Background-Inflammation and matrix degradation may play a pathogenic role in chronic heart failure (CHF), and therefore, we examined whether thalidomide, a drug with potential immunomodulating and matrix-stabilizing properties, could improve left ventricular (LV) function in patients with CHF secondary to idiopathic dilated cardiomyopathy (IDCM) or coronary artery disease (CAD). Methods and Results-Fifty-six patients with CHF and an LV ejection fraction (LVEF) Ͻ40% who were already on optimal conventional cardiovascular treatment were randomized to thalidomide (25 mg QD increasing to 200 mg QD) or placebo and followed up for 12 weeks. Our main findings were as follows: (1) During thalidomide treatment but not during placebo, there was a marked increase in LVEF (Ϸ7 EF units) along with a significant decrease in LV end-diastolic volume and heart rate. (2) This improvement in LVEF was accompanied by a decrease in matrix metalloproteinase-2 without any changes in its endogenous tissue inhibitor, suggesting a matrix-stabilizing net effect.(3) Thalidomide also induced a decrease in total neutrophil count and an increase in plasma levels of tumor necrosis factor-␣, suggesting both proinflammatory and antiinflammatory effects. (4) The effect of thalidomide on LVEF was more marked in IDCM than in CAD, possibly partly reflecting that the former group was able to tolerate a higher thalidomide dosage. Conclusions-Although our results must be confirmed in larger studies that also examine the effects on morbidity and mortality, our findings suggest a role for thalidomide in the management of CHF in addition to traditional cardiovascular medications. (Circulation. 2005;112:3408-3414.)

The occurrence of visual disturbances following cardiac catheterization with angiographies was studied in a prospective study of 2,006 consecutive adult patients. The overall incidence of visual disturbances was 1.0% and of complete blindness 0.2%. Women had higher incidence than men (2.0 versus 0.6%, p less than 0.01) and patients with a history of angina pectoris with normal coronary arteries had higher incidence than those with coronary artery stenosis (3.7 versus 0.8%, p less than 0.02). Thirteen of twenty patients also had signs of mental confusion. An abnormal electroencephalogram was found in 8 of 13 patients studied. Other neurological findings were observed in one patient only. All patients had complete recovery within 24 hours. Thus, the incidence of visual disturbances is found to be higher than earlier reported, but the visual loss is transient with a benign course.

During electrophysiological investigation of 22 patients with VT or aborted sudden cardiac death, arterial and RV pressures were measured. The time courses of mean arterial pressure (MAP), RV pulse pressure (RVPP), RV pulse pressure integral (RVPPI), and maximum right ventricular dP/dt (RV dP/dtmax) were followed during the first 15 seconds after VT induction. Compared to basal (preinduction) conditions, the RVPPI decreased by 41+/-10% (mean +/- SD) after 10-15 seconds of VT in 11 patients with stable VT and by 75+/-8% in 11 patients with unstable VT (MAP < 60 mmHg 15 s after VT onset). RVPP decreased by 13+/-11% after 10-15 seconds of VT in the stable VT group and by 50+/-16% in the unstable VT group. For RV dP/dtmax, these decreases were 4+/-22% in the stable VT group and 37+/-24% in the unstable VT group. There was a good correlation between percent decrease in MAP and percent decrease in RVPPI, RVPP, and RV dP/dtmax at 5-10 seconds (r = 0.86, 0.81, and 0.73, respectively) and 10-15 seconds (r = 0.84, 0.82, and 0.69, respectively) after VT onset. There was hardly any overlap of distributions of the individual values with the RVPPI parameter between the two VT groups. Comparing and correlating the percent decrease in mean arterial pressure with the RVPPI, RVPP, and RV dP/dtmax during induced VT, RVPPI demonstrated the most significant and specific changes in discriminating stable from unstable rhythms. However, by comparing RVPPI and RVPP using the area under the receiver operating characteristic curves, there was no significant statistical difference between the two parameters. By integrating rate criteria, electrogram signal analysis, and RVPPI or RVPP as a hemodynamic criterion, detection and treatment algorithms could improve the performance of future implantable defibrillators and avoiding shocks in VTs that can be terminated by antitachycardia pacing.

The clinical and patholgoical findings in two neonates with the malformation of the great vein of Galen are given. They both reported with serious neonatal heart failure suggesting congenital heart disease. In one of them cardiac catheterization revealed a foetal pattern of circulation causing cyanosis. A bruit and in one of them a thrill over the skull gave the clinical diagnosis of an intracranial arteriovenous aneurysm. They died 48 and 144 hours after birth in spite of medical treatment. The outlook for patients having malformation of the great vein of Galen and suffering neonatal heart failure treated conservatively, seems hopeless.