coronary artery bypass graft surgeries. However, two patients had undergone mitral valve replacement due to severe mitral regurgitation. Eight patients with recurrent ischemia had control angiography; stents were found to be patent in all 8 patients. Two patients experienced recurrent myocardial infarction (6.6%). Direct stenting strategy in thrombus-containing lesions seems to be a safe and feasible approach in avoiding no re-flow. We believe that benefits observed with direct stenting in this study should be compared to conventional stenting in the same setting with a randomized study.

Stenting of the septal perforator coronary artery.

This report describes the first application of intracoronary stenting to the septal perforator coronary artery in a patient with a totally occluded left anterior descending coronary artery (LAD) and a patent venous graft to the distal LAD. The procedure was successful and resulted in almost complete relief of class III angina. Therefore, diseased large septal perforators may cause angina and be treated effectively by intracoronary stenting in selected cases.

Primary angioplasty and stenting in a patient with primary antiphospholipid syndrome and thrombocytopenia.

Antiphospholipid syndrome is characterized by venous and arterial thrombosis, thrombocytopenia, stroke and, rarely, acute coronary syndromes. However, there are no data available regarding the management of acute myocardial infarction in primary antiphospholipid syndrome with accompanying severe thrombocytopenia and cardiogenic shock. We describe such a case, which was managed by successful primary percutaneous transluminal coronary angioplasty and stent implantation with accompanying immunosuppression therapy.

Left atrial free floating thrombus. Diagnosis by two dimensional and M-mode echocardiography.

Left atrial thrombus, which is a frequent finding in patients with mitral valve disease, is generally attached to the atrial wall. Left atrial free-floating thrombus has rarely been reported. Since the risk of peripheral emboli is fairly high, patients with such a thrombus are candidates for emergency surgery. Our first case was a 45-year-old female with mitral stenosis and regurgitation. The typically appearing free floating thrombus with a diameter of 3.4 cm was detected by two-dimensional and M-mode echocardiography, and an appropriate surgical procedure was performed. The surgical findings were consistent with the echocardiographic findings. Our second case was a 59-year-old female. A free floating thrombus with a diameter of 2 cm was detected by echocardiography when this patient with mitral stenosis was hospitalized because of right hemiplegia and aphasia. The thrombus was extracted by an immediate surgical procedure. Transthoracic echocardiographic (TTE) study was definitely specific in both cases; no other study was thus required.

A case of pericardial lipoma diagnosed by noninvasive techniques.

Intracardiac lipomas that consist of mature fat cells with fibrous and myxoid tissues are regarded as rather rare lesions. The diagnosis may frequently be established during surgical intervention or at autopsy. The patient presented is a 23-year-old male who had had no complaints. The lesion had been incidentally detected on x ray examination which had revealed an enlarged heart shadow. His physical examination revealed no abnormality except displacement of the heart to the right and sinus tachycardia. A solid mass derived from the pericardium was observed on CT scans and echocardiography. On CT scans the mass exhibited a density consistent with a lipoma. The patient was operated on and the mass, which was encapsulated and 19 x 17 x 10 cm in size, was removed. Histopathological examination revealed a lipoma.

Synergism between UK 38485 and ICI 185282 against digoxin-induced arrhythmias in guinea-pigs.

In this study, the combination of a thromboxane synthetase inhibitor (UK 38485) and a thromboxane receptor antagonist (ICI 185282) was tested for an interaction of potential therapeutic importance and the effect of acetylsalicylic acid pretreatment on this combination was evaluated in digoxin-induced arrhythmias in guinea-pigs. Drug treatments at the dose combinations used (ICI 185282: 0.2 mg/kg + 0.2 mg/kg/hr + UK 38485 0.1 mg/kg/hr and ICI 185282: 2 mg/kg + 2 mg/kg/hr + UK 38485 1 mg/kg/hr) markedly reduced the incidence of ventricular fibrillation, mortality rate and arrhythmia score. Pretreatment with acetylsalicylic acid plus drug combination resulted in a dose-dependent increase in mortality rate and arrhythmia score. The increase in mean arterial blood pressure, observed after digoxin administration, was inhibited by the combination therapy. Although heart rate values were increased, the computed pressure-rate index remained unchanged when compared with the control group. These data suggest that the combined treatment with a thromboxane synthetase inhibitor and a thromboxane receptor antagonist provides a better protection against digoxin intoxication than with either agent alone. Furthermore, the results illustrate that formation of cyclooxygenase metabolites of arachidonic acid plays an important role in this action.

Subacute rupture of the free left ventricular wall following acute myocardial infarction. Successful surgery in a case.

Free left ventricular wall rupture following acute myocardial infarction usually results in cardiac tamponade and sudden death. Occasionally, the bleeding into the pericardial sac is arrested by the surrounding pericardial tissue causing formation of a pseudoaneurysm. The case herein reported presented with a refractory pericardial effusion 1 month after an anterior myocardial infarction. While echocardiography failed to reveal a pseudoaneurysm or to localize a rupture, cineventriculography disclosed the diagnosis of a minimal rupture of the left ventricular free wall. The patient was successfully treated by surgery.

Effects of thromboxane synthetase inhibitor (UK 38,485) and thromboxane receptor antagonist (ICI 185,282) on digoxin-induced arrhythmias in anaesthetized guinea-pigs.

1. Increased local thromboxane (Tx) formation has been considered to be a contributing factor in digitalis-induced arrhythmias. 2. A potent Tx synthetase inhibitor (TxSI), UK 38,485 (0.1, 1.0 or 10.0 mg/kg per h, administered intravenously) and a Tx receptor antagonist (TxRA), ICI 185,282 (1, 2 or 10 mg/kg bolus and 1, 2 or 10 mg/kg per h, administered intravenously) were tested for their ability to reduce digoxin-induced arrhythmias in anaesthetized guinea-pigs. 3. Electrocardiograms, mean blood pressure, heart rate and arrhythmias were recorded, starting 30 min before digoxin administration and continued for 60 min afterwards. 4. ICI 185,282, at the doses used, significantly delayed the time of onset of arrhythmias, and reduced the incidence of ventricular fibrillation, mortality and arrhythmia score. In contrast, UK 38,485 was found to be effective on all measured variables only at the dose rate of 1.0 mg/kg per h, except for time required for the development of arrhythmias. These protective effects of both TxSI and TxRA were not found to be dose-dependent. 5. Arterial blood pressure and heart rate changes caused by either UK 38,485 or ICI 185,282 infusions did not have any marked effects on digoxin-induced arrhythmias. 6. These data suggest that endogenously released TxA2 and prostaglandin endoperoxides may play an important role in digoxin-induced arrhythmias in guinea-pigs.

Digoxin-induced cardiac toxicity in the anaesthetized guinea-pigs and effect of heparin infusion.

We have examined the effects of heparin infusion on the arrhythmias induced by digoxin. Digoxin treatment consisted of 0.6 mg kg-1 given i.v. 15 min after the beginning of heparin infusion. Heparin infusions (1.7 IU, 3.4 IU and 6.8 IU kg-1 min-1) were begun 15 min before digoxin injection and continued for another 30 min. ECG, blood pressure, heart rate and arrhythmias were recorded starting 15 min before and continuing for 60 min after the digoxin injection. Heparin at the infusion rates of 3.4 IU and 6.8 IU kg-1.min-1 reduced significantly the arrhythmia scores. On the other hand, heparin did not significantly alter the arterial blood pressure and heart rate values affected by digoxin.

Prevention by a carbacyclin analogue (ZK 36 374) of digoxin-induced ventricular extrasystoles in guinea-pig myocardium.

Intravenous infusion of ZK 36 374 to the anesthetized guinea-pig or addition of the compound to the perfusion medium of the isolated perfused guinea-pig heart prevented digoxin-induced ventricular premature beats without altering the prolongation of the P-R interval by the glycoside. The prevention by ZK 36 374 of the ventricular extrasystoles induced by digoxin was obtained at lower concentrations while higher doses of the compound produced a dysrhythmic effect which terminated within a few min after the cessation of drug application.